stevia, Rebaudioside A, needs more safety testing before FDA approval, MF
Jacobson, CSPI, S Kobylewski & CD Eckhert, UCLA, 26-page review 2008.08.04:
Murray 2008.09.21
http://rmforall.blogspot.com/2008_09_01_archive.htm
Sunday, September 21, 2008
http://groups.yahoo.com/group/aspartameNM/message/1559

[ See also:
FDA approval of stevia (Rebaudioside A) expected by Nov 13, from
PureCircle for $ billion world market: Coca-Cola (Truvia),
PepsiCo (PureVia), Cargill, Merisant, NutraSweet,
J.W. Childs Associates: Murray 2008.09.19
http://rmforall.blogspot.com/2008_09_01_archive.htm
Friday, September 19, 2008
http://groups.yahoo.com/group/aspartameNM/message/1557

"The sweetener is already approved in several countries such as China,
Japan, the former Soviet Union and South America and only in the last few
weeks received approval in Australia and Switzerland."

http://www.guardian.co.uk/business/feedarticle/7805653 ]


http://cspinet.org/new/200808281.html

Lab Tests Point to Problems with Trendy New Stevia Sweetener

CSPI Urges More Testing Before Stevia Extract is Used in Food, Drinks

WASHINGTON -- Coca-Cola and Pepsi are planning to introduce new drinks made with
rebiana, an extract of stevia leaves that is 200 times sweeter than sugar. But
according to a new 26-page report by toxicologists at the University of
California, Los Angeles, several, though not all, laboratory tests show that the
sweetener causes mutations and DNA damage, which raises the prospect that it
causes cancer. In a letter to the Food and Drug Administration, the Center for
Science in the Public Interest says the agency should require additional tests,
including a key animal study, before accepting rebiana as Generally Regarded as
Safe, or GRAS.

"A safe, natural, high-potency sweetener would be a welcome addition to the food
supply," said CSPI executive director Michael F. Jacobson. "But the FDA needs to
be as sure as possible that rebiana is safe before allowing it into foods that
would be consumed by tens of millions of people. It would be tragic if the
sweetener turned out to cause cancer or other problems."

One key animal study has not been conducted, according to the UCLA experts and
CSPI. The FDA's guidelines advise testing prospective major new food additives
on two rodent species, usually rats and mice. The new sweetener has only been
tested on rats, but not mice. The toxicologists' report said that because
several studies found mutations and DNA damage, a lifetime mouse study designed
to evaluate the risk of carcinogenicity and other health problems was
particularly important.

The new report was prepared for CSPI by Sarah Kobylewski, a graduate student in
the Department of Molecular Toxicology, and Curtis D. Eckhert, Ph.D., a
professor of Environmental Health Sciences and Molecular Toxicology, at UCLA.
They were assisted by Professor Joseph R. Landolph, Jr., Ph.D., of the
Department of Molecular Microbiology and Immunology, and Pathology, Keck School
of Medicine, and the School of Pharmacy at the University of Southern
California.

The UCLA toxicologists emphasized the need for more genotoxicity tests, because
of the evidence that derivatives of stevia that are closely related to rebiana
damage DNA and chromosomes. Their report noted that much of the recent research
on rebiana was sponsored by Cargill and urged the FDA to obtain independently
conducted tests to ensure that corporate biases don't influence the design,
conduct, or results of the tests.

Rebiana is shorthand for rebaudioside A, a component of stevia. It is obtained
from the leaves of a shrub native to Brazil and Paraguay. Coke, Pepsi, and other
companies are excited about rebiana, because it supposedly tastes better than
crude stevia, which is sold as a dietary supplement in health-food stores. After
all the controversies pertaining to saccharin, aspartame, and other artificial
sweeteners, the food industry expects many calorie-conscious consumers to
eagerly opt for this natural sweetener.

Two companies -- Cargill and Merisant -- have told the FDA that rebiana should
be considered GRAS, a category given less scrutiny by the FDA than ordinary food
additives. A third company, Wisdom Natural Brands, has declared that its
stevia-based sweetener is GRAS and will market it without giving evidence to, or
even notifying, the FDA. That company gave CSPI only a heavily redacted report
prepared by scientists it hired to declare its stevia derivative, which is of
unknown purity, is safe.

Stevia is legal in foods in Japan and several other countries, but the United
States, Canada, and the European Union bar stevia in foods because of older
tests that suggested it might interfere with reproduction. New tests sponsored
by Cargill did not find such problems.

"I am not saying that rebiana is harmful, but it should not be marketed until
new studies establish that it is safe," Jacobson said.

Cargill's version of rebiana is called Truvia and would be used by Coca-Cola.
Pepsi’s version is called PureVia and is produced by Merisant’s Whole Earth
Sweetener division. Merisant is best known for marketing the Equal brand of
aspartame.

CSPI has not questioned the safety of two artificial sweeteners, sucralose
(Splenda) and neotame, but says that suggestive evidence indicates that
saccharin, aspartame (Equal, NutraSweet), and acesulfame-K pose small risks of
cancer.

"The whole issue of what gets GRAS status needs to be reviewed by Congress,"
Jacobson said. "It’s crazy that companies can just hire a few consultants to
bless their new ingredients and rush them to market without any opportunity for
the FDA and the public to review all the safety evidence."

Two of the most harmful ingredients in the food supply are considered GRAS:
salt, which raises blood pressure and causes thousands of unnecessary heart
attacks and strokes every year, and partially hydrogenated oil, which is the
source of artery-clogging artificial trans fat. CSPI has long campaigned to get
partially hydrogenated oil out of the food supply and to reduce salt to safe
levels.


http://www.confectionerynews.com/Formulation/Calls-for-more-stevia-safety-tests-\
threaten-market-launches

Calls for more stevia safety tests threaten market launches
By Sarah Hills

29-Aug-2008 --

The safety of stevia has been called into question again after scientists at the
University of California said further tests were needed on potential cancer
causing properties before the sweetener is used in food and drink.

Beverage giants Coca-Cola and PepsiCo are poised to launch products containing
their own brands of rebiana, which is from the stevia plant, but it is argued
that more evidence is needed to show that the sweetener is safe.

A review of safety data was carried out by the toxicologists on behalf of the
Center for Science in the Public Interest. It said that carcinogenicity studies
have not found stevioside (which differs slightly from rebiana) to be
carcinogenic in rats but further studies on rebiana, including a study on mice,
are needed.

This is partly because several genotoxicity studies found that stevioside and
steviol cause mutations, chromosomal damage, and DNA breakage which “indicate
the need for greater reassurance of noncarcinogenicity” as rebiana might cause
similar problems, or cancer, in humans.

The Food and Drug Administration's (FDA) guidelines advise testing potential
food additives on two rodent species, usually rats and mice. But rebiana
(rebaudioside A) has only been tested on rats

The study concluded that the FDA should require carcinogenicity and toxicology
studies both in rats and mice before accepting rebaudioside A as generally
recognized as safe (GRAS) or approving it as a food additive.

The Center for Science in the Public Interest has now written to the FDA echoing
the reports conclusions.....

Rebiana is the sweetest, purest part of the leaf from the South American stevia
plant, which is approximately 200 times as sweet as sugar.

Stevia, which is permitted for sale in the US as a dietary supplement on the
basis of its low glycemic index, is yet to have FDA GRAS status for use in food
and beverages.

The US market for stevia is estimated to be worth about $60m, a figure analysts
say could triple with FDA GRAS. Currently the biggest markets for stevia are
Japan and Korea.

Last month it was announced that PepsiCo has joined with the Whole Earth
Sweetener Company to launch its rebiana sweetener PureVia.

Meanwhile Coca-Cola has teamed up with Cargill to use its rebiana brand, called
Truvia.

Cargill is already selling Truvia online as a table-top sweetener but the
beverage companies are yet to sell drinks with the sweetener in the US.

A spokesman for PepsiCo said: “Everyone agrees that no ingredient should be
marketed to consumers until its safety has been proven.

“While we believe the full body of evidence presented to the FDA by multiple
sweetener manufacturers demonstrates the safety of this ingredient, ultimately
it’s up to the FDA to decide.” .....

http://cspinet.org/
Center for Science in the Public Interest
1875 Connecticut Ave. N.W., Suite 300, Washington, D.C. 20009
Main switchboard: (202) 332-9110  Fax: (202) 265-4954

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(both U.S. and Canadian editions): circ@...

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questions about CSPI's work: cspi@...

For questions about CSPI in Canada: jefferyb@...


http://cspinet.org/new/pdf/stevia-cspi-cover-letter-8-4-08.pdf  CSPI letter to
FDA 2008.08.04

August 4, 2008

Dockets Management Branch (HFA-305)
U.S. Food and Drug Administration
5630 Fishers Lane, Room 1061
Rockville, MD 20852

Office of Food Additive Safety Center for Food Safety and Applied Nutrition Food
and Drug Administration 5100 Paint Branch Parkway College Park, MD 20740
Re: GRN No. 253 (and GRN No. 252)

Dear Sir or Madam:

Please consider the attached comment by UCLA toxicologists in your review of
GRAS notification No. 253 for rebaudioside A purified from Stevia rebaudiana
(Bertoni). The comment may also apply to notification No. 252 regarding a
similar substance (we have submitted a FOIA request for the notification, but
have not yet received the information). (Another company, Wisdom Natural Brands,
has announced that it has self-affirmed a stevia derivative as GRAS.) The
comment addresses the adequacy of testing done on rebaudioside A (and stevioside
and steviol) and the results of the tests.

Rebaudioside A, if safe, could be a welcome substitute for the various
artificial sweeteners, such as saccharin, aspartame, and acesulfame-K, that have
been the foci of great controversy, because of (inconclusive) evidence of
potential carcinogen risk. Older studies on cruder extracts of stevia indicated
potential toxic effects on reproduction in rats and hamsters.1 The newer tests
did not find similar problems with the purer rebaudioside A preparation.
However, importantly, several in vitro and in vivo genotoxicity tests of steviol
and stevioside, which are closely related to rebaudioside A, found
substance-related mutations, chromosome aberrations, and DNA breakage. Such
findings indicate that rebaudioside A might cause similar problems, or cancer,
in humans.

In addition, a high-potency sweetener like rebaudioside A will probably be
consumed in significant quantity by tens of millions of people. The FDA’s
testing guidelines (Redbook II) for

1 Yamada A, Ohgaki S, Noda T, et al. Chronic toxicity study of dietary Stevia
extracts in F344 rats. J. Food Hyg. Soc. Japan 1985;126:169-83 (Abstract in
English. Partial English translation provided); Wasuntarawat C, Temcharoen P,
Toskulkao C, et al. Drug Chem. Toxicol. 1998;21:207-22.

Page 2

food additives consumed in significant quantity indicates that, as a basic
safeguard, companies should conduct chronic feeding studies of such substances
in two rodent species, typically rats and mice. GRAS notification No. 253
indicates that rebaudioside A has been tested in only one species (rat). In the
present case, the need for a lifetime 2 feeding study in a second species
(mouse) is underscored by the positive findings in multiple genotoxicity
studies.

Furthermore, because of differences in pharmacokinetics of stevioside and
rebaudioside A, certain toxicity tests (such as carcinogenicity studies)
involving stevioside may not be predictive for rebaudioside A. Rebaudioside A is
the ingredient that would be used in food, and that is the ingredient that
should be used in tests.

Considering the genotoxic effects of rebaudioside A and the absence of a
lifetime feeding study in mice, and considering that impartial toxicologists
from UCLA (in contrast to the paid consultants to Cargill 3) are criticizing the
testing and safety of rebaudioside A, this ingredient cannot be considered
generally recognized as safe.

We urge the FDA to advise the sponsor(s) that they should submit a full food
additive petition, including the results of a new chronic feeding study on mice
and repeats of all the genotoxicity tests. The food additive route would enable
the FDA to review the safety tests in detail, rather than give them the more
perfunctory examination characteristic of GRAS reviews. Furthermore, to obtain
objective tests of this potentially widely used substance, the FDA should ask
the National Toxicology Program to conduct chronic feeding studies on rats and
mice, as well as a battery of genotoxicity tests (including repetitions of both
the positive and negative studies conducted by the notifier, as well as other
tests deemed appropriate).

Sincerely,

Michael F. Jacobson, Ph.D., Executive Director

2 Any new “lifetime” study should be not 80 or 104 weeks, but closer to 2.5
years, the actual “lifetime” of a mouse (
http://sageke.sciencemag.org/cgi/content/full/2003/25/as1 ). Huff J, Jacobson
MF, Davis DL. 2008. The limits of 2-Year Bioassay Exposure Regimens for
Identifying Chemical Carcinogens. Environ Health Perspect:
doi:10.1289/ehp.10716. [Online 30 June 2008]
http://ehp.niehs.nih.gov/docs/2008/10716/abstract.html

3 The FDA should require GRAS notifiers to disclose financial conflicts of
interest of members of their GRAS panels, just as medical journals, federal
advisory committees, and others require authors, nominees, or members to
disclose their conflicts of interest.


[ This review cites an expert mouse Comet assay genotoxicity study by YF Sasaki
et al, 2002, which I have reviewed in detail:

http://groups.yahoo.com/group/aspartameNM/message/935
Comet assay finds DNA damage from sucralose, cyclamate, saccharin in
mice: Sasaki YF & Tsuda S Aug 2002: Murray 2003.01.01
[ Also borderline evidence, in this pilot study of 39 food additives,
using test groups of 4 mice, for DNA damage from for stomach, colon,
liver, bladder, and lung 3 hr after oral dose of 2000 mg/kg aspartame--
a very high dose.]

http://groups.yahoo.com/group/aspartameNM/message/961
genotoxins, Comet assay in mice: Ace-K, stevia fine; aspartame poor;
sucralose, cyclamate, saccharin bad: Y.F. Sasaki Aug 2002:
Murray 2003.01.27 [A detailed look at the data] ]

http://groups.yahoo.com/group/aspartameNM/message/1084
26 stevia safety abstracts since 1993: aspartame vs stevia debate on
alt.support.diabetes, George Schmidt, OD: Murray 2004.05.17 ]


http://cspinet.org/new/pdf/stevia-report_final-8-14-08.pdf  26-page full text
2008.08.14
[ long detailed tables omitted ]

Toxicology of Rebaudioside A: A Review
by Sarah Kobylewski 1 and Curtis D. Eckhert, Ph.D.

1 Sarah Kobylewski is a doctoral student in the Department of Molecular
Toxicology and Curtis D. Eckhert is Professor of Environmental Health Sciences
and Molecular Toxicology at the University of California, Los Angeles.

[ Dept. of Environmental Health Sciences and Molecular Toxicology, UCLA School
of Public Health, Los Angeles, California 90095-1772.
Sarah Ellen Kobylewski, Student sarah@... 310-882-0548
Eckhert, Curtis D., Prof, Dept Chair  ceckhert@... 310-825-8429 ]


They acknowledge, with gratitude, the thoughtful contributions and counsel of
Professor Joseph R. Landolph, Jr., Ph.D., of the Department of Molecular
Microbiology and Immunology and the Department of Pathology, Keck School of
Medicine, and the School of Pharmacy at the University of Southern California.

The authors and reviewers do not have any financial conflicts of interest
related to manufacturers of rebaudioside A, stevia, and other caloric and
non-caloric sweeteners or other segments of the food industry.

Toxicology of Rebaudioside A: A Review

This review of safety data regarding high-purity rebaudioside A (rebiana), the
subject of two GRAS (generally recognized as safe) notifications,1,2 was
conducted for the Center for Science in the Public Interest. Much of the recent
research was published in a Food and Chemical Toxicology supplement on
rebaudioside
A. 3 All the rebiana used in the studies published in that supplement met all
current
specifications for steviol glycosides set by the Joint FAO/WHO Expert Committee
on
Food Additives (Carakostas et al., 2008 and JECFA, 2007). The research described
in
this supplement was peer reviewed and said to be conducted in compliance with
Good
Laboratory Practices (GLP) and Good Clinical Practices (GCP) requirements.

Background

Rebaudioside A is a steviol glycoside derived from the herb Stevia Rebaudiana
(bertoni). Rebaudioside A and stevioside (Fig. 1) are the two main steviol
glycosides
found in the S. Rebaudiana herb and are the two predominant derivatives used in
high potency
sweeteners. Stevioside differs from rebaudioside A by having one less glucose
moiety. Steviol glycosides have been used as food and medicine in Japan and
South
America for many years, but stevia in the leaf or extracted form is permitted to
be sold in
the U.S. only as a dietary supplement, as defined in section 201(ff)(1) of the
Federal
Food, Drug, and Cosmetic Act. In 2007, JECFA specified that steviol glycoside
sweeteners must be composed of at least 95% of the known steviol glycosides
(JECFA,
2007). Products that consist predominantly of rebaudioside A are referred to as
rebiana.

The temporary acceptable daily intake (ADI) for steviol glycosides set by JECFA
is 0-2
mg/kg bw/day (based on steviol content) with a steviol equivalent of 0-6 mg/kg
bw/day
of rebaudioside A (steviol equivalent=[stevioside]*(0.4); [rebaudioside
A]*(0.33)).

JECFA has concluded that there is insufficient data to give steviol glycosides a
permanent ADI. The FDA has not yet authorized stevia as a food additive nor has
the
FDA considered it to be generally recognized as safe (GRAS). (Data for the above
background information was obtained from Carakostas et al. 2008 and
correspondence by
the author with the Food and Drug Administration (FDA).)

1 GRAS notification numbers 252 and 253. We have not obtained a copy of No. 252
and
so cannot comment on any data that may have accompanied that notification.
Furthermore at least one other company, Wisdom Natural Brands, may have
self-affirmed
its stevia product as GRAS, and not notified the FDA.

2 See Appendix A for list of abbreviations

3 Authors of the supplement are affiliated with manufacturers or potential users
of
rebaudioside A (see Appendix B).

Page - 1

JECFA’s Requirements

The JECFA has made the following requests for research before it set a permanent
ADI
for rebiana and reduced the safety factor to 100 (currently 200):

- detailed information on specifications

- human studies conducted in normotensive and hypotensive subjects to gain
information on potential hypotensive effects;

- human studies with subjects with insulin-dependent and insulin-independent
diabetes to gain information on the effects on glucose homeostasis (Carakostas
et al.
2008).

Below we discuss those issues and indicate several additional concerns.

Comparative Metabolism

1. Humans

Renwick et al. (2008) reviewed the literature on the metabolism of stevioside
and
rebaudioside A by intestinal microbiota. Investigators used this review to try
to
establish that toxicity studies on stevioside are relevant for assessing the
toxicity of
rebaudioside A. Gardana et al. (2003) provided a comprehensive study on steviol
glycoside hydrolysis in the human gut. The study was carried out under anaerobic
conditions with mixed bacterial cultures from fecal samples of healthy human
volunteers.

Stevioside was completely hydrolyzed to steviol after 10 hours of incubation,
with
steviolbioside as an intermediate. Steviolbioside formation peaked at 2-4 hours
and
steviol was first detected at 3-4 hours of incubation. Rebaudioside A was
completely
hydrolyzed to steviol after 24 hours of incubation, with steviolbioside as an
intermediate.
Steviolbioside was detected at 6-7 hours and peaked at 12-15 hours of
incubation.

Steviol was unchanged by incubation with intestinal microflora after 72 hours of
incubation. Because stevioside and rebaudioside A are metabolized at different
rates,
toxicity assessments of stevioside cannot definitively be extrapolated to assess
the risk of
rebaudioside A.

Hutapea et al. (1997) reported that stevioside has a steviol-16,17-epoxide
metabolite
(Fig. 2) when incubated for 48 hours with rat intestinal microflora. Epoxides
are of
concern because they are highly reactive with nucleophiles, such as DNA. The
creation
of the steviol-16,17-expoxide metabolite that was seen in the Hutapea study
could not be
replicated by Gardana et al. (2003) and Koyama et al. (2003). Renwick et al.
(2008)
speculated that the HPLC-UV (high performance liquid chromatography-ultraviolet)
instrument used to detect the epoxide metabolite in the Hutapea study was not
highly
specific. However, given the possibility of epoxide formation from steviol
and/or its
glycosides based on their structures (Fig. 1), the creation of an epoxide
metabolite in the
human system needs to be further investigated.

Page - 2

Wheeler et al. (2008) conducted human metabolism studies that
reported similar metabolic and elimination pathways (Fig. 3) but not
identical pharmacokinetics for rebaudioside A and stevioside.

Healthy, adult, male subjects received a single oral dose of 5 mg/kg of 98.7%
pure rebaudioside A and 4.2 mg/kg of 96.6% pure stevioside (each ~1.6
mg/kg of steviol equivalents). Plasma, urine, and fecal samples were
collected during a pre-dose period and up to 72 hours post-dose. Both
glycosides were hydrolyzed in the GI tract into steviol, which was absorbed
and conjugated to a glucuronide.

Steviol glucuronide was predominantly excreted in the urine
and accounted for 59% and 62% of the
rebaudioside A and stevioside, respectively.

Steviol excreted in the urine only accounted for 0.04% and 0.02%
of rebaudioside A and stevioside, respectively.

Steviol glucuronide was not detectable in the feces,
but steviol in the feces accounted for 4.8% and 5.2% of
rebaudioside A and stevioside, respectively.

The half-life (t1/2) for both glycosides was approximately 14 hours
(Tables 1 and 2).

However, only 64.2% of rebaudioside A and
67.22% of stevioside was accounted for in the urine and feces
after 72 hours of dosing.

Plasma steviol glycosides were not measured in this study.

Geuns et al. (2003) reported low transport of rebaudioside A and stevioside in
Caco-2
cells, a human epithelial colorectal adenocarcinoma cell line often used to
detect
absorption rates of drugs, with apparent permeability coefficients of 0.11 x
10-6 and
0.16 x 10-6 cm/s, respectively. They reported that steviol was transported much
more
efficiently than the two glycosides, with an apparent permeability coefficient
for
absorptive transport of 38.6 x 10-6 cm/s. Though it is apparent that the
majority of the
stevioside and rebaudioside A are hydrolyzed into steviol, which is absorbed by
the GI
tract, it is possible that transport and/or absorption of rebaudioside A and
stevioside

Page - 3

occurs. It is also likely that steviol metabolites are not being excreted within
72 hours, and that may account for the remainder of the dose that was not
measured in the feces or urine. The unaccounted-for fraction of rebaudioside A
and stevioside after 72 hours (~5 half-lives) of dosing needs to be further
investigated. If harmful metabolites are being formed after absorption, it is
important to understand their toxicokinetics in order to properly assess their
potential toxicological relevance. A more complete study would measure plasma
concentrations and excretion of unhydrolyzed steviol glycosides.

In the human metabolism study, rebaudioside A and stevioside had different
pharmacokinetic results for certain parameters when steviol and steviol
glucuronide were measured (Tables 1 and 2). For instance, there was a longer
Tmax and lower Cmax of steviol glucuronide and steviol when the patients were
administered rebaudioside A compared to stevioside. Stevioside toxicity studies
may be a good way to predict the toxicity of rebaudioside A, but they cannot be
used in place of directly testing rebaudioside A itself. The toxicity of
stevioside and rebaudioside A should be studied individually since each will
potentially be used as ingredients in human foods.

2. Rats

Roberts et al. (2008) investigated the metabolism of stevioside, rebaudioside A,
and steviol in Sprague-Dawley rats in order to determine the toxicokinetic and
metabolic similarities between stevioside and rebaudioside A. The three
compounds were radiolabeled with 14C in the =CH2 group of the steviol moiety
(Fig. 1). The rats were given a single oral dose of 5 mg/kg bw rebaudioside A,
4.2 mg/kg bw stevioside, and 1.6 mg/kg bw steviol (molar equivalents). Even
though the investigators concluded that the pharmacokinetics of stevioside and
rebaudioside A in rats are similar, while that of steviol is different, it
appears that most of the pharmacokinetic parameters are quite different for all
three compounds in rats of the same sex (Table 3). The main radioactive
component in plasma was always steviol after rats were dosed with
14C-stevioside, 14Crebaudioside A, and 14C-steviol. Steviol glucuronide and two
unidentified metabolites were also found in the plasma in lower concentrations t
han steviol. The absorption through the gut from rebaudioside A treatment was
71% for males, 82% for females; from stevioside treatment was 78% for males and
81% for females; from steviol treatment was 97% for males and 99% for females.
Steviol was excreted predominantly
in the feces and was the primary metabolized component of the parent glycoside.
Unlike the human studies, limited urinary elimination was reported. Steviol
glucuronide was the primary form of the metabolized glycoside found in the bile
of cannulated rats.

Steviol glucuronide from the bile proceeds to the GI tract where it is
deconjugated back to steviol. Steviol is then either re-circulated back to the
liver or is excreted in the feces (Fig. 3). The investigators propose that
because of the pharmacokinetic similarities

Page - 5

between stevioside and rebaudioside A, information from stevioside safety
studies can be used to extrapolate safety data on rebaudioside A. However, the
pharmacokinetic parameters in rats are different enough that toxicity data from
stevioside may not be reliably extrapolated to rebaudioside A. Independent
toxicity studies on rebaudioside A would be needed to make any conclusive
statements about its safety.

The difference in excretion pathways between humans and rats is explained by the
different molecular weight thresholds for human and rat biliary excretion of
organic anions such as steviol glucuronide (Renwick, 2008b). Steviol and steviol
glucuronide are subject to enterohepatic re-circulation in the rat (Roberts and
Renwick, 2008).

Roberts et al. (2008) proposed that the rat is an ideal model for studying
steviol glycoside toxicity in humans due to their similarities in steviol
glycoside metabolism. However, due to the differences in steviol glycoside
metabolism between humans and rats (Fig. 3) the rat does not appear to be an
ideal model for studying steviol glycoside toxicity.

Steviol glycosides are hydrolyzed to their aglycone by similar microflora in the
guts of the two species, but steviol and its glucuronide conjugate undergo
enterohepatic circulation in the rat. The rat’s primary path of elimination is
through the feces, while in humans steviol is conjugated to glucuronide and
predominantly eliminated in the urine.

While studies in rats are certainly useful, rat studies may lead to
inappropriate conclusions because of the differences in metabolism between rats
and humans.

Page - 6

Dietary Intake Assessment

To project rebaudioside A intakes, Renwick et al. (2008) used a substitution
method that takes into account actual intake data of high consumption artificial
sweeteners (expressed as sucrose equivalents). Renwick et al. (2008) determined
that this method was conservative enough for purposes of toxicity assessments.
They found that the highest predicted intake of rebaudioside A would be in
children and diabetics, but predicted that dietary exposure would always be less
than 6 mg/kg bw/day. The estimates were calculated from published intake data of
existing artificial sweeteners which had varying age ranges for children. In
order to be conservative, Renwick et al. used data from the age group of each
study that showed the highest intake.

The predicted daily intake of rebaudioside A in average consumers was 1.3, 2.1
and 3.4 mg/kg bw in the general population, children, and children with
diabetes, respectively.

The predicted daily intake of rebaudioside A in high consumers was 3.4, 5.6, and
4.5 mg/kg bw in the general population, children, and children with diabetes,
respectively.

Hemodynamic Effects

According to a 4-week study by Maki et al. (2008a), 1,000 mg/day rebaudioside A
did not significantly alter resting, seated systolic blood pressure, diastolic
blood pressure, mean arterial pressure, heart rate, or 24-hour ambulatory blood
pressure responses in patients with low-normal to normal blood pressure compared
with a placebo.

1,000 mg/day is 7-10 times the predicted average daily intake and 2-4 times the
daily intake for high-intake consumers. A secondary analysis noted small changes
in diastolic blood pressure and mean arterial pressure. The investigators assert
that those findings are clinically insignificant.

Glucose Homeostasis

According to Maki et al. (2008b), rebaudioside A does not affect glucose
homeostasis or resting blood pressure in patients with type 2 diabetes mellitus.
The patients in this study were dosed for 16 weeks with 1,000 mg/day
rebaudioside A. The investigators found no hypoglycemia in the rebaudioside A
group compared to the placebo. However, there was a small but significant
increase in alanine transaminase (ALT) levels in the rebaudioside A group (1.7
U/L) and a decrease in the placebo group (-1.5 U/L). The investigators suggest
that the elevation in ALT levels was likely due to random variation and claim it
has no clinical significance since mean levels of ALT stayed within normal
range. No explanation of “clinically significant” or “normal range” was provided
by the investigators. Further investigation would be necessary to determine one
of the many possibly causes of the elevated ALT levels.

Page - 7

Genotoxic Effects

According to the literature review by Brusick et al. (2008) on the genotoxicity
of steviol and stevioside, two of 16 studies showed genotoxic activity for
stevioside and four of 15 studies (Brusick et al. did not include Pezzuto et
al., 1985, and TM677 results by Matsui et al., 1996a) showed genotoxic activity
for steviol (see Tables 4 and 5, respectively).

Rebaudioside A was not found to cause mutations, chromosome damage, or DNA
strand breakage in several in vitro and in vivo studies (Pezzuto et al, 1985;
Nakajima 2000a; Nakajima 2000b; Sekihashi et al, 2002). Examples of (mostly
positive) genotoxicity studies using stevioside include:

Page - 8

• Stevioside showed positive results in Salmonella typhimurium (S. typhimurium)
strain TA98 at 50 mg/plate for 99% pure stevioside (Suttajit et al., 1993). The
results showed a 4-fold increase in revertants without S9 extract and a 2-fold
increase with S9. That study used stevioside pre-incubated with and without
β-
glucosidase. The treated and untreated samples showed roughly the same mutagenic
results. Those results demonstrate that at 50 mg/plate, stevioside (without
B-glucosidase or S9), steviol (stevioside + B-glucosidase), stevioside
metabolite(s) (stevioside +S9), and steviol metabolite(s) (stevioside + B-
glucosidase + S9) are all mutagenic in TA98.

• Klongpanichpak et al. (1997) did not find stevioside to be mutagenic in TA98
at a concentration of 50 mg/plate. However, they used S9 extract from rats,
mice, hamsters, and guinea pigs; Suttajit et al. (1993) showed the strongest
results without S9 extract.

• Suttajit et al. (1993) found that stevioside did not cause chromosomal
aberrations in human lymphocytes incubated with 1, 5, and 10 mg/ml stevioside
for 24 hours.

• Using the comet assay, Nunes et al. (2007) reported DNA breakage in blood,
spleen, liver, and brain cells in Wistar rats exposed to 400 mg/kg of stevioside
in drinking water. The strongest effects of stevioside were found in the liver
cells.

• Matsui et al. (1996a) found that stevioside at doses up to 5 mg/plate was not
mutagenic in S. typhimurium strains TA97, TA98, TA100, TA102, and TA104 with or
without S9 or in S. typhimurium strains TA1535 and TA1537 and E. coli WP2
uvrA/pKM101 with S9. Stevioside was also not mutagenic in S. typhimurium strain
TM677 with or without S9 at 10 mg/ml. Stevioside also gave negative results in
the umu test with or without S9 and was negative in the spore and streak
rec-assays with or without S9 at 10 mg/disk.

Metabolically-activated steviol was found to cause dose-related positive
responses in several mutagenicity tests. These results indicate that a steviol
derivative is likely responsible for its mutagenic activity, but the metabolite
has not been identified (Brusick et al., 2008). The mutagenicity of steviol
metabolites needs to be further investigated.

• Matsui et al. (1989) showed positive results for steviol in a plasmid
mutagenesis study.

• Matsui et al. (1996a) found that steviol is mutagenic in S. typhimurium strain
TM677, caused chromosome aberrations in cultured Chinese hamster lung (CHL)
cells, and mutagenic in CHL cells in the presence of S9. In the same study,
steviol produced a weak positive response with or without S9 in the umu test.

• Matsui et al. (1996a) found that steviol at doses up to 5 mg/plate was not
mutagenic in S. typhimurium strains TA97, TA98, TA100, TA102, and TA104 with or
without S9 or in S. typhimurium strains TA1535 and TA1537 and E. coli WP2
uvrA/pKM101 with S9. In the same study, steviol was also negative for spore and
streak rec-assays and did not induce micronuclei in bone marrow erythrocytes of
mice.

• A forward mutation assay using S. typhimurium strain TM677 found mutagenicity
using 100 μg/ml steviol when assayed with S9 extract (Pezzuto et al.,
1985).

Page - 9

• Suttajit et al. (1993) showed that steviol was not mutagenic in TA98 or TA100
at doses of 1-20 mg/plate. This study also showed that steviol does not cause
chromosome aberrations at 0.1 and 0.2 mg/ml.

Page - 12

Subchronic Toxicity

Curry et al. (2008a) performed subchronic tests of rebaudioside A in a 13-week
study on Han-Wistar rats. After a 4-week palatability study, investigators dosed
rats with 12,500, 25,000, and 50,000 ppm rebaudioside A (dosing equivalents
provided in Table 6). In the 13-week study, mean body weight gain was
significantly less in the first four days for males and females in the 25,000
ppm and 50,000 ppm treatment groups compared to controls. Males in all treatment
groups had significantly less mean body weight gain than control groups for the
length of the study. Females showed similar results but only in the 25,000 ppm
and 50,000 ppm treatment groups. Investigators concluded that the reduced weight
gain was not an adverse effect due to the following considerations: the effect
of rebaudioside A on food conversion efficiency was minimal; rebaudioside A
affects food consumption and body weight gain due to palatability issues;
reduced food consumption was consistently associated with trea
tment groups that demonstrated reduced weight gain; and toxicity was not
observed over the dose-range in the 13-week study (Flamm et al., 2003). Also,
based on WHO guidance from 1987 (WHO, 1987), the body-weight-gain reductions
observed in both studies would not be considered an adverse effect.

Page - 13

Large, but inconsistent, reductions in bile acids occurred in both studies
across all treatment groups.

However, liver enzyme activities (as measured in serum) and hepatic
histopathology were within normal limits and did not differ significantly from
controls. Mean plasma urea and creatinine concentration in several treatment
groups in both studies were slightly increased from controls, but levels always
remained within
reference limits. Because of low urine volume, high urine specific gravity, and
no change in other urinalysis parameters, investigators concluded that these
results were probably not a sign of renal failure but of dehydration, possibly
from the osmotic effects of high doses of rebaudioside A. Macroscopic and
microscopic evaluation of the kidneys showed no alterations.

Absolute epidydimal weights of high-dose males and the absolute weights of the
ovaries of high-dose females were significantly lower than controls.
Spermatogenesis was unaffected by treatment and testicular atrophy was not
detected. Microscopic histopathology did not detect any other effects on the
testes.

The NOAEL for rebaudioside A in Han-Wistar rats for the 13-week study was
determined to be 50,000 ppm for the 13-week study (4,161 and 4,645 mg/kg bw/day
in males and females, respectively). This is ~2,000-fold greater than the ADI of
2.0 mg/kg bw/day of steviol glycosides established by JECFA and ~1,000-fold
greater than the predicted human exposure.

Carcinogenicity

Studies in rats have failed to produce any evidence of carcinogenicity of
stevioside, though rebaudioside A, the subject of the GRAS notification, itself
has not been tested (Carakostas et al., 2008). Three studies support
non-carcinogenicity of that substance:

• Fischer 344 rats administered 5% stevioside in their diet in a relatively
brief 36-week study showed no increased development of pre-neoplastic or
neoplastic lesions in the urinary bladders with and without an initiating dose
of the bladder carcinogen N-nitrosobutyl-N-(4-hydroxybutyl) amine (Hagiwara et
al., 1984).

• Xili et al. (1992) found no neoplastic or pre-neoplastic lesions in Wistar
rats in a 24-month chronic toxicity and carcinogenicity study with 85% pure
stevioside (600 mg/kg bw/day)
.
Page - 14

• A 24-month carcinogenicity study by Toyoda et al. (1997) did not find any
increase in non-neoplastic or neoplastic lesions in Fischer 344 rats exposed to
2.5% and 5% of 95.6% pure stevioside in the diet. JECFA used the 970 mg/kg
bw/day dose (2.5% dose in male rats) used in the Toyoda study to
set the temporary ADI of 2 mg/kg bw/day (Carakostas et al., 2008).

It is important to note that FDA normally asks for tests in two rodent species,
usually rats and mice, in a compound with such a high predicted exposure level.
Also, all three of the aforementioned studies were done with stevioside, not
rebaudioside A. It is possible that differences in metabolism and toxicokinetics
would result in different risks of carcinogenicity using the two steviol
glycosides.

Reproductive Toxicity

Older studies reported anti-fertility effects, as well as decreases in the
weights of the testes, seminal vesicle, and cauda epididymides and a reduction
in spermatozoa concentration, in rats administered crude stevia extracts
(Mazzei-Plana and Kuc 1968; Olivereira Filho et al., 1989, and Melis, 1999).
However, other studies with purified stevioside (not rebaudioside A, the subject
of the GRAS notification) failed to produce
these reproductive effects (Mori et al., 1981; Yodyingyuad and Bunyawong, 1991;
Usami et al., 1995).

In a recent study, Curry et al. (2008b) found no treatment-related effects of
rebaudioside A on mating performance, fertility, gestation lengths, and estrous
cycle in the F0 and F1 generation of rats in a two-generation study. After a
preliminary short-term study to determine appropriate dosage levels, those
investigators dosed F0 and F1 generation rats with 0, 7,500, 12,500, and 25,000
ppm rebaudioside A via the diet (dosing equivalents provided in Table 7). Female
rats in the 12,500 ppm and 25,000 ppm groups and male rats in the 25,000 ppm
group of the F1 generation and male and female rats in the 25,000
ppm group of the F2 generation showed significant decreases in body weight gains
compared to controls. The investigators considered those effects to be
toxicologically insignificant due to the lack of adverse effects on those
animals’ survival, condition of their offspring, their pre-weaning reflex
development, weight gain after 25 days, and timing of sexual maturation. The
investigators presume that the weight-gain effects were due to the nature of a
diet supplemented with high levels of intense sweeteners that normally leads to
reduced consumption and nutritional content (WHO, 1987).

Investigators found higher adjusted mean liver weights in females in the 12,500
ppm and 25,000 ppm F0 and F1 generations. There were no changes in the relative
weights of the thymus glands in treated groups compared to the control group,
but there was a reduction in relative and absolute weights of the spleens in
several animals of the F1 and F2 treatment groups. However, the investigators
did not find any clinically significant alterations in blood count or the
histopathology of other immune system organs. There was no change on the ability
of the females of the F0 and F1 generations to litter and rear their offspring
to weaning. There was also no effect on litter size, sex ratio, and pre- and
post-natal survival of offspring.

Page - 15

Curry et al. (2008b) concluded that steviol glycosides do not pose a
reproductive or developmental hazard. They found the NOAEL for rebaudioside A
for Han-Wistar rats to be 25,000 ppm for reproductive effects in the F0
generation and for survival, growth, and general condition of F1 and F2
offspring.

Summary and Discussion

Investigators demonstrated that rebaudioside A has no adverse hemodynamic
effects in people with normal to low-normal blood pressure dosed with 1,000
mg/day for 4 weeks.

Investigators also found no clinically significant effects of rebaudioside A
treatment on patients with type 2 diabetes mellitus. The only concerning finding
of the glucose homeostasis study was an increase in ALT levels. This finding is
not of great concern since it did not lead to any adverse effects, but further
investigation would be necessary to determine the cause of the increase and the
long-term effects of rebaudioside A on
ALT levels.

In both the rat and human metabolism studies, investigators demonstrate that
rebaudioside A and stevioside have similar metabolic pathways within each
species.

However, rebaudioside A’s extra glucose moiety causes differences in the two
compounds’ pharmacokinetic parameters (Tables 1, 2, and 3). Because of those
differences, toxicity data for stevioside cannot be assumed to be an appropriate
basis for assessing the safety of rebaudioside A. Separate toxicity studies on
rebaudioside A itself are necessary to make definitive conclusions about its
safety.

Investigators whose studies are published in the Food and Chemical Toxicology
supplement concluded from the metabolism studies that the rat is an ideal model
for steviol glycoside human toxicity studies. Both species hydrolyze the
glycosides into steviol by the gut microflora, but after absorption the
metabolic pathways differ (Fig. 3).

Since steviol glycoside metabolism in rats and humans is not identical, the rat
may not be an ideal model for evaluating human toxicity.

Hutapea et al. (1997) reported a steviol-16,17-epoxide stevioside metabolite.
Given the structures of stevioside and rebaudioside A, an epoxide is a likely
metabolite. The

Page - 16

possibility of a steviol glycoside forming an epoxide metabolite needs to be
investigated carefully, because epoxides may react with DNA and cause mutations.

Genotoxicity studies published in the Food and Chemical Toxicology supplement,
as well as other studies, raise significant concerns.

Suttajit et al. (1993) reported positive results for reverse mutations in the S.
typhimurium strain TA98 with and without S9 extract at a 50 mg/plate dose of
stevioside. Certain studies in that supplement cited the negative mutagenicity
results by Klongpanichpak et al. (1997) to try to discredit the work of
Suttajit, but Klongpanichpak used S9 extract while the mutagenic results from
Suttajit were highest without S9. The ability of stevioside and rebaudioside A
to cause reverse mutations as indicated by TA98 needs to be further
investigated, because such mutations suggest the possibility of carcinogenesis.

Stevioside also caused DNA breakage in blood, spleen, liver, and brain cells in
rats (Nunes et al., 2007).

The mutagenicity of this compound requires further, careful investigation.

Steviol was found positive in an umu test, mutagenic in a forward-mutation
assay, and caused chromosome aberrations and gene mutations in mammalian cells
(Matsui et al., 1996a) and plasmid mutagenesis (Matsui et al., 1989). Pezzuto et
al. (1985) found that steviol is both toxic and mutagenic in the TM677 assay
using S9 extract. Matsui’s studies were all conducted with S9.

These results indicate that steviol has a mutagenic metabolite that has yet to
be identified.

These finding are very important because rebaudioside A is hydrolyzed into
steviol before it is absorbed by the GI tract. Before rebaudioside A can be
generally regarded as safe, the mutagenic steviol intermediate needs to be
identified and further studied.

Overall, because of the warning flags raised by several studies, it is critical
that further genotoxicity testing be conducted to clarify the potential risks.

Carcinogenicity studies have not found stevioside to be carcinogenic in rats
(Hagiwara et al., 1984, Toyoda et al., 1997, Xili et al., 1992), but further
studies on rebaudioside A, including a study on mice, are needed for several
reasons:

• The rat is an imperfect model for evaluating steviol glycoside toxicity and
carcinogenicity risks in humans because of the differences in metabolism in the
two species.

• Several genotoxicity studies that found that stevioside and steviol cause
mutations, chromosomal damage, and DNA breakage indicate the need for greater
reassurance of noncarcinogenicity.

• The differences in pharmacokinetics between rebaudioside A and stevioside
indicate the need to test rebaudioside A itself in two rodent species.

• Based on a maximum estimated intake level of steviol glycosides of 1.7 mg/kg
bw/day (steviol equivalent), steviol glycosides should be considered a concern
level III chemical, for which the FDA recommends carcinogenicity studies in two
rodent species (usually mice and rats) (FDA Redbook, 2000).

The value of testing chemicals in two species is indicated by the fact that
bioassays of chemicals with a variety of structures that did not find
carcinogenicity in rats did find

Page - 17

carcinogenicity in mice (see appendix C). In sum, a lifetime carcinogenicity
study in mice of rebaudioside A must be conducted before that substance (or
other steviol glycosides) can be accepted as a GRAS ingredient that likely would
be consumed by tens of millions of people.

In conclusion, the FDA should ensure that the genetic toxicity studies that
produced either positive or conflicting results be repeated. Studies that look
at potential DNA adducts related to the potential reactive metabolites (C-13
carbonium ion or the epoxide) of steviol would be a strong addition to the
genotoxicity data.

Finally, the FDA should require carcinogenicity 4 and toxicology studies in rats
and in mice before accepting rebaudioside A as a GRAS substance or approving it
as a food additive.

Ideally, all those studies would be conducted by an independent party, such as
the National Toxicology Program of the National Institute of Environmental
Health Sciences.

4 Ideally, the studies would include an in utero phase and follow the animals
for almost their entire lives, instead of prematurely ending the study after 104
weeks. Huff J, Jacobson MF, Davis DL. 2008.
The limits of 2-year bioassay exposure regimens for identifying chemical
carcinogens.
Environ Health Perspect: doi:10.1289/ehp.10716. [Online 30 June 2008]
http://ehp.niehs.nih.gov/docs/2008/10716/abstract.html

Page - 18

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Male
NBR Rats. Technical Report Series No. 515. NIH Publication No. 04-4449. US
Department of Health and Human Services, Public Health Services, National
Institutes of
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of
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Technical Report No. 352. Battelle Columbus Laboratory. Produced from Chemtrack
Database (2001).

National Toxicology Program (NTP) (1989). Toxicology and Carcinogenesis Studies
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(Inhalation Studies). Technical Report Series No. 346. NIH Publication No.
90-2801.
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Institutes of Health, Research Triangle Park, NC.

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of
Evidence of Carcinogenicity of Diphenylhydantoin (Phenytoin) (CAS No. 57-41-0).
NTP Technical Report No. 404. Batelle Columbus Laboratory. Produced from
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National Toxicology Program (NTP) (2000). Toxicology and Carcinogenesis Studies
of
Primidone (CAS No. 125-33-7) in F344N Rats and B63CF1 Mice. Technical Report
Series No. 476. NIH Publication No. 00-3966. US Department of Health and Human
Services, Public Health Services, National Institutes of Health, Research
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Nunes, A.P.M., Ferreira-Machado, S.C., Nunes, R.M., Dantas, F.J.S., De Mattos,
J.C.P.,
Caldeira-de-Araújo, A., 2007. Analysis of genotoxic potentiality of stevioside
by comet
assay. Food Chem. Toxicol. 45, 662-666.

Oh, H., Han, E., Choi, D., Kim, J., Eom, M., Kang, I., Kang, H., Ha, K., 1999.
In vitro
and in vivo evaluation of genotoxicity of stevioside and steviol, natural
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Yakhak Hoeji 43, 614-622.

Oliveira-Filho, R.M., Uehara, O.A., Minetti, C.A., Valle, L.B., 1989. Chronic
administration of aqueous extract of Stevia rebaudiana (Bert.) Bertoni in rats:
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Pezzuto, J.M., Compadre, C.M., Swanson, S.M., Nanayakkara, N.P.D., Kinghorn,
A.D.,
1985. Metabolically activated steviol, the aglycone of stevioside, is mutagenic.
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doi:
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Renwick, A.G., The use of a sweetener substitution method to predict dietary
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doi:
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Renwick, A.G., Tarka, S.M., Microbial hydrolysis of steviol glycosides, Food and
Chemical Toxicology (2008), doi: 10.1016/j.fct.2008.05.008

Roberts, A., Renwick, A.G., Comparative toxicokinetics and metabolism of
rebaudioside
A, stevioside, and steviol in rats, Food and Chemical Toxicology (2008), doi:
10.1016/j.fct.2008.05.006

Sasaki, Y.F., Kawaguchi, S., Kamaya, A., Ohshita, M., Kabasawa, K., Iwama, K.,
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Sekihashi, K.,Saitoh, H., Sasaki, Y.F., 2002. Genotoxicity studies of stevia
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Temcharoen, P., Suwannatrai, M., Klongpanichpak, S., Apibal, S., Glinsukon, T.,
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Usami, M., Sakemo, K., Kawashima, K., Tsuda, M., Ohno, Y., 1995. Teratogenicity
study of stevioside in rats. Eisei Shikenjo Hokoku 113:31-35 [Abstract only].

Wheeler, A., Boileau, A.C., Winkler, P.C., Compton, J.C., Prakash, I., Jiang,
X.,
Mandarino, D.A., Pharmacokinetics of rebaudioside A and stevioside after single
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10.1016/j.fct.2008.04.041

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in Food. World Health Organization (WHO), International Programme on Chemical
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from: http://www.inchem.org/documents/ehc/ehc/ehc70.htm.

Yodyingyuad, V., Bunyawong, S., 1991. Effect of stevioside on growth and
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Hum. Reprod. 6, 158-165.

Xili, L., Chengjiany, B., Eryi, X., Reiming, S., Yuengming, W., Haodong, S.,
Zhiyian,
H., 1992. Chronic oral toxicity and carcinogenicity study of stevioside in rats.
Food
Chem. Toxicol. 30, 957-965.

Page - 24

Appendix A: List of Abbreviations

ADI=Acceptable Daily Intake
Aeu=amount excreted in urine
Aef=amount excreted in feces
ALT=Alanine Transaminase
AUC=Area Under the Curve
Bw=body weight
CLR=clearance rate
cm=centimeter
Cmax=maximum concentration
g=gram
GRAS=Generally Recognized as Safe
HPLC-UV=high performance liquid chromatography-ultraviolet
hr=hours
JECFA= Joint FAO/WHO Expert Committee on Food Additives
k=terminal rate constant
kg=kilogram
L=liter
LC-DAD-MS=liquid chromatography-diode array detector-mass spectrometry
LD50=lethal dose, 50%
LED=Lowest concentration tested that shows a clearly positive response according
to the
criteria of the specific test
HNED=Highest concentration tested for a study with negative results
mg=milligram
min=minute
ml=milliliter
n=number
NOAEL=No Observed Adverse Effect Level
NOEL=No Observed Effect Level
ng=nanogram
NTP=National Toxicology Program
ppm=parts per million
s=second
t1/2=half life
Tmax=time to maximum

Page - 25

Appendix B: Conflicts of Interest

Authors Bisognano, Brown, Brusick, Renwick, Roberts, and Tarka received
financial support from Cargill for consulting services.

Authors Brown, Brusick, Renwick, Roberts, Tarka, and Wheeler received financial
support form Cargill for manuscript preparation.

Authors Boileau, Curry, and Fosdick are employed by Cargill, Inc.

Authors Carakostas, Clos, DuBois, Prakash, and Wilkensare are employed by The
Coca-Cola Company.
____________________________________________________


Cargill rolling out natural, no-calorie sweetener Truvia [stevia], Martinne
Geller, Reuters.com: Murray 2008.07.10
http://rmforall.blogspot.com/2008_07_01_archive.htm
Thursday, July 10, 2008
http://groups.yahoo.com/group/aspartameNM/message/1549

new stevia products -- Truvia (Cargill), rebiana (Coca-Cola), Stevia Plus
and Sweet Leaf (Wisdom Natural Brands), Zevia (Zevia), also one due from
Pepsi: WebTV: NPICenter.com: Murray 2008.06.07
http://rmforall.blogspot.com/2008_06_01_archive.htm
Saturday, June 7, 2008
http://groups.yahoo.com/group/aspartameNM/message/1542

stevia herbal sweetener to be sold as Truvia (rebiana) by Cargill and
Coca-Cola, if blitz of 12 studies wins FDA approval in 30-90 days:
Murray 2008.05.24
http://rmforall.blogspot.com/2008_05_01_archive.htm
Saturday, May 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1540

533 mostly negative reports on sucralose in 2 1/2 years (many GI symptoms)
Mark J & Cherie Yannone, Phoenix, AZ www.FoodAndDiet.com: GI
stimulation, M Kidd et al, Yale U, AJPGLP 2008.06.12:
Rich Murray 2008.07.29
http://rmforall.blogspot.com/2008_07_01_archive.htm
Tuesday, July 29, 2008
http://groups.yahoo.com/group/aspartameNM/message/1555

formaldehyde, aspartame, and migraines, the first case series, Sharon E
Jacob-Soo, Sarah A. Stechschulte, UCSD, Dermatitis 2008 May: Rich Murray
2008.07.18
http://rmforall.blogspot.com/2008_07_01_archive.htm
Friday, July 18, 2008
http://groups.yahoo.com/group/aspartameNM/message/1553

Overlooked aspartame-induced hypertension, HJ Roberts, Southern Medical J,
2008 Sept.: Murray 2008.09.16
http://rmforall.blogspot.com/2008_09_01_archive.htm
Tuesday, September 16, 2008
http://groups.yahoo.com/group/aspartameNM/message/1556

methanol impurity in alcohol drinks [ and aspartame ] is turned into
neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol Syndrome,
BM Kapur, DC Lehotay, PL Carlen at U. Toronto, Alc Clin Exp Res 2007 Dec.
plain text: detailed biochemistry, CL Nie et al. 2007.07.18: Murray
2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524

details on 6 epidemiological studies since 2004 on diet soda (mainly
aspartame) correlations, as well as 13 other mainstream studies on
aspartame toxicity since summer 2005: Murray 2007.11.14
http://rmforall.blogspot.com/2007_11_01_archive.htm
Wednesday, November 14, 2007
http://groups.yahoo.com/group/aspartameNM/message/1490
____________________________________________________


"Of course, everyone chooses, as a natural priority, to enjoy peace, joy,
and love by helping to find, quickly share, and positively act upon evidence
about healthy and safe food, drink, and environment."

Rich Murray, MA Room For All rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com new primary archive

http://groups.yahoo.com/group/aspartameNM/messages
group with 134 members, 1,559 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1,134 members, 22,941 posts in public archive
____________________________________________________

ALS, amyotrophic lateral sclerosis, 1156 deaths in a million person study
1982-2004, correlates with years of formaldehyde exposure [ aspartame diet soda
sold after fall 1983 ], MG Weisskopf et al, Harvard SPH 2008.04.16: Rich Murray
2008.09.20
http://rmforall.blogspot.com/2008_09_01_archive.htm
Saturday, September 20, 2008
http://groups.yahoo.com/group/aspartameNM/message/1558

http://www.hsph.harvard.edu/faculty/marc-weisskopf/index.html

Marc G. Weisskopf
Mark and Catherine Winkler Assistant Professor of Environmental and Occupational
Epidemiology
Department of Environmental Health
Department of Epidemiology
401 Park Dr., Rm 3-104
Landmark Center, PO Box 15697
Boston, Massachusetts 02215
617.384.8872  mweissko@...

Education
ScB, Neuroscience, Brown University, 1989
PhD, Neuroscience, University of California, San Francisco, 1994
ScD, Epidemiology, Harvard School of Public Health, 2006

http://www.hsph.harvard.edu/faculty/marc-weisskopf/files/AAN_ALS_chem_press_rele\
ase.pdf
EMBARGOED FOR RELEASE UNTIL 2:00 P.M. CT/3:00 P.M. ET, WEDNESDAY, APRIL 16, 2008
Media Contacts:
Angela Babb, (651) 695-2789, ababb@...
Rachel Seroka, (651) 695-2738, rseroka@...
AAN Press Room 179B (April 12–18): (312) 791-7053

http://www.youtube.com/watch?v=h3ISwNRe4Xk&feature=related
4:15 minute video by John Gever, Medscape Today

http://www.4woman.gov/News/English/614428.htm
http://www.healthfinder.gov/news/newsstory.asp?docid=614428
http://www.medicinenet.com/script/main/art.asp?articlekey=88726

"...there are only about 5,500 new cases in the United States each year."

Formaldehyde Linked to Lou Gehrig's Disease
By Randy Dotinga
HealthDay Reporter

WEDNESDAY, April 16, 2008 (HealthDay News) -- New preliminary research suggests
that exposure to the chemical formaldehyde, present in a variety of workplaces,
could greatly increase a person's chances of developing Lou Gehrig's disease.

The findings aren't definitive, and only a few thousand Americans are diagnosed
with the condition  -- also known as amyotrophic lateral sclerosis (ALS) -- each
year.

Still, the study results deserve attention, especially since formaldehyde hasn't
been considered an ALS risk factor before, said study author Marc Weisskopf, an
assistant professor of epidemiology and environmental health at Harvard School
of Public Health. "It's a result that we view as very intriguing and worthy of
follow-up."

The findings were scheduled to be released Wednesday at the American Academy of
Neurology annual meeting, in Chicago.

ALS progressively causes damage to the nerve cells in the brain and spinal cord.
Patients lose the ability to control their muscles, and they typically become
paralyzed. There's no cure for ALS, and treatments have limited value.

Weisskopf and his colleagues examined statistics from an American Cancer Society
study of more than 1 million people who were followed for 15 years.

The researchers first examined the participants' responses in 1982 to questions
about exposure to 12 different chemicals, including formaldehyde. Then they
followed up between 1989 and 2004 to see what happened to those people.

The researchers found that 617 men and 539 women died of ALS during the study
period. Only those who reported exposure to formaldehyde had a higher risk -- 34
percent higher -- of developing ALS.

Formaldehyde is used in the manufacture of a variety of products, including
particle board, clothing, glues, cosmetics and shampoo. People who work in
medical facilities and mortuaries may also encounter it on the job.

The pungent chemical has already been linked to higher rates of lung cancer and
leukemia. It was not declared a probable human carcinogen at high exposure
levels by the Environmental Protection Agency until 1987.

Those who reported more than 10 years of exposure to formaldehyde were almost
four times more likely to develop ALS.

According to Weisskopf, the study design didn't allow him to estimate how many
extra people may develop ALS because they are exposed to formaldehyde. However,
he said there are only about 5,500 new cases in the United States each year.

Researchers have considered pesticides to be a possible cause of ALS, but
formaldehyde hasn't been raised as a villain before, Weisskopf said. It's not
clear how it might be linked to development of the disease, but Weisskopf said
it could set off brain damage by increasing the "stress" caused by oxygen.

It's possible that other factors besides formaldehyde may be causing ALS in the
study participants. Indeed, Weisskopf said the findings don't confirm a
cause-and-effect relationship: "That's very hard to do. But it does provide an
avenue to get more insight into the disease process, and it may give us insight
that's helpful in determining other avenues to take."

Dr. Catherine Lomen-Hoerth, director of the ALS Center at the University of
California, San Francisco, said it's too early for anyone to worry too much
about the findings.

The research "means studies can be done in ALS rats or mice to see if
formaldehyde worsens the disease process," she said, but, "I don't think we
understand environmental factors very well, and in what way they affect disease
processes."

"If we knew more about what causes ALS, we might know more about how
formaldehydes and other chemicals might [play a role]," she added.

SOURCES: Marc Weisskopf, Ph.D., assistant professor, epidemiology and
environmental health, Harvard School of Public Health, Boston; Catherine
Lomen-Hoerth, M.D., Ph.D., director, ALS Center, University of California, San
Francisco; April 16, 2008, presentation, American Academy of Neurology annual
meeting, Chicago

Copyright © 2008 ScoutNews, LLC. All rights reserved.


"Regular formaldehyde exposure increased ALS risk by 34%.
In addition, the longer the self-reported exposure to formaldehyde, the higher
the risk for ALS.
Thus, compared with those reporting no exposure, the adjusted relative risk for
ALS was
1.5 in individuals who reported less than four years of exposure,
2.1 in those with four to 10 years of exposure, and
4.1 in those with more than 10 years of exposure.
Overall, 2.6% of participants reported that they had been exposed to
formaldehyde."

"Nearly 25% of beauticians reported that they were exposed to formaldehyde.
Pharmacists, morticians, radio/lab technicians, dentists, firemen,
photographers, printers, doctors, and nurses also reported high rates of
formaldehyde exposure.
Individuals in these high-exposure jobs had a 28% greater risk for ALS."

"There are several possible mechanisms for formaldehyde neurotoxicity, said Dr.
Weisskopf.
These include hyperexcitability of dorsal horn neurons,
reduced excitability of the isolated phrenic nerve,
prefrontal cortex/hippocampal neurotoxicity,
a decrease in superoxide dismutase activity,
an increase in malondialdehyde,
and toxic tau protein misfolding."

"...other factors that might contribute to ALS were controlled for, including
sex, smoking status, military service, level of education, alcohol intake,
occupation, vitamin E supplement use, and exposure to other chemicals."

http://www.neurologyreviews.com/08june/FormaldehydeALS.html

Neurology Reviews.Com
Vol. 16, No. 6  June 2008

Formaldehyde Exposure May Pose Risk for Amyotrophic Lateral Sclerosis

CHICAGO -- Preliminary results suggest that exposure to the chemical
formaldehyde may increase the risk for amyotrophic lateral sclerosis (ALS),
according to a report at the 60th Annual Meeting of the American Academy of
Neurology. Researchers found that people with more than 10 years of exposure to
formaldehyde had a 4.1 times increased risk for ALS, compared with those who had
no exposure.

“While pesticides have been thought to contribute to the development of ALS,
this is the first time that formaldehyde has been identified as a potential risk
factor,� commented Marc Weisskopf, PhD, Assistant Professor of Environmental
and Occupational Epidemiology at Harvard School of Public Health in Boston.

Formaldehyde is used in particleboard and other wood products, permanent press
fabrics, glues, photography chemicals, and other household products, such as
cosmetics and shampoo. It is also used as a tissue preservative in medical
laboratories and mortuaries and as an industrial disinfectant. About 20 years
ago, the US Environmental Protection Agency designated high levels of
formaldehyde as a probable carcinogen.

EXPOSURE TO CHEMICALS AND RISK FOR ALS

Prior research has suggested that environmental toxins, including pesticides,
may be associated with ALS. This notion has been backed by case-control and
genetic studies implicating genes involved in pesticide detoxification, said Dr.
Weisskopf. However, the findings have been contradictory, and there have been no
large prospective studies to support this hypothesis.

In the present investigation, Dr. Weisskopf’s group prospectively examined the
relationship between regular exposure to 12 types of chemicals and ALS in
987,229 individuals who participated in the American Cancer Society-sponsored
Cancer Prevention Study II. Participants were asked about their exposure to
chemicals, including formaldehyde, in 1982, and they were then followed for
approximately 15 years. The researchers also analyzed exposure to asbestos,
acids/solvents, coal or stone dust, coal tar pitch/asphalt, diesel engine
exhaust, dyes, gasoline exhaust, pesticides/herbicides, textile fibers/dust,
wood dust, and x-ray/radioactive material.

Overall, 617 men and 539 women died from ALS during the follow-up period.
Regular formaldehyde exposure increased ALS risk by 34%.
In addition, the longer the self-reported exposure to formaldehyde, the higher
the risk for ALS.
Thus, compared with those reporting no exposure, the adjusted relative risk for
ALS was
1.5 in individuals who reported less than four years of exposure,
2.1 in those with four to 10 years of exposure, and
4.1 in those with more than 10 years of exposure.
Overall, 2.6% of participants reported that they had been exposed to
formaldehyde.
By contrast, there was limited evidence for an association between ALS and
pesticides/herbicides.

The study also found that an increased risk for ALS was seen with certain jobs.
Nearly 25% of beauticians reported that they were exposed to formaldehyde.
Pharmacists, morticians, radio/lab technicians, dentists, firemen,
photographers, printers, doctors, and nurses also reported high rates of
formaldehyde exposure. Individuals in these high-exposure jobs had a 28% greater
risk for ALS.

There are several possible mechanisms for formaldehyde neurotoxicity, said Dr.
Weisskopf.
These include hyperexcitability of dorsal horn neurons,
reduced excitability of the isolated phrenic nerve,
prefrontal cortex/hippocampal neurotoxicity,
a decrease in superoxide dismutase activity,
an increase in malondialdehyde,
and toxic tau protein misfolding

A CAUSAL RELATIONSHIP FOR ALS AND FORMALDEHYDE?

Dr. Weisskopf noted that the longitudinal design of the study minimizes the
possibility that the results are due to bias. Additional strengths of the study
include its large size and uniform case ascertainment, as well as the fact that
other factors that might contribute to ALS were controlled for, including sex,
smoking status, military service, level of education, alcohol intake,
occupation, vitamin E supplement use, and exposure to other chemicals.

Possible limitations of the study include small numbers in some exposure
categories, as well as self-assessment of exposure. In addition, only mortality
data were used to identify ALS cases. Dr. Weisskopf noted, however, that because
death certificates have been reported to accurately identify 70% to 80% of
ALS-related deaths, they might be a reasonable surrogate for ALS incidence, due
to the short survival time associated with the disease.

Dr. Weisskopf emphasized that the findings are preliminary and do not establish
a causal relationship between formaldehyde and ALS. “At the moment, it is
premature to make broad public health recommendations, and corroboration of the
data is needed,� he concluded.

NR  -- Jill Stein

Suggested Reading

Morahan JM, Pamphlett R. Amyotrophic lateral sclerosis and exposure to
environmental toxins: an Australian case-control study. Neuroepidemiology.
2006;27(3):130-135.

Morahan JM, Yu B, Trent RJ, Pamphlett R. A gene-environment study of the
paraoxonase 1 gene and pesticides in amyotrophic lateral sclerosis.
Neurotoxicology. 2007;28(3):532-540.

Neuroepidemiology. 2006; 27(3): 130-5. Epub 2006 Aug 1.
Amyotrophic lateral sclerosis and exposure to environmental toxins: an
Australian case-control study.
Morahan JM, Pamphlett R.
Department of Pathology, University of Sydney, Sydney, Australia.

It has been suggested that environmental toxins could be risk factors for
sporadic amyotrophic lateral sclerosis (SALS).
We therefore analysed epidemiological data on 179 SALS cases and 179 age-,
ethnicity- and sex-matched controls in Australia using self-reporting
questionnaires. SALS was associated with solvent/chemical exposure (OR = 1.92,
95% CI: 1.26-2.93),
overall herbicide/pesticide exposure (OR = 1.57, 95% CI: 1.03-2.41) and
industrial herbicide/pesticide exposure (OR = 5.58, 95% CI: 2.07-15.06).
Exposure to herbicides/pesticides showed a dose-response effect.
All positive findings were more statistically significant in males.
These findings support those from northern hemisphere studies, indicating that
environmental toxins can be risk factors for SALS.
Copyright (c) 2006 S. Karger AG, Basel.  PMID: 16946624

http://www.usyd.edu.au/research/opportunities/supervisors/128

Dr Morahan, Julia
position:  Postdoctoral Research Fellow
department:  Discipline of Pathology, School of Medical Sciences
phone:  +61 2 9036 7233 fax:  +61 2 9351 3429
email:  morahanj@...
location:  Level 5, Room 502a
address:  D06 - Blackburn
The University of Sydney
NSW 2006 Australia

Associate Professor Pamphlett, Roger
position:  Associate Professor
department: Discipline of Pathology, School of Medical Sciences
phone:  +61 2 9351 3318  fax:  +61 2 9351 3429
email:  rogerp@...
location:  Room 502A
address:  D06 - Blackburn
The University of Sydney
NSW 2006 Australia

About Associate Professor Roger Pamphlett

To find a genetic cause for motor neuron disease that will enable gene therapy
to halt this devastating condition.

Roger Pamphlett is a neurologist and neuropathologist who works with a team of
molecular geneticists in trying to find a genetic cause for motor neuron
disease.

Prof Pamphlett’s research in the pathogenesis of ALS started by examining the
role of environmental agents. He published 20 papers on the relationship between
heavy metals and ALS, using both human tissue and animal models. This body of
work showed that heavy metals enter motor neurons selectively, but that the
metals by themselves are unlikely to cause ALS. This raised the possibility that
genetic susceptibility to these environmental toxins may underlie ALS.

To look for genetic susceptibilities to ALS he has set up the Australian MND DNA
Bank. He travels to all Australian mainland states collecting blood samples from
people with ALS as well as controls. This Bank, supported by an NHMRC Enabling
Grant, now contains over 1,400 DNA samples. Participants fill in detailed
questionnaires to allow gene-environment studies to be undertaken. Using DNA
from this Bank it has been shown that polymorphisms in the poliovirus receptor
are more common in some forms of MND, and a variety of other genes that protect
against toxins and viruses are under investigation.

Prof Pamphlett is now interested in novel genetic mechanisms that could underlie
sporadic ALS, such as mutations that affect CNS cells predominantly (somatic
mutations). To examine these possibilities he recruits ALS patients in NSW to
donate their brains and spinal cords after they die to a Tissue Bank, and
collaborates with other Banks in Australia and the UK to obtain further tissue
samples.


Epidemiology. 2008 Mar; 19(2): 324-37.
Diet and amyotrophic lateral sclerosis.
Morozova N,
Weisskopf MG,
McCullough ML,
Munger KL,
Calle EE,
Thun MJ,
Ascherio A.
Natalia Morozova; Marc G. Weisskopf; Marjorie L. McCullough; Kassandra L.
Munger; Eugenia E. Calle; Michael J. Thun; Alberto Ascherio
Departments of *Nutrition, Harvard School of Public Health, Boston, MA 02215,
USA. nmorozov@...;
mweissko@...; marji.mccullough@...;
hpklg@...; aascheri@...; kgorham@...;
mthun@...; jcalle@...; ethacker@...;

BACKGROUND:
Several dietary factors have been associated with risk of amyotrophic lateral
sclerosis (ALS) in case-control studies, but no prospective studies have
investigated diet and ALS.
METHODS:
We prospectively assessed the association of selected foods and beverages with
ALS mortality among participants of the Cancer Prevention Study II, a cohort of
over 1 million men and women enrolled in 1982.
Habitual diet was assessed with a 44-item food frequency questionnaire.
Participant follow-up was conducted from 1989 through 2002 for ALS mortality.
RESULTS:
During the follow-up period, 862 cohort participants died of ALS.
The strongest finding was an inverse association between chicken consumption and
risk of ALS (P for trend = 0.0006).
We also observed an increased risk of ALS among study participants with a high
consumption of brown rice/whole wheat/barley (P for trend = 0.006)
and decaffeinated coffee (P for trend = 0.01),
and a decreased risk of ALS for high consumption of tea (P for trend = 0.02)
and French fries (P for trend = 0.02);
however, none of these latter associations remained significant after adjusting
for multiple comparisons.
CONCLUSIONS:
Overall, these results do not provide convincing evidence that the investigated
food items are related to ALS mortality.
The association observed between chicken consumption and ALS mortality should be
assessed in other studies.
PMID: 18300717


tobacco, alcohol drinks, and aspartame all expose people to methanol,
formaldehyde, and formic acid: Rich Murray 2008.09.20

formaldehyde, aspartame, and migraines, the first case series, Sharon E
Jacob-Soo, Sarah A Stechschulte, UCSD, Dermatitis 2008 May: Rich Murray
2008.07.18
http://rmforall.blogspot.com/2008_07_01_archive.htm
Friday, July 18, 2008
http://groups.yahoo.com/group/aspartameNM/message/1553
___________________________________________________


Dermatitis. 2008 May-Jun; 19(3): E10-1.
Formaldehyde, aspartame, and migraines: a possible connection.
Jacob SE, Stechschulte S.
Department of Dermatology and Cutaneous Surgery, University of Miami,
Miami, FL, USA.

Aspartame is a widely used artificial sweetener that has been linked
to pediatric and adolescent migraines.

Upon ingestion, aspartame is broken, converted, and oxidized into
formaldehyde in various tissues.

We present the first case series of aspartame-associated migraines
related to clinically relevant positive reactions to formaldehyde on
patch testing.  PMID: 18627677


formaldehyde from many sources, including aspartame, is major cause of
Allergic Contact Dermatitis, SE Jacob, T Steele, G Rodriguez, Skin and
Aging 2005 Dec.: Murray 2008.03.27
http://rmforall.blogspot.com/2008_03_01_archive.htm
Thursday, March 27, 2008
http://groups.yahoo.com/group/aspartameNM/message/1533

"For example, diet soda and yogurt containing aspartame (Nutrasweet),
release formaldehyde in their natural biological degradation.

One of aspartame's metabolites, aspartic acid methyl ester, is
converted to methanol in the body, which is oxidized to formaldehyde
in all organs, including the liver and eyes. 22

Patients with a contact dermatitis to formaldehyde have been seen to
improve once aspartame is avoided. 22

Notably, the case that Hill and Belsito reported had a 6-month history
of eyelid dermatitis that subsided after 1 week of avoiding diet soda.
22"


Avoiding formaldehyde allergic reactions in children, aspartame,
vitamins, shampoo, conditioners, hair gel, baby wipes, Sharon E Jacob,
MD, Tace Steele, U. Miami, Pediatric Annals 2007 Jan.: eyelid contact
dermatitis, AM Hill, DV Belsito, 2003 Nov.: Murray 2008.03.27
http://rmforall.blogspot.com/2008_03_01_archive.htm
Thursday, March 27, 2008
http://groups.yahoo.com/group/aspartameNM/message/1532

Sharon E. Jacob, MD, Assistant Professor of Medicine (Dermatology)
University of California, San Diego 200 W. Arbor Drive #8420, San
Diego, CA 92103-8420
Tel: 858-552-8585 ×3504 Fax: 305-675-8317  sjacob@...;


Dermatitis. 2008 Jan-Feb;19(1):9-15.
Systemic contact dermatitis.
Jacob SE, Zapolanski T.  tamar.zapolanski@...;
Department of Dermatology and Cutaneous Surgery, University of Miami,
Miami, FL, USA.

Systemic exposure to allergens resulting in a cutaneous eruption is
known as systemic contact dermatitis (SCD).

Once sensitization occurs, varying exposures to antigens via multiple
routes (including transepidermal routes, intravenous or intramuscular
routes, inhalation, and ingestion) can result in systemic flare.

This article highlights the different categories of common
contactants, metals, medications, and plants, exposure to which leads
to SCD.

A comprehensive approach that takes into account all possible routes
of exposure is essential in diagnosing SCD and in helping patients
successfully avoid their allergens.   PMID: 18346390


"We present a case of a medical student who presented with
erythematous eczematoid plaques on her trunk and legs and fine
vesiculation of her scalp, 3 weeks after starting anatomy class.

Of note, she routinely washed her face and arms after leaving the
anatomy lab, but remained in her scrubs for the rest of the day.

Formaldehyde and Quaternium-15 positive reactions in the same patient.
[ photo ]"

"Our patient underscores the importance of appropriate patch testing
and education.

Once we identified the allergy to formaldehyde and quaternium-15, we
provided patient education materials regarding the common and not-so-
common locations of these chemicals and cross-reactors.

We also gave the patient information on avoidance and safe
alternatives (see Table 5).

Fortunately, with technical advances, this student completed the
anatomy section via electronic learning tools.

By avoiding formaldehyde, including anatomy lab, FRP in her shampoo
and cosmetics, and aspartame in her diet, this patient dramatically
improved.

As with all contact dermatitides, the mainstay of treatment for
allergic contact dermatitis is avoidance."

http://www.skinandaging.com/article/5158  Skin & Aging Journal
ISSN: 1096-0120 - Volume 13 - Issue 12_2005 -
December 2005 - Pages: 22 - 27

Allergen Focus:
Focus on T.R.U.E. Test Allergens #21, 13 and 18:
Formaldehyde and Formaldehyde-Releasing Preservatives
-- By Sharon E. Jacob, M.D., Tace Steele, B.A., [now MD] and Georgette
Rodriguez, M.D., M.P.H.


http://www.eczemacenter.org/eczema_center/meetfacultystaff.htm
[ photo ]

The Eczema Center
Rady Children's Hospital of San Diego
8010 Frost Street, Suite 602, San Diego, CA 92123
or call... (858) 966-6774

Sharon E. Jacob , MD
Dr. Sharon E. Jacob is Assistant Clinical Professor of Pediatrics and
Medicine (Dermatology) at the University of California, School of
Medicine and Rady Children's Hospital.
She earned her medical degree from the Temple University, and
completed dermatology training at the University of Miami and advanced
contact dermatitis training at New York University (NYU).
She has been board certified in dermatology.

Dr. Jacob's clinical interests include atopic and contact dermatitis
and education.
She is considered a national expert on chemical sensitivities in the
skin and has published more than 45 journal articles, book chapters
and abstracts on this topic.
In 2005, Dr Jacob was the first to present contact dermatitis data on
U.S. pediatric patients to the American Contact Dermatitis Society
(ACDS).

She has received an excellence in teaching award from the University
of Miami Dermatology and the Clinical Research Award from the ACDS.
She is an active reviewer for the following medical publications
including Journal of the American Academy of Dermatology, Pediatric
Dermatology, Dermatitis, and the Archives of Dermatology.
Dr. Jacob also serves on the medical board of the Inflammatory Skin
Disease Institute and the Skin and Aging Journal.

Dr. Jacob enjoys taking care of children and their families and is an
advocate for children's dermatologic health.


http://www.eczemacenter.org/eczema_center/index.htm

Atopic dermatitis (AD) -- better known as eczema -- is the most common
chronic skin disorder seen in infants and children.
In fact, the prevalence of this condition has risen dramatically
during the last three decades.
Currently, 15% to 20% of children in the United States are expected to
experience this condition sometime during their lifetime, compared to
7% around 1960.

The negative impact of eczema is profound and insidious.
It affects both the patient who suffers from it and that patient's
family members, and it does so on two important levels -- physical and
emotional.

Physical:

Inflamed, itchy rashes can involve any and all of the skin surfaces
and are frequently complicated by skin breakdown and bacterial, viral,
and fungal infections.

It is linked to the development of life-long allergic conditions,
including asthma, food allergies, and rhinitis.

Any level of AD is extremely uncomfortable and, at times, painful.
Individuals with moderate to severe disease report that eczema hugely
disturbs their sleep and impacts performance of daily activities,
including adverse effects on school, sports activities, work, and peer
relationships.

In studies, individuals with eczema reported more negative impact on
quality of life than those with insulin-dependent diabetes!

Emotional:

Patients and their families experience considerable emotional
distress, anxiety, and embarrassment because of people's response to
this illness.

In fact, the emotional scarring on both patient and family members may
outlast eczema's physical effects.

Parents especially suffer because it is difficult for children
experiencing this condition to understand that their parents cannot
make the torment go away.
The stress of caring for these children is even greater than parents
caring for a child with insulin-dependent diabetes.

Patients experience considerable discrimination and social isolation
because of this illness.
People often stare, shiver with disgust or step back in fear from
those who have this condition.
The end result for patients: A life-time of struggle with their sense
of worth and self esteem.


http://aad2008.omnibooksonline.com/data/papers/CRS-113-F.pdf  lecture
with photos
___________________________________________________


similar levels of daily formaldehyde and formic acid, causes of birth
defects, come from cigarettes, aspartame, and dark wines and liquors
-- folic acid protects most people: Rich Murray 2008.07.15
http://rmforall.blogspot.com/2008_07_01_archive.htm
Tuesday, July 15, 2008
http://groups.yahoo.com/group/aspartameNM/message/1552


http://www.divine.ca/en/health-and-wellness/articles/c_16_i_3295/5-reasons-to-qu\
it-smoking-1.html

"A smoker who goes through one pack a day will smoke 7,300 cigarettes
a year, inhaling the equivalent of nearly 1 gram of formaldehyde
(yikes!)."

That's about 2.5 mg daily formaldehyde intake for 20 cigarettes, over
the 2 mg USA FDA alarm level for formaldehyde in average 2 liters
daily drinking water, while a single 12 oz can of diet soda also
results in about 2 mg formaldehyde toxic products in the body,
including formic acid, a notorious cause of birth defects.

Dark wines and liquors usually supply even more methanol, which the
body always turns into formaldehyde and formic acid -- the major cause
of "morning after" hangovers.

High levels of folic acid, a safe, affordable vitamin in fruits and
vegetables, largely prevents formaldehyde and formic acid toxicity in
most people.

It is certain that high levels of aspartame use, above 2 liters daily
for months and years, must lead to chronic formaldehyde-formic acid
toxicity.

Fully 11 % of aspartame is methanol -- 1,120 mg aspartame in 2 liters
diet soda, almost six 12-oz cans, gives 123 mg methanol (wood
alcohol). The methanol is immediately released into the body after
drinking .
Within hours, the liver turns much of the methanol into formaldehyde,
and then much of that into formic acid, both of which in time are
partially eliminated as carbon dioxide and water.

However, about 30 % of the methanol remains in the body as cumulative
durable toxic metabolites of formaldehyde and formic acid -- 37 mg
daily, a gram every month, accumulating in and affecting every tissue.

If only 10 % of the methanol is retained daily as formaldehyde, that
would give 12 mg daily formaldehyde accumulation -- about 60 times
more than the 0.2 mg from 10 % retention of the 2 mg EPA daily limit
for formaldehyde in drinking water.

Bear in mind that the EPA limit for formaldehyde in drinking water is
1 ppm, or 2 mg daily for a typical daily consumption of 2 liters of
water.


formaldehyde and formic acid in FEMA trailers and other sources
(aspartame, dark wines and liquors, tobacco smoke): Murray 2008.01.30
http://rmforall.blogspot.com/2008_01_01_archive.htm
Wednesday, January 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1508

The FEMA trailers give about the same amount of formaldehyde and
formic acid daily as from a quart of dark wine or liquor, or two
quarts (6 12-oz cans) of aspartame diet soda, from their over 1 tenth
gram methanol impurity (one part in 10,000), which the body quickly
makes into formaldehyde and then formic acid -- enough to be the major
cause of "morning after" alcohol hangovers.

Methanol and formaldehyde and formic acid also result from many fruits
and vegetables, tobacco and wood smoke, heater and vehicle exhaust,
household chemicals and cleaners, cosmetics, and new cars, drapes,
carpets, furniture, particleboard, mobile homes, buildings, leather...
so all these sources add up and interact with many other toxic
chemicals.

methanol impurity in alcohol drinks [ and aspartame ] is turned into
neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol
Syndrome, BM Kapur, DC Lehotay, PL Carlen at U. Toronto, Alc Clin Exp
Res 2007 Dec. plain text: detailed biochemistry, CL Nie et al.
2007.07.18: Murray 2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524


opportunities re BA Magnuson, GA Burdock et al., Aspartame Safety
Evaluation 2007 Sept., Critical Reviews in Toxicology:
Rich Murray 2008.07.11
http://rmforall.blogspot.com/2008_07_01_archive.htm
Friday, July 11, 2008
http://groups.yahoo.com/group/aspartameNM/message/1550
___________________________________________________


"Of course, everyone chooses, as a natural priority, to enjoy peace,
joy, and love by helping to find, quickly share, and positively act
upon evidence about healthy and safe food, drink, and environment."

Rich Murray, MA Room For All rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com  new primary archive

http://groups.yahoo.com/group/aspartameNM/messages
group with 134 members, 1,558 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1,134 members, 22,940 posts in a public archive
___________________________________________________

FDA approval of stevia (Rebaudioside A) expected by Nov 13, from PureCircle
for $ billion world market: Coca-Cola (Truvia), PepsiCo (PureVia), Cargill,
Merisant, NutraSweet, J.W. Childs Associates: Murray 2008.09.19
http://rmforall.blogspot.com/2008_09_01_archive.htm
Friday, September 19, 2008
http://groups.yahoo.com/group/aspartameNM/message/1557

"The sweetener is already approved in several countries such as China,
Japan, the former Soviet Union and South America and only in the last few
weeks received approval in Australia and Switzerland."

http://www.guardian.co.uk/business/feedarticle/7805653

PureCircle sees U.S. sweetener approval in 2 months

Reuters, Wednesday September 17 2008, by David Jones

LONDON, Sept 17 (Reuters) -- Malaysia-based sweetener group PureCircle
expects U.S. approval for its natural no-calorie sweetener Reb-A within two
months which will prompt Coca-Cola and PepsiCo to launch it in their drinks
within days.

The London AIM-listed group expects the U.S. Food and Drug Administration
(FDA) to approve the sweetener as Generally Recognised as Safe (GRAS) which
will allow the natural sweetener to be launched across the U.S. food and
beverage industry.

"We expect an FDA no-objection letter within two months. We don't foresee
any problems. Coke and PepsiCo are ready to launch products with Reb-A as
soon as possible," PureCircle's Russian managing director Magomet Malsagov
said in an interview.

Approval will allow the group to break into the lucrative U.S. market for
high intensity sweeteners which accounts for 60 percent of the global $1.3
billion market for sugar substitutes such as NutraSweet, Sweet'N Low and
Splenda.

The soft drinks industry dominated by Coca-Cola Co and PepsiCo Inc will be
key for PureCircle, and PepsiCo said it will launch a new line of its SoBe
Life drink with Reb-A, under the brand name PureVia, in Latin America where
the sweetener is already cleared for use.

Rebaudioside A (Reb-A) is made from certain compounds in the leaves of
stevia, a shrub native to Paraguay, and PureCircle is the world's largest
producer and distributor of what it says is the world's first natural high
intensity sweetener with 400 times the sweetness of sugar.

Reb-A is likely to compete with established artificial sweeteners such as
saccharin, aspartame and sucralose, which are sold under brand names Sweet'N
Low, NutraSweet and Splenda.

Sweet'N Low is made by New York-based family-owned Cumberland Packing Corp
while NutraSweet Co is owned by Boston-based private equity firm J.W. Childs
Associates.

Tate & Lyle makes the sucralose sweetener Splenda which accounts for around
one fifth of its group profits.

Chicago-based Merisant also makes aspartame products such as Equal and
Canderel.

PureCircle shares were first listed on London's junior stock market, the
Alternative Investment Market (AIM), in December 2007 at 170 pence with a
free float of over 30 percent. The shares close on Wednesday off 2 percent
at 218p.

Malsagov says Reb-A could make inroads if consumers turn to natural
alternative sweeteners with zero calories for a healthier diet, while the
product has the advantage of being heat and pH stable for the food and
drinks industry.

He says the group controls around 80 percent of the world crop of stevia,
largely grown in Chinese plantations, but is expanding in countries such as
Kenya, Uganda and Paraguay. It has an extraction plant in China and a
refinery in Malaysia.

The sweetener is already approved in several countries such as China, Japan,
the former Soviet Union and South America and only in the last few weeks
received approval in Australia and Switzerland.

Malsagov believes after FDA approval, it will take the European Union some
6-12 months to approve the product.

End-user groups such as Merisant and Cargill made the applications to the
FDA in May, and should receive answers within 180 days, meaning Merisant
should hear by Nov 13 and Cargill by Nov 28, Malsagov said.

Merisant is set to launch its PureVia Reb-A product after FDA approval,
while Cargill has already launched its Truvia Reb-A product.

Currently, aspartame holds 44 percent of the artificial high intensity
global sweetener market with sucralose on 26 percent and saccharin 11
percent, says PureCircle. (Editing by Mike Elliott)

http://www.purecircle.com/showArticle.aspx?ID=0&targetName=latestNews

PureCircle             +60 3 2093 9333
Magomet Malsagov, Managing Director
William Mitchell, Group Finance Director

College Hill             +44 20 7457 2020
Mark Garraway
Robert Pugsley

RFC Corporate Finance (Nomad)             +61 8 9480 2500
Stephen Allen

For more information about PureViaT tabletop sweetener and food and
beverages containing PureViaT visit www.purevia.com .

About Whole Earth Sweetener Company
Whole Earth Sweetener Company is committed to providing natural alternatives
to sugar and to helping people eat better and live healthier, more
fulfilling lives. The company actively supports and is involved in simple
and sustainable farming - the best method for promoting agriculture and
protecting the environment and farm workers. Formed in 2006, Whole Earth
Sweetener Company launched its first sweetener brand, Sweet Simplicity®, in
2007, and the company continues to develop a vertically integrated business
that will bring products that are perfectly sweet and perfectly natural from
the farm to consumers. Whole Earth Sweetener Company is a wholly owned
subsidiary of Merisant Company, the maker of Equal® and Canderel® and a
global leader in the manufacture, marketing and distribution of tabletop
sweeteners with sales in over 90 countries.
For more information, visit www.WholeEarthSweetener.com  31 July 2008

http://www.purecircle.com/

Unit 19-03-02, 3rd Floor, PNB Damansara
No.19, Lorong Dungun, Damansara Heights
50490 Kuala Lumpur, Malaysia
T +603  2093 9333  F +603  2093 7333  E  info@...
____________________________________________________


Cargill rolling out natural, no-calorie sweetener Truvia [stevia], Martinne
Geller, Reuters.com: Murray 2008.07.10
http://rmforall.blogspot.com/2008_07_01_archive.htm
Thursday, July 10, 2008
http://groups.yahoo.com/group/aspartameNM/message/1549

new stevia products -- Truvia (Cargill), rebiana (Coca-Cola), Stevia Plus
and Sweet Leaf (Wisdom Natural Brands), Zevia (Zevia), also one due from
Pepsi: WebTV: NPICenter.com: Murray 2008.06.07
http://rmforall.blogspot.com/2008_06_01_archive.htm
Saturday, June 7, 2008
http://groups.yahoo.com/group/aspartameNM/message/1542

stevia herbal sweetener to be sold as Truvia (rebiana) by Cargill and
Coca-Cola,
if blitz of 12 studies wins FDA approval in 30-90 days: Murray 2008.05.24
http://rmforall.blogspot.com/2008_05_01_archive.htm
Saturday, May 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1540

533 mostly negative reports on sucralose in 2 1/2 years (many GI symptoms)
Mark
J & Cherie Yannone, Phoenix, AZ www.FoodAndDiet.com: GI stimulation, M Kidd
et
al, Yale U, AJPGLP 2008.06.12: Rich Murray 2008.07.29
http://rmforall.blogspot.com/2008_07_01_archive.htm
Tuesday, July 29, 2008
http://groups.yahoo.com/group/aspartameNM/message/1555

formaldehyde, aspartame, and migraines, the first case series, Sharon E
Jacob-Soo, Sarah A. Stechschulte, UCSD, Dermatitis 2008 May: Rich Murray
2008.07.18
http://rmforall.blogspot.com/2008_07_01_archive.htm
Friday, July 18, 2008
http://groups.yahoo.com/group/aspartameNM/message/1553

Overlooked aspartame-induced hypertension, HJ Roberts, Southern Medical J,
2008
Sept.: Murray 2008.09.16
http://rmforall.blogspot.com/2008_09_01_archive.htm
Tuesday, September 16, 2008
http://groups.yahoo.com/group/aspartameNM/message/1556

methanol impurity in alcohol drinks [ and aspartame ] is turned into
neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol Syndrome,
BM Kapur, DC Lehotay, PL Carlen at U. Toronto, Alc Clin Exp Res 2007 Dec.
plain text: detailed biochemistry, CL Nie et al. 2007.07.18: Murray
2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524

details on 6 epidemiological studies since 2004 on diet soda (mainly
aspartame) correlations, as well as 13 other mainstream studies on
aspartame toxicity since summer 2005: Murray 2007.11.14
http://rmforall.blogspot.com/2007_11_01_archive.htm
Wednesday, November 14, 2007
http://groups.yahoo.com/group/aspartameNM/message/1490
____________________________________________________


"Of course, everyone chooses, as a natural priority, to enjoy peace, joy,
and love by helping to find, quickly share, and positively act upon evidence
about healthy and safe food, drink, and environment."

Rich Murray, MA Room For All rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com new primary archive

http://groups.yahoo.com/group/aspartameNM/messages
group with 134 members, 1,557 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1,133 members, 22,938 posts in public archive
____________________________________________________

Overlooked aspartame-induced hypertension, HJ Roberts, Southern Medical J, 2008
Sept.: Murray 2008.09.16
http://rmforall.blogspot.com/2008_09_01_archive.htm
Tuesday, September 16, 2008
http://groups.yahoo.com/group/aspartameNM/message/1556

South Med J. 2008 Sep; 101(9):969.
Overlooked aspartame-induced hypertension.
Roberts HJ.
PMID: 18708962

Overlooked Aspartame-Induced Hypertension

To the Editor:  As a constructive comment on the excellent article by
Trewet, C. L. and Ernst, 1 on "resistant hypertension", allow me to
mention an important factor contributing to hypertension that
continues to be overlooked:  "diet" products containing aspartame
which are being consumed by an estimated two-thirds of the population.

I reported earlier on hypertension in 64 aspartame reactors who were
not known to have had an elevated blood pressure prior to using this
chemical. 2

Its severity was impressive -- e.g., a registered nurse
with readings as high as 280/160.

The blood pressure in another nurse rose to 240/150.

Several patients were studies to rule out pheochromocytoma.

The causative role of aspartame products was indicted by
1) the striking improvement or normalization of blood pressure
after stopping aspartame, and
2) the prompt recurrence of hypertension following aspartame resumption.

The association of hypertension with the consumption of cola
beverages (Diet Coke (TM)) has been confirmed by
Winkelmayer et al in a large prospective study of female nurses --
but NOT with caffeine consumption.  They speculated that
"perhaps some other compound contained in soda-type soft drinks ....
may be responsible for the increased risk of hypertension."

I have reviewed the likely pharmacologic basis, especially the
conversion of phenylalanine (comprising half of the aspartame
molecule) to dopamine, epinephrine, and norepinephrine ... all
pressor substances. 2

Other aspartame reactors have evidenced peripheral vasomotor
features (including the Raynaud phenomenon, 2
and probable pulmonary hypertension. 4

At the very least, persons with hypertension that resist
conventional therapy ought to avoid aspartame products.

H. J. Roberts, MD, FACP, FCCP
Palm Beach Institute for Medical Research, Inc.
West Palm Beach, Florida

References

1. Trewet CL, Ernest ME.
Resistant hypertension; identifying causes and optimizing treatment regimens.
South Med J 2008; 101: 166-173.

2.  Robert HJ.
Aspartame Disease:  An Ignored Epidemic
West Palm Beach, Sunshine Sentinel Press, 2001.

3.  Winkelmayer WC, Stampfer MJ, Willett WC, et al.
Habitual caffeine intake and the risk of hypertension in women.
JAMA 2005; 294:  2330-2335.

4.  Roberts HJ.
Aspartame induced dyspnea and pulmonary hypertension.
Townsend Letter for Doctors and Patients 2003: 54-55.
____________________________________________________


Aspartame Induced Arrhythmias and Sudden Death, HJ Roberts 2004: Murray
2008.06.26
http://rmforall.blogspot.com/2008_06_01_archive.htm
Thursday, June 26, 2008
http://groups.yahoo.com/group/aspartameNM/message/1544

Aspartame Induced Arrhythmias and Sudden Death

By H. J. Roberts, M.D., F.A.C.P., F.C.C.P.
E-Mail:   HJrobertsmd@...
(c)2004 by H. J. Roberts, M.D.

A recent extensive review of sudden death in young athletes (1)
made no mention of aspartame as a primary cause or suspected
contributory factor, especially when demonstrable pathology was
absent.

This issue has assumed great public health importance because
"diet" products containing this chemical are being consumed by
over two-thirds of the population -- especially weight-conscious
persons.

I have repeatedly reported the serious cardiovascular,
'neuropsychiatric, metabolic and other adverse effects of
aspartame products. (2-4)

Among the first 1200 aspartame reactors in my data base,
193 (16%) had symptomatic arrhythmia,
85 (7%) atypical chest pain, and
64 (5%) recent or aggravated hypertension.

One hypertensive patient developed complete heart block within
hours after consuming his first diet cola.

Another had undergone unsuccessful radio frequency ablations in the
heart before awareness of having aspartame disease.

Pheochromocytoma was suspected in several aspartame reactors.

The issue of sudden death related to aspartame and its breakdown
products has been raised a number of times, particularly among
previously well individuals using such products... including pilots
and drivers, (3,4,6) and athletes.

I have detailed the release of norepinephrine, epinephrine, dopamine
and free methanol by aspartame; a host of pertinent-related
pathophysiologic conditions,
(e.g., cumulative formaldehyde adducts derived from aspartame in
tissue proteins and nucleic acids; excessive insulin release);
direct oropharyngeal absorption from gum, breath fresheners and
other products; and the increasing problem of aspartame addiction.
(4-7)

The likelihood of pulmonary hypertension induced by the
vasoconstrictive effects of aspartame products also has been
considered. (5)

It is relevant that unexplained dyspnea was experienced by 110
aspartame reactors, usually with prompt improvement after
abstinence.

Moreover, primary pulmonary hypertension was found at autopsy
in a 27 year old female aspartame reactor.

The lack of familiarity of most physicians and medical examiners
with the foregoing considerations can have serious legal
consequences.

A case in point is that of a young woman (also a Sunday School
teacher) who has been sentenced to serve 50 years in a Virginia
prison for allegedly poisoning her husband with methyl alcohol.
[ Diane and Charles Fleming ]

Elevated methanol blood concentrations were found postmortem in
this body builder/basketball player who drank ten diet drinks and
other aspartame products daily.

She remains incarcerated despite affidavits indicating that 10% of
aspartame becomes free methyl alcohol after consumption.

The need for clinicians and corporate-neutral investigators to
evaluate the contributory role of aspartame in cardiopulmonary
disorders and sudden death, and drug interactions with aspartame,
is underscored by the frequency of persons dying unexpectedly
being categorized as "death due to causes yet to be determined."

One interested resident of Orange county (California) found 192
persons listed in this category between July 11 and November 15,
2003 according to the Orange county Register.

References:

Maron BJ,
Sudden death in young athletes,
N Engl J Med 2003; 349: 1064-1075.

Roberts HJ,
Reactions to aspartame containing products: 551 cases,
J Appl Nutr l988; 40: 86-94.

Roberts HJ, Aspartame (NutraSweet): Is It Safe?
Philadelphia, The Charles Press, 1989.

Roberts HJ,
Aspartame Disease: An Ignored Epidemic.
West Palm Beach, Sunshine Sentinel Press, 2001.

Roberts HJ,
Aspartame-induced dyspnea and pulmonary hypertension,
Townsend Letter for Doctors & Patients 2003; 237 (January): 64-65.

Roberts HJ,
Ignored Health Hazards for Pilots and Drivers.
West Palm Beach, Sunshine Sentinel Press, 1998.

Roberts HJ, Aspartame (NutraSweet) addiction,
Townsend Letter for Doctors & Patients, 2000; 198 (January): 52-57.

H. J. Roberts, MD, FACP, FCCP
Palm Beach Institute for Medical Research
P. O. Box 17799
West Palm Beach, Florida 33416 USA
____________________________________________________


http://www.dorway.com/tldaddic.html 5-page review
Roberts HJ Aspartame (NutraSweet) addiction.
Townsend Letter 2000 Jan; HJRobertsMD@...
http://www.sunsentpress.com/ sunsentpress@...
Sunshine Sentinel Press P.O.Box 17799 West Palm Beach, FL 33416
800-814-9800 561-588-7628 561-547-8008 fax

http://groups.yahoo.com/group/aspartameNM/message/669
1038-page medical text "Aspartame Disease: An Ignored Epidemic"
published May 30 2001 $ 60.00 postpaid data from 1200 cases
available at http://www.amazon.com
over 600 references from standard medical research

http://groups.yahoo.com/group/aspartameNM/message/790
Moseley: review Roberts "Aspartame Disease: An Ignored Epidemic":
Murray 2002.02.07

Roberts, Hyman J., 1924- ,
Useful insights for diagnosis, treatment and public heath: an updated
anthology of original research, 2002, 798 pages,
aspartame disease, pages 627-685, 778-780

http://groups.yahoo.com/group/aspartameNM/message/859
Roberts: the life work of a brilliant clinician: aspartame toxicity:
Murray 2002.08.02
____________________________________________________


re "A Few too Many", Joan Acocella, The New Yorker, long review of hangover
research 2008.05.26 -- same levels of formaldehyde and formic acid in FEMA
trailers and other sources (aspartame, dark wines and liquors, tobacco
smoke): Murray 2008.06.05
http://rmforall.blogspot.com/2008_06_01_archive.htm
Thursday, June 5, 2008
http://groups.yahoo.com/group/aspartameNM/message/1541


formaldehyde and formic acid in FEMA trailers and other sources (aspartame,
dark wines and liquors, tobacco smoke): Murray 2008.01.30
http://rmforall.blogspot.com/2008_01_01_archive.htm
Wednesday, January 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1508

The FEMA trailers give about the same amount of formaldehyde and formic acid
daily as from a quart of dark wine or liquor, or two quarts (6 12-oz cans)
of aspartame diet soda, from their over 1 tenth gram methanol impurity (one
part in 10,000), which the body quickly makes into formaldehyde and then
formic acid -- enough to be the major cause of "morning after" alcohol
hangovers.

Methanol and formaldehyde and formic acid also result from many fruits and
vegetables, tobacco and wood smoke, heater and vehicle exhaust, household
chemicals and cleaners, cosmetics, and new cars, drapes, carpets, furniture,
particleboard, mobile homes, buildings, leather... so all these sources add
up and interact with many other toxic chemicals.

methanol impurity in alcohol drinks [ and aspartame ] is turned into
neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol Syndrome,
BM Kapur, DC Lehotay, PL Carlen at U. Toronto,  Alc Clin Exp Res 2007 Dec.
plain text: detailed biochemistry, CL Nie et al. 2007.07.18: Murray
2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524

"Of course, everyone chooses, as a natural priority, to enjoy peace, joy,
and love by helping to find, quickly share, and positively act upon evidence
about healthy and safe food, drink, and environment."

Rich Murray, MA Room For All rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com  new primary archive

http://groups.yahoo.com/group/aspartameNM/messages
group with 133 members, 1,556 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1,132 members, 22,932 posts in public archive
____________________________________________________


details on 6 epidemiological studies since 2004 on diet soda (mainly
aspartame) correlations, as well as 13 other mainstream studies on
aspartame toxicity since summer 2005: Murray 2007.11.14
http://rmforall.blogspot.com/2007_11_01_archive.htm
Wednesday, November 14, 2007
http://groups.yahoo.com/group/aspartameNM/message/1490
[ Selection ]

" When studying individual classes of caffeinated beverages, habitual
coffee consumption was not associated with increased risk of hypertension.

By contrast, consumption of cola beverages was associated with an
increased risk of hypertension, independent of whether it was sugared or
diet cola (P for trend <.001).

Conclusion
No linear association between caffeine consumption and incident
hypertension was found.

Even though habitual coffee consumption was not associated with an
increased risk of hypertension, consumption of sugared or diet cola was
associated with it.

Further research to elucidate the role of cola beverages in hypertension
is warranted. "

" The findings were consistent between the cohorts and were present
across types of soda beverages:
both sugared cola and diet cola beverages were associated with an
increased risk of hypertension (Table 5 and Table 6).

Hence, we speculate that it is not caffeine but perhaps some other
compound contained in soda-type soft drinks that may be responsible for
the increased risk in hypertension.

If these associations are causal, they may have considerable impact on
public health. "

" Finally, an examination of the possible associations between
caffeinated cola beverages and the risk of hypertension
showed that
sugared caffeinated cola (NHS I, P for trend = .03; NHS II, P for trend
<.001) (Table 5)
and diet caffeinated cola (NHS I, P for trend = .02; NHS II, P for
trend <.001) (Table 6)
were positively associated with hypertension in both cohorts. "

" Table 6. Age-Adjusted and Multivariate Relative Risks for Incident
Hypertension According to Frequency of Diet Cola Intake

Glasses or Cans of Diet Cola per Day
under 1 ------- 1 ----------- 2-3 ------- 4 and more --- P for Trend


Nurses’ Health Study I (1990-2002) 53,175 nurses, ages 44-69 in 1990

No. of cases of Incident Hypertension
17,268 ------- 1,154 ---------- 662 --------- 130
% 100 ---------- 6.7 ---------- 3.8 -------- 0.75
#% 32.5 -------- 2.2 ---------- 1.3 -------- 0.25 #% of 53,175

Person-years
479,890 ----- 30,579 --------17,316 ------- 3,173
% 100 -----------6.4 ---------- 3.6 -------- 0.66

Age-adjusted relative risk (95% CI)
1.00 -- 1.16(1.10-1.24)-- 1.23(1.13-1.33)-- 1.37(1.15-1.62)-- under .001

Multivariate relative risk (95% CI)*
1.00 -- 1.07(1.00-1.13) -- 1.06(0.98-1.15) -- 1.16(0.97-1.37)------ .02

Nurses’ Health Study II (1991-2003) 87,369 nurses, ages 27-44 in 1991


No. of cases of Incident Hypertension
10,192 -------- 1,452 ---------- 1,358 -------- 449
% 100 ---------- 14.3 ----------- 13.3 --------- 4.4
#% 11.7 --------- 1.7 ------------ 1.6 --------- 0.51 #% of 87,369

Person-years
713,971 ----- 91,144 ------- 77,398 ------- 21,265
% 100 --------- 12.8 --------- 10.8 ---------- 3.0


Age-adjusted relative risk (95% CI)
1.00 -- 1.16(1.10-1.23) -- 1.33(1.26-1.41) -- 1.63(1.49-1.80) under .001

Multivariate relative risk (95% CI)*
1.00 -- 1.05(0.99-1.11) -- 1.09(1.03-1.15) -- 1.19(1.08-1.32) under .001

Abbreviation: CI, confidence interval.
*Adjusted for age, body mass index, intake of alcohol, family history of
hypertension, oral contraceptive use (in Nurses’Health Study II only),
physical activity, and smoking status, as well as the other classes of
beverage. "

http://jama.ama-assn.org/cgi/reprint/294/18/2330?ijkey=ff7fa86b688f2c2e23d9b6185\
\
19b890439fefb9e

full text pdf

http://jama.ama-assn.org/cgi/content/abstract/294/18/2330?ijkey=ff7fa86b688f2c2e\
\
23d9b618519b890439fefb9e&keytype2=tf_ipsecsha
full text html

JAMA Vol. 294 No. 18, November 9, 2005

Online Features
Original Contribution

Habitual Caffeine Intake and the Risk of Hypertension in Women
Wolfgang C. Winkelmayer, MD, ScD; wwinkelmayer@...,
Meir J. Stampfer, MD, DrPH; stampfer@...,
Walter C. Willett, MD, DrPH; walter.willett@...,
Gary C. Curhan, MD, ScD gary.curhan@...,
JAMA. 2005; 294: 2330-2335.

Context
Caffeine acutely increases blood pressure, but the association between
habitual consumption of caffeinated beverages and incident hypertension
is uncertain.

Objective
To examine the association between caffeine intake and incident
hypertension in women.

Design, Setting, and Participants
Prospective cohort study conducted in the Nurses’ Health Studies
(NHSs) I and II of 155,594 US women free from physician-diagnosed
hypertension followed up over 12 years
(1990-1991 to 2002-2003 questionnaires).

Caffeine intake and possible confounders were ascertained from regularly
administered questionnaires.

We also tested the associations with types of caffeinated beverages.

Main Outcome Measure
Incident physician-diagnosed hypertension.

Results
During follow-up, 19.541 incident cases of physician-diagnosed
hypertension were reported in NHS I and 13,536 in NHS II.

In both cohorts, no linear association between caffeine consumption and
risk of incident hypertension was observed after multivariate adjustment
(NHS I, P for trend = .29; NHS II, P for trend = .53).

Using categorical analysis, an inverse U-shaped association between
caffeine consumption and incident hypertension was found.

Compared with participants in the lowest quintile of caffeine
consumption, those in the third quintile had a 13 % and 12 % increased
risk of hypertension, respectively (95 % confidence interval in NHS I, 8
% - 18 %; in NHS II, 6 % - 18 %).

When studying individual classes of caffeinated beverages, habitual
coffee consumption was not associated with increased risk of hypertension.

By contrast, consumption of cola beverages was associated with an
increased risk of hypertension, independent of whether it was sugared or
diet cola (P for trend <.001).

Conclusion
No linear association between caffeine consumption and incident
hypertension was found.

Even though habitual coffee consumption was not associated with an
increased risk of hypertension, consumption of sugared or diet cola was
associated with it.

Further research to elucidate the role of cola beverages in hypertension
is warranted.

Author Affiliations:
Division of Pharmacoepidemiology and Pharmacoeconomics (Dr Winkelmayer),
Renal Division (Drs Winkelmayer and Curhan),
and Channing Laboratory (Drs Stampfer, Willett, and Curhan),
Department of Medicine, Brigham and Women’s Hospital, Harvard Medical
School,
and Departments of Epidemiology (Drs Stampfer, Willett, and Curhan) and
Nutrition (Drs Stampfer and Willett), Harvard School of Public Health,
Boston, Mass.

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INTRODUCTION

Approximately 50 million people in the United States have hypertension,
and the prevalence is increasing. 1

Hypertension is a major risk factor for coronary heart disease, stroke,
and congestive heart failure. 2-3

Therefore, even small reductions in the prevalence of hypertension could
have a potentially large public health and financial impact.

Much clinical lore about the possible association between caffeine
intake and the risk of hypertension is available.

Short-term studies have demonstrated that caffeine intake acutely
increases blood pressure, but over time, attenuation of this effect does
occur. 4

Experimental studies have shown that caffeine can raise plasma levels of
several stress hormones, such as epinephrine, norepinephrine, 5-6 and
cortisol, all of which can lead to an increase in blood pressure. 6-7

However, these experiments have been limited to relatively short
periods of observation, typically less than 1 week; information on a
more sustained neuroendocrine response to regular exposure to caffeine
is not available.

A long-term effect of caffeine intake on the risk of developing
hypertension would be of substantial public health importance given the
widespread consumption of beverages containing caffeine, but currently,
studies of this association are scarce.

A recent longitudinal study in 1,017 men found a positive association
between coffee consumption and blood pressure and incident hypertension
in unadjusted analyses. 8

Although the association with blood pressure level was significant in
multivariate analyses, a nonsignificant 40 % increase in the risk of
incident diagnosis of hypertension (95 % confidence interval [CI], –6 %
to 109 %) for 3 to 4 cups per day and a 43 % increase (95% CI, –6 % to
118 %) for 5 or more cups per day vs no coffee consumption was found.

No published studies to date of the association between caffeine intake
and the risk of hypertension in women are available.

To prospectively elucidate whether caffeine intake or consumption of
certain caffeine-containing beverages is associated with the risk of
incident hypertension in women, we examined these questions in 2 large
cohort studies of women, the Nurses’ Health Studies (NHSs) I and II.

METHODS

Study Populations

The NHS I cohort was assembled in 1976 when 121,700 female registered
nurses, aged 30 to 55 years, completed and returned a mailed
questionnaire. 9

Follow-up questionnaires have been mailed every 2 years to update
information on health-related behaviors and medical events.

The NHS II began in 1989, when 116,671 female registered nurses, aged 25
to 42 years, completed and returned a mailed questionnaire.

Questionnaires have been mailed every 2 years to update exposure
information and diagnosis of new diseases.

The follow-up for both cohorts exceeds 90 %.

In this analysis, all participants who had not been diagnosed with
hypertension before the return of the 1990 NHS I or 1991 NHS II
questionnaires were included.

This study was approved by the institutional review board at Brigham and
Women’s Hospital, Boston, Mass.

Receipt of each questionnaire implies participant’s consent.

Dietary Assessment

Food frequency questionnaires were used to measure dietary intake and
were completed in 1990, 1994, and 1998 for NHS I and 1991, 1995, and
1999 for NHS II.

Participants were asked about their usual intake of foods and beverages
during the past year.

The response options for specified serving sizes were the following:
never or less than once per month;
1 to 3 times per month;
1 per week;
2 to 4 per week;
5 to 6 per week;
1 per day;
2 to 3 per day;
4 to 5 per day;
and 6 or more per day.

The relevant beverages included on the questionnaire were the following:
low-calorie cola (eg, Diet Coke or Diet Pepsi with caffeine),
regular cola (eg, Coke, Pepsi,
or other cola beverages with sugar),
tea with caffeine, tea without caffeine,
coffee with caffeine, and decaffeinated coffee.

Total caffeine intake was calculated primarily using US Department of
Agriculture food composition sources.

In these calculations, it was assumed that the content of caffeine was
137 mg per cup of coffee, 47 mg per cup of tea, 46 mg per can or bottle
of cola beverage, and 7 mg per serving of chocolate candy. 10

This method of measuring coffee intake was shown to be valid in both the
NHS I cohort and a similar cohort study of male health professionals. 11-13

Assessment of Other Variables

Data on height and family history of hypertension were collected at
baseline in both cohorts.

Information on weight was updated every 4 years.

Using each participant’s updated weight, body mass index was calculated
by dividing the weight in kilograms by height in meters squared.

Also, an updated variable for weight difference between baseline and the
time of respective follow-up questionnaire was generated.

Information on oral contraceptive use in the NHS II cohort also was
updated every 4 years.

The same semiquantitative food frequency questionnaires were used to
determine intake of alcohol, sodium, potassium, magnesium, calcium, and
phosphorus. 14

Physical activity was assessed in NHS I (1988, 1992, and 1996) and NHS
II (1989, 1993, and 1997) cohorts; energy expenditure was expressed in
metabolic equivalent tasks. 15

In addition, the frequency of analgesic drug use (aspirin, nonsteroidal
anti-inflammatory drugs, and acetaminophen) was ascertained. 16-17

Outcome Definition

The baseline and biennial follow-up questionnaires inquired about
physician-diagnosed hypertension and the year of diagnosis.

Self-reported diagnosis of hypertension was found to be reliable in the
NHS I cohort. 18

In a subset of women who reported hypertension, review of medical
records confirmed a documented systolic and diastolic blood pressure,
respectively, higher than 140 mm Hg and 90 mm Hg in 100 % and higher
than 160 mm Hg and 95 mm Hg in 77 % of participants.

Additionally, self-reported hypertension was predictive of subsequent
cardiovascular events. 18

A study participant was considered to have a history of hypertension if
she reported a diagnosis of high blood pressure on any questionnaire up
to and including the 1990 questionnaire in NHS I and the 1991
questionnaire in NHS II, and therefore was excluded from the study.

Among the remaining women in each cohort, incident cases were included
as those who first reported hypertension on any of the subsequent
biennial questionnaires and whose date of diagnosis was after the return
of the 1990 NHS I or the 1991 NHS II questionnaire.

This method recently has been used in a study of folate intake and the
risk of hypertension in women. 19

Statistical Methods

The time of observation was between return of the 1990 NHS I and 1991
NHS II and the 2002 NHS I and 2003 NHS II questionnaires.
Participants who did not return the baseline questionnaires for this
study were allowed to contribute person-time for later time intervals,
provided that they had not been diagnosed with hypertension prior to
return of the respective questionnaire.
Participants were censored after being diagnosed with hypertension or at
the time of death.
Each cohort was analyzed separately.
Age-adjusted Cox proportional hazards regression models were used to
estimate relative risks and 95% CIs.
In addition, multivariate models were constructed that adjusted for
other known risk factors of the study outcome:
age (continuous), body mass index (continuous), alcohol use (6
categories), physical activity (quintiles of metabolic equivalent
tasks), smoking status (current, past, or never), family history of
hypertension (yes/no), and current oral contraceptive use (yes/no; only
in NHS II).
In additional analyses, we ensured that sodium, magnesium, calcium,
potassium, and phosphorus intake (quintiles) did not confound the
estimates from these multivariate models.
All variables were updated to reflect the most recent value provided by
the participants on the biennial questionnaires.
Participants with missing data were assigned to a missing category for
that specific time period.
We determined P values for trend for each of the exposures of interest
by using the median for each category.
Level of significance for P values for trend was <.05.
Also the interaction between caffeine intake and the other variables was
tested.
We used SAS version 8.2 for UNIX statistical software package
(SAS Institute Inc, Cary, NC).

RESULTS

In NHS I, 53,175 women had not been diagnosed with hypertension at
baseline in 1990.

Another 7,916 participants who did not respond to the 1990 questionnaire
but who did respond to a later questionnaire disclosing that they
previously had not been diagnosed with hypertension allowed them to
contribute person-time from that point in time.

Over the 12 years (539,388 person-years of follow-up), 19,541 incident
cases of physician-diagnosed hypertension were reported.

In NHS II, 94,503 participants who were free of hypertension (87,369 in
1991 and an additional 7,134 at a later point in time) were included in
the analyses of younger women.

During 909,199 person-years of observation, 13,536 participants
responded that they were diagnosed with hypertension by a physician.

Participant characteristics by quintile of caffeine intake are presented
in Table 1.

In both cohorts, mean caffeine consumption ranged from less than 20 mg/d
in the lowest quintile to approximately 600 mg/d in the highest quintile.

Caffeine intake was correlated positively with alcohol consumption and
smoking status
r = 0.12, P < .001 for NHS I; r = 0.23, P < .001 for NHS II),
whereas all other relevant characteristics did not differ
materially across quintiles of caffeine consumption.


Table 1. Baseline Characteristics of Cohort by Quintile of Caffeine
Intake in Nurses’ Health Study I (N = 53,175)
and Nurses’ Health Study II (N = 87,369)*

Age-adjusted analyses demonstrated an inverse U-shaped relation between
caffeine intake and the incidence of hypertension in both cohorts.

Compared with participants in the lowest quintile of caffeine
consumption, the risk of incident hypertension was increased by 14 % (95
% CI, 9 % -19 % for NHS I) and 15 % (95 % CI, 9 % - 21 % for NHS II) for
those in the third quintile, whereas those in the highest quintile were
not at an increased risk of hypertension (Table 2).

Multivariate adjustment did not materially change these findings (Table 2).

Table 2. Age-Adjusted and Multivariate Relative Risks for Incident
Hypertension According to Quintile of Caffeine Intake

To further examine this inverse U-shaped association, the frequency of
use of different caffeine-containing beverages in relation to the risk
of incident hypertension was evaluated.
In multivariate models including beverage type, rather than actual
caffeine intake, no association between frequency of intake of
caffeinated coffee and incident hypertension was observed in either cohort.
Compared with NHS I participants drinking less than 1 cup per day of
caffeinated coffee, the relative risks were
1.06 (95% CI, 1.01-1.10) for those consuming 1 cup per day,
1.00 (95% CI, 0.97-1.04) for those drinking 2 to 3 cups per day,
0.93 (95% CI, 0.88-0.99) for those drinking 4 to 5 cups per day,
and 0.88 (95% CI, 0.80-0.98) for those drinking 6 or more cups per day
(Table 3).
The trend for the NHS I cohort was marginally significant for
an inverse association between coffee intake and the risk of
hypertension (Table 3; P for trend = .02).
The findings in the NHS II cohort were practically identical (P for
trend = .03).
The results for intake of decaffeinated coffee also were similar to the
data for caffeinated coffee intake (data not shown);
the trend suggested an inverse association of risk of hypertension in
the NHS I cohort (P for trend = .08)
but not in the NHS II cohort (P for trend = .67).

Table 3. Age-Adjusted and Multivariate Relative Risks for Incident
Hypertension According to Frequency of Coffee Intake

An association between caffeinated tea intake and incident hypertension
in the NHS I cohort (Table 4; P for trend = .79) was not found.
However, in the cohort of younger women in NHS II, a moderate increase
in risk of hypertension (P for trend = .01; Table 4) was detected.

Table 4. Age-Adjusted and Multivariate Relative Risks for Incident
Hypertension According to Frequency of Caffeinated Tea Intake

Finally, an examination of the possible associations between caffeinated
cola beverages and the risk of hypertension showed that
sugared caffeinated cola (NHS I, P for trend = .03; NHS II, P for trend
<.001) (Table 5)
and diet caffeinated cola (NHS I, P for trend = .02; NHS II, P for
trend <.001) (Table 6)
were positively associated with hypertension in both cohorts.

Table 5. Age-Adjusted and Multivariate Relative Risks for Incident
Hypertension According to Frequency of Sugared Cola Intake

Table 6. Age-Adjusted and Multivariate Relative Risks for Incident
Hypertension According to Frequency of Diet Cola Intake

Glasses or Cans of Diet Cola per Day
under 1 ------- 1 ----------- 2-3 ------- 4 and more --- P for Trend


Nurses’ Health Study I (1990-2002) 53,175 nurses, ages 44-69 in 1990

No. of cases of Incident Hypertension
17,268 ------- 1,154 ---------- 662 -------- 130
% 100 ---------- 6.7 ---------- 3.8 -------- 0.75
#% 32.5 -------- 2.2 ---------- 1.3 -------- 0.25 #% of 53,175

Person-years
479,890 ----- 30,579 ------17,316 ------- 3,173
% 100 -----------6.4 ---------- 3.6 -------- 0.66

Age-adjusted relative risk (95% CI)
1.00 -- 1.16(1.10-1.24)-- 1.23(1.13-1.33)-- 1.37(1.15-1.62)-- under .001

Multivariate relative risk (95% CI)*
1.00 -- 1.07(1.00-1.13) -- 1.06(0.98-1.15) -- 1.16(0.97-1.37)------ .02

Nurses’ Health Study II (1991-2003) 87,369 nurses, ages 27-44 in 1991


No. of cases of Incident Hypertension
10,192 -------- 1,452 ---------- 1,358 -------- 449
% 100 ---------- 14.3 ----------- 13.3 --------- 4.4
#% 11.7 --------- 1.7 ------------ 1.6 --------- 0.51 #% of 87,369

Person-years
713,971 ----- 91,144 --------- 77,398 ----- 21,265
% 100 --------- 12.8 ------------ 10.8 --------- 3.0


Age-adjusted relative risk (95% CI)
1.00 -- 1.16(1.10-1.23) -- 1.33(1.26-1.41) -- 1.63(1.49-1.80) under .001

Multivariate relative risk (95% CI)*
1.00 -- 1.05(0.99-1.11) -- 1.09(1.03-1.15) -- 1.19(1.08-1.32) under .001

Abbreviation: CI, confidence interval.
*Adjusted for age, body mass index, intake of alcohol, family history of
hypertension, oral contraceptive use (in Nurses’Health Study II only),
physical activity, and smoking status, as well as the other classes of
beverage.

Additional analyses adjusting for intake of sodium, magnesium,
potassium, phosphorus, and calcium or analgesic drug use did not change
the results materially for the caffeine intake or specific beverage
intake analyses. When testing the robustness of the results, such as by
limiting the analysis to those women who reported having had a routine
physical examination during the time interval or by using baseline body
mass index and updated change in weight rather than updated body mass
index, the results were virtually unchanged (data not shown).

COMMENT

In this prospective study of the association between caffeine intake and
the risk of physician-diagnosed hypertension in 2 large cohorts of
women, we found a modest inverse U-shaped association between caffeine
intake and hypertension in both cohorts.

The magnitude of the highest multivariate relative risk was 1.13 in NHS
I and 1.12 in NHS II.

To better understand this nonlinear relation between caffeine intake and
the risk of hypertension, we evaluated the individual associations of
several caffeine-containing beverages.

Neither caffeinated nor decaffeinated coffee demonstrated a positive
association with incident hypertension in either cohort.

The results for consumption of caffeinated tea were inconclusive:
although no association was observed in the NHS I cohort, a positive
trend was shown in the NHS II cohort.

By contrast, we found a highly significant association between cola
intake (sugared or low-calorie cola) and incident hypertension that was
consistent across the cohorts.

To our knowledge, this study is the first to prospectively evaluate the
putative effect of caffeine consumption on the long-term risk of
hypertension in women.

The speculation that coffee may cause hypertension was supported by
several small experiments over short periods of observation ( under 80
days). 20

If the short-term effects of caffeine on blood pressure persist, then
habitual coffee drinking might contribute to an excess risk of hypertension.

Such an effect would be of great public health importance given the
widespread use of coffee and other caffeinated beverages.

In this study with more than 1.4 million person-years of follow-up, the
relevant exposures and outcomes have been found valid and accurate,
11-13,18 and coffee intake was updated to reflect changes in individual
behavior.

We found strong evidence to refute speculation that coffee consumption
is associated with an increased risk of hypertension in women.

The associations found between caffeinated tea consumption and the risk
of hypertension differed between the 2 cohorts.

In the NHS I cohort, no association was found; however, in the NHS II
cohort, a significant positive trend was observed.

A recent study conducted among 711 men and 796 women in Taiwan found a
strong inverse association between both frequency and duration of tea
intake and hypertension. 21

Since the types of tea (green or oolong) consumed in that study are
likely different from those consumed in our study of US women, the
comparability of the findings from these 2 studies appears uncertain.

In both NHS cohorts we found a positive association between frequency of
caffeinated soft drink consumption and the risk of hypertension.

The findings were consistent between the cohorts and were present across
types of soda beverages: both sugared cola and diet cola beverages were
associated with an increased risk of hypertension (Table 5 and Table 6).

Hence, we speculate that it is not caffeine but perhaps some other
compound contained in soda-type soft drinks that may be responsible for
the increased risk in hypertension.

If these associations are causal, they may have considerable impact on
public health.

Recent studies have found an effect of the intake of cola beverages on
insulin resistance in a rat model 22; in humans, the intake of cola
beverages was associated with an increased risk of diabetes in the NHS
II cohort. 23

These studies have attributed these associations to the glycemic load of
corn syrup, which is used as sweetener in these beverages, and the
caramel coloring, which is rich in advanced glycation end products.

Further studies on the possible mechanisms underlying these associations
clearly are needed.

We acknowledge the limitations of this study.

We cannot rule out that individuals susceptible to adverse effects of
caffeinated coffee intake on their blood pressure in the past may have
reduced their consumption of beverages containing caffeine.

Patients were asked about the frequency of their food intake, but no
information was available on the daily timing of such ingestion.

We did not directly measure the participants’ blood pressure and the
diagnosis of hypertension was self-reported.

Nonetheless, self-reported blood pressure has been validated and
demonstrated to be a strong predictor of actual values. 18

Furthermore, we do not know whether these findings are generalizable
beyond populations of predominantly white women.

We also cannot exclude the possibility that the associations found are
residually confounded.

Lastly, no statement can be made on the effect of coffee intake on the
control of blood pressure among individuals already diagnosed with
hypertension.

In conclusion, consumption of coffee in women does not appear to
increase the risk of developing hypertension.

Whether caffeinated soft drinks are causally related to the risk of
hypertension and its underlying mechanism will require further study.

AUTHOR INFORMATION

Corresponding Author: Wolfgang C. Winkelmayer, MD, ScD, Division of
Pharmacoepidemiology and Pharmacoeconomics and Renal Division, Brigham
and Women’s Hospital, 1620 Tremont St, Suite 3030, Boston, MA 02120
wwinkelmayer@...,

Author Contributions: Dr Winkelmayer had full access to all of the data
in the study and takes responsibility for the integrity of the data and
the accuracy of the data analysis.

Study concept and design: Winkelmayer, Willett, Curhan.

Acquisition of data: Stampfer, Willett, Curhan.

Analysis and interpretation of data: Winkelmayer, Stampfer, Willett, Curhan.

Drafting of the manuscript: Winkelmayer.

Critical revision of the manuscript for important intellectual content:
Winkelmayer, Stampfer, Willett, Curhan.

Statistical analysis: Winkelmayer, Willett, Curhan.

Obtained funding: Willett, Curhan.

Administrative, technical, or material support: Stampfer, Willett, Curhan.

Study supervision: Curhan.

Financial Disclosures: None reported.

Funding/Support:
This study was funded by National Institutes of Health grants DK52866,
DK66574, CA87969, and CA050385.

Dr Winkelmayer is a 2004 T. Franklin Williams Scholar in Geriatric
Nephrology and a recipient of the American Society of
Nephrology-ASP-Junior Development Award in Geriatric Nephrology, jointly
sponsored by the Atlantic Philanthropies, the American Society of
Nephrology, the John A. Hartford Foundation, and the Association of
Subspecialty Professors.
He is also supported by an American Heart Association Scientist
Development grant (0535232N).

Role of the Sponsors:
None of the funding organizations had any role in the design and conduct
of the study; collection, management, analysis, and interpretation of
the data; or preparation, review, or approval of the manuscript.

Author Affiliations
Division of Pharmacoepidemiology and Pharmacoeconomics (Dr Winkelmayer),
Renal Division (Drs Winkelmayer and Curhan), and Channing Laboratory
(Drs Stampfer, Willett, and Curhan), Department of Medicine, Brigham and
Women’s Hospital, Harvard Medical School, and Departments of
Epidemiology (Drs Stampfer, Willett, and Curhan) and Nutrition (Drs
Stampfer and Willett), Harvard School of Public Health, Boston, Mass.

REFERENCES

© 2007 American Medical Association. All Rights Reserved.

1. 2002 Heart and Stroke Statistical Update. Dallas, Tex: American Heart
Association; 2001.

2. Fiebach NH, Hebert PR, Stampfer MJ, et al. A prospective study of
high blood pressure and cardiovascular disease in women. Am J Epidemiol.
1989;130:646-654. FREE FULL TEXT

3. Levy D, Larson MG, Vasan RS, Kannel WB, Ho KK. The progression from
hypertension to congestive heart failure. JAMA. 1996;275:1557-1562. ABSTRACT

4. Jee SH, He J, Whelton PK, et al. The effect of coffee on
blood-pressure: a meta-analysis of controlled clinical trials. Can J
Cardiol. 1997;13(suppl B):36B.

5. Robertson D, Frolich JC, Carr RK, et al. Effects of caffeine on
plasma renin activity, catecholamines and blood pressure. N Engl J Med.
1978;298:181-186. ABSTRACT

6. Lane JD, Adcock RA, Williams RB, Kuhn CM. Caffeine effects on
cardiovascular and neuroendocrine responses to acute psychosocial stress
and their relationship to level of habitual caffeine consumption.
Psychosom Med. 1990;52:320-336. FREE FULL TEXT

7. Lovallo WR, Pincomb GA, Sung BH, et al. Caffeine may potentiate
adrenocortical stress response in hypertension-prone men. Hypertension.
1989;14:170-176. ABSTRACT

8. Klag MJ, Wang NY, Meoni LA, et al. Coffee intake and risk of
hypertension: the Hopkins precursors study. Arch Intern Med.
2002;162:657-662. FREE FULL TEXT

9. Colditz GA. The Nurses’ Health Study: a cohort of US women followed
since 1976. J Am Med Womens Assoc. 1995;50:40-44. PUBMED

10. Willett WC, Sampson L, Stampfer MJ, et al. Reproducibility and
validity of a semiquantitative food frequency questionnaire. Am J
Epidemiol. 1985;122:51-65. FREE FULL TEXT

11. Salvini S, Hunter DJ, Sampson L, et al. Food-based validation of a
dietary questionnaire: the effects of week-to-week variation in food
consumption. Int J Epidemiol. 1989;18:858-867. FREE FULL TEXT

12. Rimm EB, Giovanucci EL, Stampfer MJ, Colditz GA, Litin LB, Willett
WC. Reproducibility and validity of an expanded self-administered
semiquantitative food frequency questionnaire among male health
professionals. Am J Epidemiol. 1992;135:1114-1126. FREE FULL TEXT

13. Grobbee DE, Rimm EB, Giovanucci E, et al. Coffee, caffeine, and
cardiovascular disease in men. N Engl J Med. 1990;323:1026-1032. ABSTRACT

14. Willett WC. Nutritional Epidemiology. 2nd ed. New York, NY: Oxford
University Press; 1998.

15. Ainsworth BE, Haskell WL, Leon AS, et al. Compendium of physical
activities: classification of energy costs of human physical activities.
Med Sci Sports Exerc. 1993;25:71-80. ISI | PUBMED

16. Curhan GC, Willett WC, Rosner B, Stampfer MJ. Frequency of analgesic
use and risk of hypertension in younger women. Arch Intern Med.
2002;162:2204-2208. FREE FULL TEXT

17. Dedier J, Stampfer MJ, Hankinson SE, et al. Nonnarcotic analgesic
use and the risk of hypertension in US women. Hypertension.
2002;40:604-608. FREE FULL TEXT

18. Colditz GA, Martin P, Stampfer MJ, et al. Validation of
questionnaire information on risk factors and disease outcomes in a
prospective cohort study of women. Am J Epidemiol. 1986;123:894-900.
FREE FULL TEXT

19. Forman JP, Rimm EB, Stampfer MJ, Curhan GC. Folate intake and the
risk of incident hypertension among US women. JAMA. 2005;293:320-329.
FREE FULL TEXT

20. Jee SH, He J, Whelton PK, Klag MJ. The effect of chronic coffee
drinking on blood pressure: a meta-analysis of controlled clinical
trials. Hypertension. 1999;33:647-652. FREE FULL TEXT

21. Yang YC, Lu FH, Wu JS, et al. The protective effect of habitual tea
consumption on hypertension. Arch Intern Med. 2004;164:1534-1540. FREE
FULL TEXT

22. Choi SB, Park CH, Park S. Effect of cola intake on insulin
resistance in moderate fat-fed weaning male rats. J Nutr Biochem.
2002;13:727-733. FULL TEXT | ISI | PUBMED

23. Schulze MB, Manson JE, Ludwig DS, et al. Sugar-sweetened beverages,
weight gain, and incidence of type 2 diabetes in young and middle-aged
women. JAMA. 2004;292:927-934. FREE FULL TEXT
____________________________________________________

533 mostly negative reports on sucralose in 2 1/2 years (many GI symptoms) Mark
J & Cherie Yannone, Phoenix, AZ www.FoodAndDiet.com: GI stimulation, M Kidd et
al, Yale U, AJPGLP 2008.06.12: Rich Murray 2008.07.29
http://rmforall.blogspot.com/2008_07_01_archive.htm
Tuesday, July 29, 2008
http://groups.yahoo.com/group/aspartameNM/message/1555
___________________________________________________


http://www.foodanddiet.com/splenda/symptom-list.html

Food and Diet, Mark J. and Cherie Yannone
1421 E Charleston Ave
Phoenix AZ 85022
Phone  602-569-9632  foodanddiet@...;
Site designed and maintained by webDedication webDesign Studios
© 2002-2007 webDedication webDesign Studios and Cherie Yannone.
All rights reserved

All of the symptoms listed on this page may be caused by something other than
sucralose consumption. Be certain to speak with your physician to discuss your
symptoms and to get treatment for allergies, illnesses, diseases, or conditions
that require medical attention.

Having clarified that, based upon the more than 500 stories received from our
visitors, we have compiled a list of the most frequently reported symptoms
resulting from the use of sucralose (Splenda). The list, expanding almost
monthly, may not contain your particular symptom.  That does not mean you aren't
suffering side effects from Splenda consumption, but may mean that the side
effect has not been reported often enough for us to add it to the list (yet).

* bloating
* abdominal pain
* gas, sometimes painful
* nausea
* heartburn
* diarrhea
* headaches
* migraines (severe headaches)
* heart palpitations (fluttering, irregular heartbeats)
* shortness of breath
* depression
* anxiety and panic attacks
* spaced-out or drugged sensation
* joint pain, especially in the knees
* dizziness

http://www.foodanddiet.com/splenda/story-index.html
Index 7 -- 18, from  2005.04.26 to 2006.06.21

Each of the following links will take you to an individual index containing 25
stories from Splenda users.
Some stories are positive, as indicated by a bright yellow happy face.
Some stories are negative, as indicated by a sickly green unhappy face.
Note that the indices start at Index 7.
Previous indices are found on our main website.

In addition, the following side effects are being reported more often, although
not with the same degree of frequency as those above:

* lone atrial fibrillation
* extreme fatigue
* muscle weakness
* tingling mouth or tongue
* tingling in fingers and hands
* numbness in the lips and tongue
* swollen lips or tongue
* swollen face
* redness or welts on face
* mouth sores
* blurred vision

If you believe you are suffering ill effects after consuming Splenda, we
strongly suggest you conduct the two-week test:

For two weeks, double-check every package label (from bottled waters to OTC
medications) to ensure you consume absolutely nothing with Splenda (sucralose).
Not every product containing sucralose will display the now-familiar Splenda
logo, so read every label.
If, during the two-week period your symptoms stop and don't return, try
consuming something with Splenda as you did previously.
If the symptoms return, you've likely discovered the source of your illness.
If the symptoms don't abate, worsen, or do not return with a return to Splenda
consumption, you may have another illness or problem.
In either case, be certain to speak with your physician and discuss your
suspicions about sucralose as it relates to your condition.

[ The last four stories, after which no more stories are collected, are:

http://www.foodanddiet.com/splenda/stories-500-599/splenda-story533.html

On 18 June 2006, we received this note from E.L. concerning their use of
sucralose.

"Approximately one month ago, I drank a diet lemonade. It must have had Splenda
in it because one day later I had severe cramping and diarrhea. It lasted for
two days. At first, I thought I had a bug.

A few days ago, I drank another lemonade drink (only about 2 ounces this time).
It was so sweet and so awful I threw most of it away. One night later, I had
severe stomach cramps and diarrhea. It took two days to get over it. I almost
went to the ER I was so sick.

Now that I know it's the Splenda, I will watch what I drink.

My friend ate one piece of dietetic chocolate candy. She had diarrhea before she
could get home! She knew exactly what caused it. She didn't even get home before
it hit her!

I will not touch that stuff any more."

Thank you E.L. for sharing your story with our visitors.

If you have experienced any side effects, whether you are sure it is Splenda or
not, be sure to speak with your physician and discuss all possibilities.

You can also use the search function at the bottom of the page to find stories
based solely on a particular side effect or symptom.

http://www.foodanddiet.com/splenda/stories-500-599/splenda-story534.html

On 19 June 2006, we received this note from L. concerning their use of
sucralose.

"I have been using Splenda for probably two years. I have always loved it
because it didn't leave an aftertaste. But it seemed every month before my
menstrual cycle my breasts would become extremely tender, so much that it was
almost unbearable. I knew that caffeine could cause this, but I was drinking
half-caf coffee and really didn't feel like I was drinking too much to cause the
breast tenderness.

I decided to experiment a little.  I stopped using Splenda in my coffee about a
month ago and started using saccharin to sweeten my coffee. I just started my
cycle today. It totally caught me off-guard because before I knew when I was
going to start my cycle because of the breast tenderness. I had NO breast
tenderness at all this month!!!

I am totally shocked.

I have also been having headaches a lot in the past. So I will see if stopping
the Splenda will help that as well. Just thought I should share my story.

Thanks so much for your website!"

http://www.foodanddiet.com/splenda/stories-500-599/splenda-story535.html

On 20 June 2006, we received this note from B. concerning their use of
sucralose.

"I was searching for a website about sucralose and found your site.

I have problems with this sucralose that are among your list. I have experienced
bloating, abdominal pain (real bad), redness on my face, swollen itchy bumps on
my face, and diarrhea. I have also had a symptom that is not on your list:
clumsiness. It's like my feet don't go where they are supposed to go. I trip and
stumble.

I know these problems are caused by the sucralose because I tested myself. The
days I drank flavored water with sucralose, I had the symptoms. A couple of days
without sucralose and the symptoms disappeared. I tried the drinks a week later,
and the symptoms reoccurred.

I'm really disappointed because I hate the taste of regular water, but it seems
everything now has sucralose in it.  When Fruit 2-0 first came out, I
experienced the above symptoms. I called the company to ask if Splenda could be
causing it or if they had any complaints of side effects.  I was told there had
been no adverse effects at all. BULL!

It's like I now haven't any choie except to be very careful of what I eat and
drink. I read every word on labels. What ever happened to just plain sugar?!
Doesn't anyone care what this stuff is doing to people?!

Thank you for your website."

http://www.foodanddiet.com/splenda/stories-500-599/splenda-story536.html

On 21 June 2006, we received this note from N.H. in Northern California
concerning their use of sucralose.

"Quite a few years ago, I was diagnosed by my physician as having reactive
hypoglycemia. My blood sugar dropped to 43 during the testing. I struggled with
that off and on over the years depending on how careful I was about what I ate.

About three years ago, I was diagnosed as hypothyroid. I was avoiding caffeine
and taking Synthroid (50, the white ones). I was actually feeling better than I
had in a long time. I don't remember when I first tried Splenda, but I didn't
like it because it seemed to cause my blood sugar to shoot up and then crash so
I could barely stay awake. I didn't buy anything with it, but I may have had
some occasionally at a restaurant or at someone's house.

Last Thanksgiving, I bought some flavored instant decaf coffee. When I was
drinking that I was not having the sleepy crash so I didn't suspect the Splenda.
But I was not feeling well. I was anxious and depressed, especially in the
mornings. The coffee was the only thing I was eating or drinking that was
different. When I stopped drinking the coffee, I felt much better.  I didn't
associate the problem with the Splenda, though, and thought it may have been
related to the process of removing the caffeine.

Since then, I occasionally had soda with Splenda and didn't seem to be bothered,
although as I look back, my hypoglycemia seemed worse at times and I had
symptoms with lower amounts of carbs. Last month, at the end of the school year
(I am a teacher), when I was under more stress than usual to get everything
done, I bought some sugar-free ice cream with Splenda. The stress and the
Splenda together caused real problems. I felt terrible. I was nervous and
depressed, especially in the mornings.  I could feel my heart beat and my
thyroid started working overtime, so I had to stop taking my thyroid medication.
After less than a week without Splenda, I was feeling much better, and after a
week the symptoms were gone.

I think, in my case, the Splenda aggravated the hypoglycemia. I'm not sure why
it made my thyroid work overtime, but it certainly seems that it did."  ]

http://www.foodanddiet.com/NewFiles/splenda.html
Index 1 -- 6, from 2003.12.28 to 2005.04.16
___________________________________________________


http://ajpgi.physiology.org/cgi/content/abstract/00056.2008v1

"Mechanisms by which gut luminal content regulates secretion and motility is
ill-understood.
... the artificial sweetener, sucralose, stimulated (EC50 = 9.2nM and 0.38nM)."

Am J Physiol Gastrointest Liver Physiol. 2008 Jun 12. [Epub ahead of print]
The luminal regulation of normal and neoplastic human EC cell serotonin release
is mediated by bile salts, amines, tastants and olfactants.
Kidd M, Modlin IM, Gustafsson BI, Drozdov I, Hauso O, Pfragner R.
Surgery, Yale University School of Medicine, New Haven, Connecticut, United
States.

Introduction:
Mechanisms by which gut luminal content regulates secretion and motility is
ill-understood.

We evaluated whether neuroendocrine enterochromaffin (EC) cells act as
luminal-sensors for a wide variety of nutrients and defined the secretory
mechanisms of this process.

Methods and Results:
Pure (98-99%) FACS-sorted human EC cells and neoplastic EC cells (KRJ-I) were
studied.

RT-PCR identified transcripts for T2R1 (bitter), OR1G1 (class II olfactory) and
trace amine (TAR1) GPCRs, and transporters for glutamine (SNAT1/2), glucose
(GLUT1/3/SGLT1) and bile salts (ABST).

Glutamine and sodium deoxycholate stimulated 5HT release (EC50 =
0.002-0.2microM; 2-fold release) but were 10-100x more potent in neoplastic EC
cells which also secreted 6-13x more 5HT.

Tastants (caffeine, tyramine, octopamine) and olfactants (thymol/eugenol), also
stimulated normal and neoplastic EC cell 5HT secretion (EC50 = 1.2nM-2.1microM
and 0.05nM-0.1microM release, respectively) while 2-deoxyglucose and the
artificial sweetener, sucralose, stimulated (EC50 = 9.2nM and 0.38nM).

5HT release was associated with ERK phosphorylation (1.5-fold, p<0.02) and could
be inhibited by a somatostatin analogue (IC50: 10(-12)M).

Eleven secretory associated genes including the vesicle docking inhibitor,
STXBP3, were up-regulated in response to glutamine and bile salt stimulation in
neoplastic EC cells.

Targeting STXBP3 expression using antisense knockdown significantly (p<0.05)
reduced 5HT secretion.

Conclusions:
EC cells express GPRCs and transporters for luminal tastants, olfactants,
glutamine, glucose and bile salts.

Activation includes a panel of secretory genes, ERK phosphorylation and 5HT
secretion.

Luminal EC cell regulation is likely to be as important as the G cell regulation
in gastric acid secretion; development of agents to target EC cell function is a
critical therapeutic goal.

Key words: gastrointestinal, luminal, neuroendocrine, secretion, tastant.
PMID: 18556422

Mark S. Kidd 1, mark.kidd@...;
Irvin M. Modlin 2*,  imodlin@...;   Telephone: +1-203-7855429     Fax:
+1-203-7374067
Bjorn I Gustafsson 3, bjorn.gustafsson@...;
Ignat Drozdov 1,  ignat.drozdov@...;
Oyvind Hauso 4,  oyvind.hauso@...;
and Roswitha Pfragner 5  roswitha.pfragner@...;

1 Surgery, Yale University School of Medicine, New Haven, Connecticut, United
States
2 Surgery, Yale University School of Medicine, New Haven, Connecticut, United
States; United States
3 Surgery, Yale University School of Medicine, New Haven, Connecticut, United
States; Internal Medicine, Gastroenterology, St Olavs University Hospital HF,
Trondheim, Norway
4 Molecular Biology and Cancer Research, NTNU, Trondheim, Norway
5 Institute of Pathophysiology, Centre for Molecular Medicine, Medical
University of Graz, Graz, Austria; Institute of Pathophysiology and Immunology,
Centre for Molecular Medicine, Medical University of Graz, Graz, Austria
* To whom correspondence should be addressed. E-mail: imodlin@...;
___________________________________________________


http://en.wikipedia.org/wiki/Sucralose

http://groups.yahoo.com/group/aspartameNM/message/1481
Australia official report 2001.12.10 finds arsenic impurity in sucralose
at 15 % of USA EPA adult ADI limits for daily drinking water, also 67 %
of child lead alarm limits -- evidence for claims by D.L. Dewey and G.N.
Ferebee petition (some typos): Murray 2007.10.25

http://groups.yahoo.com/group/aspartameNM/message/1413
sucralose, aspartame, sugar legal melee, How Sweet It Isn't, Avery
Johnson, Wall Street Journal: Murray 2007.04.06

http://groups.yahoo.com/group/aspartameNM/message/1412
sucralose (an earnest effort at a neutral summary of both sides of the
Splenda toxicity debate), Wikipedia 2007.03.26: Murray 2007.03.29

adroit PR firm Qorvis Communications, hired by Sugar Association, coyly
sets up Citizens For Health front to attack sucralose (Splenda):
Murray 2007.03.22
http://groups.yahoo.com/group/aspartameNM/message/1411

http://groups.yahoo.com/group/aspartameNM/message/1328
Migraine from sucralose, Bigal ME & Krymchantowski AV,
Headache 2006 March; formaldehyde from 11% methanol part of
aspartame or from red wine causes same toxicity (hangover) harm:
Murray 2006.04.24

http://groups.yahoo.com/group/aspartameNM/message/1257
Comet assay tests groups of 4 mice to show sucralose genotoxicity
in stomach, colon, lung, Yu F Sasaki et al, Mutation Research 2002,
full plain text: Murray 2005.11.22

http://groups.yahoo.com/group/aspartameNM/message/1152
reply to Ferne Hudson, Tate & Lyle PLC, re Splenda (sucralose) policy:
Murray 2005.02.08
"This weekend I found a large, competent website by Mr. Mark J. Yannone, a
programmer, who in email on 2001.01.22 reported that his seizures were cured
by giving up aspartame. Aspartame and sucralose are only a small fraction
of the issues listed on his voluminous site.

http://www.foodanddiet.com/ foodanddiet@... Mark J. & Cherie Yannone
1421 E Charleston Ave, Phoenix AZ 85022
Phone 602-569-9632 Fax 602-569-9635

http://www.foodanddiet.com/NewFiles/splenda-story-list.html lists an
ever-growing archive, now 236 reports in a year, of posts about symptoms from
sucralose -- about 10% of the posts said they had no problems. The
sophistication, size, organization, and clarity of this site far exceeds what
aspartame activists offered six years ago, as does the amount of user
information.

Here are the first titles:

"I woke up with my very first migraine ever...
There has never been any negative side effect...
I have been headache free for two weeks now...
Using Splenda for a year now with no problem...
Uncontrollable bouts with gas...
I'll continue with the Splenda...
Hot and cold flashes, but also depressed for no reason...
I plan to throw out the entire box...
It IS the sucralose making me ill...
At no point would I have ever put two-and-two together...
We recently changed our way of eating...
I can relate to the symptoms I have read...
I know I feel better now, and I know how I was feeling then...
Splenda was like a kick in the stomach...
I felt so terrible I was not even able to go to work...
My focus seems to be returning...
I'm still in awe of my experience...
I have had a whopping headache for hours now...
I had one encounter with the use of Splenda...
Splenda is not so splendid...
I truly cannot attribute negative side effects to the sweetener...
I can't believe that I have been poisoning myself ...
I also stopped losing weight after adding sucralose...
I found myself spinning into a dark depression...
I started feeling "not myself"...
I have only used Splenda a few times...
I noticed incredible fatigue and sleepiness...
I am not happy with the results...
I didn't even realize it might be the Splenda ...
I had the worst feeling...
Two weeks ago, my wife decided to use Splenda ...
What a terrible mistake!...
I have had no side effects at all...
I decided to try Splenda again...
I wanted to pass along my story about sucralose...
I started using Splenda in small doses..."

"Based upon information supplied to us by our visitors, we note the
following possible side effects from consumption of sucralose:

bloating
abdominal pain
gas
nausea
diarrhea
headaches
migraines (severe headaches)
heart palpitations (fluttering)
shortness of breath
depression or overwhelming anxiety
spaced-out or drugged sensation
joint pain
dizziness"

I notice that these are also common symptoms reported by aspartame reactors."
___________________________________________________


"Of course, everyone chooses, as a natural priority, to enjoy peace,
joy, and love by helping to find, quickly share, and positively act
upon evidence about healthy and safe food, drink, and environment."

Rich Murray, MA Room For All rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com  new primary archive

http://groups.yahoo.com/group/aspartameNM/messages
group with 126 members, 1,555 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1,126 members, 22,843 posts in public archive
___________________________________________________

excellent long essay on universal core values for world reform, Nichola Torbett,
The Network of Spiritual Progressives 2007.02.14: Rich Murray 2008.07.28
http://rmforall.blogspot.com/2008_07_01_archive.htm
Monday, July 28, 2008
http://groups.yahoo.com/group/aspartameNM/message/1554
http://groups.yahoo.com/group/rmforall/messages/83


Rich Murray rmforall@...  505-501-2298
___________________________________________________


http://www.spiritualprogressives.org/

http://www.spiritualprogressives.org/article.php?story=20061207101937278

Core Vision  Posted Wednesday, February 14 2007
by Nichola Torbett, Director of National Programs

Updated information on membership dues to the NSP can be found by going to
www.spiritualprogresives.org

You can join online or contact us at:
The Network of Spiritual Progressives, c/o TIKKUN Magazine
2342 Shattuck Avenue, Suite 1200, Berkeley, CA 94704.
Tel: (510) 644-1200
(call during business hours 9:30 a.m. -5:30 p.m. M-F, Pacific Standard Time).

Email: RabbiLerner@... or generosity@...

Many of us are involved in or greatly admire the accomplishments of social
change movements like the peace movement, the women's movement, the
environmental movement, the movement for economic justice, the civil rights
movement, the gay rights movement, the labor movement, struggles for civil
liberties, and the disability rights movement, to name just a few.

And yet, we believe that these movements have tended to underplay or even deny a
very important dimension of human life -- the spiritual dimension. And this
deficit has limited the potential impact that all these movements could have. It
will take a very different kind of movement -- one founded on and giving central
focus to a spiritual vision -- to create a real alternative to the political
Right, to the fundamentalists (religious and political), and to our society’s
ethos of selfishness, materialism, and cynicism.

We seek to create that alternative. We are a community of people from many
faiths and traditions, called together by the Spiritual Covenant with America
(see www.spiritualprogressives.org ) and its vision of healing and transforming
our world. We include in this call both the outer transformation needed to
achieve social justice, ecological sanity, and world peace, and the inner
healing needed to foster loving relationships, a generous attitude toward the
world and toward others unimpeded by the distortions of our egos. Our movement
will encourage a habit of generosity and trust, and the ability to respond to
the grandeur of creation with awe, wonder and radical amazement.

We are guided in our work by our belief in the principle of solidarity. For some
of us, this principle has spiritual roots in the Jewish commandment to remember
that we were all slaves in Egypt; we believe that we are all harmed by
oppression directed at any group or individual. This is a message which is
common to most of the religious and spiritual traditions of the human race for
the past several thousand years, and is part of the tradition also of many
secular and even "orthodox atheist" groups that came into existence in the past
few hundred years when the religious and spiritual communities that supposedly
were committed to these values actually failed to take them seriously and
became, instead, embedded in economic and political realities that were
oppressive.

We in the Network of Spiritual Progressives use the word "spiritual" to include
all those whose deepest values lead them to challenge the ethos of selfishness
and materialism that has led people into a frantic search for money and power
and away from a life that places love, kindness, generosity, peace,
non-violence, social justice, awe and wonder at the grandeur of creation,
thanksgiving, humility and joy at the center of our lives.

We believe that many of the secular movements that exist in the world today
actually have deep spiritual underpinnings, but often they are themselves
unaware of those foundations, unable or unwilling to articulate them and
sometimes even holding a knee-jerk antagonism to explicit spiritual or religious
language. This antagonism limits their effectiveness, though it derives from
legitimate anger at the way that the language of spirituality and religion has
been sometimes used to justify war, oppression, sexism, racism, homophobia,
ecological indifference, or insensitivity to the suffering of the poor and the
homeless of the world.

Solidarity means that we affirm our responsibility towards each other within our
families, within our nation, and within our spiritual/religious community -- and
also beyond the narrow boundaries of ethnicity, religion, and geography. We
affirm the obligation to actively resist injustice and refuse to take part in it
even when we can't prove that our resistance will produce change. In solidarity
with the oppressed, we wish to see the democratization of economic and political
institutions and a redistribution of wealth so that all people can share equally
and sustainably in the benefits of the planet.

We hope to have the courage -- in the tradition of the Jewish prophets and
interpreters of Torah, in the spirit of Jesus and the early Christian
communities of resistance to Rome, in the spirit of Muhammed, in the spirit of
the activists of the labor & civil rights and feminist and gay rights movements
-- to speak truth to power. The Network of Spiritual Progressives is an
interfaith organization (and welcoming to agnostics and atheists as well).

At the same time, we will challenge the lack of a spiritual dimension in the
agendas of our allies in progressive social change movements. That gap has
allowed the Right to present itself as the force that cares about spiritual
issues. And the Left’s failure to address spirituality has led many to believe
their hunger for a larger framework of meaning and purpose must be separated
from their involvement with social transformation.

Social change activity gets focused on a narrow political agenda that lacks the
depth that can inspire sustained commitment or nourishing involvement. Imagine
an international group of people who would see themselves as allies to each
other in advancing this way of thinking, people who are unashamedly utopian and
willing to fight for their highest ideals, yet unashamedly humble in knowing
that we don't know all that we need to know to do the healing that needs to be
done.

Imagine that this group would help each other in our individual as well as group
activities, affirming what is good and brainstorming with us about how to create
a movement that gives equal priority to our inner lives and to social justice,
that takes loving and caring as serious goals for social healing, and that
rejects the utilitarian and materialistic assumptions of the contemporary world
and actively fosters awe and wonder in its participants. Imagine that you could
be part of creating that.

You can -- by helping us create the Network of Spiritual Progressives (NSP). The
NSP starts from this fundamental recognition: The sources of external injustice,
suffering, and ecological numbness are to be found not only in economic and
political arrangements, but also in our alienation from one another, in our
inability to experience and recognize ourselves and each other as holy, in our
inability to respond to the call of the universe which bids us to deeper levels
of consciousness and love, and in our inability to overcome our own egos and see
ourselves as part of the Unity of All Being.

We need a spiritual consciousness along with a political consciousness if we are
to heal and transform the world. Some of us in the NSP are atheists or
secularists, some of us belong to traditional religious communities, some of us
are just beginning to work out our relationship to Spirit. But all of us
understand that we need a movement that can address spiritual needs.

It is our contention that social change and inner change go hand in hand. We are
building a movement in which we can talk about love and caring for each other --
and this is the only way we can overcome the old left/right dichotomies and dead
policy debates that fill academic journals, leftie magazines, the insipid
television confrontations between shouting talking heads, the vacuity of so many
of the speeches at leftie anti-war demonstrations, and the rhetoric of elected
officials. For too long these predictable slogans and divisions have paralyzed
American politics and made most of us feel like withdrawing into a purely
personal life.

At this moment, we are particularly excited by and supportive of the upsurge of
social justice activism aimed both at promoting environmental sanity and at
challenging the destructive impact of globalization. But we hope to play a role
in deepening those and other social change movements to integrate into their
core the kind of spiritual awareness that can make it possible for them to reach
a much wider audience and thus be able to actually achieve their social justice
goals.

To do so we must talk at a far deeper level than merely repeating or reframing
the traditional leftist demands for economic and political rights. While we
support those demands and thus welcome any advances that provide adequate food,
clothing, shelter, health care, child care, and other basic rights, we also
believe that these will only be won on a global level when the social change
movements are able to address the spiritual consequences of the triumph of
corporate globalization: a society-wide depression and repression of what we can
variously call the life-force, eros, God-energy or Spirit.

Please note that this is very different from those who talk about spiritual
politics but actually mean only this: that it would be politically advantageous
and opportune to take the traditional liberal agenda and dress it up with some
spiritual or “values” language. So they take the existing liberal/left agenda,
with its primary focus on social justice, inclusion of those who have been left
out, economic redistribution, and peace -- and then they find some Biblical
quotes to bolster the case for the pre-existing liberal/progressive agenda. We
support all that, but our movement goes much deeper. We don’t believe that the
liberal agenda can be won simply by reframing it in spiritual language.

For a large section of the American public, the primary source of pain in their
lives is not about economic deprivation or non-inclusion, but about the way that
the ethos of selfishness and materialism plays out in their personal lives and
in the lives of people around them in ways that are destructive and feel
terrible. They can’t stand being part of the manipulative, narrowly utilitarian
way people treat each other and themselves and the earth. They want a framework
of meaning to their lives and to the lives of those around them that speaks of
higher meaning to life, shows a path to a life that is not only about maximizing
money but about maximizing a meaningful life -- in short, they want and need a
politics of meaning, and need a meaning-oriented movement that can counter the
spiritual depression that surrounds them.

Don’t confuse this with those who simply are trying to put some Biblical quotes
in front of the same old Democratic Party or liberal agenda -- we are seeking a
much deeper change. Our challenge is not only to the Right -- but also to the
liberals and progressives, to the Greens and the Democrats, who have not allowed
themselves to get beyond their knee-jerk antagonism to religion and
spirituality, and whose openness to religious or spiritual people is only
utilitarian and does not include a willingness to learn about the actual
dimensions of the spiritual deprivation which is endemic to the way global
capitalism functions today, and the ways that it generates a global emotional
depression.

This spiritual depression and emotional repression that suffuse contemporary
life are the near-universal responses to the globalization of a
self-congratulatory individualism, obsessive materialism, and consumption -- all
provided as compensation for the meaninglessness of our present-day culture. The
one-dimensional technocratic consciousness, speed-up of work, perception that we
have "no time" to do what we really believe in, and our inability to recognize
others in terms that go beyond what they can do for us to advance our own
agendas as rational maximizers of self-interest -- all these combine to create
human beings who, if they don’t explode in violence or self-destructive alcohol
and drug abuse, find themselves in varying degrees of disconnection to their
inner selves, their feelings, and their capacities to be loving towards others
and responding to the universe with joy.

In contrast to this, we encourage an engagement with the Sacred, an Emancipatory
Spirituality which affirms pleasure and joy and the recognition that "there is
enough," a replacement of postmodernist self-alienation with a renewal of Being
based on awe, wonder and radical amazement at the mystery of the universe and
the mystery of every human being on the planet as a manifestation of the sacred.
Our economic, social and political institutions need to be replaced and
rethought not only because they are unjust, but because they foster a
consciousness that keeps us from connecting to the deepest truths of the
universe and make it harder for us to recognize each other as fully free, fully
conscious, self-creating, loving beings. In this sense, the globalization of
Spirit is the antidote to the globalization of Capital.

We reach out for a spiritual dimension not as a replacement for, but as a
deepening, of our understanding of social action, and not as a replacement for
but a deepening of our understanding of informed science. Our spirituality does
not reject the value of rational thought nor does it suspend scientific inquiry.

Why is it that people who live in the advanced industrial societies of North
America, Europe and Japan, the richest societies that history has ever known,
believe we "can’t afford" to share what we have with the rest of the world so as
to eliminate poverty, hunger and homelessness? It is partly because of our
collective paranoia that no one will be there for us if we should ever really
need their help that leads us to think our only security lies in endless
accumulation, to protect our isolated self-interest in face of a deep inner
certainty that others can’t be counted on. And partly because we have a deep
emptiness inside and we have come to believe that only material goods can fill
it. We buy things to buy happiness, to compensate ourselves for the alienated
work, the disconnection from each other, and the estrangement from our own inner
selves that constitute the texture of our daily lives.

In our spiritually impoverished world, acquiring ever more things provides an
illusion of fulfillment -- and a replacement for the deep connection with each
other and to the spiritual realities of the universe for which we both hunger
and simultaneously deny to ourselves (lest we re-experience the pain and
disappointment we had at earlier points in our lives when we allowed ourselves
to be vulnerable and then failed to receive the loving and recognition we needed
but didn’t fully get).

In addition, almost every child in our culture gets strong messages to focus
attention on that which can be useful, and away from the spiritual dimension
which has no "practical application." Indeed, this message has been so deeply
ingrained in many of us that we instinctively shy away from the spiritual realm
as though it were as dirty as not being toilet trained. We fear that were we to
acknowledge to ourselves or others that we actually wish for connection with
that which cannot be used or made practical, cannot be subject to empirical
observation or turned into a commodity or something that will make us more
attractive or salable on the job or relationship marketplace, we would subject
us to ridicule and humiliation.

Fearful that we will experience that pain once again, we often build strong
external walls to keep us out of touch with this deep yearning for connection to
each other and to the universe. Instead of drawing on our own inner resources,
we too often find ourselves looking to the media-dominated mass culture for
fulfillment and reassurance that our scaled-down sense of possibility is "what
everybody else is doing" and hence "the only possible path for us too." The
media is one of the many institutions that speeds up time -- protecting us from
the quiet moments in which we might doubt the whole way our lives our being
lived.

Instead of finding our own pace, we find ourselves rushing about, seeking
machines and gadgets that make things go faster, becoming accustomed to media
and technology which speed the pace while “shallow-ing” the intellectual and
emotional level of our daily consciousness. We learn to forget the past and
focus only on the new while devaluing the old, which leads to decreasing
literacy and an increasing difficulty in following a complex discussion,
sustaining a long-term relationship, or committing to social goals that can't be
accomplished immediately.

Sadly, our social institutions only reinforce this materialist view. Our
institutions provide us with the illusion of permanency (pretending we won’t
die) and the illusion that the "real world" is the world of power and wealth.
Compound this with the patriarchal assumption that we should be tough and ignore
our feelings, and we are left with a "common sense" that dismisses the relevance
of our inner lives. We are told that spirituality should be left in the home,
relegated to the weekend, kept separate from the pragmatic decisions that should
shape politics and the business world.

In the NSP, we refuse this kind of "realism." We will unashamedly use and learn
from the language and practices of spiritual communities. The spiritual life can
give us a level of mindfulness, focus, and calm so that we can re-center
ourselves and discover what we truly value.

One reason we are proud to have the NSP draw upon the spiritual wisdom of
Judaism is because we think that the spiritual practice of Shabbat, a
twenty-five hour meditation focused on turning our energies from "getting things
done" to a "celebration of all that is," can empower us in the struggle to heal
our planet. This is one example of the kinds of spiritual practices that we
encourage among our members and for the larger world -- even as we say this in a
non-coercive way without implication that you must be doing a particular
spiritual practice to be part of our community.

So too the Biblical idea of a Sabbatical Year for all and the Biblical idea of
Jubilee with its call for a redistribution of land and wealth back to a basic
equality once every fifty years provide us with inspiration for how to learn
from the wisdom of sacred texts.

Although our organization will speak at times in the name of the best in the
Jewish tradition, we will also honor all major spiritual traditions represented
in our membership. We are a multi-ethnic, multi-religious, multi-spiritual
community -- and we believe that there are many paths to spiritual truth, and we
want to honor all of those which are open to an Emancipatory Spirituality as
presented in TIKKUN magazine. So we draw upon the richness of Christianity,
Buddhism, Islam, Hinduism, spiritual truths from indigenous peoples and from the
often ignored spiritual wisdom of women.

We do not believe that every particularistic tradition must be totally left
behind in some new globalized spiritual mush. While we support the attempts
within existing religious and spiritual traditions to renew their foundations,
we do not seek a spiritual melting pot but a world in which plurality and
difference can be respected, even as we affirm the Unity of All Being, the
interconnectedness of all with all.

At the same time, we will challenge reactionary spirituality that privileges one
group above all others while demeaning those who are not part of the group. We
will challenge forms of spirituality which seek to impose racist, sexist, or
homophobic values. And we will challenge forms of spirituality which lead people
into quietism or a de facto accommodation to a world of oppression. In this and
other respects we want to be clear that we do not embrace a vapid "tolerance"
which refuses to make moral distinctions or a deconstructionist logic which sees
all forms of discourse as little more than strategies for some group or other to
gain power over others. We are not tolerant of religious reactionaries who
manipulate the language of God in the service of an oppressive status quo or to
restore patriarchy and authoritarian forms of government.

Our goal is to build a community of people who share a common
intellectual/spiritual perspective -- an intellectual/spiritual cadre of
activist social healers -- even as they retain their own particular religious
and spiritual practices. We will work together to bring a progressive spiritual
politics into the various arenas in which we work. For example, we will bring
our perspective into existing social change movements in the hopes of
strengthening them and making them more successful. Our task is to support each
other as we bring ideas into the public sphere that are often dismissed as "too
idealistic" or "too spiritual" -- and to help each other sustain a commitment to
a transformative agenda against all the pressures to be "more realistic" and
settle for much less than we actually believe in.

In this work, we see ourselves as fundamentally connected to the thinking being
done in TIKKUN magazine. We connect with all who hope for a real TIKKUN (the
Hebrew word for healing, repair and transformation).

The NSP will not be a traditional organization -- certainly not an organization
that would compete with or take resources away from other social action groups.

We are trying to create something which doesn't have an exact analogue in
contemporary life. The truth of the matter is, many of us are wary of any
organization -- they remain human institutions, susceptible to the ever-present
reality of human frailty. The capacity to under-whelm, frustrate, disappoint,
and madden is common to all human organizations, whether spiritual or secular,
whether on the left or the right or in the middle.

Particularly when people start hoping for a loving reality, we often get so
scared -- because we have been so deeply shaped by the pathogenic belief that we
don't really deserve to be loved -- that we try to prove to ourselves that a
better world isn't really possible. That’s when we find people in our
organizations hurting each other in the name of love, being brutal and lacking
compassion, creating endless fights over theoretical differences, or clinging to
ego at the cost of finding real solidarity with others. We will do what we can
to provide a supportive context, but we will also not hesitate to ask people to
leave our organization who would prefer to fight with each other than to
lovingly support each other. Creating an international community of people who
start with agreement on the points in this document can generate generous
amounts of comradely love and solidarity.

We expect that in the NSP we will find ourselves learning from our dialogue with
each other, having intense conversations, listening to each other's formal
presentations but also, and equally importantly, each other's life experiences
and current struggles. Our community will only be sustainable if it provides
many opportunities to laugh with each other, to meditate or pray together, to
sing and dance together, and to experience each other as sources of surprise,
joy and transcendence. So, our expectation is that this commitment will be fun
and joyous.

If you are interested in joining us, please look over the fundamental principles
printed below. Are they principles you share? If so, please become a dues-paying
member of Tthe NSP (you can join on-line at www.tikkun.org or by calling our
national office at 510 644 1200). And we will contact you to find ways to
integrate you into our growing organization.

1. INTERDEPENDENCE AND ECOLOGICAL SANITY

We are one mutually interdependent human race, and we have a responsibility to
be stewards of the planet and of all other life forms. Our well-being depends on
the well-being of every other human being on the planet and on the well-being of
our environment. It is time to overcome all forms of national, religious, and
ethnic chauvinism. It’s time to realize that it is in our own personal
self-interest to ensure a world in which everyone is invited to be part of
loving, spiritually deep, emotionally satisfying, and materially thriving
communities of their own choice, and to live in a world in which mutual respect
and care are the common sense truths by which we live.

As Americans we can no longer worry only about what is "best for America," as
Jews we can no longer worry only about what is "best for the Jews," as
Christians we can no longer worry only about what is "best for the Christians,"
etc. We need to see ourselves as manifestations of Spirit -- the unfolding of
the love and goodness of the universe as it becomes conscious through us. The
world is entering a new period in which this understanding of ourselves as
fundamentally aligned with all other human beings on the planet becomes the
prerequisite for building a global political and economic movement capable of
challenging corporate power and saving the planet from ecological destruction.

To recognize our mutual interdependence does not require us to abandon cultural
difference. We reject the view that says that real peace can only be achieved if
everyone is alike, part of a leveling universal culture fostered by a
melting-pot of preexisting cultures.

We do not seek to obliterate all differences, but to build a multi-cultural
world based on mutual recognition and respect for difference. The world is
better served by a diversity of religious, ethnic and cultural traditions --
each of which has learned to respect and honor this diversity and to divest
itself of those elements in its tradition that lead to hatred or the demeaning
of others. Our responsibility to the planet requires us to make dramatic
transformations in our patterns of production and consumption. We must:

Take all necessary steps to halt and reverse global warming (really, global
scorching). Encourage graceful simplicity in living. We must commit to sharing
the resources of this planet equally with all six billion other human beings
while also committing ourselves to the planet’s ecological sustainability. This
commitment requires that we alter our notions of private property in ways that
give adequate attention to the needs of the whole, rather than approaching the
world first and foremost from the standpoint of our individual rights without
sensitivity to the needs of others.

Adopt a new attitude of caring toward animals and other life forms, and a
recognition that stewardship implies responsibility to take all necessary steps
to preserve the diversity and integrity of life forms on this planet, to the
greatest extent possible consistent with protecting human life (we don't
"respect" the "rights" of cancer or forms of life that are aggressively
destructive to human beings).

Exercise extreme caution in the uses of biotechnology. We should immediately
remove the profit motive and ensure that all significant decisions are made
within a context of democratic control. A new sense of humility should govern
any decision that might potentially alter the biosphere or the genetic
structures of plants, animals or humans. Science must be harnessed to serve the
highest values of the human race, not the profit-motives of corporations or the
military needs of governments.

Commit ourselves to Ethical Consumption or what the Jewish Renewal movement
calls eco-kashrut, (building on the traditional Jewish concern with the origins
of the food we eat as a tool to actualize the environmentalism of our
tradition). Ethical Consumption requires that all purchasing decisions,
including but not limited to those necessary for physical sustenance, be made in
a way that has the least negative environmental impact. We hope to enlist many
people in religious and spiritual communities to participate in the formulation
of standards and the ongoing observance of ethical consumption.

Ethical Consumption is a direction for our communal aspiration, but in this area
as in every other we are super-careful to not let our ideals become a club to
beat each other up with (as in "you own an SUV so you can’t be part of our
movement" or "you have too big a house" or "you shouldn’t take vacations"). As
in all things, spiritual balance is critical: recognizing a direction for our
energies, but being compassionate and tolerant of the different paces at which
people move toward that goal. Tolerant to individuals -- but not tolerant toward
social and corporate policies that are environmentally destructive. Not tolerant
of societal decisions like opposing sensible constraints on ozone destroying
emissions and not tolerant of environmentally hazardous global trade accords.

2. A NEW BOTTOM LINE IN OUR ECONOMIC AND SOCIAL INSTITUTIONS

Productivity and efficiency must no longer be judged solely by the degree to
which any corporation or institution maximizes profits or power, but also by the
degree to which a corporation, school, government institution, or social
practice tends to :
support ethical, spiritual, and ecological sensitivity and to promote the
sustainability of our environment;
support human beings to be loving, caring and capable of sustaining long-term
loving relationships;
promote the well-being of everyone on the planet;
help people overcome a narrow utilitarian attitude toward each other or toward
the universe and encourages them instead to see other people in a
non-utilitarian way, and to view the physical world not primarily as something
that can be used for human purposes but also through the lens of awe and wonder
at the grandeur of creation.

Beyond all definitions of efficiency and productivity, we seek to shape a
society in which there is time not only to Do and to Make but there is time also
to Be and to Love -- time for family, community, and spiritual exploration.

We want this New Bottom Line brought into all aspects of our public life, so
that we can begin to reshape our schools and hospitals, our government, our
professions, our media in ways that encourage people to see each other as
fundamentally valuable and deserving of love and caring. We reject the notion
that values should be kept out of public life, and instead seek to champion the
values articulated in this statement, and to encourage social change that would
foster these values throughout the society.

So, for example, we want schools to be assessed as successful or as failures not
only to the extent that they produce students who can read and write but also to
the extent that they tend to foster caring human beings who are ethically and
ecologically sensitive, who excel at taking care of others and at developing
their own inner resources, and who have developed the capacity to respond to the
universe with awe and wonder.

We want corporate charters to be dependent on their ability to prove a history
of social responsibility as measured by an Ethical Impact Report. We want all of
our economic and social institutions to be judged successful to the extent that
they foster caring and respect for all peoples and for the planet. While some of
the direction for this thinking has already been developed in Rabbi Michael
Lerner’s book Spirit Matters: Global Healing and the Wisdom of the Soul, we
believe that a full vision can best emerge when people in their own workplaces
and professions can form consciousness raising small groups which will develop
concrete and detailed answer to the question: “What would this workplace or
profession look like if it did in fact have a ‘New Bottom Line’ like that called
for by The Tikkun Community -- and how do we begin to take the first steps to
struggle for that new bottom line, both in our own workplace and by uniting with
others in other workplace and professions to seek
  support for these changes?” This conversation will become a central task of
people in building a new spiritual politics in the coming decades.

There are some who believe that the New Bottom Line we seek can be instituted
inside corporations and within the evolving framework of global capital. There
are others who believe that it will take a whole new economic system to get a
New Bottom Line. We welcome both within our organization -- our commitment is to
this New Bottom Line, and encourage anyone who is serious about struggling for
that New Bottom Line to be part of our organization as long as they don’t
sacrifice that struggle to “realism” (which is a way of saying, that they don’t
give up the struggle in order to accommodate to the power of the capitalist
system as currently constituted). What matters to us is what happens when the
decisions are actually being made: what are the criteria being used?  If, in the
heat of decision making, the decision makers put the development of loving and
caring human beings above the maximization of profits, if hey consistently use
the criteria of our New Bottom Line specified above (n
ot just in their language but in the actuality of their considerations and
deliberations), we don’t care what you call the name of the economic system that
is using these criteria or who formally owns the stocks in those companies.

3. SUPPORTING THE STRUGGLES FOR SOCIAL JUSTICE AND PEACE

We are committed to the efforts to create peace and social justice throughout
the world. We insist that hunger and poverty can be eliminated -- and that this
be given a very high priority in allocating our taxes. We support the struggles
for adequate health care and access to medicine, for child care and elder care,
and for other fundamental human rights including the right of working people to
meaningful work with a living wage, the right to organize in defense of their
own interests, the protection of children from exploitation, and the end to all
forms of slavery, forced labor, and sweatshops.

We support efforts to give primacy to ecological and social justice concerns in
all global economic arrangements. We align ourselves with the efforts to
challenge the kind of globalization that is being forged by the world's elites
of wealth and power. We stand in strong opposition to the use of torture or
violence, and all forms of abuse (physical, sexual, and emotional) and insist
that children be treated with respect and nonviolence. We call for an end to
imprisoning drug users and for the creation of a sane drug policy that mixes
prevention and treatment with a recognition that some of the psychedelic drugs
currently illegal have positive medical and/or psychological benefits and should
be made responsibly available rather than having their use criminalized. We
oppose the War on Drugs and its use as an instrument of assault against young
African Americans (jailing them for use of drugs that whites also use without
facing similar penalties) and as an excuse to intervene in Colom
bia and other countries.

We support disarmament both on an international level and on a societal level.
We support the enforcement of international human rights. And we support efforts
to create an international peace force to intervene with techniques of
nonviolence to prevent wars and violence. But we insist that peace depends also
on economic security and feelings of respect and open-heartedness toward "the
Other," and that these need to be an intrinsic part of our conception of
international assistance and aid. We join with the Jubilee 2000 in calling for a
worldwide agreement to abolish all third world debt and instead call for a
guarantee that loans in the future will go directly to the development of
education, training, health care, and housing of the people in recipient
countries. And we support massive funding from the Western world to fight AIDS,
poverty, homelessness, and inadequate education and health care.

We are committed to advancing the struggles of women in all spheres of life for
full equality. Women’s experience and wisdom must become a shaping force as we
build a more liberatory and more nurturing culture and work world. We support
the struggles of gays, lesbians, bisexuals, and transgendered people who seek
full equality, respect, and opportunity to live their lives without being bound
to traditional ideas about gender and sexuality. We see the oppression of gender
as inextricably linked to the oppression that takes place within the categories
of race and class, so we support those who are seeking to build healing in all
three realms simultaneously.

We call upon the United States to move toward an honest recognition and
repentance for slavery, for post-slavery segregation, and for the long history
of oppression and racism toward peoples of color, most particularly with regard
to African Americans but also including its treatment of people from Mexico,
Central and South America, its treatment of Japanese, Chinese and other Pacific
Island immigrants, and its treatment of American Indians. In this regard a
society-wide strategy must include education of the entire population on the
realities of how racism functions in our society, as well as an honest and
serious plan to provide a meaningful rectification of this history of oppression
(which may include, for example, reparations to African Americans and to Native
Americans). Similarly, we call for reparations and rights of return (where doing
so would not cause even greater levels of suffering) for all populations around
the world who have been forced from their homes by war and
oppression (we think particularly of the people of Central Africa, the people of
Chechnya, the people of Tibet, and tens of millions of other refugees around the
world). Where reparations or return are not the best means to rectify past
oppression without creating new forms of dislocation and oppression, we commit
to other strategies to provide rectification -- and these must not only be
economic, but involve public and systematic atonement on the part of societies
that have materially benefited from the misuse of or oppression of others. This
same principle should be applied in matters of class oppression as well as
racial oppression.

We don't seek here to list all forms of oppression which must end -- that
laundry list concept of politics usually leads nowhere. So we will resist the
efforts of some to join our community and spend their time adding new issues to
our list of oppression and claiming that somehow we are oppressing someone or
some group if we didn’t mention them at this point. That kind of discourse is
usually a way to avoid taking any of these principles seriously, by spending all
of one’s time debating them.

On the other hand, we do at least want to give special attention in this
founding statement to what has become a particularly egregious focus of
right-wing energy: the assault on gays and lesbians. TIKKUN magazine has long
championed the transformation of Jewish practices that demean queers or that
limit marriage to heterosexual unions. The NSP will oppose all use of state
power, in the United States, Canada, England, Israel and other countries both,
to disadvantage queer relationships or to limit marriage or family to
traditional heterosexual forms. We honor those who are developing what they call
a "queer politics" that forces all of us to rethink gender relationships, even
while rejecting any attempts to privilege any one approach as "the politically
correct way" for sexual life. Our community also affirms support and honor to
heterosexuality as an equally valid form of family and marriage. We seek to
create a society which is supportive of families and of people making and sust
aining long-term loving commitments, and we will do our best to support people
to work through the inevitable difficulties that emerge in all loving
relationships. And we also will provide emotional support to those who have
chosen to remain single or who have chosen communal forms of living. For those
who are single but don't wish to be, we believe that a community of caring
people should give time and attention to helping such people find appropriate
partners of whatever gender they seek, rather than abandoning them to face the
problem of finding a partner as a kind of lone entrepreneur in a marketplace of
relationships. Similarly, we will give warm welcome to bisexuals and those who
are cross-gendered.

We also want to emphasize the central importance we give to creating a loving
and spiritually rich environment for children, recognizing their right to have
education that is stimulating and meaningful, to be involved in loving and
caring relationships, and to be introduced to the spiritual practices and social
transformation movements that can enrich their lives. In part, this means
learning from our children, trusting them, and giving them opportunities to
shape their own paths. In part, this means that we have an obligation to impart
to the young (and not just our own children) all that we have learned about the
joys and excitements of life, the joys and excitement of intellectual activity
and the life of the mind, the joy of learning skills and disciplines. We have a
responsibility to keep children from inflicting lasting hurt on themselves or
others. Within that context of responsibility, we also wish to affirm pleasure,
not only for ourselves but also for our children, as an
important aspect of life. Similarly, we wish to create contexts for them to
learn the wisdom of our elders, the wisdom and great knowledge accumulated in
science and humanities. We also need to provide forms of support that show them
respect and caring, affirm their right to deepen their own knowledge, affirm
their right to pleasure and sexual and spiritual fulfillment, and provide
opportunities to use their creativity in service to the community.

4. PEACE, JUSTICE AND RECONCILIATION FOR ISRAEL AND PALESTINE

We are committed to full and complete reconciliation between Israel and the
Palestinian people within the context of social justice for the Palestinians and
security for Israel. We call upon Israel to end the Occupation, to return
settlers to the pre-1967 borders of Israel (providing them with decent housing),
and to take major (though not total) responsibility for Palestinian refugees. We
oppose Israel’s violations of Palestinian human rights and we insist that Israel
adopt a strategy based on open-heartedness toward the Palestinians, repentance
for past misdeeds, reparation, and genuine acknowledgement of the ways that some
Israelis were oppressive, murderous, and oblivious to the legitimate needs of
the Palestinian people. We call for an end to the teachings in Jewish and
Israeli schools and media which demean or demonize the Palestinian people;
instead we seek to replace those with teachings that emphasize the humanity and
goodness of the Palestinian people, Arabs and Muslims.
Although we affirm Israel as a Jewish state side by side with Palestine, we
believe that all non-Jews in Israel, including most importantly Arab or
Palestinian citizens of Israel, should have full civil rights in Israel and
equal economic entitlements to any Israeli who has served in the army.

We call upon the Palestinian people to acknowledge the right of Jews to maintain
their own homeland in the pre-1967 borders of the state of Israel, with Jewish
control over the Jewish section of Jerusalem (including French Hill and Mt.
Scopus and the Jewish Quarter of the Old City) and the Western Wall, and
unimpeded access to the cemetery on the Mount of Olives. We call upon the
Palestinian people to stop acts of terror against Israel and to listen and heed
the growing number of Palestinian voices that are calling for a strategy of
nonviolent civil disobedience We call upon Palestinians to end all teachings in
their schools and media which demean or demonize the Jewish people or Israel and
to replace those with teachings that emphasize the humanity and goodness of the
Jewish people.

We recognize that some Palestinians will respond by pointing out the structural
violence inherent in the presence of the Israeli Occupation and the settlements.
We agree with these points, but still believe that the breakthrough necessary to
free Palestinians from Occupation will only come when the Israeli people feel
enough safety to contemplate arrangements based on trust. Just as Israelis must
demonstrate that they see Palestinians as created in the image of God and
deserving of full respect, so the Palestinians must demonstrate that they see
Israelis as created in the image of God and are deserving of full respect.

Both sides need to recognize a need for repentance for past deeds that were
hurtful and oppressive. Jews must understand why Palestinians were fearful that
the more highly organized and politically sophisticated Zionist movement that
began to emerge in the period 1920-1948 might lead to the disenfranchisement of
Palestinians, and why Palestinians today feel that "the right to return" to
their homes is no different from the right of return that was at the basis of
Zionism.

Similarly, Palestinians need to acknowledge their own role in helping create the
conflict by their armed resistance to Jewish immigration to Palestine in the
years when Jews were being annihilated or when Jews were stumbling out of the
death camps of Europe.

This is just a sample of the stories we must learn from each other so that we
can build reconciliation of the heart, based on genuine compassion for each
other. Political arrangements cannot be trusted until there is a serious
commitment on both sides to compassionate listening to each other. Its only when
both sides can tell the other side's story with compassion and conviction, and
both sides recognize that in some important respects both sides are wrong and
both sides are right, that we can hope to move to a real reconciliation of the
heart.

All the fancy agreements and all the political maneuvering is secondary to
developing an open-heartedness and generosity in both peoples to the legitimate
needs of the other. We believe an important step in that process is for both
sides to learn how to tell the other other side's narrative in a convincing and
compassionate way. This has been done in part in Rabbi Michael Lerner’s book
Healing Israel/Palestine, and in the works of various Israeli and Palestinian
thinkers who are able to transcend their own community’s demand for proving that
their side is the “righteous victim” and the other side is “the evil oppressor.”

We call upon the United States and other world powers to intervene with all
their influence and economic power both to stop the cycle of violence and to
achieve the creation of a demilitarized Palestinian state in all of the West
Bank and Gaza (minus the most minimal border alterations), an end to the
Occupation, and an end to acts of terror. We will support efforts to convince
the United States to condition aid to Israel on the end of the Occupation. We
call upon the peoples of the world to come to Israel and Palestine and actively
interpose ourselves between the warring sides to provide protection to civilians
on both sides. And we call for all parties to adopt the nonviolent philosophies
and strategies of Martin Luther King Jr. and Mahatma Gandhi.

Although we do not support any form of nationalism as an ultimate good, we
understand why, in this historical moment, the Jewish people need a state of our
own. With memories of the murder and genocide of our people still fresh and the
perception that we would have been far less vulnerable had we had a state and an
army -- with the persistence of virulent anti-Semitism in the world today -- the
Jewish people cannot be asked to be the first to voluntarily eliminate the
protections of the nation state. That’s why, at this point in time, the TIKKUN
Community is supporting a two-state rather than a bi-national solution to the
Israel-Palestinian crisis, even though some members of our community believe
that such a bi-national state is the only way to achieve social justice for
Palestinians.

After what Jews have been through, it is not reasonable to expect them to be the
first to give up the protections of an armed state. On the other hand, we see
nationalism as a perverting influence in Jewish life -- and one that must be
overcome. So we do hope Israel will become one of the first 20 percent of
countries of the world to overcome the trappings of national chauvinism,
militarism, and excessive focus on boundaries -- say, for example, after the
United States, Russia, China, Japan, Iraq, Iran, Syria, India, Pakistan,
England, France, Germany, Italy, Egypt, Poland, Argentina, Chile, Mexico, Libya,
Saudi Arabia, Algeria, Nigeria, Ethiopia, Uganda, and South Africa have
pioneered that path by abolishing borders and accomplished full disarmament.
Until then, the Jewish people have a right to their own state, which we hope
will eventually move in the direction of confederation with Palestine and Jordan
for economic and political cooperation.

A state with many Jews in it is not a Jewish state unless it embodies an ethos
of love and justice and becomes a living proof that healing and transformation
is possible. Israel is not yet a Jewish state in this sense, so we will support
the forces that will help it evolve in that direction. To make it possible for
Jewish values of love, justice, and peace to triumph inside its own society, and
to open the possibility that Israelis could rediscover the deep spiritual truths
of Judaism, Israel will have to eliminate all forms of religious control of the
state, end all religious coercion, and allow people to find their own religious
and spiritual path, giving equal rights and treatment to non-Jews.

We oppose all attempts by some sectors of the Orthodox world to use the Israeli
government as a vehicle to impose their own particular perspective about
Judaism, including who is "really" Jewish, what counts as a legitimate wedding,
divorce or conversion, etc. We support instead the fostering of a climate of
mutual tolerance and respect among all sectors of the Jewish people. We reject
all practices which lead to unequal treatment of Palestinians or other
non-Jewish minorities within the State of Israel.

So, when we affirm preserving "the Jewish character" of Israel, we do not mean
merely a demographically Jewish state but a state which lives up to the highest
Jewish values of "love the neighbor," "love the stranger," and "justice, justice
shalt thou pursue." In the short term, the greatest obstacle to the creation of
a state living up to the values of an ethically and spiritually renewed Judaism
are the Occupation, the settlements, and what is described in Michael Lerner's
book Jewish Renewal as the "Settler Judaism" mentality.

Settler Judaism sees the world as always against the Jews, always ready to hurt
us -- and hence rejects universal ethical standards and equates "good" with
"what’s good for the Jews." Similarly, settler Judaism assumes that Jewish
interests can be achieved through the use of power and coercion, the
obliteration of those with whom we disagree, and believes that Jews have some
special right to the Land of Israel that allows them to be insensitive to others
who live there.

The greatest obstacle to Jewish values in Israel as in the United States lies in
the triumph of the ethos of selfishness and materialism. Those who respect
Judaism and wish to see it retain its integrity in a Jewish state must reject
the vision of an Israel which finds its ultimate mission in becoming "the
globalization miracle and new technology and finance headquarters of the Middle
East." Rather, we support those who favor a genuinely Jewish society built on
principles of love, justice, peace, and caring for others, including non-Jewish
others. This path requires rejecting those themes and currents within the Jewish
tradition or interpretations of Jewish history which tend to bring out
chauvinism or a narrow focus on the well being of Jews to the exclusion of
others, and instead renewing Judaism to focus on those parts of the tradition
and Jewish history that bring out in Jews greater empathy for others, and
develop the capacities of Jews as loving, generous, open-hearted and co
mpassionate human beings. And it is this same kind of renewal that we support in
every other religious and spiritual tradition.

5. A SPIRITUAL MOVEMENT

The world we want to see cannot be created solely by external economic and
political changes. We wish to see the democratization of our economic and
political institutions, and a redistribution of wealth so that all people can
share equally in the benefits of this planet. But as we indicated above, the
sources of our worldwide economic and political problems are not solely external
in nature, but reflect also distortions in how we experience ourselves and each
other So work on changing our own inner selves and our ideas about the world is
an important aspect of changing the world -- not a diversion from the healing
that is necessary, but an important component of it.

We need to engage in activity that aims at fostering a new consciousness and the
development of an inner life that is not merely private and individual in
nature, but is rather both social and spiritual in nature -- an inner life that
is also an interconnected life with other human beings and with the Unity of All
Being.

In short, the political must have a spiritual dimension. This is a dimension of
life which is rarely given attention in social change movements, but it is a
central concern of the NSP.

Among the central building blocks of such a spiritual dimension:

the development of a personal spiritual practice such as meditation or prayer,
the practice of generosity and sharing what we have with others,
compassion toward others and toward oneself,
including the open-hearted acceptance of one's own and other's flaws,
developing the habit of affirming the being of others even when we may disagree
with some of their beliefs or practices,
careful attention to one's speech so as to not say hurtful things towards
others,
joyfulness and the affirmation of pleasure,
treasuring our bodies through conscious eating and exercising (but without
politically correct guilt trips),
the practice of forgiveness and repentance,
giving to give and not to get,
letting go of fantasies that we can control everything,
and recognizing that there is enough and that we are enough.

We are particularly sensitive to the ways that social movements in the past have
used their own ideals as clubs with which to beat up themselves and those who
are not part of the "in" group, so we want to insist that our movement have a
compassionate attitude toward its own members as well as toward those who do not
agree with us, while simultaneously rejecting a mindless moral relativism which
makes everything OK or acceptable. Building this balance between compassion and
striving for transformation requires practical wisdom, and so our movement
rejects the anti-leadership tendencies that have often been associated with
progressive politics and embraces the notion of spiritual leadership based on
inner depth, compassionate understanding, practical wisdom, and a powerful sense
of humor.

WHY CREATE A NEW ORGANIZATION?

There are many organizations doing good work in each of the areas discussed
above, and we intend to support all of them. We especially encourage the
creation and strengthening of truly transnational grassroots movements focused
not only on resisting corporate globalism but on creating a new democratic
"globalization" -- a planetary movement that is not controlled either by
national governments or by corporations. We especially support efforts to
require that corporations serve the public good such as the proposed Social
Responsibility Amendment to the U.S. Constitution.

What does not exist is an organization that brings all these concerns together
within the context of a unified worldview (there are many groups who have
laundry lists of demands, but these demands do not flow from a shared
theoretical perspective). As a result, many people involved in one or another of
the concerns described above don't really recognize themselves as part of a
larger movement for healing and transformation of the planet, don't see these
others as their allies, and don't inject into their own activities a larger
understanding that could deepen their specific important work, the NSP can
provide that larger framework.

We are people who share the basic ideas of an Emancipatory Spirituality as
described in Michael Lerner's Spirit Matters: Global Healing and the Wisdom of
the Soul -- a book which provides our basic framework.

We also see as foundational the writings of
Peter Gabel, particularly as articulated in The Bank Teller and Other Essays on
the Politics of Meaning, Judith Plaskow's Standing Again at Sinai
and Arthur Waskow's Down to Earth Judaism.

We draw upon the wisdom of many teachers, including the work of
Abraham Joshua Heschel and Zalman Schachter Shalomi,
Marcia Prager and Rachel Adler,
Rumi and St. Francis and the Kabbalists,
Susannah Heschel and Lawrence Kushner,
Art Green and Judith Antonelli,
Jerry Mander and David Korten,
Ken Wilber and Jim Wallis,
Thomas Merton and Matthew Fox and Zygmunt Bauman,
Thich Nhat Hanh and The Dalai Lama,
the Ishbitzer Rebbe and Teilhard de Chardin,
Mordecai Kaplan and Adrienne Rich,
Roger Gottlieb and Walter Bruegemann,
and the work of Catholic liberation theologians, feminist theologians, Socially
Engaged Buddhists, and many more.

What the NSP seeks to offer is a vision that positions the quest for economic
and social justice, peace and ecological sanity within the framework of a
spiritual consciousness and a practice of open-heartedness, generosity, caring
for others and outpouring of loving kindness. The NSP is for anyone who shares
the perspective articulated here.

The NSP’s major organizational contribution to the worldwide movement for social
justice and spiritual well-being will be:

To provide a support mechanism for people who wish to bring this new way of
thinking into the world. When people try to do this by themselves, they often
find themselves burning out or becoming "realistic," that is, adjusting to the
frame of reference of the larger society. We will provide support to each other
to remain focused on a larger and more utopian vision.
To do consciousness-raising in the larger world and in social change movements,
so that they can begin to incorporate our perspective and they strengthen their
ability to survive the burnout, cynicism, and despair that often debilitate
those who wish for social change.
To change the intellectual framework within which most Americans view
contemporary social reality and their own possibilities for a fulfilling life.
To provide ongoing education and the development of theory and practice that
could become models for social healing.  We do not intend to replace or
duplicate existing social change movements. But there are many arenas even in
those movements where a more coherent worldview, and an organization linking
them intellectually and spiritually would only strengthen rather than detract
from their important work.
To provide a context within which older and seasoned activists and those
involved in social healing in their work can interact with the new and exciting
generation of younger activists -- and both can learn from each other.
To be a national think-tank for social change movements -- a think-tank that can
help them move beyond narrow economistic frameworks and begin to incorporate a
spiritual wisdom and framework both in their conceptualizing the issues they
address and in building a support community for their own activists.
To be an information-gathering network that can provide an alternative to the
polling done by establishment-oriented groups -- and to ask the questions that
reflect a psychological and spiritual sophistication rarely brought to the task
of understanding what is happening in our society.
We see the educational, consciousness-raising, and linking work we do as a
critical contribution to social healing.

We see ourselves as a corps of spiritual transformers -- that is, a cadre of
people who share a fundamentally similar perspective and wish to work more
effectively by supporting each other, learning from each other's experience, and
more deeply internalizing the ideas and ideals we hold. This is one reason why
we place a great deal of emphasis on agreement with the details of this founding
document -- because intellectual coherence is only possible if we start from the
same place.

Like a new kind of non-sectarian spiritual Order, perhaps like the Franciscans
fused with a Hasidic sect fused with the skills of a guild for social change and
maybe even the willingness to commit to taking care of each other that is
manifested by the Jesuits and by Skull and Bones and by some Native American
tribes, we will make a life-long commitment to supporting the people who join
and stay involved in the NSP, and do what we can to make sure that we help them
in any way we can. For some, that may mean helping someone get a job or
promotion, for others it may mean helping someone get the health care they need,
or introducing someone to a life partner, or advancing their literary or
political career, or assisting them in playing a leadership role. The commitment
is based on the recognition that as members of the NSP people are themselves
making a commitment to be involved in using our own talents, skills, and life
energies to promote the kind of healing and transformation envisi
oned in this Core Vision. So of course we are going to want to do everything we
reasonably and morally and legally can do to help each other advance through our
lives, and give each other companionship, love, caring, generosity and
compassion as we face life's challenges from the time we are in college to the
time we may be facing aging and death. It is this kind of commitment to each
other that can only be made real by our own individual actions and which becomes
the ultimate glue to holding together a vanguard of love.

We see TIKKUN magazine, along with the spiritualprogressives.org website and
Love Embodied e-zine, as the primary vehicle through which we can communicate
with each other about the new thinking and activity that the NSP develops.

So How Do I Get Involved?

There are many ways to be involved in the NSP. We imagine that in a few years
these will be the answers some of us will be giving about what we've been doing
to build the NSP:

Some of us are seeking to bring these ideas into our professional or workplace
contexts and to campaign for a "New Bottom Line."

We are creating groups of like-minded people at our annual meetings of
professional associations, at national conventions of unions and political
parties, or at the national gatherings of our religious communities.

Some of us are business people introducing these ideas into our businesses and
experimenting with new ways to work -- or we are developing communities of
people who infuse their philanthropic activities with this kind of orientation.

Some of us are working in foundations and some of us are working in universities
and some of us are working in media and some of us are working in local churches
and synagogues and mosques, and wherever we are, we are raising the kinds of
issues raised in this founding statement.

Some of us are creating local NSP chapters -- essentially chapters or salons of
the NSP in which we can work to educate people in our local areas about this
perspective and deepen our understanding of our principles in monthly
conversations.

Some of us are participating by talking about these ideas in every context in
which we find ourselves and by convincing others to read TIKKUN magazine

Some of us are students who are seeking to create campus chapters of the NSP.

Some of us are engaged in solidarity work with the Israeli peace movement or in
developing local initiatives to challenge the Occupation. Some of us are
developing teach-ins about Israel-Palestinian peace, and in other ways
challenging the mainstream interpretation of that struggle.

Some of us are bringing these ideas into the anti-globalization, ecological, and
social justice movements or affinity groups of which we are part. Some of us are
trying to do that in the Democratic Party, the Natural Law Party, the Green
Party and other political parties.

Some of us are intellectuals working in academia or in policy institutes or in
media and seeking to foster an understanding of this perspective.

Some of us are artists, poets, writers, musicians and others who will be
participating by using our skills and talents to advance the consciousness
described here.

Some of us are challenging local and national media, insisting that they
recognize the distorted and cynical nature of their presentations, and educating
the public to alternative ways to think about reality. Some of us are retirees
who are making phone calls and writing letters to the media or to neighbors
about these ideas.

Some of us are trying to influence foundations to adopt and support this
perspective. Others of us are involved in fundraising projects to support the
NSP and fund educational work. Some of us are trying to change the way people
think about philanthropy, or the way they use their charitable donations -- so
that they become a force to convince social change movements to incorporate this
broader perspective.

Some of us are working in communities of seniors and developing spiritual
eldering projects to support the ways that retired people can provide spiritual
leadership for the society.

Others are working in schools and pushing for a new bottom line there. Still
others are working to get the Social Responsibility Amendment to the U.S.
Constitution on the ballots of local and state elections (requiring corporations
to get a new charter which would only be rewarded if they could prove a history
of social responsibility). Some of us are helping shape a spiritually oriented
political party, while others are working within existing parties.

For all of us, the NSP is a place where we can talk about these ideas and give
each other mutual support for being unequivocally utopian and committed to large
scale TIKKUN olam (transformation of the world). We get this nurturance through
TIKKUN magazine, the spiritualprogressives.org website and email groups, the
Love Embodied e-zine, and through NSP national gatherings.

What will the National Organization Do?

We will hold national conferences/trainings which will be aimed at exploring
more fully the ideas put forward in this statement and applying them to current
social, political and spiritual realities. Meetings of our conference will not
be about passing resolutions or debating policies, but rather about developing
our own inner spiritual resources, thinking through ideas together, and learning
from cutting-edge thinkers, spiritual leaders, social activists and
practitioners of healing and transformation.

We will provide an email discussion groups for those who want daily briefings on
current national happenings and priorities. Right now, we don’t have the
resources for a moderated bulletin board, but that could happen in the future.

We will develop educational material that will help people do organizing around
the national priorities for that year.

We will seek publicity in national and local media to highlight the perspectives
articulated in this founding statement.

We will take public stands on issues that connect to this founding vision and
publicize those stands, organize public gatherings or other events to forward
those ideals, develop a corps of speakers who can speak to these issues,
encourage artists, film and video people, and writers to integrate our
perspective into their works, and find other creative ways to provoke public
discussion of the NSP perspective.

We will assist in the formation of coalitions and partnerships and national
campaigns (including media campaigns) to advance these ideas.

On leadership: Our organization rejects both the anti-leadership tendencies of
some parts of the Left and the Guru/Great Man tendencies of various spiritual
movements. We want to give full and strong support to leadership -- leadership
not chosen on the basis of “representing” either a constituency or a cohort of
the population, but rather a spiritual leadership based on inner depth, wisdom,
deep understanding of the world and of spiritual disciplines, compassionate
understanding, practical wisdom and powerful sense of humor. We seek leaders who
encourage the growth of these qualities and skills in our members.

We are all too familiar with organizations in which concern about democratic
process paralyzes leadership so that they never feel capable of taking creative
action or making public statements for the organization. That’s why we do not
model ourselves on the “consensus building” organizations that predominate today
-- even as we admire the democratic impulse that underlies that practice. Nor do
we accept the leveling that fails to recognize inequalities in levels of
intellectual or spiritual or emotional development among people (based in part
on differences in life experience). There are people among us who know more, or
who have had unique experiences that they can articulate in ways that are
helpful to all of us, and not everyone is in that position. So we want to treat
our leaders and teachers with genuine respect, but not with uncritical
subservience to their views when we disagree.

Not everyone in the NSP agrees with every point in this statement. What they do
agree with is this: that this statement is the foundational position of this
organization, and that insofar as we function within the context of the NSP or
act as its public representatives to the public or to other organizations we
acknowledge ourselves as bound by the approach articulated here. Since our
primary organizational goal is to be a force that will educate others to the
perspective articulated here in this Core Vision, and to the ideas that underlie
it, it is reasonable for us to want people within the organization to really be
enthusiastic about its perspective and for its leaders and spokespeople to share
all of its major points articulated here (but not necessarily all the ways that
these get elaborated in the future).

The NSP is committed to fostering a new consciousness so that we allow ourselves
to know that the most significant and rewarding part of our lives comes through:

Acts of love and generosity

Kindness to humans and animals

Caring for and giving to others without expectation of reward or a “return on
the investment of our time and enegy”

Work that is fulfilling both in its process and in the sense it gives us that we
are contributing to the public good

Awe at the grandeur of creation

The experience of being recognized on the deepest level of our being and
recognizing others in that way

Acknowledging our connection to something larger than ourselves and seeing our
lives in the context of service to the ultimate triumph of love, goodness,
justice and peace.

We hope you join us, and we pray for guidance and wisdom, humor and love as we
build this exciting venture.
___________________________________________________

formaldehyde, aspartame, and migraines, the first case series, Sharon E
Jacob-Soo, Sarah A. Stechschulte, UCSD, Dermatitis 2008 May: Rich Murray
2008.07.18
http://rmforall.blogspot.com/2008_07_01_archive.htm
Friday, July 18, 2008
http://groups.yahoo.com/group/aspartameNM/message/1553
___________________________________________________



Dermatitis. 2008 May-Jun; 19(3): E10-1.
Formaldehyde, aspartame, and migraines: a possible connection.
Jacob SE, Stechschulte S.
Department of Dermatology and Cutaneous Surgery, University of Miami, Miami, FL,
USA.

Aspartame is a widely used artificial sweetener that has been linked to
pediatric and adolescent migraines.

Upon ingestion, aspartame is broken, converted, and oxidized into formaldehyde
in various tissues.

We present the first case series of aspartame-associated migraines related to
clinically relevant positive reactions to formaldehyde on patch testing.  PMID:
18627677


formaldehyde from many sources, including aspartame, is major cause of Allergic
Contact Dermatitis, SE Jacob, T Steele, G Rodriguez, Skin and Aging 2005 Dec.:
Murray 2008.03.27
http://rmforall.blogspot.com/2008_03_01_archive.htm
Thursday, March 27, 2008
http://groups.yahoo.com/group/aspartameNM/message/1533

"For example, diet soda and yogurt containing aspartame (Nutrasweet), release
formaldehyde in their natural biological degradation.

One of aspartame's metabolites, aspartic acid methyl ester, is converted to
methanol in the body, which is oxidized to formaldehyde in all organs, including
the liver and eyes. 22

Patients with a contact dermatitis to formaldehyde have been seen to improve
once aspartame is avoided. 22

Notably, the case that Hill and Belsito reported had a 6-month history of eyelid
dermatitis that subsided after 1 week of avoiding diet soda. 22"


Avoiding formaldehyde allergic reactions in children, aspartame, vitamins,
shampoo, conditioners, hair gel, baby wipes, Sharon E Jacob, MD, Tace Steele, U.
Miami, Pediatric Annals 2007 Jan.: eyelid contact dermatitis, AM Hill, DV
Belsito, 2003 Nov.: Murray 2008.03.27
http://rmforall.blogspot.com/2008_03_01_archive.htm
Thursday, March 27, 2008
http://groups.yahoo.com/group/aspartameNM/message/1532

Sharon E. Jacob, MD, Assistant Professor of Medicine (Dermatology)
University of California, San Diego 200 W. Arbor Drive #8420, San Diego, CA
92103-8420
Tel: 858-552-8585 ×3504 Fax: 305-675-8317  sjacob@...;
seves@...;


Dermatitis. 2008 Jan-Feb;19(1):9-15.
Systemic contact dermatitis.
Jacob SE, Zapolanski T.  tamar.zapolanski@...;
Department of Dermatology and Cutaneous Surgery, University of Miami, Miami, FL,
USA.

Systemic exposure to allergens resulting in a cutaneous eruption is known as
systemic contact dermatitis (SCD).

Once sensitization occurs, varying exposures to antigens via multiple routes
(including transepidermal routes, intravenous or intramuscular routes,
inhalation, and ingestion) can result in systemic flare.

This article highlights the different categories of common contactants, metals,
medications, and plants, exposure to which leads to SCD.

A comprehensive approach that takes into account all possible routes of exposure
is essential in diagnosing SCD and in helping patients successfully avoid their
allergens.   PMID: 18346390


"We present a case of a medical student who presented with erythematous
eczematoid plaques on her trunk and legs and fine vesiculation of her scalp, 3
weeks after starting anatomy class.

Of note, she routinely washed her face and arms after leaving the anatomy lab,
but remained in her scrubs for the rest of the day.

Formaldehyde and Quaternium-15 positive reactions in the same patient. [ photo
]"

"Our patient underscores the importance of appropriate patch testing and
education.

Once we identified the allergy to formaldehyde and quaternium-15, we provided
patient education materials regarding the common and not-so-common locations of
these chemicals and cross-reactors.

We also gave the patient information on avoidance and safe alternatives (see
Table 5).

Fortunately, with technical advances, this student completed the anatomy section
via electronic learning tools.

By avoiding formaldehyde, including anatomy lab, FRP in her shampoo and
cosmetics, and aspartame in her diet, this patient dramatically improved.

As with all contact dermatitides, the mainstay of treatment for allergic contact
dermatitis is avoidance."

http://www.skinandaging.com/article/5158Skin & Aging Journal
Skin & Aging - ISSN: 1096-0120 - Volume 13 - Issue 12_2005 -
December 2005 - Pages: 22 - 27

Allergen Focus:
Focus on T.R.U.E. Test Allergens #21, 13 and 18:
Formaldehyde and Formaldehyde-Releasing Preservatives
-- By Sharon E. Jacob, M.D., Tace Steele, B.A., [now MD] and Georgette
Rodriguez, M.D., M.P.H.


http://www.eczemacenter.org/eczema_center/meetfacultystaff.htm [ photo ]

The Eczema Center
Rady Children's Hospital of San Diego
8010 Frost Street, Suite 602, San Diego, CA 92123
or call... (858) 966-6774

Sharon E. Jacob , MD
Dr. Sharon E. Jacob is Assistant Clinical Professor of Pediatrics and Medicine
(Dermatology) at the University of California, School of Medicine and Rady
Children’s Hospital.
She earned her medical degree from the Temple University, and completed
dermatology training at the University of Miami and advanced contact dermatitis
training at New York University (NYU).
She has been board certified in dermatology.

Dr. Jacob's clinical interests include atopic and contact dermatitis and
education.
She is considered a national expert on chemical sensitivities in the skin and
has published more than 45 journal articles, book chapters and abstracts on this
topic.
In 2005, Dr Jacob was the first to present contact dermatitis data on U.S.
pediatric patients to the American Contact Dermatitis Society (ACDS).

She has received an excellence in teaching award from the University of Miami
Dermatology and the Clinical Research Award from the ACDS.
She is an active reviewer for the following medical publications including
Journal of the American Academy of Dermatology, Pediatric Dermatology,
Dermatitis, and the Archives of Dermatology.
Dr. Jacob also serves on the medical board of the Inflammatory Skin Disease
Institute and the Skin and Aging Journal.

Dr. Jacob enjoys taking care of children and their families and is an advocate
for children’s dermatologic health.


http://www.eczemacenter.org/eczema_center/index.htm

Atopic dermatitis (AD) -- better known as eczema -- is the most common chronic
skin disorder seen in infants and children.
In fact, the prevalence of this condition has risen dramatically during the last
three decades.
Currently, 15% to 20% of children in the United States are expected to
experience this condition sometime during their lifetime, compared to 7% around
1960.

The negative impact of eczema is profound and insidious.
It affects both the patient who suffers from it and that patient's family
members, and it does so on two important levels -- physical and emotional.


Physical:

Inflamed, itchy rashes can involve any and all of the skin surfaces and are
frequently complicated by skin breakdown and bacterial, viral, and fungal
infections.

It is linked to the development of life-long allergic conditions, including
asthma, food allergies, and rhinitis.

Any level of AD is extremely uncomfortable and, at times, painful.
Individuals with moderate to severe disease report that eczema hugely disturbs
their sleep and impacts performance of daily activities, including adverse
effects on school, sports activities, work, and peer relationships.

In studies, individuals with eczema reported more negative impact on quality of
life than those with insulin-dependent diabetes!

Emotional:

Patients and their families experience considerable emotional distress, anxiety,
and embarrassment because of people’s response to this illness.

In fact, the emotional scarring on both patient and family members may outlast
eczema's physical effects.

Parents especially suffer because it is difficult for children experiencing this
condition to understand that their parents cannot make the torment go away.
The stress of caring for these children is even greater than parents caring for
a child with insulin-dependent diabetes.

Patients experience considerable discrimination and social isolation because of
this illness.
People often stare, shiver with disgust or step back in fear from those who have
this condition.
The end result for patients: A life-time of struggle with their sense of worth
and self esteem.


http://aad2008.omnibooksonline.com/data/papers/CRS-113-F.pdf  lecture with
photos
___________________________________________________


similar levels of daily formaldehyde and formic acid, causes of birth defects,
come from cigarettes, aspartame, and dark wines and liquors -- folic acid
protects most people: Rich Murray 2008.07.15
http://rmforall.blogspot.com/2008_07_01_archive.htm
Tuesday, July 15, 2008
http://groups.yahoo.com/group/aspartameNM/message/1552


http://www.divine.ca/en/health-and-wellness/articles/c_16_i_3295/5-reasons-to-qu\
it-smoking-1.html

"A smoker who goes through one pack a day will smoke 7,300 cigarettes a year,
inhaling the equivalent of nearly 1 gram of formaldehyde (yikes!)."

That's about 2.5 mg daily formaldehyde intake for 20 cigarettes, over the 2 mg
USA FDA alarm level for formaldehyde in average 2 liters daily drinking water,
while a single 12 oz can of diet soda also results in about 2 mg formaldehyde
toxic products in the body, including formic acid, a notorious cause of birth
defects.

Dark wines and liquors usually supply even more methanol, which the body always
turns into formaldehyde and formic acid -- the major cause of "morning after"
hangovers.

High levels of folic acid, a safe, affordable vitamin in fruits and vegetables,
largely prevents formaldehyde and formic acid toxicity in most people.

It is certain that high levels of aspartame use, above 2 liters daily for months
and years, must lead to chronic formaldehyde-formic acid toxicity.

Fully 11 % of aspartame is methanol -- 1,120 mg aspartame in 2 liters diet soda,
almost six 12-oz cans, gives 123 mg methanol (wood alcohol). The methanol is
immediately released into the body after drinking .
Within hours, the liver turns much of the methanol into formaldehyde, and then
much of that into formic acid, both of which in time are partially eliminated as
carbon dioxide and water.

However, about 30 % of the methanol remains in the body as cumulative durable
toxic metabolites of formaldehyde and formic acid -- 37 mg daily, a gram every
month, accumulating in and affecting every tissue.

If only 10 % of the methanol is retained daily as formaldehyde, that would give
12 mg daily formaldehyde accumulation -- about 60 times more than the 0.2 mg
from 10 % retention of the 2 mg EPA daily limit for formaldehyde in drinking
water.

Bear in mind that the EPA limit for formaldehyde in drinking water is 1 ppm, or
2 mg daily for a typical daily consumption of 2 liters of water.


formaldehyde and formic acid in FEMA trailers and other sources (aspartame, dark
wines and liquors, tobacco smoke): Murray 2008.01.30
http://rmforall.blogspot.com/2008_01_01_archive.htm
Wednesday, January 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1508

The FEMA trailers give about the same amount of formaldehyde and formic acid
daily as from a quart of dark wine or liquor, or two quarts (6 12-oz cans) of
aspartame diet soda, from their over 1 tenth gram methanol impurity (one part in
10,000), which the body quickly makes into formaldehyde and then formic acid --
enough to be the major cause of "morning after" alcohol hangovers.

Methanol and formaldehyde and formic acid also result from many fruits and
vegetables, tobacco and wood smoke, heater and vehicle exhaust, household
chemicals and cleaners, cosmetics, and new cars, drapes, carpets, furniture,
particleboard, mobile homes, buildings, leather... so all these sources add up
and interact with many other toxic chemicals.

methanol impurity in alcohol drinks [ and aspartame ] is turned into neurotoxic
formic acid, prevented by folic acid, re Fetal Alcohol Syndrome, BM Kapur, DC
Lehotay, PL Carlen at U. Toronto, Alc Clin Exp Res 2007 Dec. plain text:
detailed biochemistry, CL Nie et al. 2007.07.18: Murray 2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524


opportunities re BA Magnuson, GA Burdock et al., Aspartame Safety Evaluation
2007 Sept., Critical Reviews in Toxicology: Rich Murray 2008.07.11
http://rmforall.blogspot.com/2008_07_01_archive.htm
Friday, July 11, 2008
http://groups.yahoo.com/group/aspartameNM/message/1550
___________________________________________________


"Of course, everyone chooses, as a natural priority, to enjoy peace, joy, and
love by helping to find, quickly share, and positively act upon evidence about
healthy and safe food, drink, and environment."

Rich Murray, MA Room For All rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com  new primary archive

http://groups.yahoo.com/group/aspartameNM/messages
group with 127 members, 1,553 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1,125 members, 22,826 posts in public archive
___________________________________________________

similar levels of daily formaldehyde and formic acid, causes of birth defects,
come from cigarettes, aspartame, and dark wines and liquors -- folic acid
protects most people: Rich Murray 2008.07.15
http://rmforall.blogspot.com/2008_07_01_archive.htm
Tuesday, July 15, 2008
http://groups.yahoo.com/group/aspartameNM/message/1552
___________________________________________________


"A smoker who goes through one pack a day will smoke 7,300 cigarettes a year,
inhaling the equivalent of nearly 1 gram of formaldehyde (yikes!)."

That's about 2.5 mg daily formaldehyde intake for 20 cigarettes, over the 2 mg
USA FDA alarm level for formaldehyde in average 2 liters daily drinking water,
while a single 12 oz can of diet soda also results in about 2 mg formaldehyde
toxic products in the body, including formic acid, a notorious cause of birth
defects.

Dark wines and liquors usually supply even more methanol, which the body always
turns into formaldehyde and formic acid -- the major cause of "morning after"
hangovers.

High levels of folic acid, a safe, affordable vitamin in fruits and vegetables,
largely prevents formaldehyde and formic acid toxicity in most people.

It is certain that high levels of aspartame use,
above 2 liters daily for months and years,
must lead to chronic formaldehyde-formic acid toxicity.

Fully 11 % of aspartame is methanol -- 1,120 mg aspartame
in 2 liters diet soda, almost six 12-oz cans, gives 123 mg methanol
(wood alcohol). The methanol is immediately released
into the body after drinking .
Within hours, the liver turns much of the methanol into formaldehyde,
and then much of that into formic acid, both of which in time
are partially eliminated as carbon dioxide and water.

However, about 30 % of the methanol remains in the body
as cumulative durable toxic metabolites of formaldehyde
and formic acid -- 37 mg daily,
a gram every month, accumulating in and affecting every tissue.

If only 10 % of the methanol is retained daily as formaldehyde,
that would give 12 mg daily formaldehyde accumulation -- about
60 times more than the 0.2 mg from 10 % retention
of the 2 mg EPA daily limit for formaldehyde in drinking water.

Bear in mind that the EPA limit for formaldehyde in drinking water is
1 ppm, or 2 mg daily for a typical daily consumption of 2 liters of water.


formaldehyde and formic acid in FEMA trailers and other sources
(aspartame, dark wines and liquors, tobacco smoke):
Murray 2008.01.30
http://rmforall.blogspot.com/2008_01_01_archive.htm
Wednesday, January 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1508

The FEMA trailers give about the same amount of formaldehyde
and formic acid daily as from a quart of dark wine or liquor,
or two quarts (6 12-oz cans) of aspartame diet soda,
from their over 1 tenth gram methanol impurity
(one part in 10,000), which the body quickly makes into
formaldehyde and then formic acid -- enough to be the major cause
of "morning after" alcohol hangovers.

Methanol and formaldehyde and formic acid also result from
many fruits and vegetables, tobacco and wood smoke, heater
and vehicle exhaust, household chemicals and cleaners, cosmetics,
and new cars, drapes, carpets, furniture, particleboard,
mobile homes, buildings, leather... so all these sources add up
and interact with many other toxic chemicals.

methanol impurity in alcohol drinks [ and aspartame ] is turned into
neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol
Syndrome, BM Kapur, DC Lehotay, PL Carlen at U. Toronto,
Alc Clin Exp Res 2007 Dec. plain text: detailed biochemistry,
CL Nie et al. 2007.07.18: Murray 2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524
___________________________________________________


http://www.divine.ca/en/health-and-wellness/articles/c_16_i_3295/5-reasons-to-qu\
it-smoking-1.html

Canada's Online Women's Magazine
http://www.divine.ca/en/divineca/contact-us/c_271/

5 Reasons to Quit Smoking NOW
By Mariève Inoue

It’s common knowledge that smoking is bad for you.
Shocking, even horrifying pictures of what smoking can do to your body are
placed strategically on packs of cigarettes in an effort to encourage people to
quit, and the price of cigarettes is constantly being increased.
Yet according to the Canadian Tobacco Use Monitoring Survey, about 5.3 million
Canadians aged 15 and over were current smokers in 2003.

If you’ve never been a smoker, or have quit successfully, our hats go off to you
-- but if you’re still stepping out for that cigarette break, we’ve got some
facts and stats to give you an extra nudge towards quitting for good.

Reason #1: Tobacco kills an estimated 45,000 Canadians every year.
This number is higher than the number of deaths caused by AIDS, car accidents,
suicide, murder, fires and accidental poisonings combined.

Reason #2: Tobacco smoke contains over 4,000 chemicals.
These include carbon monoxide (what comes out of the car exhaust), arsenic (rat
poison), ammonia (found in many window cleaners), naphthalene (used in
mothballs), lead, formaldehyde, and butane.

A smoker who goes through one pack a day will smoke 7,300 cigarettes a year,
inhaling the equivalent of nearly 1 gram of formaldehyde (yikes!).

Reason #3: Smoking puts you at risk for lung cancer… among other things.
It’s a known fact: smoking puts you at risk for developing lung cancer.
But did you know it also puts you at a higher risk of developing pancreas,
breast, cervical, stomach, kidney, and bladder cancer, as well as leukemia,
coronary heart disease, circulatory, high blood pressure, high cholesterol,
tooth decay, gum disease, osteoporosis and cataracts?

Reason #4: It’s not only about you.
Second hand smoke exposure is the number two cause of lung cancer (the number
one cause being smoking), which means that by smoking you’re not only putting
yourself in danger, but also the people around you and your loved ones.

Reason #5: It’s never too late to quit.
Within eight hours of not having smoked, carbon monoxide levels decrease, and
the oxygen levels in your blood increase.
After having quit for two days, your sense of taste and smell start to improve.
Between two weeks and three months after having quit, your lungs work better,
making it a lot easier to do a vital action: breathe.
And only one year after having quit, your risk of having a smoking-related heart
attack is reduced by half.

Sources: Health Canada, Canadian Cancer Society, and The Lung Association
___________________________________________________


re "A Few too Many", Joan Acocella, The New Yorker, long review of hangover
research 2008.05.26 -- same levels of formaldehyde and formic acid in FEMA
trailers and other sources (aspartame, dark wines and liquors, tobacco
smoke): Murray 2008.06.05
http://rmforall.blogspot.com/2008_06_01_archive.htm
Thursday, June 5, 2008
http://groups.yahoo.com/group/aspartameNM/message/1541

[ See also:
There really is no controversy, Adrienne Samuels PhD, letter re
evident toxicity of aspartame EJCN 2008.06.11:
Murray 2008.06.30
http://rmforall.blogspot.com/2008_06_01_archive.htm
Monday, June 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1546

former key Hillary Clinton staff Mark Penn and Patti Solis Doyle
use much neurotoxic aspartame Diet Coke -- also many other
politicians: Murray 2008.06.30
http://rmforall.blogspot.com/2008_06_01_archive.htm
Monday, June 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1545

opportunities re BA Magnuson, GA Burdock et al., Aspartame Safety Evaluation
2007 Sept., Critical Reviews in Toxicology: Rich Murray 2008.07.11
http://rmforall.blogspot.com/2008_07_01_archive.htm
Friday, July 11, 2008
http://groups.yahoo.com/group/aspartameNM/message/1550 ]

http://www.newyorker.com/reporting/2008/05/26/080526fa_fact_acocella?currentPage\
=all

Annals Of Drinking
A Few Too Many
Is there any hope for the hung over?
by Joan Acocella May 26, 2008  themail@...

"Wayne Jones, of the Swedish National Laboratory of Forensic Medicine"
[ http://groups.yahoo.com/group/aspartameNM/message/1469
highly toxic formaldehyde, the cause of alcohol hangovers, is
made by the body from 100 mg doses of methanol from
dark wines and liquors, dimethyl dicarbonate, and aspartame:
Murray 2007.08.31 ]

http://groups.yahoo.com/group/aspartameNM/message/1286
methanol products (formaldehyde and formic acid) are main cause
of alcohol hangover symptoms [same as from similar amounts of
methanol, the 11% part of aspartame]: YS Woo et al, 2005 Dec:
Murray 2006.01.20

Addict Biol. 2005 Dec;10(4): 351-5.
Concentration changes of methanol in blood samples during
an experimentally induced alcohol hangover state.
Woo YS, Yoon SJ, Lee HK, Lee CU, Chae JH, Lee CT, Kim DJ.
Chuncheon National Hospital, Department of Psychiatry,
The Catholic University of Korea, Seoul, Korea.
http://www.cuk.ac.kr/eng/ sysop@...
Songsin Campus: 02-740-9714 Songsim Campus: 02-2164-4116
Songeui Campus: 02-2164-4114
http://www.cuk.ac.kr/eng/sub055.htm eight hospitals

[ Han-Kyu Lee ]

A hangover is characterized by the unpleasant physical and mental
symptoms that occur between 8 and 16 hours after drinking alcohol.

After inducing experimental hangover in normal individuals,
we measured the methanol concentration prior to
and after alcohol consumption
and we assessed the association between the hangover condition
and the blood methanol level.

A total of 18 normal adult males participated in this study.

They did not have any previous histories of psychiatric
or medical disorders.

The blood ethanol concentration prior to the alcohol intake
(2.26+/-2.08) was not significantly different from that
13 hours after the alcohol consumption (3.12+/-2.38).

However, the difference of methanol concentration
between the day of experiment (prior to the alcohol intake)
and the next day (13 hours after the alcohol intake)
was significant (2.62+/-1.33/l vs. 3.88+/-2.10/l, respectively).

A significant positive correlation was observed
between the changes of blood methanol concentration
and hangover subjective scale score increment when covarying
for the changes of blood ethanol level (r=0.498, p<0.05).

This result suggests the possible correlation of methanol
as well as its toxic metabolite to hangover. PMID: 16318957

[ The toxic metabolite of methanol is formaldehyde, which in turn
partially becomes formic acid -- both potent cumulative toxins
that are the actual cause of the toxicity of methanol.]

This study by Jones AW (1987) found next-morning hangover
from red wine with 100 to 150 mg methanol
(9.5 % w/v ethanol, 100 mg/l methanol, 0.01 %).
Fully 11% of aspartame is methanol --
1,120 mg aspartame in 2 L diet soda,
almost six 12-oz cans, gives 123 mg methanol (wood alcohol).

Pharmacol Toxicol. 1987 Mar; 60(3): 217-20.
Elimination half-life of methanol during hangover.
Jones AW. wayne.jones@...;
Department of Forensic Toxicology,
University Hospital, SE-581 85 Linkoping, Sweden.

This paper reports the elimination half-life of methanol in human
volunteers.
Experiments were made during the morning after the subjects had
consumed 1000-1500 ml red wine
(9.5 % w/v ethanol, 100 mg/l methanol)
the previous evening. [ 100 to 150 mg methanol ]
The washout of methanol from the body
coincided with the onset of hangover.
The concentrations of ethanol and methanol in blood were
determined indirectly by analysis of end-expired alveolar air.
In the morning when blood-ethanol dropped
below the Km of liver alcohol dehydrogenase (ADH)
of about 100 mg/l (2.2 mM),
the disappearance half-life of ethanol was 21, 22, 18 and 15 min.
in 4 test subjects respectively.
The corresponding elimination half-lives of methanol
were 213, 110, 133 and 142 min. in these same individuals.
The experimental design outlined in this paper can be used
to obtain useful data on elimination kinetics of methanol
in human volunteers without undue ethical limitations.
Circumstantial evidence is presented to link methanol
or its toxic metabolic products, formaldehyde and formic acid,
with the pathogenesis of hangover. PMID: 3588516 ]
___________________________________________________


"Of course, everyone chooses, as a natural priority, to enjoy peace,
joy, and love by helping to find, quickly share, and positively act
upon evidence about healthy and safe food, drink, and
environment."

Rich Murray, MA Room For All rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com  new primary archive

http://groups.yahoo.com/group/aspartameNM/messages
group with 127 members, 1,552 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1,121 members, 22,820 posts in public archive
___________________________________________________

The Spin on Aspartame, hirelings of Ajinomoto, including Dr. C. Wayne Callaway:
Lynn Stratton: Rich Murray 2008.07.13
http://rmforall.blogspot.com/2008_07_01_archive.htm
Sunday, July 13, 2008
http://groups.yahoo.com/group/aspartameNM/message/1551


http://aconstantineblacklist.blogspot.com/2008/07/spin-on-aspartame.html

Alex Constantine's Blacklist

"We suffer primarily ... from our illusions. We are haunted, not by reality, but
by those images we have put in place of reality. America went to war nearly five
years ago after an orchestrated campaign of false statements by the nation's top
officials, a war begun under the illusion of an imminent national security
threat. We are haunted by a war begun, in other words, under false pretenses." -
Daniel Boorstin, The Image (1961)

Friday, July 11, 2008
The Spin on Aspartame

Government Agencies, Health Experts Join Forces to Push Aspartame Safety
http://www.emediawire.com/releases/2008/7/prweb1081414.htm

The FDA, the USDA, and medical experts from such powerhouses as the Mayo Clinic
and Harvard Medical School have worked together for years to convince the
American public that aspartame, the artificial sweetener commonly known as
NutraSweet, is safe, despite numerous studies showing it causes a host of
ailments, including brain tumors and lesions. Even worse, the research that
these federal agencies, health associations and medical experts use to back up
their safety claims has, in fact, been paid for by the aspartame industry
itself.

St. Petersburg, Fl (PRWEB) July 9, 2008 -- New information from an independent
reporter shows that the FDA, the USDA and even high-ranking government officials
have worked in concert with nationally recognized health experts for years to
convince the American public that aspartame, the artificial sweetener commonly
known as NutraSweet, is safe, despite medical research showing it causes brain
tumors and lesions.

In a well documented study, the author has traced the connections between such
medical powerhouses as the Mayo Clinic, Harvard Medical School and the American
Dietetic Association and the two biggest producers of aspartame in the world,
the NutraSweet Company, in the U.S., and Ajinomoto, a global operation.

The complete article, The Spin on Aspartame (
http://healthy-holistic-living.com/spin-on-aspartame.html ) is available on
healthy-holistic-living.com a site dedicated to offering tips and information
for those wishing to live a healthier lifestyle. ...
••••••

The Spin on Aspartame

If you google "aspartame," the results will take you literally days to wade
through -- believe me, I know. I've been sifting through it for days. There's
more than enough information, research, and speculation out there on the subject
to fill volumes, and this is just a small article.

So rather than simply rehash everything that has been written about aspartame
(I've included some links at the end of this article, and within it, for those
who want more information), I wanted to take a different approach. I wanted to
focus on a small part of the debate, and then follow it through to wherever it
took me.

I wanted to look at the folks who keep assuring us that it's safe: the experts.
Experts in the government, experts in the medical field, the people who keep
patting us on the head and telling us not to worry, that if aspartame was
dangerous, they'd tell us.

The problem was, I've always been something of a skeptic. The more someone pats
me on the head, the more I start looking for something up his sleeve.

But, as skeptical as I am, what I found startled me: a concerted effort, on the
part of those at the highest levels of our government and those at the highest
levels of the medical community, to mislead us about the safety of aspartame.

Let me be clear: We have been deceived about the safety of a dangerous product,
and all in the name of corporate profits.
* * *

Where did aspartame come from? It was first developed by the pharmaceutical
company G.D. Searle. But Searle had difficulty getting their product approved by
the Food and Drug Administration, the federal agency responsible for making sure
our food and drugs are safe: Apparently, the monkeys and mice the substance was
tested on developed brain lesions, tumors, and seizures, and even died from it.
The company's applications for approval were rejected for 16 years, but they
persisted in offering their "proof" that aspartame was safe until the FDA
finally asked the Department of Justice to prosecute G.D. Searle for submitting
fraudulent test data in their efforts to get the substance approved. (An FDA
senior toxicologist, Dr. Adrian Gross, once told Congress, "Beyond a shadow of a
doubt aspartame triggers brain tumors.")

But then G.D. Searle, producer of aspartame, made Donald Rumsfeld its CEO-yes,
that Donald Rumsfeld. When Ronald Reagan took office and brought Rumsfeld with
him as part of his transition team, a new FDA commissioner was appointed
immediately. In one of his first acts as head of the federal agency, the new FDA
commissioner approved aspartame, the artificial sweetener made by the company
that Donald Rumsfeld was now the head of, over the objections of the FDA
scientific board.

And here's a strange bit of trivia: When it looked like aspartame would be
approved later on for use in carbonated beverages, the National Soft Drink
Association itself objected, saying it wouldn't be safe because aspartame is
very unstable in liquid form and breaks down into, among other things,
formaldehyde. Monsanto bought G.D. Searle and Co. in 1985, and the NutraSweet
Company operated as part of Monsanto until 2000, when Monsanto sold it to J.W.
Childs Equity Partners, where it remains today.

And in all this time, the FDA has compiled a list of 92 symptoms associated with
aspartame consumption, including nausea, dizziness, blindness, deafness, weight
gain, and even death. And aspartame is still here, and it's showing up in more
and more products.

In fact, the Aspartame Resource Center, at www.aboutaspartame.com , notes that
it is found in more than 6,000 products worldwide. And they should know: the
Aspartame Resource Center is actually a public relations and "information" arm
of Ajinomoto, one of the world's largest producers of aspartame, the other being
the NutraSweet Company. (Ajinomoto is also known for its other additive,
monosodium glutamate, or MSG.) The ARC site is full of cheerful information on
the safety of aspartame, and they even have a section labeled "Meet the
doctors," which lists their "medical advisory board."

In that section, the ARC says, "The Aspartame Information Center Expert Medical
Advisory Board was created to help guide the Center's communications to health
professionals and the public about aspartame benefits, safety and role in a
healthy diet. The board members provide counsel on current medical and nutrition
science, as well as insight on tools that help address the needs of health
professionals in their work. Their backgrounds span critical areas of medicine
and science, and each has unique experience in health and nutrition."

But, wait. Are they confused about who they are? What is this "Aspartame
Information Center" they mention? I looked it up: www.aspartame.org . They, too,
have a laundry list of "experts" they use to back up their claims that aspartame
is safe, including our very own FDA and something called the Calorie Control
Council. In fact, the Calorie Control Council owns the Aspartame Information
Center site and is listed on the bottom of every page as the copyright holder.

But back to the ARC. The Aspartame Resource Center offers all sorts of "fact"
sheets you can download, including one called "Straight Answers About
Aspartame." It was prepared by the American Dietetic Association . . . and the
Calorie Control Council. At the bottom, the fact sheet notes that it has been
sponsored by aspartame.org, that is, the Aspartame Information Center, a.k.a.
the Aspartame Resource Center, a.k.a. Ajinomoto, one of the world's biggest
producers of aspartame.

Ajinomoto, in cahoots with the American Dietetic Association? Let's see who's
behind the Calorie Calorie Control Council. Here's what their own site, at
www.caloriecontrol.org, says: "The Calorie Control Council, established in 1966
. . . represents 60 manufacturers and suppliers of low-calorie, low-fat and
light foods and beverages, including the manufacturers and suppliers of more
than a dozen different dietary sweeteners . . ."

Go further, and you'll see another site connected to the Calorie Contol Council,
called Calories Count, at www.caloriescount.com , which lists as its sponsors .
. . wait for it . . . Ajinomoto, NutraSweet, Splenda, and Sweet 'N Low. You can
take a look at their sponsorship page here:
http://www.caloriescount.com/support.html .

Because it's hard to keep the players straight in the aspartame follies, let's
recap. The folks at the FDA thought aspartame was dangerous, so they wouldn't
approve it. They changed their minds when the president at that time and his
buddy, Donald Rumsfeld, who just happened to be the head of the company that
made aspartame, appointed a new head of the FDA. Miraculously, aspartame was
approved not long afterward, after sixteen years of being rejected. And when we
look for information on aspartame, to allay our concerns, we find Web sites full
of comforting information showing us how safe the stuff is, written by reliable
organizations like the American Dietetic Association, and sponsored by . . .
aspartame.

Got that? Okay, but there's more. Because I was trying not to get lost in the
organizational rabbit hole, I backed out again to the Aspartame Resource Center
and its expert medical advisors. After all, these were the medical
professionals, the people who had the scientific knowledge, not to mention the
connections with both the governmental agencies that protect our health and the
largest medical and health organizations. Surely, they were to be trusted.

Skeptical, I started with the first name on the list, and I fell into yet
another rabbit hole that seems, even now, to have no end. In fact, I never got
past that first name.

The first name on the list? C. Wayne Callaway, M.D.

I went first to his own Web site. Once you get past the introductory quote from
Hippocrates, you can find all sorts of interesting information there. In fact,
he has very helpfully posted his entire curriculum vitae for all and sundry to
see.

C. Wayne Callaway, M.D., received his medical training at Northwestern
University, Mayo Graduate School of Medicine and Harvard University. Very
impressive. He's board certified in Internal Medicine, Clinical Nutrition, and
Endocrinology, Diabetes and Metabolism and has held academic appointments at
Harvard Medical School, Mayo Medical School, and George Washington University.

He also works with the Mayo Clinic, the National Institutes of Health, the U.S.
Department of Health and Human Services, and the USDA; he was an advisor to the
U.S. Surgeon General and helped develop dietary guidelines for the USDA. He
served as chair of the Public Information Committee of the American Society for
Clinical Nutrition and the American Society for Nutrition Sciences, has been a
member of the Board of Directors of the American Board of Nutrition, has been a
committee member at the American Heart Association, has been an adviser to the
American Medical Association.

And he's served on the editorial boards of the American Journal of Clinical
Nutrition, among other medical journals. Whew -- busy man. Want more? His
publications have appeared in the Journal of the American Medical Association,
the Annals of Internal Medicine, the Journal of the American Dietetic
Association, and the International Journal of Obesity, among others.

The separate biography on his site tells us that Dr. Callaway "has offered his
expert views on nutrition on NBC, ABC, CBS, CNN, PBS, ESPN, and numerous
affiliates, and has appeared on the McNeill-Lehrer Newshour, the Today Show,
Good Morning America, Phil Donahue, Larry King Live, and other nationally
syndicated news and talk programs." His opinions on nutrition and health are
"frequently published in the New York Times, Washington Post, Chicago Tribune,
LA Times, and Wall Street Journal, as well as in numerous magazines (Time,
Newsweek, U.S. News & World Report, Business Week, Vogue, Elle, Glamour, People,
Self, Health, Prevention, and others)." You know, the mainstream media.

Callaway's bio says, "Dr. Callaway is a member of the American Society for
Clinical Nutrition." And remember, we also saw that he served as chair of the
Public Information Committee of the American Society for Clinical Nutrition. But
looking for the American Society for Clinical Nutrition takes you directly to
the American Society for Nutrition, www.nutrition.org . They publish the
American Journal of Clinical Nutrition, "the highest ranked peer-reviewed
journal in nutrition and dietetics," and the Journal of Nutrition, "which
provides the latest research on a broad spectrum of topics of vital interest to
researchers, students, policymakers and all individuals with interests in
nutrition."

Sounds impressive, until you start poking at it, as I did. If you keep going
deeper down that particular rabbit hole, you find that the American Society for
Clinical Nutrition, A.K.A. the American Society for Nutrition, is supported by
what they call "sustaining members," which, they say, "[provide] corporate
financial support for the society's activities in education/training, scientific
programs and professional outreach." The site says that sustaining members have
"the ability to sponsor educational opportunities, grants and other items."
Oddly, they don't specify what those "other items" might be, but I'd be willing
to bet that research is one of them.

Would you like to know who some of the sustaining members are? Get ready: The
National Cattlemen's Beef Association. Cadbury Schweppes. Campbell Soup Company.
ConAgra Foods. Dannon. Eli Lilly. General Mills. Gerber. GlaxoSmithKline.
Kellog. Kraft. Mars. McCormick. Monsanto (of course!). The National Dairy
Council. Nestle. PepsiCo. POM Wonderful (maker of those nifty pomegranate
juices). Procter & Gamble. The Sugar Association. Unilever. Wrigley. Wyeth.

To recap, because the players are getting a bit confusing now, Dr. C. Wayne
Callaway is a recognized expert in nutrition, such an expert, in fact, that he
testifies before Congress and appears on national television to expound on his
views on food and nutrition. His views are published nationally, and frequently.
He is, in short, a national expert, and his views are taken very, very
seriously, and published in well respected medical journals. And he pats us on
the back and tells us not to worry, aspartame is safe.

And he works with and writes for the folks who are "supported," a.k.a. "paid
by," the food industry that uses aspartame. Indeed, he is a "medical expert" on
the safety of aspartame, one hired by the aspartame industry to go before the
mainstream media and tell us how safe aspartame is.

Dr. Callaway's resume lists these as government agencies that he consults for:
the Department of Health & Human Services; the National Insitutes of Health, or
NIH; the National Research Council/National Academy of Sciences; the U.S.
Congress; the USDA, and, oddly, the U.S. Postal Service, to catch us, perhaps,
if we try to send stevia through the mail.

Oh, and one more agency he consults for: the FDA. His Web site also helpfully
lists the industry folks he consults for, a.k.a. "is paid by." They include the
American Institute of Wine and Food; Mars; Mead Johnson Nutritional Group; the
Milk Industry Foundation; the Monsanto Corporation; Nabisco, Inc.; the National
Dairy Council; the Nestle Foundation for Nutrition and Health; Ocean Spray;
Parke-Davis; Proctor & Gamble; Quaker Oats; the United Dairy Industry.

Oh, and one more: NutraSweet.

To recap once again, a nationally recognized expert on nutrition who says, in
his extraordinarily frequent public appearances, that aspartame is safe, is paid
by Ajinomoto and NutraSweet, the two largest producers of aspartame, to say that
aspartame is safe. (And, this may be helpful for some of you, he's also spoken
about the safety of Olestra. Just, you know, fyi.) I said earlier that we were
being misled in the name of corporate profits. Where do the profits come in? It
is projected that the U.S. market for artificial sweeteners, with aspartame
leading the charge, will be about $1.1 billion by 2010. That's in this country,
only; worldwide, it's projected to be over $3 billion. That's a lot of money for
an easily concocted chemical.
* * *

So how do you know if a product contains aspartame? The Aspartame Resource
Center says simply looking at the ingredient list will tell you if the product
contains aspartame, and indeed, the FDA requires that aspartame be listed on the
label. Right, that ARC, that FDA. But just in case a company hasn't listed it,
if the label mentions "phenylalanine" at all, which is a component of aspartame,
then the product contains aspartame.

But you'll need to be vigilant, especially given the tiny print on most
ingredient labels. And given the propensity of aspartame to turn up where you
least expect it, such as in the vitamins you give to your child, or your liquid
antibiotics, or your Metamucil.

The bottom line is, your vigilance is the only thing standing between you and
your unwilling ingestion of a dangerous product. Our government and our medical
experts are in the very deep pockets of the industry that makes and sells that
dangerous product, and no help is going to come from them. None.
* * *

At the top of the home page for the Aspartame Information Center -- which, don't
forget, is actually Ajinomoto, one of the two biggest producers of aspartame --
we see this quote: "Few compounds have withstood such detailed testing and
repeated, close scrutiny, and the process through which aspartame has gone
should provide the public with additional confidence of its safety."

It's attributed to the U.S. Food & Drug Administration.

Pat, pat, pat.

If you would like to learn more you may want to read other articles on aspartame
and the potential health risks associated with its use.

Aspartame- The Silent Killer
Aspartame Side Effects
Aspartame Poisoning
Aspartame and Pregnancy
Aspartame and Diabetes

Below is a list of links that you may find helpful in sorting out the facts:

www.aspartamesafety.com
http://aspartame.worldwidewarning.net/
http://www.holisticmed.com/aspartame/
http://www.sweetpoison.com/

About the Author:

Lynn Stratton worked for the St. Petersburg Times as a news archivist, copy
editor and staff writer until recently, when she started her own writing and
editing business. Before that, she taught at USF for 15 years. Originally from
NYC, she spends her spare time walking her standard poodle, Harry, and working
in her butterfly garden, where she's had 6 species of caterpillars so far this
year. lstratton@...
[ http://www.healthy-holistic-living.com/msg.html  MSG: The Hidden Danger in
Your Children's Food ]

Posted by Alex Constantine at 4:50 AM

Contact; The brute physics of time rule out long-winded responses, but I can be
reached at: alexx1984@...
___________________________________________________


http://www.doctorcallaway.com/noflash.html
C. Wayne Callaway, M.D.  Endocrinologist / Diabetes Specialist
Dr. C. Wayne Callaway
2311 M St Nw Ste 301
Washington, DC 20037
(202) 331-3330

Clifton W. Callaway, MD  callawaycw@...;
University of Pittsburgh Physicians
Department of Emergency Medicine
UPMC Presbyterian Emergency Department
200 Lothrop Street

http://www.nextbio.com/b/literature/literature.nb;jsessionid=A1BF9F859040CFD441E\
95E9D2D942D21?author=CW+Callaway
over 100 papers listed 2008 - 1974

http://www.aboutaspartame.com/professional/board.asp
Expert Medical Advisory Board
C. Wayne Callaway, M.D. callawaycw@...;
John D. Fernstrom, Ph.D.  fernstromjd@...;
Sue Y.S. Kimm, M.D., M.P.H. skimm@...;
Ronald E. Kleinman, M.D. rkleinman@...;
___________________________________________________



folic acid prevents harm from formaldehyde and formic acid,
formed from methanol from many sources:
Rich Murray 2008.07.13

re "A Few too Many", Joan Acocella, The New Yorker, long review of hangover
research 2008.05.26 -- same levels of formaldehyde and formic acid in FEMA
trailers and other sources (aspartame, dark wines and liquors, tobacco
smoke): Murray 2008.06.05
http://rmforall.blogspot.com/2008_06_01_archive.htm
Thursday, June 5, 2008
http://groups.yahoo.com/group/aspartameNM/message/1541

[ See also:
There really is no controversy, Adrienne Samuels PhD, letter re
evident toxicity of aspartame EJCN 2008.06.11:
Murray 2008.06.30
http://rmforall.blogspot.com/2008_06_01_archive.htm
Monday, June 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1546

former key Hillary Clinton staff Mark Penn and Patti Solis Doyle
use much neurotoxic aspartame Diet Coke -- also many other
politicians: Murray 2008.06.30
http://rmforall.blogspot.com/2008_06_01_archive.htm
Monday, June 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1545

opportunities re BA Magnuson, GA Burdock et al., Aspartame Safety Evaluation
2007 Sept., Critical Reviews in Toxicology: Rich Murray 2008.07.11
http://rmforall.blogspot.com/2008_07_01_archive.htm
Friday, July 11, 2008
http://groups.yahoo.com/group/aspartameNM/message/1550 ]


formaldehyde and formic acid in FEMA trailers and other sources
(aspartame, dark wines and liquors, tobacco smoke):
Murray 2008.01.30
http://rmforall.blogspot.com/2008_01_01_archive.htm
Wednesday, January 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1508

The FEMA trailers give about the same amount of formaldehyde
and formic acid daily as from a quart of dark wine or liquor,
or two quarts (6 12-oz cans) of aspartame diet soda,
from their over 1 tenth gram methanol impurity
(one part in 10,000), which the body quickly makes into
formaldehyde and then formic acid -- enough to be the major cause
of "morning after" alcohol hangovers.

Methanol and formaldehyde and formic acid also result from
many fruits and vegetables, tobacco and wood smoke, heater
and vehicle exhaust, household chemicals and cleaners, cosmetics,
and new cars, drapes, carpets, furniture, particleboard,
mobile homes, buildings, leather... so all these sources add up
and interact with many other toxic chemicals.

methanol impurity in alcohol drinks [ and aspartame ] is turned into
neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol
Syndrome, BM Kapur, DC Lehotay, PL Carlen at U. Toronto,
Alc Clin Exp Res 2007 Dec. plain text: detailed biochemistry,
CL Nie et al. 2007.07.18: Murray 2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524
___________________________________________________


In fact the FDA brought suit against Searle for its radically biased, improper
scientific studies.

The industry won by persuading the FDA's two attorneys to let the legal process
languish.

Soon, the attorney's inexplicably found pleasant, prosperous futures in the
industry's networks.

Similar adroit exercises in corporate realpolitic were led by the CEO of Searle,
none other than that modest American hero, Donald Rumsfeld, who used Reagan's
victory to immediately manipulate the FDA's approval by a brand new
Commissioner, Arthur Hull Hayes, in July, 1981, of aspartame in dry foods, and
soon in beverages two years later, whereupon the fortunate Commissioner,
troubled by hints of political corruption, found a gracious life with the
industry's PR agency.

Donald Rumsfeld CEO 1977-85 G.D. Searle & Co., got new President Reagan to
prohibit FDA opposition to aspartame 1981.01.25, history by lawyer James S.
Turner: Murray 2007.10.29
http://groups.yahoo.com/group/aspartameNM/message/1483

aspartame history Part 1/4 1964-1976: Gold: Murray 1999.11.06
http://groups.yahoo.com/group/aspartameNM/message/53
http://www.dorway.com/enclosur.html

aspartame expose 96K Oct 1987 Part 1/3: Gregory Gordon, UPI reporter: Murray
2000.07.10
http://groups.yahoo.com/group/aspartameNM/message/262
http://www.dorway.com/upipart1.txt

revolving door, Monsanto, FDA, EPA: NGIN: Murray 2002.12.23
http://groups.yahoo.com/group/aspartameNM/message/928
____________________________________________________


"Of course, everyone chooses, as a natural priority, to enjoy peace, joy, and
love by helping to find, quickly share, and positively act upon evidence about
healthy and safe food, drink, and environment."

Rich Murray, MA Room For All rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com  new primary archive

http://groups.yahoo.com/group/aspartameNM/messages
group with 127 members, 1,551 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1,123 members, 22,811 posts in public archive
___________________________________________________

opportunities re BA Magnuson, GA Burdock et al., Aspartame Safety Evaluation
2007 Sept., Critical Reviews in Toxicology: Rich Murray 2008.07.11
http://rmforall.blogspot.com/2008_07_01_archive.htm
Friday, July 11, 2008
http://groups.yahoo.com/group/aspartameNM/message/1550
____________________________________________________


"Of course, everyone chooses, as a natural priority, to enjoy peace, joy, and
love by helping to find, quickly share, and positively act upon evidence about
healthy and safe food, drink, and environment."

Rich Murray, MA Room For All rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com  new primary archive

http://groups.yahoo.com/group/aspartameNM/messages
group with 127 members, 1,550 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1,125 members, 22,796 posts in a public archive
____________________________________________________


[ See also:
two detailed critiques of industry affiliations and biased science in 99
page review with 415 references by BA Magnuson, GA Burdock and 8 more,
Critical Reviews in Toxicology, 2007 Sept.: Mark D Gold 13 page: also Rich
Murray 2007.09.15: 2008.03.24
http://rmforall.blogspot.com/2008_07_01_archive.htm
Monday, March 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1531 ]


Introduction:

As a volunteer medical layman information activist, ( note that all citizens
are laymen outside the domain of their specific areas of expertise ) who for
over nine years has earnestly provided detailed, long, fair, civil reviews
on the Net of mainly mainstream aspartame toxicity research and related
topics, as well as responsible world media and Net sources, I submit a
version of my 240 KB critical review of an aspartame approving, Ajinomoto
funded review by BA Magnuson, GA Burdock, et al. 2007, (which herein is
designated as "ASE"), to the world public.

I welcome cogent criticism, which usually I will promptly add uncensored to
my public archive.

bias, omissions, incuriosity = opportunity, aspartame safety evaluation,
Magnuson BA, Burdock GA, Williams GM, 7 more, 2007 Sept, Ajinomoto funded 98
pages html [ $ 32 pdf ]: Murray 2007.09.15
http://rmforall.blogspot.com/2007_09_01_archive.html
Saturday, September 15, 2007  240 KB

"Of course, everyone chooses, as a natural priority, to enjoy peace, joy,
and love by helping to find, quickly share, and positively act upon evidence
about healthy and safe food, drink, and environment."

Rich Murray, MA Room For All rmforall@... 505-501-2298 1943 Otowi
Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com  new primary archive

http://groups.yahoo.com/group/aspartameNM/messages
group with 127 members, 1,550 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1,124 members, 22,793 posts in a public archive

My inspiring mentor since January 1999 has been another conscientious
medical layman, Mark David Gold, gives an excellent 13-page critique of ASE
that details undue industry affiliations by the authors and specific faults
in their opus:
http://www.HolisticMed.com/aspartame mgold@...
Aspartame Toxicity Information Center, Mark D. Gold
12 East Side Drive #2-18 Concord, NH 03301 603-225-2100

two detailed critiques of industry affiliations and biased science in 99
page review with 415 references by BA Magnuson, GA Burdock and 8 more,
Critical Reviews in Toxicology, 2007 Sept.: Mark D Gold 13 page: also Rich
Murray 2007.09.15: 2008.03.24
http://rmforall.blogspot.com/2008_03_01_archive.htm
Monday, March 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1531

http://www.holisticmed.com/aspartame/burdock/

"Nearly every section of the Magnuson (2007) review has research that is
misrepresented and/or crucial pieces of information are left out.

In addition to the misrepresentation of the research, readers (including
medical professionals) are often not told that this review was funded by the
aspartame manufacturer, Ajinomoto, and the reviewers had enormous conflicts
of interest."

[ See also:

http://groups.yahoo.com/group/aspartameNM/message/957
safety of aspartame Part 1/2 12.4.2: EC HCPD-G SCF:
Murray 2003.01.12 EU Scientific Committee on Food, a whitewash

http://groups.yahoo.com/group/aspartameNM/message/1045
http://www.holisticmed.com/aspartame/scf2002-response.htm
Mark Gold exhaustively critiques European Commission Scientific Committee on
Food re aspartame ( 2002.12.04 ): 59 pages, 230 references ]

www.informaworld.com/smpp/section?content=a781888262&fulltext=713240928  $
32

Bernadene A. Magnuson,
George A. Burdock,
John Doull,
Robert M. Kroes, [deceased]
Gary M. Marsh,
Michael W. Pariza,
Peter S. Spencer,
William J. Waddell,
Ronald Walker,
Gary Murray Williams.
"Aspartame: A Safety Evaluation Based on Current Use Levels, Regulations,
and Toxicological and Epidemiological Studies,"
Critical Reviews in Toxicology, 37(8), 629-727, 2007 Sept [415 references]


http://www.utoronto.ca/nutrisci/faculty/Magnuson/
Bernadene A. Magnuson, Ph.D.
Adjunct Associate Professor, Department of Nutritional Sciences
Senior Scientific and Regulatory Consultant, Cantox Health Science
International, 2233 Argentia Road, Suite 308, Mississauga, ON L5N 2X7
Tel: (905) 542 2900 Fax: (905) 542 1011 BMagnuson@...;
Research
My research interests have been in the area of diet and cancer and I am now
interested in the new and exciting area of nanotechnology and its role in
nutrition. ]
____________________________________________________


details on 6 epidemiological studies since 2004 on diet soda (mainly
aspartame) correlations, as well as 13 other mainstream studies on aspartame
toxicity since summer 2005: Murray 2007.11.14
http://rmforall.blogspot.com/2007_11_01_archive.htm
Wednesday, November 14, 2007
http://groups.yahoo.com/group/aspartameNM/message/1490

http://groups.yahoo.com/group/aspartameNM/message/1340
aspartame groups and books: updated research review of 2004.07.16: Murray
2006.05.11


formaldehyde and formic acid in FEMA trailers and other sources (aspartame,
dark wines and liquors, tobacco smoke): Murray 2008.01.30
http://rmforall.blogspot.com/2008_01_01_archive.htm
Wednesday, January 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1508

The FEMA trailers give about the same amount of formaldehyde and formic acid
daily as from a quart of dark wine or liquor, or two quarts (6 12-oz cans)
of aspartame diet soda, from their over 1 tenth gram methanol impurity (one
part in 10,000), which the body quickly makes into formaldehyde and then
formic acid -- enough to be the major cause of "morning after" alcohol
hangovers.

Methanol and formaldehyde and formic acid also result from many fruits and
vegetables, tobacco and wood smoke, heater and vehicle exhaust, household
chemicals and cleaners, cosmetics, and new cars, drapes, carpets, furniture,
particleboard, mobile homes, buildings, leather... so all these sources add
up and interact with many other toxic chemicals.

methanol impurity in alcohol drinks [ and aspartame ] is turned into
neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol Syndrome,
BM Kapur, DC Lehotay, PL Carlen at U. Toronto, Alc Clin Exp Res 2007 Dec.
plain text: detailed biochemistry, CL Nie et al. 2007.07.18: Murray
2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524


http://www.blackwell-synergy.com/doi/abs/10.1111/j.1530-0277.2007.00541.x

Alcoholism: Clinical and Experimental Research
Volume 31 Issue 12 Page 2114-2120, December 2007

Bhushan M. Kapur,  b.kapur@...;
Arthur C. Vandenbroucke, PhD, FCACB
Yana Adamchik,
Denis C. Lehotay,  dlehotay@...;
Peter L. Carlen  carlen@...;
(2007) Formic Acid, a Novel Metabolite of Chronic Ethanol Abuse, Causes
Neurotoxicity, Which Is Prevented by Folic Acid
Alcoholism: Clinical and Experimental Research 31 (12), 2114-2120.
doi:10.1111/j.1530-0277.2007.00541.x

Abstract

Background:
Methanol is endogenously formed in the brain and is present as a congener in
most alcoholic beverages.

Because ethanol is preferentially metabolized over methanol (MeOH) by
alcohol dehydrogenase, it is not surprising that MeOH accumulates in the
alcohol-abusing population.

This suggests that the alcohol-drinking population will have higher levels
of MeOH's neurotoxic metabolite, formic acid (FA).

FA elimination is mediated by folic acid.

Neurotoxicity is a common result of chronic alcoholism.

This study shows for the first time that FA, found in chronic alcoholics, is
neurotoxic and this toxicity can be mitigated by folic acid administration.

Objective:
To determine if FA levels are higher in the alcohol-drinking population and
to assess its neurotoxicity in organotypic hippocampal rat brain slice
cultures.

Methods:
Serum and CSF FA was measured in samples from both ethanol abusing and
control patients, who presented to a hospital emergency department.  [ CSF =
Cerebral Spinal Fluid ]

FA's neurotoxicity and its reversibility by folic acid were assessed using
organotypic rat brain hippocampal slice cultures using clinically relevant
concentrations.

Results:
Serum FA levels in the alcoholics (mean ± SE: 0.416 +- 0.093 mmol/l, n = 23)
were significantly higher than in controls (mean ± SE: 0.154 +- 0.009
mmol/l, n = 82) (p < 0.0002).

FA was not detected in the controls' CSF (n = 20), whereas it was >0.15
mmol/l in CSF of 3 of the 4 alcoholic cases.

Low doses of FA from 1 to 5 mmol/l added for 24, 48 or 72 hours to the rat
brain slice cultures caused neuronal death as measured by propidium iodide
staining.

When folic acid (1 umol/l) was added with the FA, neuronal death was
prevented. [ umol = micromole ]

Conclusions:
Formic acid may be a significant factor in the neurotoxicity of ethanol
abuse.

This neurotoxicity can be mitigated by folic acid administration at a
clinically relevant dose.

Key Words:
Formic Acid, Folic Acid, Methanol, Neurotoxicity, Alcoholism.

From the Department of Clinical Pathology (BMK), Sunnybrook Health Science
Centre, Division of Clinical Pharmacology and Toxicology, The Hospital for
Sick Children, Toronto, Ontario, Canada;

St. Michael's Hospital (ACV), Toronto, Canada;

Department of Laboratory Medicine and Pathobiology, (BMK, ACV), Faculty of
Medicine, University of Toronto, Toronto, Ontario, Canada;

Departments of Medicine (Neurology) and Physiology (YA, PLC), Toronto
Western Research Institute, University of Toronto, Toronto, Ontario, Canada;

and University of Saskatchewan (DLC), Saskatchewan, Canada.

Received for publication May 1, 2007; accepted September 24, 2007.

Reprint requests: Dr. Bhushan M. Kapur, Department of Clinical Pathology,
Sunnybrook Health Science Centre, 2075 Bayview Ave, Toronto, Ontario, M4N
3M5, Canada;
Fax: 416-813-7562; E-mail: b.kapur@...;

Copyright  2007 by the Research Society on Alcoholism. DOI:
10.1111/j.1530-0277.2007.00541.x
Alcoholism: Clinical and Experimental Research 2007 Dec.
Alcohol Clin Exp Res, Vol. 31, No 12, 2007: pp 2114-2120

NEUROTOXICITY AND BRAIN damage are common concomitants findings of chronic
alcoholism (Carlen and Wilkinson, 1987; Carlen et al., 1981; Harper, 2007).

The cause of ethanol-induced neurotoxicity is still unclear.

We present here a novel hypothesis for neurotoxicity: increased formic acid
(FA) levels produced from methanol (MeOH), whose catabolism is blocked by
ethanol.

Axelrod and Daly (1965) demonstrated the endogenous formation of MeOH from
S-adenosylmethionine (SAM) in the pituitary glands of humans and various
other mammalian species.

Presence of MeOH in the breath of human subjects was reported by Ericksen
and Kulkarni (1963).

Most alcoholic beverages also have a small amount of MeOH as a congener
(Sprung et al., 1988).

As ethanol (EtOH) has a higher affinity for alcohol dehydrogenase (ADH) than
MeOH, EtOH is preferentially metabolized (Mani et al., 1970).

As a result, MeOH accumulation from endogenously produced MeOH, and/or, that
consumed as part of an alcoholic beverage, has been reported in
concentrations up to 2 mmol/l in heavy drinkers (Majchrowicz and Mendelson,
1971).

Toxicity resulting from MeOH consumption is extensively documented in both
humans and animals and has been attributed to its metabolite, FA (Benton and
Calhoun, 1952; Roe, 1946, 1955; Wood, 1912; Wood and Buller, 1904).

The rate of formate oxidation and elimination is dependent on adequate
levels of hepatic folic acid, particularly hepatic tetrahydrofolate (THF)
(Johlin et al., 1987; Tephly and McMartin, 1974).

Significantly higher formate levels were obtained when folate-deficient
animals were exposed to MeOH as compared with folate-sufficient animals (Lee
et al., 1994; McMartin et al., 1975; Noker et al., 1980).

To understand ethanol's toxicity, one must consider FA produced from MeOH,
and its elimination mediated by folic acid.

We postulate that in the chronically drinking patient, we will find higher
levels of FA than in the nondrinking population, and that formate is
neurotoxic.

We also hypothesize that treatment with folic acid, which is a critical
factor in the catabolism of FA, can prevent or diminish FA neurotoxicity.
____________________________________________________


Pondering how to proceed for two months, I realized the value of  my
existing opus and modus operandi.  It is best to submit this text as a
working preprint, in the public domain, allowing readers to access the
wonderful opportunities today on the Net for immediate, full, unlimited,
detailed, uncensored, global public collaboration, forever archived, freely
accessible, and very conveniently searchable.  Thus, the text is a portal to
aid agile readers in hopping quickly in any direction and depth they want,
with hyperlinked references throughout.

The focus here, largely bypassing the isolated fortress islands of vested
interest operations, vainly entrenched to impede open-ended investigation,
shut down debate, defend narrowly construed self-interest, spread confusion,
instill propaganda -- all the dull, tedious, pious pleadings of false
authority, the mistakable artifice of modern PR spin artists, in the service
of criminal capitalism -- is opportunity.

Opportunity is not optional.  Just as new collaborations of responsibility
arose in the face of nuclear and thermonuclear bombs after 1945, so again
now with the current chemical catastrophe:


http://groups.yahoo.com/group/aspartameNM/message/1453
Souring on fake sugar (aspartame), Jennifer Couzin, Science 2007.07.06: 4
page letter to FDA from 12 eminent USA toxicologists re two Ramazzini
Foundation cancer studies 2007.06.25: Murray 2007.07.18

Dr. Kamal M. Abdo, PhD,
Carlos A. Camargo, Jr., MD, DrPH,
Devra Lee Davis, PhD, MPH,
David E. Egilman MD, MPH,
Samuel S. Epstein, MD,
John R. Froines, PhD,
Dale Hattis, PhD,
Kim Hooper, PhD,
James Huff, PhD,
Michael F. Jacobson, PhD,
Peter F. Infante, DDS, DrPH.
Letter to U.S. FDA commissioner. Questions about the safety of the
artificial sweetener aspartame.
Int J Occup Environ Health. 2007 Oct-Dec; 13(4): 449-50. No abstract
available. PMID: 18085059

" In light of the new aspartame study, which extends and corroborates the
finding from an earlier study, we urge the FDA to immediately commence a
careful review of the new study.

Considering how widely aspartame in consumed by young children, as well as
adults, in the United States and abroad, it is essential that this review be
done as expeditiously as possible.

If that review confirms that aspartame caused cancer in the laboratory
animals, the FDA must invoke the Delaney amendment and revoke its approval
for the artificial sweetener. 8 "

www.ramazzini.it/fondazione/pdfUpload/Science_06.07.2007.pdf

SCIENCE VOL 317 6 JULY 2007 page 31

Souring on Fake Sugar

Fearful it causes cancer, 12 U.S. environmental health experts last week
asked the U.S. Food and Drug Administration (FDA) to review the potential
health risks of the artificial sweetener aspartame, which appears in
everything from medicines to diet sodas.

A study published last month in Environmental Health Perspectives found
somewhat more leukemias and lymphomas in male rats receiving less aspartame
than the recommended maximum for humans; at higher doses, the rats had a
marked increase in cancers throughout the body.

Pregnant rats were fed the sweetener, and animals received it once they'd
been weaned. The work, by scientists at the European Ramazzini Foundation of
Oncology and Environmental Sciences in Bologna, Italy, is "more sensitive
and more realistic" than earlier aspartame studies, says James Huff of the
National Institute of Environmental Health Sciences, who signed onto the FDA
letter drafted by the
Washington, D.C.-based watchdog group Center for Science in the Public
Interest.

But because the study conflicts with earlier work, FDA spokesperson Michael
Herndon says that the agency finds the study unpersuasive and that
"aspartame is safe."

FDA's European counterpart has not responded publicly to the study. --
Jennifer Couzin

www.cspinet.org/new/200706251.html
www.cspinet.org/new/200706251_print.html
http://cspinet.org/new/pdf/aspartame_letter_to_fda.pdf


http://health.groups.yahoo.com/group/GFCFKids/messages

This group, after nine years, has 12,708 members and 335,599 posts in a
public archive:  "This list is unmoderated and unrestricted. The principle
aim of this list is to provide a discussion forum for parents of children on
the autism spectrum who are avoiding gluten and casein and other substances
in their children's diets. "


British Columbia guidelines against "any drinks with artificial sweeteners"
in January 2008 in school vending machines, stores, cafeterias or
fundraisers -- also recently in Ontario and Quebec, Janet Steffenhagen
2007.12.28 Vancouver Sun:  Murray 2008.04.10
http://rmforall.blogspot.com/2008_04_01_archive.htm
Thursday, April 10, 2008
http://groups.yahoo.com/group/aspartameNM/message/1537

http://groups.yahoo.com/group/aspartameNM/message/1426
ASDA (unit of Wal-Mart Stores WMT.N) and Marks & Spencer will join Tesco and
also Sainsbury to ban and limit aspartame, MSG, artificial flavors dyes
preservatives additives, trans fats, salt "nasties" to protect kids from
ADHD: leading UK media: Murray 2007.05.15

http://groups.yahoo.com/group/aspartameNMmessage/1451
Artificial sweeteners (aspartame, sucralose) and coloring agents will be
banned from use in newly-born and baby foods, the European Parliament
decided: Latvia ban in schools 2006: Murray 2007.07.12

http://groups.yahoo.com/group/aspartameNM/message/1341
Connecticut bans artificial sweeteners in schools, Nancy Barnes, New Milford
Times: Murray 2006.05.25

http://groups.yahoo.com/group/aspartameNM/message/1369
Bristol, Connecticut, schools join state program to limit artificial
sweeteners, sugar, fats for 8800 students, Johnny J Burnham, The Bristol
Press: Murray 2006.09.22


Summary:

1. The preceding items indicate a few facets of exponentially evolving
global responses on many levels to chemical catastrophe.  AspartameNM was
set up nine years ago to facilitate this process with detailed, thorough,
referenced information, civil discourse based on reason and public evidence,
and openness to dialogue among diverse and opposed points of view.  It may
well evolve into a new type of scientific journal, with an unusually broad
membership, allowing fully democratic co-evolution of articles, discussions,
research and public affairs proposals, funding, project implementations,
completely transparent and perpetually archived communication during all
phases, constant sharing of data,  conclusions, and open questions to
consider, with constantly co-created traditions of organization,
responsibility, and ownership, naturally allied with other "open source"
service societies, like Wikipedia and Citizendium, and the many 12-Step
communities.

This review exists within and serves this context of a wider global society,
extremely diverse yet complexly unified, aided by service societies not
bound by past concepts: national, political, economic, educational,
governmental, legal, medical, spiritual, scientific.  Multiple exponential
emergencies mandate multiple exponential service societies.

  Here, it is helpful for the specific case of aspartame toxicity to present
salient capsules, with full references and texts given in the rest of this
text.

2. Aspartame is a triple toxin, since all three of its loosely bound
components along with their complex metabolites are toxic, especially for
the many vulnerable groups who are also long-term, heavy users, above 6 cans
diet soda, 1,200 mg aspartame, daily for years:
Phenylalanine 50%, aspartic acid 39%, methanol 11% -- methanol likewise owes
its toxicity entirely to its rapid conversion in humans to formaldehyde and
thence to formic acid.  About 30-40% of the methanol remains in human
tissues as cumulative, toxic products, as yet largely unobserved and
unexplored.

3. It is fruitless to study aspartame without tracking its actual metabolic
fate in specific tissues in individual humans.

4. There is extreme individual variation -- involving genetics, diet, health
status, drugs and medicines, age, sex, stress, other toxins and protective
factors like adaquate folic acid levels.

5. According, studies that focus on averages, such as much of epidemiology
and double blind experimental tests, are completely blind to the realities.

6. Therefore, it is essential to do deep, detailed, exhaustive studies on
individuals, starting with case histories.

7. It is necessary to thoroughly integrate all studies on methanol,
formaldehyde, formic acid, folic acid, acetaldehyde, alcohol hangover,
addiction studies, and all sources of methanol and formaldehyde, including
alcohol drinks, tobacco and wood smoke, air pollution, degradation of
pectins from fruits and vegetables by bacteria in the colon, and the modern
diet and environment.  The toxic level of concern for formaldehyde  from air
in mobile homes is about the same as the dose from 3 cans of diet soda.

8.  Folic acid in most people expedites the safe metabolism of methanol and
formaldehyde, so it must be included in most research. It is urgent to
immediately assess and publicize its value.  Its presence in fruits and
vegetables may account for the low level of reported symptoms.

9.  There are many, many other such co-factors.

10. Behavioral measures for neurotoxicity show immediate harm at much lower
doses, compared to biochemical and genetic effects.

11. Thus, current safety levels are too high by an order of magnitude or
more for methanol, formaldehyde, formic acid, and so on.

12.  During the Stone Age, high levels of methanol from fermented fruit and
of formaldehyde from wood fires may have have helped humans survive fungi,
germs, and viruses.  These possible benefits should be evaluated for many
kinds of people and conditions.

13. Thus, evolution may have operated to make alcohol, acetaldehyde,
formaldehyde, and formic acid addictive.

14. A small population in the Stone Age may have evolved overproduction of
brain cells to counter neurotoxicity, leading to larger brains overall and a
thus a major survival gain.  Then, overall positive selection pressure would
also promote addiction to nonlethal levels of neurotoxins, as is common
today for caffeine, alcohol, tobacco, cocaine, heroin, marihuana, etc.

15. Formaldehyde is well known as an initial and subsequent trigger for
hypersensitivity, Multiple Chemical Sensitivity.

16. The Comet assay enables fast, inexpensive, subtle measures of genetic
damage from neurotoxins in single cells.

17. ASE reference  (Larsen and Richold, 1999):  re survey of teenage
diabetics

3.5.  "Methanol generated from aspartame is estimated to average 33 mg/day
or 0.55 mg/kg bw/day for a 60-kg individual.

For individuals in the 95th percentile the estimated methanol consumption
figures are 93.9 mg/day or 1.57 mg/kg bw/day for a 60-kg individual." [
three times more than the average ]

[ Thus, 114% of the European ADI of 40 mg/kg bw/day for a 60-kg teenager
gives 2,736 mg aspartame daily, with the 11% methanol 301 mg daily, so 30%
retention of cumulative durable toxic products of formaldehyde and formic
acid would be 90 mg daily -- 2700 mg a month.

About 150 mg methanol impurity in ordinary liquors is a major cause of
"morning after" hangovers, due to the conversion of methanol into
formaldehyde and formic acid, with methanol blood levels
reduced to about 3%, 5 mg/l, 13 h after drinking.

However, almost all of the methanol from aspartame is quickly released into
the blood.

It is urgent to assess the specific health status of this "small
subpopulation" of teenage diabetics who endure these remarkable toxic
exposures.

18. Table 1. NIH-AARP Diet and Health Study aspartame intake levels from
beverages, 1995-2000 (N = 473,984)
[ adapted from article -- a 12-oz can diet soda has 200 mg aspartame ]

0 -- under 100 -- 100-200 -- 200-400 -- 400-600 -- 600-1200 -- over 1200
mg/d
[ highest value 3400 mg ]

cohort %
46 -------- 25 -------- 13 ---------- 7 -------- 5 ----- about 3 ---- under
1


This is the first good data about the percentage of aspartame users who use
over 3 cans daily, averaging 5 cans daily at 200 mg per 12 oz can diet soda.

About 4 % of 473,984 is 19,000 people, with a peak intake of 17 cans daily,
and average 5 cans daily.

It would be worthwhile to investigate a wide variety of symptoms for the 0.1
% of highest level users, about 500 people.

18. Besides their recent studies on lifetime aspartame carcinogenicity, the
Ramazzini team in 2002 found similar cancers from studies with alcohol,
acetaldehyde, methanol, and formaldehyde at levels corresponding to those
from conversion from aspartame.


Critique:

Naturally, I want to cut to the chase with pertinent critical comments,
often giving quotes from the ASE text and its 415 references, and then my
comments in square brackets.

ASE 6.  "As aspartame is completely hydrolyzed following intake, studies
employing either intraperitoneal administration or direct exposure of cells
in vitro to intact aspartame do not reflect human exposures and therefore,
must be carefully interpreted." [ Spot on! ]

ASE 3.1.1 [ They state that 22 mg ingested aspartame releases 2.4 mg
methanol, Stegink, 1987 -- i.e., which is 11% of the aspartame.

Fully 11% of aspartame is methanol -- 1,120 mg aspartame in 2 L diet soda,
almost six 12-oz cans, gives 123 mg methanol (wood alcohol). If 30 % of the
methanol is turned into formaldehyde, the amount of formaldehyde, 37 mg, is
18 times the USA EPA limit for daily formaldehyde in drinking water, 2 mg in
2 L water.

For instance, hangover researchers claim that it is the ~150 mg/L methanol
impurity, about one part in 10,000, twice the level from aspartame in diet
sodas, in dark wines and liquors that, turned into formaldehyde and then
formic acid, is the major cause of the common symptoms of "morning after"
hangover.

In addition, the half-life of methanol in blood is about 2.5 h,  (SE Jones
et al. 1987) and hangover symptoms occur 13 hours later, five half-lives, so
by then the methanol blood level is reduced about 32 fold, to about 3 %, or
5 mg/L (YS Woo et al. 2005)  -- whereas the methanol from aspartame is
quickly available in full. ]


[ ASE reference 254:  Oppermann JA, Muldoon E, Ranney RE.
Metabolism of aspartame in monkeys.
J. Nutrition 1973 Oct; 103(10): 1454-1459. [ free full text via PubMed ]
Dept. of Biochemistry, Searle Laboratories,
Division of G.D. Searle and Co. Box 5110, Chicago, IL 60680

They found that about 70% of the radioactive methanol in aspartame put into
the stomachs of 3 to 7 kg monkeys was eliminated within 8 hours, with little
additional elimination, as carbon dioxide in exhaled air and as water in the
urine.

They did not mention that this meant that about 30% of the methanol must
transform into formaldehyde and then into formic acid, both of which must
remain as toxic products in all parts of the body.

They did not report any studies on the distribution of radioactivity in body
tissues, except that blood plasma proteins after 4 days held 4% of the
initial methanol.

This study did not monitor long-term use of aspartame. ]


ASE 3.1.5.  "Ilback et al. (2003) surveyed 1120 diabetics and reported that
average daily intakes of aspartame by children and adult diabetics were
below the ADI, for both the top 5% and 10% consumers.

Worst-case intakes were calculated for the 10 diabetic children [ 1.1% of
adults and children ] consuming the highest amounts of artificially
sweetened foods and using the highest concentrations of
sweetener allowed in food products.

The worst-case calculation was based on the following assumptions:
(1) All sweeteners found in the diet were replaced by aspartame;
(2) the level of aspartame in foods was the maximum allowed by regulations,
not the concentration actually used in the foods; and
(3) the intake was based on the highest reported consumption of 10 diabetic
children consuming the highest amounts of artificially sweetened foods.

These worst-case calculations showed that consumption by this small
subpopulation would exceed the ADI by only a small percentage (about 114% of
the ADI), and thus the authors concluded that there is a sufficient safety
margin for aspartame, even in high consuming diabetics in a single time
point (Ilback et al., 2003). "

"Therefore, a short period of exposure slightly above the ADI is not
considered to pose any significant risk (Larsen and Richold, 1999)."

ASE 3.3.  "Methanol generated from aspartame is estimated to average 33
mg/day or 0.55 mg/kg bw/day for a 60-kg individual.

For individuals in the 95th percentile the estimated methanol consumption
figures are 93.9 mg/day or 1.57 mg/kg bw/day for a 60-kg individual." [
three times more than the average ]

[ Thus, 114% of the European ADI of 40 mg/kg bw/day for a 60-kg teenager
gives 2,736 mg aspartame daily, with the 11% methanol 301 mg daily, so 30%
retention of cumulative durable toxic products of formaldehyde and formic
acid would be 90 mg daily -- 2700 mg a month.

About 150 mg methanol impurity in ordinary liquors is a major cause of
"morning after" hangovers, due to the conversion of methanol into
formaldehyde and formic acid, with methanol blood levels
reduced to about 3%, 5 mg/L, 13 h after drinking.

It is urgent to assess the specific health status of this "small
subpopulation" of teenage diabetics who endure these remarkable toxic
exposures.

Many aspartame reactors used over 12 12-oz cans daily diet soda for years.
At 200 mg each, this is 2400 mg daily aspartame, 264 mg methanol, and at
30%, 80 mg retained formaldehyde and formic acid products -- disposition,
biochemistry, and concentrations unknown as yet to world science.

This fundamental crucial ignorance is hardly grounds for disingenuously
dismissing every one of hundreds of mainstream research reports and
thousands of individual cases by informed professionals and affected people.

Yet, this is all that is offered the ASE review, by a paid expert panel set
up by the Burbank Group, funded by Ajinomoto.  Should not the
"remuneration," past or continuing be disclosed, along with any contractual
obligations?

The greatest gift of science to humanity since 1600 is the vision of
unfettered, yet disciplined, curiosity, publicly and respectfully shared,
about all aspects and levels of our infinite reality.

Questions raised generate partial answers, which open up ever expanding
frontiers of more questions, within a overall richness of understanding and
subtlety of communication that is profoundly meaningful, awesomely
beautiful, and of the greatest practical value.

Like all the other previous reviews, invariably committee work at its worst,
the ASE review, fails totally at being curious, at spotting telling details
(where frisky devils cavort), acknowledging fundamental unknowns, and
raising pointed questions to inspire their peers.

Once again, good, intelligent, trained, experienced, dedicated, earnest
scientists have failed themselves and science, by acquiescing to
participation, true, very well paid, in a ceremonial public ritual dance of
groupthink to support vast vested interests.

Once again, the good tidings are immediately proclaimed in a global media
campaign, a Katrina deluge of relentless, repetitious, pious, preaching --
Our witch doctors have met and burned much incense, the baleful concerns are
all laid to rest, so go ye villagers and consume ye yet more in peace.

Once again, but with some progress.

Now, there are many times more references, with ever more on recent studies.

Now, there is explicit discussion, or at least mention, of areas of
ignorance.

Now, at least on the edge of the table of discourse, are closely related
fields of methanol, formaldehyde, formic acid, alcohol hangover, MSG,
additives, tobacco, addiction, vehicle exhaust, diet, genetic variation,
drug interactions, the many new modern diseases, whole population
epidemiology, global data bases mining -- all growing exponentially, all
intimately, instantly linked on the Net.

Now, every match sets off fire.

Now, there are Net groups with permanent, open archives, where citizens and
experts collaborate on every problem, i.e. opportunity.

AspartameNM -------------------- 127 members ---- 1,550 posts
Aspartame ---------------------- 1,124 members --- 22,793 posts
GlutenFreeCaseinFreeKids ---- 12,708 members -- 335,599 posts

The ASE review will ignite a new level of creative world collaboration to
finally remove gratuitous toxins.

This is the purpose of this critical review.

Now, corporations are inevitably competing to maximize the health, energy,
clarity, intelligence, sanity, and creative productivity not only of their
staff, but their customers, and all people.

A huge opportunity: find a safe, inexpensive process to remove all methanol
from alcohol beverages, solving the billion-dollar disease of alcohol
hangovers.

In this regard, it is tragic to delay study of the role of folic acid as a
safe, inexpensive preventive of toxicity from methanol and formaldehyde.

A corporate tipping point: whether to continue the mistake of continuing to
bet the ranch on a single highly profitable, but sadly toxic product, in a
radically uncontrolled information environment that can this year produce an
Enron-level meltdown, with tedious, hundred billion dollar civil and
criminal liabilities, a la tobacco, or immediately shut down the operation,
release all secret files and research, and set up hundred billion dollar
funds to recompense individuals and governments, while funding independent
groups to definitively study the health issues -- which can rapidly lead to
good business opportunities.

Corporations probably best cooperate to expedite this forward moving
retreat.

ASE members and Burdock Group: The ASE review should be made available for
free on the Net, along with the full text of the references and many more
related studies and a open, public archive, unedited public action group for
civil discussion and collaboration.

All financial and secrecy contracts should be made public, along with the
details of the history of meetings and communications, especially how
dissent and conflict were managed.

The ASE review should best evolve into a on-going public collaboration like
Wikipedia or Citizendium. ]


ASE 3.2.  "Thus there is no established UL for either aspartic acid or
phenylalanine (Institute of Medicine, 2005)."


ASE 3.3,  "Taucher et al. (1995) estimated that humans produce approximately
1000 mg of methanol daily from [pectins in] fruits and vegetables."

[ ASE reference 375:
Taucher J, Lagg A, Hansel A, Vogel W, Lindinger W.
Methanol in human breath.
Alcohol Clin Exp Res. 1995 Oct; 19(5): 1147-50.
Institut fur Ionenphysik, Universitat Innsbruck, Austria.

Using proton transfer reaction-mass spectrometry for trace gas analysis of
the human breath, the concentrations of methanol and ethanol have been
measured for various test persons consuming alcoholic beverages and various
amounts of fruits, respectively.

The methanol concentrations increased from a natural (physiological) level
of approximately 0.4 ppm up to approximately 2 ppm a few hours after eating
about 1/2 kg of fruits, and about the same concentration was reached after
drinking of 100 ml brandy containing 24% volume of ethanol and 0.19% volume
of methanol. [ 24 ml = 61 g ethanol, and 0.19 ml = 0.34 g = 340 mg
methanol ]
PMID: 8561283

The high folic acid levels in many fruits and vegetables may protect most
people from resulting conversion of methanol into formaldehyde and formic
acid. ]


ASE 3.3.1.  "Exposure to Formaldehyde From Methanol in Aspartame

As is described later, methanol is metabolized to formaldehyde, which is
rapidly further metabolized."

"For example, the demethylation of the caffeine found in one cup of coffee
produces 30 mg of formaldehyde (Imbus, 1988)."

[ These important, surprising results demand thorough, immediate, definitive
research into the disposition of these apparently highly toxic sources of
methanol (formaldehyde) in various vulnerable groups of people -- rather
than be used as an insipid ploy to insinuate that any methanol from
aspartame is non-issue. ]


[ http://groups.yahoo.com/group/aspartameNM/message/835
ATSDR: EPA limit 1 ppm formaldehyde in drinking water July 1999:
Murray 2002.05.30

"The EPA recommends that an adult should not drink water containing more
than 1 milligram of formaldehyde per liter of water (1 mg/L) for a lifetime
exposure, and a child should not drink water
containing more than 10 mg/L for 1 day or 5 mg/L for 10 days."

http://groups.yahoo.com/group/aspartameNM/message/1140
EPA Preliminary Remedial Goals, PRGs, 2003 Oct, air and tap water --
methanol, formaldehyde, formic acid -- not mentioned is methanol from
aspartame, dark wines and liquors: Murray 2004.11.20

http://groups.yahoo.com/group/aspartameNM/message/1108
faults in 1999 July EPA 468-page formaldehyde profile: Elzbieta Skrzydlewska
PhD, Assc. Prof., Medical U. of Bialystok, Poland, abstracts -- ethanol,
methanol, formaldehyde, formic acid, acetaldehyde, lipid peroxidation, green
tea, aging: Murray 2004.08.08 2005.07.11 ]

"The 1999 July EPA 468-page formaldehyde profile admits that four states
substantially exceed the federal EPA limit:

Environmental Protection Agency 2.00 mg in 2 L daily drinking water
California and Maine ----------------- 0.06 mg
Maryland ---------------------------- 0.02 mg
New Jersey -------------------------- 0.20 mg"

Maryland's limit is ten times more stringent than the EPA's." ]



[ This study by Jones AW (1987) found next-morning hangover from red wine
with 100 to 150 mg methanol (9.5 % w/v ethanol, 100 mg/l methanol, 0.01 %).
Fully 11% of aspartame is methanol --
1,120 mg aspartame in 2 L diet soda, almost six 12-oz cans, gives 123 mg
methanol (wood alcohol).

Jones AW. wayne.jones@...
Elimination half-life of methanol during hangover.
Pharmacol Toxicol. 1987 Mar; 60(3): 217-20.
Department of Forensic Toxicology,
University Hospital, SE-581 85 Linkoping, Sweden.

This paper reports the elimination half-life of methanol in human
volunteers.

Experiments were made during the morning after the subjects had consumed
1000-1500 ml red wine
(9.5 % w/v ethanol, 100 mg/l methanol) the previous evening. [ 100 to 150 mg
methanol ]

The washout of methanol from the body coincided with the onset of hangover.

The concentrations of ethanol and methanol in blood were determined
indirectly by analysis of end-expired alveolar air.

In the morning when blood-ethanol dropped below the Km of liver alcohol
dehydrogenase (ADH)
of about 100 mg/l (2.2 mM), the disappearance half-life of ethanol was 21,
22, 18 and 15 min.
in 4 test subjects respectively.

The corresponding elimination half-lives of methanol were 213, 110, 133 and
142 min. in these same individuals.

The experimental design outlined in this paper can be used to obtain useful
data on elimination kinetics of methanol in human volunteers without undue
ethical limitations.

Circumstantial evidence is presented to link methanol or its toxic metabolic
products, formaldehyde and formic acid, with the pathogenesis of hangover.
PMID: 3588516


http://groups.yahoo.com/group/aspartameNM/message/1052
DMDC: Dimethyl dicarbonate 200mg/L in drinks adds methanol 98 mg/L ( becomes
formaldehyde in body ): EU Scientific Committee on Foods 2001.07.12: Murray
2004.01.22

[ DMDC would be a very useful alternative source of methanol for human
studies, as controls to compare with aspartame and wines. ] ]


http://groups.yahoo.com/group/aspartameNM/message/1286
methanol products (formaldehyde and formic acid) are main cause of alcohol
hangover symptoms [same as from similar amounts of methanol, the 11% part of
aspartame]: YS Woo et al, 2005 Dec: Murray 2006.01.20

Woo YS, Yoon SJ, Lee HK, Lee CU, Chae JH, Lee CT, Kim DJ.
Concentration changes of methanol in blood samples during an experimentally
induced alcohol hangover state.
Addict Biol. 2005 Dec;10(4): 351-5.
Chuncheon National Hospital, Department of Psychiatry,
The Catholic University of Korea, Seoul, Korea.
http://www.cuk.ac.kr/eng/ sysop@...
[ Han-Kyu Lee ]

A hangover is characterized by the unpleasant physical and mental symptoms
that occur between 8 and 16 hours after drinking alcohol.

After inducing experimental hangover in normal individuals, we measured the
methanol concentration prior to and after alcohol consumption and we
assessed the association between the hangover condition
and the blood methanol level.

A total of 18 normal adult males participated in this study.

They did not have any previous histories of psychiatric or medical
disorders.

The blood ethanol concentration prior to the alcohol intake (2.26+/-2.08)
was not significantly different from that 13 hours after the alcohol
consumption (3.12+/-2.38).

However, the difference of methanol concentration between the day of
experiment (prior to the alcohol intake) and the next day (13 hours after
the alcohol intake) was significant (2.62+/-1.33/l vs. 3.88+/-2.10/l,
respectively).

A significant positive correlation was observed between the changes of blood
methanol concentration and hangover subjective scale score increment when
covarying for the changes of blood ethanol level (r=0.498, p<0.05).

This result suggests the possible correlation of methanol as well as its
toxic metabolite to hangover. PMID: 16318957

[ The toxic metabolite of methanol is formaldehyde, which in turn partially
becomes formic acid -- both potent cumulative toxins that are the actual
cause of the toxicity of methanol.] ]



ASE 4.1.  "Formic acid is ultimately converted to CO2 and water, via the
formation of 10-formyl tetrahydrofolate (Barceloux et al., 2002)."

ASE 6.9.2.1.  "Formic acid accumulates in the blood because its half-life
(t1/2 = 3.4-6 h) is very much longer than is that of formaldehyde (t1/2 =
1.5 min) (Hantson et al., 2005).

Formic acid accumulation is considered the mechanism of toxicity of high
doses of methanol, which induces metabolic acidosis, ophthalmic toxicity and
central nervous system depression (Barceloux et al., 2002)."

[ In a few pages, I give many details about formaldehyde and formic acid
dispositions in blood and tissues of 4 small monkeys from a single damage
level methanol dose:

Kenneth E. McMartin, Gladys Martin-Amat, Patricia E. Noker and Thomas R.
Tephly
Lack of a role for formaldehyde in methanol poisoning in the monkey.
Biochemical Pharmcacology 1979: 28; 645-649.
The Toxicology Center, Dept. of Pharmacology,
University of Iowa, Iowa City, Iowa 52242
K.E. McMartin and T.R. Tephly, authors of many pro-aspartame studies, in
Biochemical Pharmacology (1979) remarked, "It is now generally accepted that
the toxicity of methanol is due to the formation of toxic metabolites,
either formaldehyde or formic acid."

"Methanol was administered [ by nasogastric tube ] either to untreated
cynomolgus monkeys [ 2-3.5 kg ] or to a folate-deficient cynomolgus monkey
which exhibits exceptional sensitivity to the toxic effects of methanol.

Marked formic acid accumulation in the blood and in body fluids and tissues
was observed." ]

Ernstgård L, Shibata E, Johanson G.
Uptake and disposition of inhaled methanol vapor in humans.
Toxicol Sci. 2005 Nov; 88(1): 30-8. Epub 2005 Aug 10.
Work Environment Toxicology, Institute of Environmental Medicine, Karolinska
Institutet, Stockholm, Sweden. Lena.Ernstgard@...
http://toxsci.oxfordjournals.org/cgi/content/full/88/1/30  free full text

Methanol is a widely used solvent and a potential fuel for motor vehicles.

Human kinetic data of methanol are sparse.

As a basis for biological exposure monitoring and risk assessment, we
studied the inhalation toxicokinetics of methanol vapor in four female and
four male human volunteers during light physical exercise (50 W) in an
exposure chamber.

The relative uptake of methanol was about 50% (range 47-53%).

Methanol in blood increased from a background level of about 20 to 116 and
244 microM/l after 2 h exposure at 0, 100 ppm (131 mg/m3), and 200 ppm (262
mg/m3), respectively.

Saliva showed substantially higher levels than blood immediately after
exposure.

This difference disappeared in a few minutes; thereafter the concentrations
and time courses in blood, urine, and saliva were similar, with half times
of 1.4, 1.7, and 1.3 h, respectively.

The postexposure decrease of methanol in exhaled air was faster, with a half
time of 0.8 h.

The methanol concentrations were approximately twice as high in all four
types of biological samples at 200 compared to 100 ppm.

No increase in urinary formic acid was seen in exposed subjects.

Our study indicates non-saturated, dose-proportional kinetics of methanol up
to 200 ppm for 2 h.

No gender differences were detected.

Similar, parallel patterns were seen with regard to the methanol time
courses in blood, urine, and saliva, whereas the concentration in exhaled
air decreased markedly faster.

Thus, apart from blood and urine, saliva also seems suitable for
biomonitoring of methanol exposure. PMID: 16093526


"Symptom ratings.
The subjects rated the level of perceived discomfort immediately before,
during (10, 50, 80, and 104 min), and after (126 and 210 min) each exposure
session.

Ten questions were answered, related to irritative symptoms (eyes, nose, and
throat or airways), the central nervous system (headache, fatigue, nausea,
dizziness, feeling of intoxication), difficulty in breathing, and smell of
solvent.

The ratings were performed using a 100-mm visual analogue scale (Kjellberg
et al., 1988)
graded from "not at all" (corresponding to 0 mm) through "hardly,"
"slightly," "fairly," "much," to "almost unbearable" (100 mm).

The same questionnaire has been used in several chamber inhalation studies
performed with organic solvent vapors in our laboratory (see for example,
Ernstgård et al., 1999, 2002; Järnberg et al., 1996; Nihlén et al., 1998b)."

"Background levels of methanol were detected in all samples during control
exposure: blood range 9-76 µM/l, saliva 4-76 µM/l, urine 13-86 µM/l, and
exhaled air 0.0005-0.01 µM/l.

For each individual and time point, the exposure-related methanol
concentrations were calculated as the difference between the concentrations
measured at methanol exposure and that measured at clean air exposure.

No difference between genders was seen with respect to background methanol
in blood.

Background methanol levels in urine were higher in men than in women (35.9
vs. 21.5 mcM/l, p = 0.03 in t-test).

Similar difference was seen for saliva (39.3 vs. 19.0 mcM/l, p = 0.008).

Methanol was rapidly absorbed by inhalation.

The relative uptake remained stable throughout the exposure and was
approximately 50% at both exposure levels (range 47-53%) (Table 1).

The blood methanol concentrations reached 116 (94-144) mcM/l after 2 h
exposure at 100 ppm and 244 (228-260) µM/lat 200 ppm methanol.

These levels are consistent with linear, nonsaturated metabolism of
methanol.

Linear (i.e., dose-proportional) kinetics is also indicated when comparing
the AUC (0-6 h) of blood methanol at the different exposure levels (Fig.
1A).

Blood methanol increased in a monoexponential fashion during exposure (Fig.
2A).

The postexposure decline was also monoexponential, considering the
background methanol.

According to the toxicokinetic model, the elimination half time in blood was
about 1.4 h, and the apparent total clearance 0.2-0.3 l/min.

The steady-state level of methanol at continuous exposure to methanol was
calculated to be 186 and 394 mcM at 100 and 200 ppm, respectively (Table 1),
again an indication of linear kinetics."


ASE reference 133: Hantson PE.
[Acute methanol intoxication: physiopathology, prognosis and treatment]
[Article in French]
Bull Mem Acad R Med Belg. 2006;161(6):425-34; discussion 434-6.
Département des Soins Intensifs, Cliniques St-Luc-U.C.L.

Acute methanol poisoning is mainly the consequence of voluntary or
accidental ingestion.

The mortality and morbidity rates remain very high despite intensive care
therapy.

Methanol by itself is poorly toxic.

Methanol is transformed in the liver into formaldehyde and thereafter formic
acid

Metabolic acidosis is the main biological feature of poisoning.

Acidosis is related to formic acid accumulation, and also to a less extent
to lactate production.

In contrast to rodents, primates are relatively deficient in
tetrahydrofolate reductase and therefore formic acid is usually the final
metabolite.

Formic acid is able to inhibit cytochrome oxidase activity in the
mitochondria, leading to histotoxic hypoxia.

The most sensitive organs to the effects of formic acid are the brain and
the visual pathway, while other organs may also be seriously damaged
according to the severity of metabolic acidosis.

Hemodialysis remains indicated for the removal of both methanol and formic
acid.

Fomepizole is a recently approved antidote. It appears safe and effective.

Analysis of its cost-effectiveness ratio is still ongoing in methanol
poisoning. PMID: 17288275


Bebarta VS, Heard K, Dart RC.
Inhalational abuse of methanol products: elevated methanol and formate
levels without vision loss.
Am J Emerg Med. 2006 Oct; 24(6): 725-8.
Department of Emergency Medicine, Wilford Hall Medical Center, San Antonio,
TX, USA. vikbebarta@...

Inhalant abuse of methanol-containing products has increased over the last
decade.

We performed a prospective observational study of 7 subjects who presented
to an ED after inhalant abuse of methanol-containing hydrocarbon products.

Four patients had a methanol level greater than 24 mg/dl and 2 had an anion
gap greater than 17 mEq/l. [ 240 mg/l blood ]

The mean formic acid level was 71 microg/ml, and 1 patient had a level
considered high enough to induce retinal toxicity (>200 microg/ml). [ 71
mg/l blood]

No patient had an abnormal ophthalmologic examination.

All patients were treated with intravenous folate, 2 received alcohol
dehydrogenase blockade, and no patient received hemodialysis or intravenous
bicarbonate.

All patients' acidosis resolved within 4 hours.

The methanol and formic acid levels are lower than those reported after
methanol ingestion.

These preliminary data suggest that inhalant abusers of methanol products
may have significantly elevated methanol and formic acid levels, but are at
low risk for methanol induced complications of visual dysfunction and
refractory acidosis. PMID: 16984844


Hovda KE, Urdal P, Jacobsen D.
Increased serum formate in the diagnosis of methanol poisoning.
J Anal Toxicol. 2005 Sep; 29(6): 586-8.
Department of Acute Medicine, Ullevaal University Hospital,
NO-0407 Oslo, Norway. knov@...

Early diagnosis is essential for successful treatment in methanol poisoning.

Methanol detection by gas chromatography is not available in most hospitals.

Methanol increases the osmolal gap in serum and its metabolite formate
increases the anion gap.

The sensitivity of these indirect diagnostic methods is not good at low
concentrations of methanol or formate.

We therefore studied the usefulness of formate measurement in diagnosing
methanol poisoning.

In 15 patients poisoned with methanol, serum formate was measured
enzymatically on a Cobas Mira analyzer using formate dehydrogenase and
nicotinamid adenine dinucleotid.

Day-to-day coefficient of variation was 5%, and the upper reference limit
was 2 mg/dl (0.4 mmol/l). [ 20 mg/l blood serum = 0.4 mmol/l ]

Methanol was detected in all 15 patients of whom 14 had elevated serum
formate concentrations.

Anion gap was increased in 11 of 11, and osmolal gap in 11 patients of 15
examined.

Metabolic acidosis was present in 12 of 15 patients, but pH was below 7.30
in only 9 of them.

Four patients with no symptoms had formate concentrations in the range 2-38
mg/dl (0.5-8.3 mmol/l), indicating that increased serum formate was a
sensitive indicator of methanol poisoning.
[ 20-380 mg/l blood serum = 0.5-8.3 mmol/l]

Our results proved formate analyzes to be a simple, sensitive, and specific
way of diagnosing methanol poisoning.

Confounders are patients admitted early, or concomitant ethanol ingestion,
and therefore no acidosis.

This problem may, however, be omitted by repeated formate analysis in
patients developing metabolic acidosis. PMID: 16168185


[ It is remarkable how little is known about the disposition of formaldehyde
and formic acid in human tissues, according to a sober review by Bouchard M,
2001:

"Exposure to methanol also results from the consumption of certain
foodstuffs (fruits, fruit juices, certain vegetables, aspartame sweetener,
roasted coffee, honey) and alcoholic beverages (Health Effects Institute,
1987; Jacobsen et al., 1988)."

"A biologically based dynamic model was developed to simulate the uptake and
disposition of methanol and its metabolites (formaldehyde, formate, CO2) in
animals and humans."

"Systemic methanol is extensively metabolized by liver alcohol dehydrogenase
and catalase-peroxidase enzymes to formaldehyde, which is in turn rapidly
oxidized to formic acid by formaldehyde dehydrogenase enzymes (Goodman and
Tephly, 1968; Heck et al., 1983; Røe, 1982; Tephly and McMartin, 1984)."

"Formaldehyde, as it is highly reactive, forms relatively stable adducts
with cellular constituents (Heck et al., 1983; Røe, 1982)."

"Thus, in monkeys and plausibly humans, a much larger fraction of body
formaldehyde is rapidly converted to unobserved forms rather than passed on
to formate and eventually CO2."

"Inversely, in monkeys and in humans, a larger fraction of body burden of
formaldehyde is rapidly transferred to a long-term component.

The latter represents the formaldehyde that (directly or after oxidation to
formate) binds to various endogenous molecules..."

"However, fits to the available data in rats and monkeys of Horton et al.
1992) and Dorman et al. (1994) show that, once formed, a substantial
fraction of formaldehyde is converted to unobserved forms.

This pathway contributes to a long-term unobserved compartment.

The latter, most plausibly, represents either the formaldehyde that
(directly or after oxidation to formate) binds to various endogenous
molecules (Heck et al., 1983; Røe, 1982)...

That substantial amounts of methanol metabolites or by-products are retained
for a long time is verified by Horton et al. (1992) who estimated that 18 h
following an iv injection of 100 mg/kg of
14C-methanol in male Fischer-344 rats, only 57% of the dose was eliminated
from the body.

From the data of Dorman et al. (1994) and Medinsky et al. (1997), it can
further be calculated that 48 h following the start of a 2-h inhalation
exposure to 900 ppm of 14C-methanol vapors in female cynomolgus monkeys,
only 23% of the absorbed 14C-methanol was eliminated from the body.

These findings are corroborated by the data of Heck et al. (1983) showing
that 40% of a 14C-formaldehyde inhalation dose remained in the body 70 h
postexposure."

Michèle Bouchard *, #,1, michele.bouchard@...;
Robert C. Brunet, # brunet@...
Pierre-Olivier Droz, #
Gaétan Carrier* gaetan.carrier@...
A Biologically Based Dynamic Model for Predicting the Disposition of
Methanol and Its Metabolites in Animals and Humans
Toxicological Sciences 64, 169-184 (2001)
http://www.toxsci.oupjournals.org/cgi/content/full/64/2/169  free full text

http://groups.yahoo.com/group/aspartameNM/message/1143
methanol (formaldehyde, formic acid) disposition, Bouchard M et al, full
plain text, 2001 -- substantial sources are degradation of fruit pectins,
liquors, aspartame, smoke: Murray 2005.01.05 ]


http://groups.yahoo.com/group/aspartameNM/message/1067
eyelid contact dermatitis by formaldehyde from aspartame,
AM Hill & DV Belsito, Nov 2003: Murray 2004.03.30 [150 KB]

[ In this 2003 critique, I added a long critique of industry research,
including this study, not in the ASE review:

Biochemical Pharmcacology 1979: 28; 645-649. [ No abstract in PubMed ]
Kenneth E. McMartin, Gladys Martin-Amat, Patricia E. Noker and Thomas R.
Tephly
Lack of a role for formaldehyde in methanol poisoning in the monkey.
The Toxicology Center, Dept. of Pharmacology,
University of Iowa, Iowa City, Iowa 52242 PMID: 109089

K.E. McMartin and T.R. Tephly, authors of many pro-aspartame studies, in
Biochemical Pharmacology (1979) remarked, "It is now generally accepted that
the toxicity of methanol is due to the formation of toxic metabolites,
either formaldehyde or formic acid."

They put damage doses of methanol into the stomachs of three monkeys, and,
using insensitive tests, found no formaldehyde in many tissues -- except for
a single datum in the midbrain, 1.5 times the detection limit.

They did report widespread accumulation of formic acid in five tissues.

The use of inadequate tests is common in industry research that is funded to
claim the safety of profitable toxins.

Since then, industry scientists have been very wary of doing studies on
primates, which all too easily show the dangers to humans.

"Abstract [ not given in PubMed ]: [ My briefer comments are in square
brackets. ]

Methanol was administered [ by nasogastric tube ] either to untreated
cynomolgus monkeys [ 2-3.5 kg ] or to a folate-deficient cynomolgus monkey
which exhibits exceptional sensitivity to the toxic effects of methanol.

Marked formic acid accumulation in the blood and in body fluids and tissues
was observed.

No formaldehyde accumulation was observed in the blood and no formaldehyde
was detected in the urine, cerebrospinal fluid, vitreous humor, liver,
kidney, optic nerve, and brain in these monkeys at a time when marked
metabolic acidosis and other characteristics of methanol poisoning were
observed.

Following intravenous infusion into the monkey, formaldehyde was rapidly
eliminated from the blood with a half-life of about 1.5 min and formic acid
levels promptly increased in the blood.

Since formic acid accumulation accounted for the metabolic acidosis and
since ocular toxicity essentially identical to that produced in methanol
poisoning has been described after formate treatment, the predominant role
of formic acid as the major metabolic agent for methanol toxicity is
certified.

Also, results suggest that formaldehyde is not a major factor in the toxic
syndrome produced by methanol in the monkey."

"It is now generally accepted that the toxicity of methanol is due to the
formation of toxic metabolites (1,2), either formaldehyde or formic acid."

So, this is an acute toxicity study, with little relevance for chronic
long-term, low-level exposure.

Monkeys, like people, are susceptible to methanol toxicity.

This team cites their six previous methanol in monkey studies, from 1975 to
1977.

The report is difficult to understand, since the three monkeys were treated
differently, and different assays were used.

For the methanol sensitive, folate-deficient monkey A, the assay used was
the chromatropic acid method, with a detection limit of .025 mmol/l.

None of the five tissues showed any formaldehyde with this assay, except the
midbrain, 0.14 mmol/kg wet weight tissue [ units converted from their 0.14
micromole/gm ] -- just 1.5 times the detection limit of .09 mmol/kg wet
tissue weight (given on p. 648).
[ Since 1 kg of water is 1 liter, 1 mmol/kg is equivalent to 1 mmol/l. ]

Meanwhile, in the methanol sensitive, folate-deficient monkey A, the blood
formate level rose by 18 hours from 0.18 to 10.02 mEq/l. [ I assume that a
mEq is equivalent to a mmol -- let me know if I'm wrong. ]

The formate detection limits for the assays were not given in this report.

The formate level in the vitreous humor of the eye of monkey A was 7.90
mEq/l.

It is well known that formate is extremely damaging to the eye.

For unexplained reasons, formate levels in the five tissues and
cerebrospinal fluid were not measured in the methanol sensitive,
folate-deficient monkey A., in the cerebrospinal fluid of monkey B, or in
the optic nerve of monkey C.

Formaldehyde was not measured in the optic nerve of Monkey A.

The kidney formate level for monkey B was 6.33 and for C was only 0.44, with
no comment or explanation given.

The experiment seems arbitrary, capricious, and erratic.

For monkey A, after 18 hours, the urine formaldehyde level was below
detection level, while urine formate was 115.80 mEq/l -- so much of the
formaldehyde had been converted into formic acid, another cumulative, potent
toxin.

"In the presence of high formate values and definitive evidence of toxicity
in methanol-poisoned monkeys, no measurable formaldehyde was found in the
body tissues that were tested."

It is reasonable to surmise that more sensitive assays would have found
formaldehyde and formate bound to and reacted with a variety of cellular
substances in all tissues -- just as the 1998 Trocho study confirmed.
(Appendix E)

Monkeys B and C were normal, not extra vulnerable to methanol, and were
given 3,000 mg/kg methanol, and samples taken at 18 hr.

Formaldehyde was detected only in the blood of Monkey B, while formate was
found in 8 and 10, respectively, of the 10 fluid and tissue samples in
Monkeys B and C.

For instance, the lowest value of formate, except for zero-time blood, for
each monkey was in the midbrain, 2.16 mmol/kg for Monkey B (24 times the
detection limit for the chromatropic acid method) and 1.02 mmol/kg (1.3
times the detection for the dimedon method) for Monkey C.

This shows accumulation of formate in liver, kidney, optic nerve, cerebrum,
and midbrain.

"Thus, whereas one can associate formate intimately with ocular toxicity in
the monkey, no association of formaldehyde with ocular toxicity can be made
at this time. It is not possible to completely eliminate formaldehyde as a
toxic intermediate because formaldehyde could be formed slowly within cells
and interfere with normal cellular function without ever obtaining levels
that were detectable in body fluids..."

"Acknowledgements -- This research was supported by NIH grant GM 19420 and
GM 12675." [not funded by the industry]


Appendix F:

The exponential fragmentation of science into a fractile structure of ever
more atomized specialties ensures that every expert is a layman outside his
own specialty.

Capable laymen play an essential role by summarizing and integrating
scattered lines of inquiry that certain vested interests have long-term
campaigns for obscuring, since outright opposition would tend to attract
discussion and scrutiny that would soon vitiate billion dollar products.
Most professionals simply do not have the free time to investigate such
arcane, but possibly crucial, details.  Capable laymen now join together on
the Net to establish credibility by common sense, polite mobilization of
specialized research, backed by support from informed specialists.

For instance, I started investigating aspartame in early January 1999 and
within two months was being given papers by Woodrow C. Monte and Ralph G.
Walton.

The route of aspartame to methanol to formaldehyde to formic acid is a
classic example.  Were this line of inquiry already suspected to be sure to
establish the harmlessness of aspartame, then the industry would have every
motive to spend a few paltry millions to both complete the research in
humans and widely publicize the results.

The fact that on the contrary, there is no industry funded research in
humans at all in the public domain on the specific biochemical and tissue
outcomes of formaldehyde and formic acid from aspartame leads to a
reasonable surmise that the industry has reason to fear, obscure, and derail
this inquiry.

Following the crooked but unmistakable trail of missing research, i.e.,
avoided, ignored, misstated, discounted, obscured, explained away, or simply
never mentioned, is an excellent strategy for uncovering the lurking secret.

In spring 1999, an eminent pro-aspartame scientist Christian Tschanz had
NutraSweet Co. give me their $ 130 review text of their research, "The
Clinical Evaluation of a Food Additive: Assessment of Aspartame" (1996), by
Christian Tschanz, Harriett H. Butchko, W. Wayne Stargel, and Frank N.
Kotsonis, all aspartame stalwarts.

Chapter 5: "Metabolism and Pharmacokinetics of Radiolabeled Aspartame in
Normal Subjects", by Aziz Karim and Thomas Burns, has 10 pages and 10
citations. Page 63, Figure 4, Metabolic products derived from aspartame,
beta-aspartame, and DKP, does not list formaldehyde or formic acid.

The tangle of black arrows includes two paths from Aspartame to Methanol to
"CO2 + Body Constituents". Now, that's pretty good public relations spin,
eh?  "Body Constituents", indeed? This is systematic and persistent deceit,
as pernicious as it is profitable.

Aziz Karim, PhD is a "Distinguished Research Fellow and Sr. Director,
Clinical Research, G.D. Searle and Company, Skokie, Illinois", where Thomas
Burns, M.S. is a "Clinical Research Manager".

They state that "in monkeys" with methanol or aspartame labeled in the
methyl ester, both with 14C, "...excretion of 14CO2 in the expired air
occurred to the same extent (about 70% of the 14C dose) with both compounds,
indicating complete hydrolysis of the methyl ester moiety of aspartame
(Figure 6)."

They said nothing about resulting levels in blood plasma, urine, feces, or
any body tissues.

This is the typical commission by omission strategy of industry research on
aspartame.

ASE reference 254:
Oppermann JA, Muldoon E, Ranney RE.
Metabolism of aspartame in monkeys. [ No abstract in PubMed ]
J. Nutrition 1973 Oct; 103(10): 1454-1459.
Dept. of Biochemistry, Searle Laboratories,
Division of G.D. Searle and Co. Box 5110, Chicago, IL 60680
http://jn.nutrition.org/cgi/reprint/103/10/1454 free full text

They found that 68.67% of the radioactive methanol in aspartame put into the
stomachs of 3 to 7 kg monkeys was eliminated within 8 hours, with little
additional elimination afterwards, as carbon dioxide in exhaled air and in
the urine.

They did not mention that this meant that about 31.33% of the methanol must
transform into formaldehyde and then into formic acid, both of which must
remain as toxic products in all parts of the body.

They did not report any studies on the distribution of radioactivity in body
tissues, nor give the absolute levels for declining blood plasma proteins.

This study did not monitor long-term use of aspartame, which might reveal
cumulative effects.

Their low oral dose of aspartame and for methanol was 0.068 mmol/kg, about 1
part per million [ppm] of the acute toxicity level of 2,000 mg/kg, 67,000
mmol/kg, used by McMartin (1979).

Two liters daily use of diet soda provides 123 mg methanol, 2 mg/kg for a 60
kg person, a dose of 63 mmole/kg, a thousand times more than the dose in
this study.

By eight hours excretion of the dose in air and urine had leveled off at
67.1 +-2.1% as CO2 in the exhaled air and 1.57+-0.32% in the urine, so 68.7%
was excreted, and 31.3% was retained. [This data is the average of 4
monkeys.]  ...the 14C in the feces was negligible."  "That fraction not so
excreted (about 31%) was converted to body constituents through the
one-carbon metabolic pool."

"All radioactivity measurements were counted to +-1% accuracy..."  This
indicates that the results could not be claimed to have a precision of a
tenth of a percent. OK, so this is a nit-pick -- but I believe espousing
spurious accuracy is a sign of scientific insecurity.

The abstract ends, "It was concluded that aspartame was digested to its
three constituents that were then absorbed as natural constituents of the
diet."  Thus, the concept is very subtly insinuated that methanol, as a
constituent of aspartame, is absorbed as a natural constituent of the diet.
"Dietary methanol is derived in large part from fresh fruits and
vetetables."  Nowhere in this report, or in the book chapter are mentioned
the dreaded words, "formaldehyde" and "formic acid".


Searle Laboratories team in 1976 reported that in 4 monkeys fed aspartame,
by 12 hours: "...the major fraction (70 %) of the [aspartate] label appeared
in the expired air (Fig.6)... Urinary and fecal 14C\
[ aspartate derived ] amounted to 4 - 6 % of the administered [ aspartate ]
label."

This gives a total of a maximum 76 % excreted aspartate from the aspartame,
indicating that 24 % of this excitotoxin was retained in the body.  It is
reasonable to conclude that daily use of aspartame must lead to substantial
accumulation of this excitotoxin, aspartate, in body tissues.

Their 1979 review said: "Aspartame... is hydrolyzed in the gut to yield
aspartic acid, phenylalanine, and methanol.... Aspartate may also be
incorporated into body constituents such as other amino acids, proteins,
pyrimidines, asparagine, and N-acetylaspartic acid."

ASE reference 276:
Ranney RE, Oppermann JA.
A review of the metabolism of the aspartyl moiety of aspartame in
experimental animals and man.
J Environ Pathol Toxicol. 1979 Mar-Apr; 2(4): 979-85.
Department of Drug Metabolism and Radiochemistry,
Searle Laboratories, Skokie, Illinois.
Division of G.D. Searle and Co. Box 5110, Chicago, IL 60680

Aspartame (3-amino-N-(alpha-carboxyphenethyl) succinamic acid, methyl ester;
the methyl ester of aspartylphenylalanine, SC-18862) is hydrolyzed in the
gut to yield aspartic acid, phenylalanine, and methanol.

This review of the literature describes the metabolic paths followed by
aspartate in its conversion to CO2 or its incorporation into body
constituents.

About 70 percent of 14C from [asp-14C]-aspartame is converted in the monkey
to 14CO2.

Some of the aspartate is converted at the intestinal mucosal level to
alanine by decarboxylation.

This amino acid may be oxidized to CO2 by entering the tricarboxylic acid
cycle via pyruvate and acetyl CoA.

In addition, transamination of aspartate to oxaloacetate permits this
product also to enter the tricarboxylic acid cycle.

Aspartate may also be incorporated into body constitutents such as other
amino acids, proteins, pyrimidines, asparagine, and N-acetylaspartic acid.

It is concluded that the aspartate moiety of aspartame is metabolized in a
manner similar to that of dietary aspartic acid.  Publication Types: Review
PMID: 376770


J. A. Oppermann et al, plus F.G. McMahon of Tulane University Medical
School, published a follow-up study, "Comparative metabolism of aspartame in
experimental animals and humans", J. Toxicology and Environmental Health 2:
441-451, 1976.

The abstract says, "Hydrolysis of the methyl group by intestinal esterases
yielded methanol, which was oxidized in the one-carbon metabolic pool to
CO2."

"The hypothetical pathways of metabolism, which aspartame was expected to
follow, are diagrammed in Fig. 1.... The principle used to test the validity
of this hypothetical description of the metabolism of aspartame..."

Figure 1. shows in an nice orderly sequence that: (a) MeOH ---> one-carbon
metabolic pool ---> CO2 + formyl metabolites .

Meanwhile, this sentence jumps from p. 441 to 442 under Figure 1., "The
absorbed methanol would be incorporated into the one-carbon pool and would
be converted [ page jump in sentence ] primarily to CO2 (Makar et.al., 1968;
Tephly et al, 1964), although a small fraction might be incorporated into
body constituents."

The graphs present the same methanol in monkey data as in 1973, but the
nowhere is the specific percentage of exhaled CO2 mentioned.

Methanol and aspartame were also given to a few [ unspecified ] number of
rats: "The major fraction of the 14C was excreted in the expired air (Fig.
2)...Plasma levels of 14C reached a peak [ absolute data not given ] at
about 3 hr..."

In this follow-up report, for methanol and the methyl group in aspartame,
excretion in urine and feces were not mentioned in either the former monkey
or the new rat studies, the absolute plasma levels were not given, and, of
course, no measures were taken of 14C in body tissues.

The only hint of the possible role of formaldehyde and formic acid was the
rather diffident term "formyl metabolites" in Figure 1.

Overall, we see consistent patterns of avoiding any focus on the actual
disposition of extremely toxic formaldehyde and formic acid, both persistent
and cumulative, products in body tissues.

Subtle equivocation and qualification was expressed by such words as
"hypothetical", "was expected to follow", "would be", "primarily", "although
a small fraction might be incorporated into body constituents", "major
fraction".

Methanol from aspartame was not studied in the other species: rabbits, dogs,
and humans.

It pays to investigate early studies, because then the coverup was less well
organized, more patchy.

The loosely organized world-wide exponential growth of science ensures that
the line of inquiry of methanol to formaldehyde and formic acid will pop up
here and there, but no one is encouraged to make the connection with
aspartame, widely proclaimed as "the most thoroughly tested food additive in
history" -- until the momentous, unheralded Trocho study established
explosive results in June 1998. (Appendix E)


C. Trocho (1998): "In all, the rats retained, 6 hours after administration,
about 5 % of the label, half of it in the liver."

They used a very low level of aspartame ingestion, 10 mg/kg, for rats, which
have a much greater tolerance for aspartame than humans.

So, the corresponding level for humans would be about 1 or 2 mg/kg.

Many headache studies in humans used doses of about 30 mg/kg daily.

http://groups.yahoo.com/group/aspartameNM/message/925
aspartame puts formaldehyde adducts into tissues, Part 1 of 2 full text,
Trocho & Alemany 1998.06.26: Murray 2002.12.22

Sra. Carme Trocho, Sra. Rosario Pardo, Dra. Immaculada Rafecas, Sr. Jordi
Virgili, Dr. Xavier Remesar, Dr. Jose Antonio Fernandez-Lopez, Dr. Marià
Alemany [male]
Formaldehyde derived from dietary aspartame binds to tissue components in
vivo.
Life Sci June 26 1998; 63(5): 337-49.
Departament de Bioquimica i Biologia Molecular,
Facultat de Biologia, Universitat de Barcelona, Spain.
http://www.bq.ub.es/cindex.html Línies de Recerca: Toxicitat de
l'aspartame http://www.bq.ub.es/grupno/grup-no.html
Fac. Biologia Tel.: (93)4021544, Fac. Biologia Tel.: (93)4021521, FAX:
(93)4021559
Sra. Carme Trocho "Trok-ho" FAX: (93)4021559 alemany@...;
bioq@...;
http://ww.presidiotex.com/barcelona/index.html full text

Abstract:

Adult male rats were given an oral dose of 10 mg/kg aspartame, 14C-labeled
in the methanol carbon.
[ 1.1 mg/kg methanol, with likely 30% retained as durable toxic cumulative
products of formaldehyde and formic acid, 0.3 mg/kg. ]

At timed intervals of up to 6 hours, the radioactivity in plasma and several
organs was investigated.

Most of the radioactivity found (>98 % in plasma, >75 % in liver) was bound
to protein.

Label present in liver, plasma and kidney was in the range of 1-2 % of total
radioactivity administered per g or ml, changing little with time.

Other organs (brown and white adipose tissues, muscle, brain, cornea and
retina) contained levels of label in the range of 1/12th to 1/10th of that
of liver.

In all, the rats retained, 6 hours after administration, about 5% of the
label, half of it in the liver.

The specific radioactivity of tissue protein, RNA and DNA was quite uniform.

The protein label was concentrated in amino acids, different from
methionine, and largely coincident with the result of protein exposure to
labeled formaldehyde.

DNA radioactivity was essentially in a single different adduct base,
different from the normal bases present in DNA.

The nature of the tissue label accumulated was, thus, a direct consequence
of formaldehyde binding to tissue structures.

The administration of labeled aspartame to a group of cirrhotic rats
resulted in comparable label retention by tissue components, which suggests
that liver function (or its defect) has little effect on formaldehyde
formation from aspartame and binding to biological components.

The chronic treatment of a series of rats with 200 mg/kg of non-labeled
aspartame during 10 days results in the accumulation of even more label when
given the radioactive bolus, suggesting that the amount of formaldehyde
adducts coming from aspartame in tissue proteins and nucleic acids may be
cumulative.

It is concluded that aspartame consumption may constitute a hazard because
of its contribution to the formation of formaldehyde adducts. PMID: 9714421

[ Extracts ]
"The high label presence in plasma and liver is in agreement with the
carriage of the label from the intestine to the liver via the portal vein.

The high label levels in kidney and, to a minor extent, in brown adipose
tissue and brain are a consequence of their high blood flows (45).

Even in white adipose tissue, the levels of radioactivity found 6 hours
after oral administration were 1/25th those of liver.

Cornea and retina, both tissues known to metabolize actively methanol
(21,28) showed low levels of retained label.

In any case, the binding of methanol-derived carbon to tissue proteins was
widespread, affecting all systems, fully reaching even sensitive targets
such as the brain and retina....

The amount of label recovered in tissue components was quite high in all the
groups, but especially in the NA rats.

In them, the liver alone retained, for a long time, more than 2 % of the
methanol carbon given in a single oral dose of aspartame, and the rest of
the body stored an additional 2 % or more.

These are indeed extremely high levels for adducts of formaldehyde, a
substance responsible of chronic deleterious effects (33), that has also
been considered carcinogenic (34,47).

The repeated occurrence of claims that aspartame produces headache and other
neurological and psychological secondary effects -- more often than not
challenged by careful analysis -- (5, 9, 10, 15, 48) may eventually find at
least a partial explanation in the permanence of the formaldehyde label,
since formaldehyde intoxication can induce similar effects (49).

The cumulative effects derived from the incorporation of label in the
chronic administration model suggests that regular intake of aspartame may
result in the progressive accumulation of formaldehyde adducts.

It may be further speculated that the formation of adducts can help to
explain the chronic effects aspartame consumption may induce on sensitive
tissues such as brain (6, 9, 19, 50).

In any case, the possible negative effects that the accumulation of
formaldehyde adducts can induce is, obviously, long-term.

The alteration of protein integrity and function may needs some time to
induce substantial effects.

The damage to nucleic acids, mainly to DNA, may eventually induce cell death
and/or mutations.

The results presented suggest that the conversion of aspartame methanol into
formaldehyde adducts in significant amounts in vivo should to be taken into
account because of the widespread utilization of this sweetener.

Further epidemiological and long-term studies are needed to determine the
extent of the hazard that aspartame consumption poses for humans."


Jack Dwayne Thrasher, Alan Broughton, Roberta Madison.
Immune activation and autoantibodies in humans with long-term inhalation
exposure to formaldehyde.
Archives of Environmental Health. 1990; 45: 217-223.
http://www.drthrasher.org/formaldehyde_1990.html full text

"Immune activation, autoantibodies, and anti-HCHO-HSA antibodies are
associated with long-term formaldehyde inhalation." PMID: 2400243

"Inhalation exposure to formaldehyde (HCHO) is associated with symptoms of
irritation to mucous membranes, (1,2) chronic health problems (e.g., asthma,
(2) nasopharyngeal cancer, (3) and multiple subjective health complaints.
(4,5)

Recent observations have shown that both humoral-and cell-mediated
immunologic mechanisms occur in humans with long-term HCHO exposure.

Antibodies of all isotypes to HCHO conjugated human serum albumin (HCHO-HSA)
are demonstrable in HCHO anaphylaxis, (6) hemodialysis patients, (7) mobile
home residents, (4) persons with occupational exposures, (5,8) office
workers, (9) and in persons in other environments. (4)

In addition, changes in cell-mediated immunity include increases in
eosinophils, basophils, and T-suppressor cells following acute exposure of
patients with HCHO asthma. (10)

Moreover, individuals with multiple subjective health complaints associated
with long-term HCHO inhalation have evidence of immune activation and the
presence of autoantibodies. (4,5)

The patients in our study had symptoms and complaints related to several
organs, as described previously, (4,5,9) which were similar to symptoms of
workers with multiple chemical sensitivity,(11) cacosmia,(12) and other
chemical exposures. (13-15)

We report on the differences in humoral and cell-mediated immunity in humans
with long-term inhalation exposure to HCHO vs. asymptomatic students
(controls) who experienced short-term, periodic exposure to the chemical."

[ http://lassesen.com/cfids/cacosmia.htm
Cacosmia (a.k.a. Multiple Chemical Sensitivity) Details:
* Chemical odour intolerance induced headache, itching eyes, irritated or
congested nose, dry and/or sore throat, cough, dizziness, and itching or
rash.
* Cacosmics reported increased prevalence of physician-diagnosed nasal
allergies, breast cysts, hypothyroidism, sinusitis, food sensitivities,
irritable bowel, and migraine headache. Resource: http://www.mcsrr.org ]

"Symptoms.
All patients in this study had sought continuous medical attention because
of multiple organ symptoms involving the central nervous system (CNS)
(headaches, memory loss, difficulty completing tasks,
dizziness), upper- and lower-respiratory symptoms, skeletal-muscle
complaints, and gastroenteritis.

Three common symptoms were expressed:
[1.] and initial flu-like illness from which they had not fully recovered;
[2.] chronic fatigue; and
[3.] an olfactory sensitivity to ambient conditions containing low
concentrations of chemicals. (4,9,11)"

"It is recognized that chemicals and therapeutic drugs are associated with a
Lupus-like syndrome. (28,29 )  The observations made on the patients in this
study support this concept."

"Five groups of subjects exposed to HCHO, who gave informed consent, were
included in this study.
[1.] Controls consisted of students of chiropractic medicine (16 males, 12
females), mean age = 29 +- 9 y) exposed to HCHO for 13 h/wk for 28 wk while
studying human anatomy.
Immunologic tests were performed 12 mo following the last classroom
exposure.
No measurements of HCHO concentrations were made.
It is assumed that classroom ambient concentrations were at least 0.43 ppm.
(1)

The students stated that during exposure they experienced eye, nose and
throat irritation and that there was a pungent odor of HCHO.

They did not have residual health complaints (symptoms), and they were
asymptomatic at the time blood was taken.

[2.] Mobile home residents consisted of 19 patients (6 males, 13 females),
mean age 41+-20 y) who currently lived in mobile homes.  The patients had
lived in their environments for 2-7 y and reported multiple symptoms. (4,9)
Measured HCHO concentrations ranged from 0.05 to 0.5 ppm at the time blood
samples were taken.

[3.] Office workers included 21 patients (5 males, 16 females, mean age of
40 +-10 y) who worked in new office buildings where there was inadequate
ventilation (closed buildings).  The patients had multiple health
complaints. (9)  It was determined from medical histories that their
symptoms commenced with employment, waned when away from work (i.e.,
weekends, holidays, vacations) and became worse upon return to work.  No HCO
measurements were done; however, closed buildings have ambient
concentrations ranging from 0.01 to 0.77 ppm. (1,16)

[4.] This group included 21 patients (10 males, 11 females, mean age of 35
+ -17 y) who had multiple symptoms and who had been removed from their
original sources of HCHO exposure (mobile homes
and/or particleboard subflooring) for at least 1 y.  The HCHO concentrations
measured during their exposures ranged from 0.14 to 0.81 ppm.

[5.] Ocupationally exposed patients (6 males, 2 females, mean age of 45
+ -11 y) had HCHO exposures from the following: biology and human anatomy
classes, mortuary, pathology, physical therapy, formica furniture
(particleboard), and carbonless copy paper.  Information on six of these
patients was previously published. (5)"

"In conclusion, measurements of changes in WBCs, T cells, and H/S ratios in
individuals with apparent chemical sensitivities appear to be inadequate
immune parameters to examine.

If one assumes that these individuals respond immunogically to environmental
chemicals, investigations into autoimmunity and immune activation and
perturbations in the interleukins, luekotreines, prostglandins, and other
immunologic mediators appear to be fruitful areas for further research.
(29-32)

Thus, it appears that HCHO sensitivity is a real phenomenon and requires
further research. (4,27-32 )" ]


ASE 6.5.  "Therefore, aspartame is considered to have no reproductive or
teratogenic activity, and no effect on lactation.

In these studies, effects have been observed at exceedingly high doses, and
were secondary to reduced body weights."

[  Thrasher JD, Kilburn KH. toxicologist1@...
Embryo toxicity and teratogenicity of formaldehyde. [100 references]
Arch Environ Health 2001 Jul-Aug; 56(4): 300-11.
Sam-1 Trust, Alto, New Mexico, USA.  (702) 987-4590 (505) 937-1150
http://www.drthrasher.org/formaldehyde_embryo_toxicity.html full text

"The major difference is that the Japanese demonstrated the incorporation of
FA and its metabolites into the placenta and fetus.  The quantity of
radioactivity remaining in maternal and fetal tissues
at 48 hours was 26.9 % of the administered dose." [ Ref. 14-16 ]  The DNA
fraction contained 20 % and 50% of total incorporated radioactivity in the
maternal and fetal liver at 6 and 24 hours when compared to the acid
insoluble fraction (Fig. 1).  Of primary interest is that the incorporated
radioactivity persisted longer in the fetal liver and brain when compared to
the mothers."

Abstract:

C-14 [radioactive labelled] formaldehyde crosses the placenta and enters
fetal tissues.
The incorporated radioactivity is higher in fetal organs (i.e., brain and
liver) than in maternal tissues.
The incorporation mechanism has not been studied fully, but formaldehyde
enters the single-carbon cycle and is incorporated as a methyl group into
nucleic acids and proteins.

Also, formaldehyde reacts chemically with organic compounds (e.g.,
deoxyribonucleic acid, nucleosides, nucleotides, proteins, amino acids) by
addition and condensation reactions, thus forming adducts and
deoxyribonucleic acid-protein crosslinks.

The following questions must be addressed:
What adducts (e.g., N-methyl amino acids) are formed in the blood following
formaldehyde inhalation?
What role do N-methyl-amino adducts play in alkylation of nuclear and
mitochondrial deoxyribonucleic acid, as well as mitochondrial peroxidation?

The fact that the free formaldehyde pool in blood is not affected following
exposure to the chemical does not mean that formaldehyde is not involved in
altering cell and deoxyribonucleic acid characteristics beyond the nasal
cavity.

The teratogenic effect of formaldehyde in the English literature has been
sought, beginning on the 6th day of pregnancy (i.e., rodents)
(Saillenfait AM, et al. Food Chem Toxicol 1989, pp 545-48;
Martin WJ. Reprod Toxicol 1990, pp 237-39;
Ulsamer AG, et al. Hazard Assessment of Chemicals; Academic Press,
1984, pp 337-400;
and U.S. Department of Health and Human Services. Toxicological Profile
of Formaldehyde; ATSDR, 1999 [references 1-4, respectively, herein]).

The exposure regimen is critical and may account for the differences in
outcomes. Pregnant rats were exposed
(a) prior to mating,
(b) during mating,
(c) or during the entire gestation period.
These regimens
(a) increased embryo mortality;
(b) increased fetal anomalies (i.e., cryptochordism and aberrant
ossification centers);
(c) decreased concentrations of ascorbic acid; and
(d) caused abnormalities in enzymes of mitochondria, lysosomes, and the
endoplasmic reticulum.

The alterations in enzymatic activity persisted 4 mo following birth.

In addition, formaldehyde caused metabolic acidosis, which was augmented by
iron deficiency.

Furthermore, newborns exposed to formaldehyde in utero had abnormal
performances in open-field tests.

Disparities in teratogenic effects of toxic chemicals are not unusual.
For example, chlorpyrifos has not produced teratogenic effects in rats when
mothers are exposed on days 6-15
(Katakura Y, et al. Br J Ind Med 1993, pp 176-82
[reference 5 herein]) of gestation
(Breslin WJ, et al. Fund Appl Toxicol 1996, pp 119-30;
and Hanley TR, et al. Toxicol Sci 2000, pp 100-08
[references 6 and 7, respectively, herein]).

However, either changing the endpoints for measurement or exposing neonates
during periods of neurogenesis (days 1-14 following birth) and during
subsequent developmental periods produced adverse effects. These effects
included neuroapoptosis, decreased deoxyribonucleic acid and ribonucleic
acid synthesis, abnormalities in adenylyl cyclase cascade, and
neurobehavioral effects
(Johnson DE, et al. Brain Res Bull 1998, pp 143-47;
Lassiter TL, et al. Toxicol Sci 1999, pp 92-100;
Chakraborti TK, et al. Pharmacol Biochem Behav 1993, pp 219-24;
Whitney KD, et al. Toxicol Appl Pharm 1995, pp 53-62;
Chanda SM, et al. Pharmacol Biochem Behav 1996, pp 771-76;
Dam K, et al. Devel Brain Res 1998, pp 39-45;
Campbell CG, et al. Brain Res Bull 1997, pp 179-89;
and Xong X, et al. Toxicol Appl Pharm 1997, pp 158-74
[references 8-15, respectively, herein]).

Furthermore, the terata caused by thalidomide is a graphic human example in
which the animal model and timing of exposure were key factors
(Parman T, et al. Natl Med 1999, pp 582-85;
and Brenner CA, et al. Mol Human Repro 1998, pp 887-92
[references 16 and 17, respectively, herein]).

Thus, it appears that more sensitive endpoints (e.g., enzyme activity,
generation of reactive oxygen species, timing of exposure) for the
measurement of toxic effects of environmental agents on embryos,
fetuses, and neonates are more coherent than are gross terata observations.

The perinatal period from the end of organogenesis to the end of the
neonatal period in humans approximates the 28th day of gestation to 4 wk
postpartum. Therefore, researchers must investigate
similar stages of development (e.g., neurogenesis occurs in the 3rd
trimester in humans and neonatal days occur during days 1-14 in rats and
mice, whereas guinea pigs behave more like humans).

Finally, screening for teratogenic events should also include exposure of
females before mating or shortly following mating. Such a regimen is
fruitful inasmuch as environmental agents cause adverse effects.
Publication Types: Review Review, Tutorial PMID: 11572272

Discussion and Analysis of the Papers:

FA was distributed to all organs in the adult, the placenta and fetus (Table
1), which was similar to that reported in male F344 rats, guinea pigs and
monkeys. (25,26).

The major difference is that the Japanese demonstrated the incorporation of
FA and its metabolites into the placenta and fetus.  The quantity of
radioactivity remaining in maternal and fetal tissues at 48 hours was 26.9%
of the administered dose.

The DNA fraction contained 20 % and 50% of total incorporated radioactivity
in the maternal and fetal liver at 6 and 24 hours when compared to the acid
insoluble fraction (Fig. 1).

Of primary interest is that the incorporated radioactivity persisted longer
in the fetal liver and brain when compared to the mothers.

Also, since FA is a precursor of a number of biological compounds, it would
have been of prime interest to determine what fraction resulted from either
metabolic incorporation or from chemical reactivity of FA (e.g. crosslinks,
adduction, methylation) with biological molecules (DNA, proteins,
polypeptide, amino acids, etc.).

FA undergoes addition (adducts and alkylation) and condensation (methene
bridges) reactions with proteins and amino acids (27) as well as nucleic
acids and nucleosides/tides. (28)  It is a mutagen, crosslinking agent and
an immunogen (28-30).

Free FA concentrations in the blood are 2.24+- 0.07 (rats), 1.84+- 0.15
(Rhesus monkeys) and 2.61+- 0.14 (humans) ug/g of blood [ppm], which did not
change following either acute or subchronic inhalation of FA. (31,32)

Thus, it appears that additional information is required on addition and
condensation products of amino acids, polypeptides, nucleoside, etc., of the
blood, generated by FA exposure.

An increase of N-methyl amino acids would produce endogenous FA, which may
have a significant role in mitotic and apoptosis processes.

FA generators are responsible for FA formation in tumors and have an
impairment of liver antioxidant mechanisms and functional integrity of
mitochondria. (33-41)

FA had adverse effects on zygotes/embryos and bone marrow cells (Tables 2
and 3). The embryos showed cytological injury and high rate of mortality,
while bone marrow cells had increased rates of chromosome aberrations and
aneuploidy.

Similar observations on chromosomes of peripheral lymphocytes have been
reported for anatomy and mortuary students. (42-44)  Classroom exposure to
FA at 1.5 to 3.17 mg/m3 was associated with
increased frequency of sister chromatid exchanges, aberrations and
micronuclei.  Concentrations less 1 mg/m3 had no effect on lymphocyte
chromosomes, but caused micronuclei in nasal and oral exfoliative cells and
changes in lymphocyte subsets (increase in CD19 and decreases in CD4, CD5
and H/S ratio. (45,46)

With respect to the effect of FA on embryos additional research is needed.

FA is an alkylating agent. Treatment of C3H transplacentally with
N-ethyl-N-nitrosourea (alkylating agent) has caused primordial germ cell
mutations. (47)

Also, treatment of female mice within hours after mating with ethyl
methanesulfanate, ethyl nitrosourea and ethylene oxide resulted in fetal
deaths and malformations. (48-51)

Thus, further investigation into the zygote/embryonic effects of FA should
follow the protocols established for other alkylating agents with attention
to the role of potential methyl donors, e.g. N-methyl amino acids.

FA exposure throughout gestation caused a decreased DNA and RNA
concentrations, increased weights of bodies and organs (thymus, heart,
kidneys and adrenals) and decreased in the weights of lung and liver (Table
3).

Microscopy and histochemical observations revealed other abnormalities:
involution of lymphoid tissue, numerous extra-medullary hemopoietic centers,
decreased glycogen content (myocardium) and liver, decreased AA content of
whole fetus and fetal and maternal liver.

AA is an antioxidant, produced from glucuronate via the uronic acid pathway,
which also is the intermediary route for synthesis of pentoses.

The decreased AA content may have resulted from either the utilization of AA
as an antioxidant or by interference (inhibition?) of the uronic pathway.

It is difficult to interpret the meaning of the decreased DNA and the
increased RNA contents of the organs.  However, treatment of adult male rats
by FA injection was reported to decrease the DNA content of testis and
prostate and a decrease of protein content of the prostate and epididymus.
(52)

Cytopathology of organs and alterations of mitochondria,  ER and lysosome
enzymatic were observed in fetuses following FA inhalation (Table 4).  Organ
cytopathology included increased ploidy, micronecrotic loci, extramedullary
hematopoeitec enters, and degeneration of kidney glomeruli. Concomitant were
changes in enzymatic activity of as follows:  mitochondria (MDH, SDH, LDH
decreased, while GDH increased);  ER and lysosomes (ATPase increased while
inosine diphosphatase and b-glucorinidase decreased).  The impairment lasted
in the organs to 4 months of age.  In addition, N-acetylneuraminic
concentration increased in maternal and fetal tissues. The changes in the
enzymatic activity and N-acetyleneuraminic acid correlated with increased
fetal mortality.  Finally, the development of postnatal behavior was also
adversely affected (Table 6).

FA has effects on mitochondrial enzymes, glutathione concentrations and bile
production in the liver of many species, including humans. (53)

FA inhibits the uptake of phosphate by mitochondria, (54,55) and causes the
release of GPT, SDH, GSSG and malondialdehyde into the perfusate of isolated
livers. (56)

Intraperitoneal injection results in a 2-fold increase in bile and a
significant decrease in glutathione of the liver, lungs and brains. (57)

An electron microscopic investigation of the perfused isolated livers showed
destruction of the mitochondria (ruptured membranes, loss of the cristae)
and some damage to the endoplasmic reticulum. (56)

The protection of the liver from FA toxicity appears to be dependent upon
glutathione by formation of the adduct S-hydroxymethylglutathione. (58)

Thus, the observed effect of FA on mitochondrial and ER functions during
embryo/fetal development is also demonstrable in the adult liver.

FA caused preimplantation, prenatal and postnatal abnormalities.

The prenatal effects were demonstrable as anomalies and aberrancies in blood
buffering capacity with metabolic (formate?) acidosis.

The major anomalies were an increased frequency of cryptochordism, a
decrease/delay in ossification centers of the hyoid, metacarpus and
metatarsal bones, delay in eruption of incisors and a decrease in body
weight.

Blood pH decreased in the fetus, while the pCO2 (hypercapnia) increased in
the fetus and the mother.
The true bicarbonates and CO2 were unaffected by FA alone, but increased
with iron-deficiency in the fetus and mother.

The presence of iron-induced deficiency augmented these abnormalities, along
with increased embryo mortality.

The postnatal effect of FA was tested by maze performance.  Open field tests
demonstrated an increase in motor activity, increase in standing and
appearance of emotion.  In sexually mature rats there was an increase in
search activity.

FA is metabolized to formate.

Alcohols, particularly methanol and ethanol, are metabolized to formate and
lactate via an aldehyde.

The toxicity of alcohols and formalin in humans and animals includes
metabolic acidosis (59-61).

Alcohol toxicity generates free radicals, cause an increase in
malondialdehyde, and induce lipid peroxidation resulting in DNA single
strand breaks (62-66).

FA and alcohols probably affect embryos and the fetus via mitochondrial
damage.

Ethanol and environmental agents trigger apoptotic neurodegeneration in the
developing brain (67,68).

Oxygen stress, such as that caused by free radical generation, is associated
with apoptotic cell death and fragmentation of mitochondrial genome (69-71).

Moreover, FA via formaldehyde generators, e.g. alkylating agents, initiates
apoptosis (72-74).
Mitochondria are the suicide organelles and control apoptosis (75-78).

Thus, subtle birth defects (autism, low birth weight, fetal alcohol
syndrome, etc.) are probably best understood by investigating in utero
oxidative stress and mitochondrial damage, rather than by standard FA
teratogenic research (79-83). ]



ASE references 293, 294, 295 were published studies by HJ Roberts.

[ Roberts HJ
Aspartame (NutraSweet) addiction.
Townsend Letter 2000 Jan; HJRobertsMD@...
http://www.sunsentpress.com/ sunsentpress@...
Sunshine Sentinel Press P.O.Box 17799 West Palm Beach, FL 33416
800-814-9800 561-588-7628 561-547-8008 fax
http://www.dorway.com/tldaddic.html 5-page review full text

http://groups.yahoo.com/group/aspartameNM/message/669
1038-page medical text "Aspartame Disease: An Ignored Epidemic"
published May 30 2001 $ 60.00 postpaid data from 1200 cases
available at http://www.amazon.com
over 600 references from standard medical research

http://groups.yahoo.com/group/aspartameNM/message/790
Moseley: review Roberts "Aspartame Disease: An Ignored Epidemic": Murray
2002.07.02

http://groups.yahoo.com/group/aspartameNM/message/883
three texts by H.J. Roberts, 1958, 1971, 1979: Murray 2002.11.06

http://groups.yahoo.com/group/aspartameNM/message/880
Roberts 45 clinical research reports in mainstream journals: Murray
2002.10.20 ]


ASE 6.4.2.3.  [ They stretched to argue away this study, and concluded with
a grudging admission:

"There are two studies that, when using only one dose and only one measure
of learning, interpreted their findings to indicate an impairment of
learning by aspartame at doses of 250 and 500 mg/kg/day." ]


ASE 6.4.2.3. " Recently, Christian et al. (2004) used a T-maze to test for
memory loss in male Sprague-Dawley rats receiving aspartame (250 mg/kg
bw/day) in drinking water for 120 days.

Twelve rats per group were tested periodically during the treatment period
for the time required to find a reward (chocolate) in the T-maze.

Rats were tested every 2 weeks.

Although no differences were noted during the measurements occurring
approximately every 2 weeks up to about 72 weeks, rats receiving aspartame
took significantly longer to find the reward after 90 days.

The next measurement shown is at 120 days, when rats again took longer to
find the reward.

Rats were then killed and levels of brain cholinergic receptors and
NaK-ATPase levels were determined.

Muscarinic cholinergic receptor density, measured using radiolabeled
quinuclindinyl benzilate, was significantly higher in several areas of the
brain of rats receiving aspartame compared to rats receiving only water.

NaK-ATPase levels were similar in all areas of the brain, except for the
midbrain where levels were higher in aspartame-treated rats.

The authors (Christian et al., 2004) speculate that the increase in time to
find a reward in the T-maze indicates that chronic aspartame consumption
results in memory loss and this was mediated by the change in cholinergic
receptor density.

However, they also acknowledge that the relationship between memory and
receptor density is not well understood.

The authors suggest that an alternative explanation for the increased time
in the T-maze test is that rats treated with aspartame may have a reduced
desire for the chocolate reward.

As rats do not recognize aspartame as a sweet substance, it is not clear how
this may occur.

One possibility is that as aspartame is also used to modify the flavors of
other substances (when given below the sweetness threshold in humans), it is
possible that while the rats might not taste aspartame as sweet, aspartame
could have modified the taste of the chocolate (e.g., making it more
bitter).

Major limitations of this study are the use of only one tool or task to
measure memory and the use of only one dose of aspartame.

The majority of studies designed to detect an effect of aspartame on
learning or memory have used multiple doses and multiple tests to evaluate
these parameters.

These studies report no effect, at doses as high as 4% aspartame in the
diet, even when exposed from conception to 90 days postnatally.

Higher doses have been reported to affect various indices of learning
behavior.

There are two studies that, when using only one dose and only one measure of
learning, interpreted their findings to indicate an impairment of learning
by aspartame at doses of 250 and 500 mg/kg/day.

In summary, well-designed studies using a range of approaches to evaluate
learning and memory consistently demonstrate no effect of aspartame
consumption at levels up to 4000 mg/kg/day, indicating little likelihood
that aspartame will have an effect on memory or learning in humans."

[  ASE reference 52:

http://groups.yahoo.com/group/aspartameNM/message/1088
chronic aspartame in rats affects memory, brain cholinergic receptors, and
brain chemistry, Christian B, McConnaughey M et al, 2004 May, full plain
text & critique: Murray 2004.06.05

Christian B, McConnaughey K, Bethea E, Brantley S, Coffey A, Hammond L,
Harrell S, Metcalf K, Muehlenbein D, Spruill W, Brinson L, McConnaughey M.
Chronic aspartame affects T-maze performance, brain cholinergic receptors
and Na(+),K(+)-ATPase in rats.
Pharmacol Biochem Behav. 2004 May; 78(1): 121-7.
Department of Pharmacology, Brody School of Medicine,
East Carolina University, Greenville, NC 27858, USA;
North Carolina School of Science and Mathematics, Durham, NC 27811.
http://www.ecu.edu/pharmacology/faculty/mcconnaughey.html
Mona M. McConnaughey, Ph.D. Research Assistant Professor
Department: PHARMACOLOGY & TOXICOLOGY
Office: Brody Medical Science 6E-120A 252-744-2756
MCCONNAUGHEYM@...

This study demonstrated that chronic aspartame consumption in rats can lead
to altered T-maze performance and increased muscarinic cholinergic receptor
densities in certain brain regions.

Control and treated rats were trained in a T-maze to a particular side and
then periodically tested to see how well they retained the learned response.

Rats that had received aspartame (250 mg/kg/day) [ 27.5 mg methanol, and at
30%, 8.25 mg formaldehyde and formic acid retention ] in the drinking water
for 3 or 4 months showed a significant increase in time to reach the reward
in the T-maze, suggesting a possible effect on memory due to the artificial
sweetener.

Using [(3)H]quinuclidinyl benzilate (QNB) (1 nM) to label muscarinic
cholinergic receptors and atropine (10(-6) M) to determine nonspecific
binding in whole-brain preparations, aspartame-treated rats showed a 31 %
increase in receptor numbers when compared to controls.
In aspartame-treated rats, there was a significant increase in muscarinic
receptor densities in the frontal cortex, midcortex, posterior cortex,
hippocampus, hypothalamus and cerebellum of 80 %, 60 %, 61 %, 65 %, 66 % and
60 %, respectively.

The midbrain was the only area where preparations from aspartame-treated
rats showed a significant increase in Na(+),K(+)-ATPase activity.

It can be concluded from these data that long-term consumption of aspartame
can affect T-maze performance in rats and alter receptor densities or
enzymes in brain. PMID: 15159141


This extraordinary result demands replication, because it implies a much
lower No Observed Effect Level (NOEL), which is customarily divided by 1000
to set an Acceptible Daily Limit for humans.

A formaldehyde NOEL of about 8 mg/kg bw/day would set a human formaldehyde
ADL much lower at .008 mg/kg bw/day, which for a 60 kg person would be 0.5
mg daily, if 30 % retention of formaldehyde and formic acid durable
cumulative toxic products is allowed.

Recall that 12 cans daily diet soda gives 2400 mg aspartame, 264 mg
methanol, and at 30% retention of formaldehyde and formic acid cumulative
durable toxic products, 80 mg daily, 160 times the ADL
suggested by the results of Christian et al, 2004.

A single 12-oz can of diet soda gives 200 mg aspartame, 22 mg methanol, and
toxic products 7 mg, 13 times above this possible ADL.

Accordingly, we should give much more respectful attention to the thousands
of case reports of toxic symptoms, especially neurological, by professionals
and citizens. ]


ASE 6.4.2.4.  "Effects on Aggression.

Male Long-Evans rats received single intraperitoneal injections of 0, 200,
400, and 800 mg/kg bw aspartame in vehicle (saline plus Tween 80) and then
were exposed to an intruder rat and observed for aggression (Goerss et al.,
2000).

Eleven rats were tested with all aspartame doses delivered in ascending then
descending order with a minimum of 1 day between tests.

Contrary to an expected enhancement of aggressive behavior based on the
hypothesis that aspartame is neuroexcitatory, when rats received aspartame
doses of 200 mg/kg bw or higher, the time to attack an intruder rat
increased, the number of bites decreased, and fewer rats engaged in
aggressive attacks.

Rats treated with 200 and 400 mg/kg bw aspartame had higher levels of
serotonin (5-hydroxytryptamine) and its metabolite, 5-hydroxyindolacetic
acid, in the brain compared to rats receiving vehicle, but this effect was
not evident in rats treated with 800 mg/kg bw aspartame.

Dopamine and its metabolites, dihydroxyphenylacetic acid and homovanillic
acid, were not affected by aspartame treatments.

The authors (Goerss et al., 2000) were unable to explain how aspartame
administration would result in increased serotonin levels in these groups.

The rationale for intraperitoneal administration of aspartame was not given.

An intraperitoneal exposure is an irrelevant route of administration when
aspartame is extensively metabolized prior to absorption, and the only human
exposure is via oral administration.

In summary, there has been extensive investigation of the possibility of
neurotoxic effects due to consumption of aspartame.

The data from these studies, in general, do not support the hypothesis that
aspartame in the human diet will affect neuronal function, learning or
behavior."

[ This 2000 study demands careful replication, using even lower oral doses,
determination of the actual disposition of toxic metabolites in specific
tissues, and more tests of behavioral changes. Dimethyl dicarbonate would
make an ideal control.

It's possible that the toxic effects of intraperitoneal injection of
aspartame were depressing the rat's overall energy level.

Anxiety, restlessness, and irritability, or depression, fatigue, and dulled
affect are major symptoms for aspartame reactors and alcohol hangover.

Behavioral studies may confirm the very low ADL of 4.8 mg formaldehyde for a
60 kg person, as reasonably suggested by the results from Christian et al,
2004.

It is not surprising that researchers are not readily funded to do simple,
low cost, fast studies that would compel steep limitations on billions of
dollars annual business of world vested interests for products ranging from
diet and alcohol beverages to buildings and mobile homes to methanol vehicle
fuels, and perhaps an entire new field of concerns about the otherwise ideal
fruits and vegetables. ]


ASE 6.3.2.  Lifetime Studies

[ The ASE review has devoted section 6.3.2 to many detailed criticisms of
the two Ramazzini lifetime cancer rat studies.

As a medical layman, never educated in biochemistry, I am not qualified to
address these matters, and I welcome comments pro and con, which I will put
on my aspartameNM group public archive:

aspartameNM@yahoogroups.com

I am qualified, however, to remind scientists that effective collaboration
between opposed viewpoints has to based on an ethic of going out of one's
way to present the best expressions by others of their evidence.

In fact, the Ramazzini Foundation has a large network of eminent supporters,
some of whom have taken an unusual public position in support of their two
cancer studies:

Abdo KM, Camargo CA Jr, Davis D, Egilman D, Epstein SS, Froines J, Hattis D,
Hooper K, Huff J, Infante PF, Jacobson MF, Teitelbaum DT, Tickner JA.
Letter to U.S. FDA commissioner. Questions about the safety of the
artificial sweetener aspartame.
Int J Occup Environ Health. 2007 Oct-Dec; 13(4): 449-50. No abstract
available.  PMID: 18085059

http://groups.yahoo.com/group/aspartameNM/message/1453
Souring on fake sugar (aspartame), Jennifer Couzin, Science 2007.07.06: 4
page letter to FDA from 12 eminent USA toxicologists re two Ramazzini
Foundation cancer studies 2007.06.25: Murray 2007.07.18


In addition, Ramazzini Foundation proved carcinogenity by similar studies in
Dec., 2002 for alcohol, aldehyde, methanol, and formaldehyde, and the
results are very compatible with their first aspartame cancer study, 2005,
and with their second aspartame study, 2007:

http://groups.yahoo.com/group/aspartameNM/message/1186
aspartame induces lymphomas and leukaemias in rats, free full plain text, M
Soffritti, F Belpoggi, DD Esposti, L Lambertini, 2005 April, 2005.07.14:
main results agree with their previous methanol and formaldehyde studies,
Murray 2005.07.19

""Yellowing of the coat was observed in animals exposed to APM, mainly at
the highest concentrations.

This change was previously observed in our laboratory in rats exposed to
formaldehyde administered with drinking water 9."

http://groups.yahoo.com/group/aspartameNM/message/1441
Lifetime exposure to low doses of aspartame beginning during prenatal life
increases cancer effects in rats, Morando Soffritti et al, European
Ramazzini Foundation, USA EPA Environmental Health Perspectives 2007.06.13
free full text 24 pages: Murray 2007.06.16
www.ehponline.org/members/2007/10271/10271.pdf free full text 24 pages

Soffritti M, Belpoggi F, Lambertini L, Lauriola M.
Results of long-term experimental studies on the carcinogenicity of
formaldehyde and acetaldehyde in rats. In: Mehlman MA, Bingham E, Landrigan
PJ, et al.
Carcinogenesis bioassays and protecting public health.
Commemorating the lifework of Cesare Maltoni and colleagues.
Ann NY Acad Sci 2002; 982: 87-105.

Formaldehyde was administered for 104 weeks in drinking water supplied ad
libitum at concentrations of 1500, 1000, 500, 100, 50, 10, or 0 mg/L to
groups of 50 male and 50 female Sprague-Dawley rats beginning at seven weeks
of age.  Control animals (100 males and 100 females) received tap water
only.

Acetaldehyde was administered to 50 male and 50 female Sprague-Dawley rats
beginning at six weeks of age at concentrations of 2,500, 1,500, 500, 250,
50, or 0 mg/L.  Animals were kept under observation until spontaneous death.

Formaldehyde and acetaldehyde were found to produce an increase in total
malignant tumors in the treated groups and showed specific carcinogenic
effects on various organs and tissues. PMID: 12562630

Soffritti M, Belpoggi F, Cevolani D, Guarino M, Padovani M, Maltoni C.
Results of long-term experimental studies on the carcinogenicity of methyl
alcohol and ethyl alcohol in rats. In: Mehlman MA, Bingham E, Landrigan PJ,
et al.
Carcinogenesis bioassays and protecting public health.
Commemorating the lifework of Cesare Maltoni and colleagues.
Ann NY Acad Sci 2002; 982: 46-69.

Cancer Research Center, European Ramazzini Foundation for Oncology and
Environmental Sciences, Bologna, Italy. crcfr@...

Methyl alcohol was administered in drinking water supplied ad libitum at
doses of 20,000, 5,000, 500, or 0 ppm to groups of male and female
Sprague-Dawley rats 8 weeks old at the start of the experiment.
Animals were kept under observation until spontaneous death.
Ethyl alcohol was administered by ingestion in drinking water at a
concentration of 10% or 0% supplied ad libitum to groups of male and female
Sprague-Dawley rats; breeders and offspring were included in the experiment.
Treatment started at 39 weeks of age (breeders), 7 days before mating, or
from embryo life (offspring) and lasted until their spontaneous death.
Under tested experimental conditions, methyl alcohol and ethyl alcohol were
demonstrated to be carcinogenic for various organs and tissues.
They must also be considered multipotential carcinogenic agents.
In addition to causing other tumors, ethyl alcohol induced malignant tumors
of the oral cavity, tongue, and lips.
These sites have been shown to be target organs in man by epidemiologic
studies. Publication Types: Review Review, Tutorial PMID: 12562628


Here I have combined fairly equivalent data from their two aspartame, one
methanol, and one formaldehyde studies.

Aspartame groups were 100-150 rats each, methanol 100 rats each, and
formaldehyde 50 rats each (formaldehyde control groups 100 rats each).

Aspartame and methanol are directly comparable, since the 11% methanol
component of aspartame upon ingestion is immediately and fully released into
the GI tract, and then much of that quickly turned into formaldehyde and
then formic acid, both of which account for the toxicity of methanol.

Comparison of two aspartame, one methanol, one formaldehyde studies:

Males
Females
Males + Females

Animals with lymphomas and leukaemias [hemolymphoreticular neoplasias] % of
each group of animals

Group
100 rats each
70 rats each 2nd cancer study 2007

aspartame dose ppm a
[400 ppm in 20 gm feed = 20 mg/kg rat body weight for 0.4 kg rats)

--------equivalent methanol dose (11% of aspartame)
----------------roughly equivalent formaldehyde dose (30% of methanol)

-------------------------20,000-40.0
---------------------------------28.0 #^
-------------------------------- 34.0

I--100,000--29.0
--------------25.0**
--------------27.0

II--50,000----0.0-------5,000-36.0-----1,500-46.0 **
--------------25.0**-----------24.0------------20.0*
--------------22.5--------------30.0------------33.0

------------------------------------------1,000-22.0*
--------------------------------------------------22.0*
--------------------------------------------------22.0

---------------------------------------------500-24.0*
--------------------------------------------------14.0
--------------------------------------------------19.0

III-10,000---15.0
--------------19.0*
--------------17.0

---------------------------500-35.0
--------------------------------24.0
--------------------------------29.5

---------------------------100-26.0**
--------------------------------16.0
--------------------------------21.0

---------------------------------------------50-20.0
-------------------------------------------------14.0
-------------------------------------------------17.0

IV---2,000--22.0
--------------18.7*
--------------20.3

------2,000--17.1 70 rats, 2nd study 2007
--------------31.4
--------------24.3


V------400--16.7
--------------20.0**
--------------18.3

--------400--15.7 70 rats, 2nd study 2007
--------------17.1
--------------16.4


-----------------------------------------------10--8.0
--------------------------------------------------10.0
---------------------------------------------------9.0

----------------------------15-20.0 [-50 rats ]
--------------------------------10.0 [-50 rats ]
--------------------------------15.0 [100 rats ]

VI------80---15.3
--------------14.7
--------------15.0

VII-------0--20.7------------0-28.0--------0----8.0 [ control groups ]
---------------8.7--------------13.0--------------7.0
--------------14.7--------------20.5--------------7.5

-----------0---9.5 2nd cancer study 2007 95 rats each control group
--------------12.6
--------------11.0 190 rats, combined male and female control groups

a ppm Considering the life-span average weight of a rat (male and female) as
400 g and the average consumption of food as 20 g per day

* aspartame, statistically significant p= 0.05;
** aspartame, statistically significant p= 0.01 using poly-k test (k = 3)

# methanol, p<0.05 using X2 test
^ methanol, p<0.05 using Cochrane-Armitage test for dose-response
relationship

   * formaldehyde, p<0.05 using X2 test
** formaldehyde, p<0.01 using X2 test

The control groups vary widely, with the percentage of rats with these most
common cancers, present at natural death, ranging from 7.0 % to 28.0 %.

A layman can only speculate as to the possible causes in a uniform
population of rats in the same huge laboratory facility for decades, such as
various viruses, bacteria, or molds, or variable impurities in the tap
water.

Formaldehyde at 50 ppm shows a doubling of the percentage of rats with these
cancers, for groups of just 50 rats.

It is a safe bet that studies using groups of 100 to 200 rats would
establish significance at this 50 ppm level, which in turn would mandate the
reduction of the present USA EPA level (1999) from 1 ppm for lifetime
exposure to formaldehyde in drinking water to 0.05 ppm, since the human
limit is estimated by dividing the lowest harmful animal level by 1000.

The various standards for methanol and formaldehyde are not in harmony:

We can grasp the main picture by studying the results at a high level of
exposure:

II--50,000----0.0-------5,000-36.0------1,500-46.0 **
--------------25.0**-----------24.0-------------20.0*
--------------22.5--------------30.0-------------33.0

The results amount to 1.3 to 5.75 times their control group levels.
Aspartame, methanol, and formaldehyde results broadly agree.
Unknown factors are causing differences between males and females.


JC Caldwell et al.  2007 refuted major, widely publicized criticisms of the
Ramazzini research by the European Food Safety Authority:
Environ Mol Mutagen. 2008 Mar; 49(2): 155-64.
Evaluation of evidence for infection as a mode of action for induction of
rat lymphoma.
Caldwell JC, Jinot J, DeVoney D, Gift JS.
National Center for Environmental Assessment, U.S. Environmental Protection
Agency, Washington, DC, USA. caldwell.jane@...

The European Food Safety Authority (EFSA) released a 2006 report questioning
the relationship of aspartame exposure with increased incidence of
lymphomas/leukemias in a European Ramazzini Foundation (ERF) rat study.

The EFSA report suggested that the lymphoma/leukemia findings were most
likely explained by infection in the rat colony.

The ERF has also conducted the only available long-term oral study of methyl
tertiary-butyl ether (MTBE).

Thus, using the EFSA report as support, some have now raised questions about
the human relevance of MTBE-associated hemolymphoreticular tumors reported
by the ERF in female rats as well as whether their incidence was elevated
above background levels.

In this report, we discuss the hypothesized mode of action (MOA) of
infection-induced lymphoma and its relevance to MTBE-associated lymphomas.

We address the relationship of rat strain and study duration to lymphoma
susceptibility and review evidence of low background rates of this tumor in
control animals at the ERF, similar survival rates for female rats at the
ERF and National Toxicology Program (NTP), and chemical- and
gender-specificity of tumor induction for this type of tumor in studies at
the ERF.

We find that the background incidence of hemolymphoreticular tumors in
female rats in the MTBE study is consistent with contemporaneous studies at
the ERF and that there is an exposure-related effect, which is unlikely to
be due to infections.

We examine more recent tumor classification schemes for lymphomas, which
support the combination of lymphoblastic leukemias and lymphomas reported by
Belpoggi et al. ([1995] Toxicol Ind Health 11: 119-149; [1998]  Eur J Oncol
3: 201-206). Published 2007 Wiley-Liss, Inc.  PMID: 18095346


M Soffritti of Ramazzini Foundation answers critique by Ajinomoto funded BA
Magnuson and GM Williams re aspartame (methanol) carcinogenicity,
Environmental Health Perspectives 2008 May: Murray 2008.06.24
http://rmforall.blogspot.com/2008_06_01_archive.htm
Tuesday, June 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1543
____________________________________________________



19,000 people, the 4 % of users of aspartame who drink average 5 cans daily,
have more problems in NIH AARP study of 474,000 people: Murray 2007.09.21
http://rmforall.blogspot.com/2007_09_01_archive.htm
September 21, 2007
http://groups.yahoo.com/group/aspartameNM/message/1475


Table 1. NIH-AARP Diet and Health Study aspartame intake levels from
beverages, 1995-2000 (N = 473,984)
[ adapted from article -- a 12-oz can diet soda has 200 mg aspartame ]

0 - under 100 - 100-200 - 200-400 - 400-600 - 600-1200 - over 1200 mg/d

cohort %
46 ------- 25 ------ 13 ------ 7 -------- 5 -- about 3 --- under 1


This is the first good data about the percentage of aspartame users who use
over 3 cans daily, averaging 5 cans daily at 200 mg per 12 oz can diet soda.

About 4 % of 473,984 is 19,000 people, with a peak intake of 17 cans daily,
and average 5 cans daily.

It would be worthwhile to investigate a wide variety of symptoms for the 0.1
% of highest level users, about 500 people.

For about 200 million USA aspartame users, this would be 200,000 people.

Table 1 reveals consistent increase in problems from

--------------------- zero to  (400-600) to (over 600) mg/d
aspartame intake:

% of cohort ------------ 46 --------- 5 -------- 4 %

mean aspartame mg/d --- 0 -------441 ------ 986

16+ education ---------- 37 ------- 40 ------- 34 %

diabetes history ---------- 3 ------- 22 ------- 26 %

alcohol g/d -------------- 14 ------- 11 ------- 13

never smoke ------------ 36 ------- 31 ------- 29 %

Body Mass Index ------- 26 ------- 29 ------- 29

18.5 - 25 --------------- 42 ------- 21 ------- 19 %

30 - 35 ----------------- 13 ------- 23 ------- 26 %

over 35 -----------------  4 ------- 10 ------- 13 %

Physical activity %:

under 3-4/mo ----------- 32 ------- 32 ------- 37 %

under 1-2/wk ----------- 22 ------- 21 ------- 19 %

over 3-4/wk ------------ 45 ------- 45 ------- 43 %

Calories kcal -------- 1,919 ---- 1,855 ---- 2,044 %

Caffeine  mg/d --------- 393 ------ 364 ------ 424

There do seem to be many increases of problems from the second to third row,
as mean aspartame use doubles.

Granted, this is cherry picking the data, selecting interesting patterns.

Correlations alone do not prove any direction of causation.

Nevertheless, it may be of value to study the correlations for increasing
aspartame intake among the 4 % using over 600 mg, the equivalent of 3 cans
12-oz cans diet soda daily.  The average use for this group is 5 cans daily.

For instance, are a minority of these heavy users displaying the great
majority of the problems that are reflected in the mean for each level of
use, with most users only having little or no increase in problems?

This is a group of about 20,000 people.


http://groups.yahoo.com/group/aspartameNM/message/1141
Nurses Health Study can quickly reveal the extent of aspartame (methanol,
formaldehyde, formic acid) toxicity: Murray 2004.11.21

The Nurses Health Study is a bonanza of information about the health of
probably hundreds of nurses who use 6 or more cans daily of diet soft
drinks -- they have also stored blood and tissue samples from their immense
pool of subjects, over 100,000 for decades.


Cancer Epidemiol Biomarkers Prev. 2006 Sep; 15(9): 1654-9.
Comment in:
Cancer Epidemiol Biomarkers Prev. 2007 Jul; 16(7): 1527-8;
author reply 1528-9.
Consumption of aspartame-containing beverages and incidence of hematopoietic
and brain malignancies.
Lim U, Subar AF, Mouw T, Hartge P, Morton LM, Stolzenberg-Solomon R,
Campbell D, Hollenbeck AR, Schatzkin A.
Division of Cancer Control and Population Sciences, National Cancer
Institute, 6130 Executive Boulevard, EPN 4005, Rockville, MD 20852-7344,
USA.   PMID: 16985027

Unhee Lim 1,
Amy F. Subar 2,  subara@...,
Traci Mouw 1,
Patricia Hartge 1,
Lindsay M. Morton 1,
Rachael Stolzenberg-Solomon 1,
David Campbell 3,
Albert R. Hollenbeck 4
and Arthur Schatzkin 1

1 Division of Cancer Epidemiology and Genetics,

2 Division of Cancer Control and Population Sciences, National Cancer
Institute, NIH, Department of Health and Human Services;

3 Information Management Services, Inc., Rockville, Maryland; and

4 AARP, Washington, District of Columbia

Requests for reprints: Amy Subar,
Division of Cancer Control and Population Sciences,
National Cancer Institute,
6130 Executive Boulevard, EPN 4005, Rockville, MD 20852-7344.
Phone: 301-594-0831; Fax: 301-435-3710. E-mail: subara@...,

http://cebp.aacrjournals.org/cgi/content/full/15/9/1654  free full text

BACKGROUND:
In a few animal experiments, aspartame has been linked to hematopoietic and
brain cancers.

Most animal studies have found no increase in the risk of these or other
cancers.

Data on humans are sparse for either cancer.

Concern lingers regarding this widely used artificial sweetener.

OBJECTIVE:
We investigated prospectively whether aspartame consumption is associated
with the risk of hematopoietic cancers or gliomas
(malignant brain cancer).

METHODS:
We examined 285,079 men and 188,905 women ages 50 to 71 years in the
NIH-AARP Diet and Health Study cohort

Daily aspartame intake was derived from responses to a baseline
self-administered food frequency questionnaire that queried consumption of
four aspartame-containing beverages (soda, fruit drinks, sweetened iced tea,
and aspartame added to hot coffee and tea) during the past year.

Histologically confirmed incident cancers were identified from eight state
cancer registries.

Multivariable-adjusted relative risks (RR) and 95% confidence intervals (CI)
were estimated using Cox proportional hazards regression that adjusted for
age, sex, ethnicity, body mass index, and history of diabetes.

RESULTS:
During over 5 years of follow-up (1995-2000), 1,888 hematopoietic cancers
and 315 malignant gliomas were ascertained.

Higher levels of aspartame intake were not associated with the risk of
overall hematopoietic cancer (RR for over 600 mg/d, 0.98; 95 % CI,
0.76-1.27),
glioma (RR for over 400 mg/d, 0.73; 95 % CI, 0.46-1.15);  P for inverse
linear trend = 0.05,
or their subtypes in men and women.

CONCLUSIONS:
Our findings do not support the hypothesis that aspartame increases
hematopoietic or brain cancer risk.  PMID: 16985027

"We cannot exclude the possibility that higher aspartame consumption than
that observed in this study may be associated with an elevated risk of
hematopoietic or brain cancers.

In the laboratory study with positive findings, animals were fed doses
starting from 4 mg up to 5,000 mg per kg body weight.

Significantly elevated lymphomas and leukemias were observed in female rats
fed 20 mg of aspartame and higher (e.g., 1,200 mg for humans weighing 60 kg
or 132 lb; refs. 13, 14).

The reported aspartame intake in our data ranged from 0 to 3,400 mg/d with
sparse numbers in the upper intake categories (under 1 % consuming over
1,200 mg/d).

However, we did not detect any increase in risk estimates in the highest
categories (over 1,200 or 2,000 mg/d, which is equivalent to about 7 to 11
cans of soft drinks daily) compared with the lowest
categories, and the associations were similarly null in both men and women."



ASE 6.6.1.  "Mice Male ddY mice 2000 mg/kg bw Negative in Comet assay Sasaki
et al. (2002)"

ASE 6.6.2.  "Sasaki et al. (2002) assessed the genotoxicity of 39 food
additives using the comet assay of tissues collected from male ddY mice
administered 1 oral dose at up to one half of the LD50 or 2000 mg/kg bw.

For aspartame, a dose of 2000 mg/kg bw was used and mice (n = 4/group) were
killed after 3 and 24 h.

Nuclei were obtained from glandular stomach, colon, liver, kidney, urinary
bladder, lung, brain, and bone marrow.

No changes were found in the comet lengths of nuclear DNA from tissues from
aspartame-treated mice.

Thus, aspartame was found to be nongenotoxic in this assay."

[ The ASE review missed the actual details of this provokative study by an
experienced team that continues to use the sensitive, fast, low cost
automated Comet assay to measure DNA damage.

The team tested 39 food additives, including 7 sweeteners, using groups of
just 4 mice at a uniform oral dose of 2000 mg/kg bw, testing 8 organs at 3
or 24 hours later.

However, each test group had an assigned control group, somehow selected
from a total of 21 4-rat control groups.

Although the aspartame control levels happened to be much higher than the
averages for all 21 control groups, the aspartame values were about twice
the control values, close to statistical significance, 3 hours after the
oral dose, for stomach, colon, liver, bladder, and lung.

Results for DNA damage for Ace-K and stevia were nil, while sucralose,
cyclamate, and saccharin were significant for many tissues.

This result, once again, cries out for thorough replication, with much
larger groups of mice, using a variety of dose levels and test times, and
testing many more tissues.

A separate report confirmed that stevia was not genotoxic. ]


http://groups.yahoo.com/group/aspartameNM/message/935
Comet assay finds DNA damage from sucralose, cyclamate, saccharin in mice:
Sasaki YF & Tsuda S Aug 2002: Murray 2003.01.01
[ Also borderline evidence, in this pilot study of 39 food additives, using
test groups of 4 mice, for DNA damage from for stomach, colon, liver,
bladder, and lung 3 hr after oral dose of 2000 mg/kg aspartame -- a very
high dose. Methanol is the only component of aspartame that can lead to DNA
damage. ]


http://groups.yahoo.com/group/aspartameNM/message/961
genotoxins, Comet assay in mice: Ace-K, stevia fine; aspartame poor;
sucralose, cyclamate, saccharin bad: Y.F. Sasaki Aug 2002: Murray 2003.01.27
[A detailed look at the data] ]

"Comparing the mean control values [average of all 21 control groups] to the
values for the other 7 sweeteners:

Best is acesulfame K, with no significant or high values.

Good is glycyrrhizin (derived from licorice), two 1.4 ratios for Stomach and
Brain.

Next is stevia, with one high value [above ratio 1.4], 9.48+-1.99 for
Bladder, 2000 mg 3 hr, ratio 1.8 .

Aspartame has high values for 2000 mg 3 hr for Stomach, Colon, Liver,
Bladder, Lung.

Sucralose has 3 significant values and 13 high values, for Stomach, Colon,
Kidney, Bladder, Lung, Brain.

Sodium cyclamate has 4 significant values and 10 high values for Stomach,
Colon, Liver, Kidney, Bladder, Lung, Brain, Bone.

Saccharin has 3 highly significant values for Colon, and 13 high values for
Stomach, Colon, Kidney, Lung, Brain, Bone.

Sodium saccharin has 5 highly significant values for Stomach and Colon, and
14 high values for Stomach, Liver, Kidney, Bladder, Lung, Brain, Bone."


"For Liver, 5 of the 21 control groups, with values 1.67, 1.63, 1.29, 1.06,
1.65 would make some 3 hr aspartame values approach or reach significance.

Ratios about 2 for different tissues with aspartame that would be close to
significant would exist for many of the 21 control groups: Stomach 1 Colon 5
Liver 5 Bladder 11 Lung 5 .

The aspartame values at 3 hr are compared with the mean values for the 21
control groups:

Somach ---- Colon ---- Liver ---- Kidney ---- Bladder ---- Lung

DNA Migration at 3 hr from 2000 mg/kg dose
8.49+-0.48, 9.18+-0.56, 3.26+-0.16, 1.91+-0.26, 10.7+-2.77, 4.13+-1.26

mean of 21 control groups
6.31,------ 5.81,------ 2.15,------ 2.25, ------ 5.40, ----- 2.61,

range of values for 21 control groups
4.3-8.6 --- 4.0-8.1 --- 1.1-3.6 --- 1.2-2.9 ---- 3.6-7.1 --- 1.6-4.7

ratio = DNA Migration/control mean
1.4, ------ 1.6, ------ 1.5, ------ 0.9, ------- 2.0, ------ 1.6

Brain ---------- Bone [marrow]

0.37+-0.70, ---- 1.01+-0.59 DNA Migration at 3 hr from 2000 mg/kg dose


1.48, ---------- 1.12, mean of 21 control groups


0.8-2.6 -------- 0.6-1.9 range of values for 21 control groups


0.3 ----------------- 0.9, ratio = DNA Migration/control mean

Wouldn't the average of all the 21 control groups be the best control values
to use?

What would then be the appropriate statistical test?

How many mice would it take to reach significance for the 5 tissues with
ratios over 1.4: Stomach, Colon, Liver, Bladder, Lung?

Aspartame at 24 hours had levels too low to reach significance with any of
the 21 control groups."


ASE reference 306:
Mutat Res 2002 Aug 26; 519(1-2): 103-19
The comet assay with 8 mouse organs: results with 39 currently used food
additives.
Sasaki YF, Kawaguchi S, Kamaya A, Ohshita M, Kabasawa K, Iwama K, Taniguchi
K, Tsuda S.
Laboratory of Genotoxicity, Faculty of Chemical and Biological Engineering,
Hachinohe National College of Technology, Tamonoki Uwanotai 16-1, Aomori
039-1192, Japan.
yfsasaki-c@... ; s.tsuda@...

We determined the genotoxicity of 39 chemicals currently in use as food
additives.  They fell into six categories-dyes, color fixatives and
preservatives, preservatives, antioxidants, fungicides, and sweeteners.

We tested groups of four male ddY mice once orally with each additive at up
to 0.5xLD(50) or the limit dose (2000 mg/kg) and performed the comet assay
on the glandular stomach, colon, liver, kidney, urinary bladder, lung,
brain, and bone marrow 3 and 24 h after treatment.

Of all the additives, dyes were the most genotoxic.
Amaranth, Allura Red, New Coccine, Tartrazine, Erythrosine, Phloxine, and
Rose Bengal induced dose-related DNA damage in the glandular stomach, colon,
and/or urinary bladder.
All seven dyes induced DNA damage in the gastrointestinal organs at a low
dose (10 or 100 mg/kg).

Among them, Amaranth, Allura Red, New Coccine, and Tartrazine induced DNA
damage in the colon at close to the acceptable daily intakes (ADIs).

Two antioxidants (butylated hydroxyanisole (BHA) and butylated
hydroxytoluene (BHT)), three fungicides (biphenyl, sodium o-phenylphenol,
and thiabendazole), and four sweeteners (sodium cyclamate, saccharin, sodium
saccharin, and sucralose) also induced DNA damage in gastrointestinal
organs.

Based on these results, we believe that more extensive assessment of food
additives in current use is warranted. PMID: 12160896


[ The following critiques will be appreciated by the few who have the
tenacity to plow through the tedious mazes of red herrings, omitted studies,
incuriosity, bias, cursory dismissals, unexamined details, ignored
opportunities, spiced with sonorous PR spin:
"...the most tested food additive in history,"
"...used in over 6,000 products worldwide,"
"...approved by FDA, WHO, EU FSA, American Diabetes Assc., ect,"
"...components are part of normal foods and metabolism in much greater
amounts,"
"...finally put to rest all the rumors on the Net, using a tiny minority of
allergic individuals to opportunistically impugn distinguished experts, who
are valiantly protecting diabetics and the obese against the ravages of
sugar."


industry scientists praise aspartame safety and benefits in Paris on
2006.05.30, Herve Nordmann, Andrew G. Renwick, Carlo La Vecchia, Tommy
Visscher, Jaap Seidell, France Bellisle, Adam Drewnowski, Margaret Ashwell,
Anne de la Hunty, Sigrid A. Gibson, Alan R. Boobis: Murray 2007.11.18
http://groups.yahoo.com/group/aspartameNM/message/1491

http://groups.yahoo.com/group/aspartameNM/message/1108
faults in 1999 July EPA 468-page formaldehyde profile: Elzbieta Skrzydlewska
PhD, Assc. Prof., Medical U. of Bialystok, Poland, abstracts -- ethanol,
methanol, formaldehyde, formic acid, acetaldehyde, lipid peroxidation, green
tea, aging: Murray 2004.08.08 2005.07.11

American Dietetic Association.
Position of the American Dietetic Association: use of nutritive and
nonnutritive sweeteners.
J Am Diet Assoc. 2004 Feb; 104(2): 255-75.
http://www.eatright.org/Nutritive(1).pdf

http://groups.yahoo.com/group/aspartameNM/message/1068
critique of aspartame review by American Dietetic Association Feb 2004,
Valerie B. Duffy & Madeleine J. Sigman-Grant: Murray 2004.05.14

http://groups.yahoo.com/group/aspartameNM/message/1070
critique of aspartame review, French Food Safety Agency AFSSA 2002.05.07
aspartamgb.pdf (18 pages, in English), Martin Hirsch: Murray 2004.04.13

http://groups.yahoo.com/group/aspartameNM/message/957
safety of aspartame Part 1/2 12.4.2: EC HCPD-G SCF: Murray 2003.01.12 EU
Scientific Committee on Food, a whitewash

http://groups.yahoo.com/group/aspartameNM/message/1045
http://www.holisticmed.com/aspartame/scf2002-response.htm
Mark Gold exhaustively critiques European Commission Scientific Committee on
Food re aspartame ( 2002.12.04 ): 59 pages, 230 references


[ Here's a useful list... ]

ASE reference 42:
Butchko HH,
Stargel WW,
Comer CP,
Mayhew DA,
Benninger C,
Blackburn GL,
de Sonneville LM,
Geha RS,
Hertelendy Z,
Koestner A,
Leon AS,
Liepa GU,
McMartin KE,
Mendenhall CL,
Munro IC,
Novotny EJ,
Renwick AG,
Schiffman SS,
Schomer DL,
Shaywitz BA,
Spiers PA,
Tephly TR,
Thomas JA,
Trefz FK.
Regul Toxicol Pharmacol. 2002 Apr; 35(2 Pt 2): S1-93.
Medical and Scientific Affairs, The NutraSweet Company, Mt Prospect,
Illinois 60056, USA. harriett.h.butchko@...

Over 20 years have elapsed since aspartame was approved by regulatory
agencies as a sweetener and flavor enhancer.

The safety of aspartame and its metabolic constituents was established
through extensive toxicology studies in laboratory animals, using much
greater doses than people could possibly consume.

Its safety was further confirmed through studies in several human
subpopulations, including healthy infants, children, adolescents, and
adults; obese individuals; diabetics; lactating women; and individuals
heterozygous (PKUH) for the genetic disease phenylketonuria (PKU) who have a
decreased ability to metabolize the essential amino acid, phenylalanine.

Several scientific issues continued to be raised after approval, largely as
a concern for theoretical toxicity from its metabolic components -- the
amino acids, aspartate and phenylalanine, and methanol -- even though
dietary exposure to these components is much greater than from aspartame.

Nonetheless, additional research, including evaluations of possible
associations between aspartame and headaches, seizures, behavior, cognition,
and mood as well as allergic-type reactions and use by potentially sensitive
subpopulations, has continued after approval.

These findings are reviewed here.

The safety testing of aspartame has gone well beyond that required to
evaluate the safety of a food additive.

When all the research on aspartame, including evaluations in both the
premarketing and postmarketing periods, is examined as a whole, it is clear
that aspartame is safe, and there are no unresolved questions regarding its
safety under conditions of intended use.  PMID: 12180494


ASE  6.3.1.  "Two-Year Bioassay Studies

Aspartame was first approved by FDA as a nonnutritive sweetener in 1974,
based on the toxicity studies that were conducted by the Searle
Laboratories.

Chronic toxicity studies with aspartame, and its decomposition product, DKP,
were conducted in mice, rats, and dogs.

A 46-week study with aspartame was also performed with hamsters.

Table 15 provides a summary of these studies.

The carcinogenic potential of these compounds is discussed in the next
sections.

Following the approval of aspartame, a formal objection was submitted to the
FDA (FDA, 1981) questioning the conclusions from the rodent studies on
aspartame conducted by Searle, and proposing that aspartame may have the
potential to cause brain tumors in humans.

This objection resulted in FDA staying the regulation approving the
marketing of aspartame in 1975, and the establishment of a Public Board of
Inquiry to reexamine the studies submitted by Searle to the FDA.

Prior to the evaluation by the Board, the 15 studies submitted by Searle
were thoroughly audited by the Universities Associated for Research and
Education in Pathology, Inc. (UAREP) and by the FDA.

The findings of the UAREP, the FDA, and the Public Board of Inquiry were
considered and evaluated by the Commissioner of Food and Drugs, resulting in
the issuance of the commissioner's Final Decision that at projected levels
of consumption, aspartame would not pose a risk of brain damage and will not
cause brain tumors (FDA docket, 75F-0355, 1981) (FDA, 1981).

This decision resulted in FDA vacating the stay of the original 1974
regulation.

Objections to the of the use of aspartame were again filed with the FDA in
1983; however, the regulations approving the use of aspartame was not stayed
following these objections, as the FDA stated that they failed to create
sufficient doubt about the safety of aspartame.

A response to the objections and a denial for a hearing was issued in 1984
by the Acting Commissioner of Food and Drugs (FDA docket 75F-0355 and
82F-0305) (FDA, 1984; Wurtman and Maher, 1987). "

[ In fact the FDA brought suit against Searle for its radically biased,
improper scientific studies.

The industry won by persuading the FDA's two attorneys to let the legal
process languish.

Soon, the attorney's inexplicably found pleasant, prosperous futures in the
industry's networks.

Similar adroit exercises in corporate realpolitic were led by the CEO of
Searle, none other than that modest American hero, Donald Rumsfeld, who used
Reagan's victory to immediately manipulate the FDA's approval by a brand new
Commissioner, Arthur Hull Hayes, in July, 1981, of aspartame in dry foods,
and soon in beverages two years later, whereupon the fortunate Commissioner,
troubled by hints of political corruption, found a gracious life with the
industry's PR agency.

Donald Rumsfeld CEO 1977-85 G.D. Searle & Co., got new President Reagan to
prohibit FDA opposition to aspartame 1981.01.25, history by lawyer James S.
Turner: Murray 2007.10.29
http://groups.yahoo.com/group/aspartameNM/message/1483

aspartame history Part 1/4 1964-1976: Gold: Murray 1999.11.06
http://groups.yahoo.com/group/aspartameNM/message/53
http://www.dorway.com/enclosur.html

aspartame expose 96K Oct 1987 Part 1/3: Gregory Gordon, UPI reporter: Murray
2000.07.10
http://groups.yahoo.com/group/aspartameNM/message/262
http://www.dorway.com/upipart1.txt

revolving door, Monsanto, FDA, EPA: NGIN: Murray 2002.12.23
http://groups.yahoo.com/group/aspartameNM/message/928
____________________________________________________



formaldehyde from many sources, including aspartame, is major cause of
Allergic Contact Dermatitis, SE Jacob, T Steele, G Rodriguez, Skin and Aging
2005 Dec.: Murray 2008.03.27
http://rmforall.blogspot.com/2008_03_01_archive.htm
Thursday, March 27, 2008
http://groups.yahoo.com/group/aspartameNM/message/1533

"For example, diet soda and yogurt containing aspartame (Nutrasweet),
release formaldehyde in their natural biological degradation.

One of aspartame's metabolites, aspartic acid methyl ester, is converted to
methanol in the body, which is oxidized to formaldehyde in all organs,
including the liver and eyes. 22

Patients with a contact dermatitis to formaldehyde have been seen to improve
once aspartame is avoided. 22

Notably, the case that Hill and Belsito reported had a 6-month history of
eyelid dermatitis that subsided after 1 week of avoiding diet soda. 22"

" Allergic Contact Dermatitis is an important disease with a high impact
both in terms of patient morbidity and economics.

The contact dermatitides include irritant contact dermatitis, contact
urticaria and allergic contact dermatitis.

Irritant contact dermatitis, the most common form, accounts for
approximately 80% of environmental-occupational based dermatoses.

Contact urticaria (wheal and flare reaction) represents an IgE and mast
cell-mediated immediate-type hypersensitivity reaction that can lead to
anaphylaxis, the foremost example of this would be latex hypersensitivity.

While this is beyond the scope of this section, we acknowledge this form of
hypersensitivity due to the severity of the potential reactions and direct
the reader to key sources. 1,2

Allergic contact dermatitis, on the other hand, is a delayed type IV
hypersensitivity reaction. The primary focus of this section is to highlight
the educational component of allergic contact dermatitis.

We present a case of a medical student who presented with erythematous
eczematoid plaques on her trunk and legs and fine vesiculation of her scalp,
3 weeks after starting anatomy class.

Of note, she routinely washed her face and arms after leaving the anatomy
lab, but remained in her scrubs for the rest of the day.

Formaldehyde and Quaternium-15 positive reactions in the same patient."

"Our patient underscores the importance of appropriate patch testing and
education.

Once we identified the allergy to formaldehyde and quaternium-15, we
provided patient education materials regarding the common and not-so-common
locations of these chemicals and cross-reactors.

We also gave the patient information on avoidance and safe alternatives (see
Table 5).

Fortunately, with technical advances, this student completed the anatomy
section via electronic learning tools.

By avoiding formaldehyde, including anatomy lab, FRP in her shampoo and
cosmetics, and aspartame in her diet, this patient dramatically improved.

As with all contact dermatitides, the mainstay of treatment for allergic
contact dermatitis is avoidance."

http://www.skinandaging.com/article/5158Skin & Aging Journal
Skin & Aging - ISSN: 1096-0120 - Volume 13 - Issue 12_2005 -
December 2005 - Pages: 22 - 27

Allergen Focus:
Focus on T.R.U.E. Test Allergens #21, 13 and 18:
Formaldehyde and Formaldehyde-Releasing Preservatives
-- By Sharon E. Jacob, M.D., Tace Steele, B.A., [now MD]
and Georgette Rodriguez, M.D., M.P.H.

[ See also:

Avoiding formaldehyde allergic reactions in children, aspartame,
vitamins, shampoo, conditioners, hair gel, baby wipes,
Sharon E Jacob, MD, Tace Steele, U. Miami, Pediatric Annals
2007 Jan.: eyelid contact dermatitis, AM Hill, DV Belsito,
2003 Nov.: Murray 2008.03.27
http://rmforall.blogspot.com/2008_03_01_archive.htm
Thursday, March 27, 2008
http://groups.yahoo.com/group/aspartameNM/message/1532

Sharon E. Jacob, MD, Assistant Professor of Medicine (Dermatology)
University of California, San Diego 200 W. Arbor Drive #8420, San Diego, CA
92103-8420
Tel: 858-552-8585 ×3504 Fax: 305-675-8317  sjacob@...; ]


FDA deficiencies, Alexis Jetters, Reader's Digest, Vera Hassner Sharav,
blog, Alliance for Human Research Protection 2008.03.23: Murray 2008.04.02
http://rmforall.blogspot.com/2008_04_01_archive.htm
Tuesday, April 2, 2008
http://groups.yahoo.com/group/aspartameNM/message/1535
http://ahrp.blogspot.com/2008/03/readers-digest-crisis-in-fda-and.html


two aspartame toxicity research studies by Resia Pretorius, U. Pretoria,
South Africa, debate with JD Fernstrom: Murray 2008.04.04
http://rmforall.blogspot.com/2008_04_01_archive.htm
Friday, April 4, 2008
http://groups.yahoo.com/group/aspartameNM/message/1536
____________________________________________________



http://groups.yahoo.com/group/aspartameNM/message/1459
third study by expert Greek team of neurotoxicity in infant rats by
aspartame (or its parts, methanol, phenylalanine, aspartic acid), KH
Schulpis et al, Food Chem Toxicol 2007.06.16: Murray 2007.08.05

http://groups.yahoo.com/group/aspartameNMmessage/1447
second study by expert Greek team of neurotoxicity in infant rats by
aspartame (or its parts, methanol, phenylalanine, aspartic acid), KH
Schulpis et al, Toxicology 2007.05.18: Murray 2007.07.04

http://groups.yahoo.com/group/aspartameNMmessage/1444
expert Greek group finds aspartame (or its parts, methanol, phenylalanine,
aspartic acid) harm infant rat brain enzyme activity, KH Schulpis et al,
Pharmacol. Res. 2007.05.13: Murray 2007.06.23

http://groups.yahoo.com/group/aspartameNM/message/939
aspartame (aspartic acid, phenylalanine) binding to DNA: Karikas July 1998:
Murray 2003.01.05
Karikas GA, Schulpis KH, Reclos GJ, Kokotos G
Measurement of molecular interaction of aspartame and its metabolites with
DNA.
Clin Biochem 1998 Jul; 31(5): 405-7.
Dept. of Chemistry, University of Athens, Greece
http://www.chem.uoa.gr gkokotos@...
K.H. Schulpis inchildh@... ; G.J. Reclos reklos@...

5 recent aspartame reports by S Tsakiris, KH Schulpis, I Simintzi, with
responses to critiques by AG Renwick and by EB Abegaz, RG Bursey, 2005-2008
2008.03.05

Pharmacological Research 57 (2008) 89-90
Letter to the Editor
Answer to Letter sent to the Editor by Drs. E. Abegaz and R. Bursey
(Ajinomoto Corporate Services LLC, Washington, USA) related to Simintzi et
al. report published in Pharmacol Res 2007; 56: 155-9
Letter to the Editor / Pharmacological Research 57 (2008) 89-90

Stylianos Tsakiris a,? stsakir@...;
Kleopatra H. Schulpis b inchildh@...;
a Department of Experimental Physiology, Medical School, Athens University,
P.O. Box 65257, GR-15401 Athens, Greece
b Inborn Errors of Metabolism Department, Institute of Child Health,
Research Center, Greece
? Corresponding author.

Pharmacological Research 57 (2008) 87-88
Response to "The effect of aspartame on the acetylcholinesterase activity in
hippocampal homogenates of suckling rats" by Simintzi et al.
Eyassu G. Abegaz ?
Robert G. Bursey
Ajinomoto Corporate Services LLC, Scientific & Regulatory Affairs, 1120
Connecticut Ave., N.W., Suite 1010, Washington, DC 20036, United States
? Corresponding author. Tel.: +1 202 457 0284; fax: +1 202 457 0107. E-mail
addresses: abegazee@...; (E.G. Abegaz), burseyb@...; (R.G.
Bursey)
Keywords: Aspartame; Aspartate; Phenylalanine; Methanol; AChE activity

Tsakiris S, Schulpis KH.
Answer to letter sent by Professor A.G. Renwick (University of Southampton,
UK) related to Simintzi et al. report published in Food and Chemical
Toxicology 2007; 45(12): 2397-401.
Food Chem Toxicol. 2008 Mar; 46(3): 1208-9.
Epub 2007 Oct 25. No abstract available. PMID: 18054419
doi:10.1016/j.fct.2007.10.016 Copyright  2007 Elsevier Ltd All rights
reserved.
____________________________________________________


http://foodqualitynews.com/news/ng.asp?n=84424-aspartame-sweetener
recent news re E Pretorius aspartame and brain review


Direct and indirect cellular effects of aspartame on the brain.
Humphries P, Pretorius E, Naude H, U. Pretoria, South Africa,
Eur J Clin Nutr. 2007 Aug 8: Murray 2007.08.12
http://groups.yahoo.com/group/aspartameNM/message/1463

"The aim of this study was to discuss the direct and indirect cellular
effects of aspartame on the brain, and we propose that excessive aspartame
ingestion might be involved in the pathogenesis of certain mental disorders
(DSM-IV-TR 2000) and also in compromised learning and emotional
functioning."

Eur J Clin Nutr. 2007 Aug 8; [Epub ahead of print]
Direct and indirect cellular effects of aspartame on the brain.
Humphries P,
Pretorius E, resia.pretorius@...;
Naude H.
[1] Department of Anatomy, University of Pretoria, Pretoria, Gauteng, South
Africa
[2] Department of Anatomy, University of the Limpopo, South Africa.

The use of the artificial sweetener, aspartame, has long been contemplated
and studied by various researchers, and people are concerned about its
negative effects.

Aspartame is composed of phenylalanine (50%), aspartic acid (40%) and
methanol (10%).

Phenylalanine plays an important role in neurotransmitter regulation,
whereas aspartic acid is also thought to play a role as an excitatory
neurotransmitter in the central nervous system.

Glutamate, asparagines and glutamine are formed from their precursor,
aspartic acid.

Methanol, which forms 10% of the broken down product, is converted in the
body to formate, which can either be excreted or can give rise to
formaldehyde, diketopiperazine (a carcinogen) and a number of other highly
toxic derivatives.

Previously, it has been reported that consumption of aspartame could cause
neurological and behavioural disturbances in sensitive individuals.

Headaches, insomnia and seizures are also some of the neurological effects
that have been encountered, and these may be accredited to changes in
regional brain concentrations of catecholamines, which include
norepinephrine, epinephrine and dopamine.

The aim of this study was to discuss the direct and indirect cellular
effects of aspartame on the brain, and we propose that excessive aspartame
ingestion might be involved in the pathogenesis of certain mental disorders
(DSM-IV-TR 2000) and also in compromised learning and emotional functioning.

European Journal of Clinical Nutrition advance online publication, 8 August
2007; doi:10.1038/sj.ejcn.1602866. PMID: 17684524

Keywords: astrocytes; aspartame; neurotransmitters; glutamate; GABA;
serotonin; dopamine; acetylcholine

Received 25 October 2006; revised 26 April 2007; accepted 27 April 2007
Correspondence: Professor E Pretorius, Department of Anatomy, University of
Pretoria, BMW Building, Dr Savage Street, PO Box 2034, Pretoria 0001,
Gauteng, South Africa.  resia.pretorius@...
copyright 2007 Nature Publishing Group, All rights reserved 0954-3007/07
$30.00 www.nature.com/ejcn


http://groups.yahoo.com/group/aspartameNMmessage/1452
phenylalanine and aspartic acid from low dose aspartame in rabbits interfere
with blood coagulation, Pretorius E and Humphries P, U. of Pretoria,
Ultrastruct Pathol 2007 March: Murray 2007.07.14

"The authors conclude by suggesting that aspartame usage may interfere with
the coagulation process and might cause delayed fibrin breakup after clot
formation.

They suggest this, as the fibrin networks from aspartame-exposed rabbits are
more complex and dense, due to the netlike appearance of the minor, thin
fibers.

Aspartame usage should possibly be limited by people on anti-clotting
medicine or those with prone to clot formation."

Ultrastruct Pathol. 2007 Mar-Apr; 31(2): 77-83.
Ultrastructural changes to rabbit fibrin and platelets due to aspartame.
Pretorius E,
Humphries P.
Department of Anatomy, Faculty of Medicine, University of Pretoria, South
Africa.
[ Humphries P also at Department of Anatomy, University of Limpopo. Medunsa
Campus, Garankuwa. South Africa ]
____________________________________________________



old tiger roars -- Woodrow C Monte, PhD -- aspartame causes many breast
cancers, as ADH enzyme in breasts makes methanol from diet soda into
carcinogenic formaldehyde -- same in dark wines and liquors, Fitness Life
2008 Jan.: Murray 2008.02.11
http://rmforall.blogspot.com/2008_02_01_archive.htm
Monday, February 11, 2008
http://groups.yahoo.com/group/aspartameNM/message/1517

"Alcohol dehydrogenase ADH is required for the conversion of methanol to
formaldehyde (112).

ADH is not a common enzyme in the human body -- not many cells in the human
body contain this enzyme.

The human breast is one of the few organs in the body with a high
concentration of ADH (190b), and it is found there exclusively in the
mammary epithelial cells, the very cells known to transform into
adenocarcinoma (190c) (breast cancer).

The most recent breast cancer scientific literature implicates ADH as
perhaps having a pivotal role in the formation of breast cancer, indicating
a greater incidence of the disease in those with higher levels of ADH
activity in their breasts (190a)."

Methyl alcohol ingestion as a model etiologic agent in multiple sclerosis,
WC Monte, D Glanzman, C Johnston; Methanol induced neuropathology in the
mammalian central nervous system, Woodrow C.
Monte, Renee Ann Zeising, both reports 1989.12.04: Murray 2007.12.28
http://rmforall.blogspot.com/2007_12_01_archive.htm
Friday, December 28 2007
http://groups.yahoo.com/group/aspartameNM/message/1499

role of formaldehyde, made by body from methanol from foods and aspartame,
in steep increases in fetal alcohol syndrome, autism, multiple sclerosis,
lupus, teen suicide, breast cancer, Nutrition Prof. Woodrow C. Monte,
retired, Arizona State U., two reviews, 190 references supplied, Fitness
Life, New Zealand 2007 Nov, Dec: Murray 2007.12.26
http://rmforall.blogspot.com/2007_12_01_archive.htm
Wednesday, December 26 2007
http://groups.yahoo.com/group/aspartameNM/message/1498
____________________________________________________


There really is no controversy, Adrienne Samuels PhD, letter re evident
toxicity of aspartame EJCN 2008.06.11: Murray 2008.06.30
http://rmforall.blogspot.com/2008_06_01_archive.htm
Monday, June 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1546
___________________________________________________

Cargill rolling out natural, no-calorie sweetener Truvia [stevia], Martinne
Geller, Reuters.com: Murray 2008.07.10
http://rmforall.blogspot.com/2008_07_01_archive.htm
Thursday, July 10, 2008
http://groups.yahoo.com/group/aspartameNM/message/1549


http://www.reuters.com/article/marketsNews/idUSN0930999220080709?pageNumber=2&vi\
rtualBrandChannel=10216&sp=true

Cargill rolling out natural, no-calorie sweetener Truvia [stevia]
Wed Jul 9, 2008 9:11am EDT
By Martinne Geller

NEW YORK (Reuters) -- Agribusiness giant Cargill Inc is starting to roll out
Truvia, its natural, no-calorie sweetener on Wednesday, and expects the
product to be on grocery shelves across the U.S. sometime this fall.

Truvia is made from certain compounds in the leaves of stevia, a shrub
native to Paraguay, and will provide a natural alternative to artificial
sweeteners including Sweet 'N Low, Equal and Splenda.

Truvia is going on sale first at a handful of D'Agostino supermarkets in
Manhattan, and will eventually be sold at grocery stores and big box
retailers across the country, said Steve Snyder, vice president and business
director of Cargill's Truvia business.

Snyder declined to name specific retailers, but said it will be "widely
available" in stores and from a company website.

A box of 40 green and white packets of Truvia will have a suggested retail
price of $ 3.99, which Snyder said is a little more expensive than older,
artificial sweeteners, such as saccharin, aspartame and sucralose, which are
sold under the respective brand names of Sweet'N Low, NutraSweet and Equal,
and Splenda, which is made by Tate & Lyle Plc.

Sweet'N Low is manufactured by Brooklyn, New York-based Cumberland Packing
Corp while Chicago-based Merisant owns Equal. The NutraSweet Co is owned by
Boston-based private equity firm J.W. Childs Associates.

Truvia also will be used as a sweetener in beverages and foods -- such as
yogurts, cereals and snack bars -- in early 2009, Snyder said.

Coca-Cola Co co-developed the product with Cargill and has exclusive rights
to use Truvia in beverages. Rivals including PepsiCo Inc and Dr Pepper
Snapple Group Inc are working on their own versions of natural, no-calorie
sweeteners.

According to a May release from Cargill and Coke, Truvia, also known as
rebiana, is "the first consistent, high-purity sweetener composed of
rebaudioside A, the best-tasting part of the stevia leaf."

Stevia is approved as a food additive in a dozen countries including Japan,
Brazil and China, but not in the European Union or the United States. Yet it
is sold in the U.S. as a dietary supplement, since supplements are not
subject to the same regulations.

Cargill is using various suppliers that are growing the plants in China and
South America. One supplier, GLG Life Tech Corp, said in May that it started
building a 500-metric-ton stevia processing facility in Qindao, China.

The U.S. Food and Drug Administration classifies stevia as an "unsafe food
additive," saying on its website that "available toxicological information
on stevia is inadequate to demonstrate its safety as a food additive or to
affirm its status as a GRAS (generally recognized as safe)."

According to a story in May in the Wall Street Journal, studies of stevia's
health effects have revealed potential mutations in livers of rats and
concerns about fertility problems in men.

But Cargill, which handled the growing of the plants and consultations with
the FDA, stands by the safety of Truvia and reiterated that it is made from
certain compounds in stevia leaves and not the whole leaf.

"Although stevia today is sold in the U.S. as a dietary supplement, rebiana
will be the first available sweetener ... that has been purified from the
stevia plant. Unlike many existing stevia products, which generally contain
crude extracts of the plant, rebiana is ... consistent in quality," the
company said in May.

Cargill said it worked in consultation with the FDA for three years to make
sure all health questions and concerns about Truvia were addressed.

There is no formal approval process for natural substances, but an
"independent panel of experts met, reviewed the science, and made the
statement that the product is safe," according to Cargill spokeswoman Ann
Tucker. She added that the FDA has copies of the data proving that Truvia is
safe.

(Editing by Phil Berlowitz and Carol Bishopric)
copyright Thomson Reuters 2008 All rights reserved
____________________________________________________


stevia herbal sweetener to be sold as Truvia (rebiana) by Cargill and
Coca-Cola, if blitz of 12 studies wins FDA approval in 30-90 days:
Murray 2008.05.24
http://rmforall.blogspot.com/2008_05_01_archive.htm
Saturday, May 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1540

http://groups.yahoo.com/group/aspartameNMmessage/1488
Coca-Cola, Cargill Inc., PureCircle global operations market stevia
for foods and drinks: Murray 2007.11.12

http://groups.yahoo.com/group/aspartameNM/message/1438
Coca-Cola and Cargill Inc., after years of development,
with 24 patents, will soon sell rebiana (stevia)
in drinks and foods: Murray 2007.05.31
[ gives links to reviews of previous stevia studies ]

http://groups.yahoo.com/group/aspartameNMmessage/1437
stevia to be approved and cyclamates limited by Food Standards
Australia New Zealand: JMC Geuns critiques of two recent stevia
studies by Nunes: Murray 2007.05.29
Jan.Geuns@...;

http://groups.yahoo.com/group/aspartameNM/message/1436
FDA's corrupt war against safe herbal sweetener stevia,
Mary Nash Stoddard, 2006 January,
Aspartame Consumer Safety Network: Murray 2007.05.24

http://groups.yahoo.com/group/aspartameNM/message/1430
stevia, balanced factual detailed review in Wikipedia: Murray
2007.05.19
http://en.wikipedia.org/wiki/Stevia

http://groups.yahoo.com/group/aspartameNM/message/1419
two recent warning studies on stevia toxicity on rats and bacteria, AP
Nunes et al, 2007 April, 2006 Dec, links to 18 positive abstracts from
2000 February to 2004 January: Murray 2007.05.03

At the end of this post, I link to my 5 previous reviews in 2005
August that give 18 full abstacts in PubMed on stevia toxicity from
2000 February to 2004 January, which do not find that stevia is
practically toxic to humans in ordinary use -- and give an opposite
positive abstract using the Comet assay in 2002 December, and then
share the conclusion from the full text of another study on
mutagenicity, T Terai et al 2002 July. ]

Planta Med. 2001 Dec; 67(9): 796-9.
Inhibitory effect of stevioside on calcium influx to produce
antihypertension.
Lee CN, Wong KL, Liu JC, Chen YJ, Cheng JT, Chan P.
Department of Medicine, Taipei Medical University-Wan Fang
Hospital, Wen Shan, Taipei, Taiwan.

Antiviral Res. 2001 Jan; 49(1): 15-24.
Analysis of anti-rotavirus activity of extract from Stevia rebaudiana.
Takahashi K, Matsuda M, Ohashi K, Taniguchi K, Nakagomi O,
Abe Y, Mori S, Sato N, Okutani K, Shigeta S.
Department of Microbiology, School of Medicine, Fukushima
Medical University, 1 Hikarigaoka, Fukushima-shi 960-1295,
Japan. k-t...@...

Metabolism. 2000 Feb; 49(2): 208-14.
Stevioside acts directly on pancreatic beta cells to secrete insulin:
actions independent of cyclic adenosine monophosphate and
adenosine triphosphate-sensitive K+-channel activity.
Jeppesen PB, Gregersen S, Poulsen CR, Hermansen K.
Department of Endocrinology and Metabolism, Aarhus University
Hospital, Denmark.

http://groups.yahoo.com/group/aspartameNM/message/1201
here's three more stevia abstracts: lowers blood pressure, Lee CN
2001 Dec: antiviral, Takashashi K 2001 Jan: antihyperglycemic,
Jeppesen PB, 2000 Feb: Murray 2005.08.07

http://groups.yahoo.com/group/aspartameNM/message/1199
yet three more stevia abstracts: mutagenic in bacteria, Terai T, 2002
July: lowers blood pressure in rats, Hsu YH, 2002 Jan:
antihyperglycaemic, insulinotropic and glucagonostatic benefits in
rats, Jeppesen PB 2002 Jan; Murray 2005.08.07

http://groups.yahoo.com/group/aspartameNM/message/1198
three more stevia abstracts: no genotoxicity in mice, Sekihashi K,
Saitoh H, Sasaki Y 2002 Dec: lowers blood pressure in dogs,
Liu JC 2003 Jan: inhibits tumors in mice, Yasukawa K 2002 Nov:
Murray 2005.08.05

http://groups.yahoo.com/group/aspartameNM/message/1197
three abstracts on expert stevia research: hypertension, Chan P
2000 Sept; microflora, Gardana C 2003.10.22; helps blood pressure
and glucose level, Jeppesen PB 2003 Mar: Murray 2005.08.05

http://groups.yahoo.com/group/aspartameNM/message/1196
Alan in alt.support.diabetes re Stevia and Glycemic and Hypertension
Control 2004.05.14: 2 year large scale blood pressure study,
Hsieh MH, 2003 Nov: insulin in muscles, Lailerd N 2004 Jan:
glucose in diabetics, Gregersen S 2004 Jan: Murray 2005.08.04

http://groups.yahoo.com/group/aspartameNM/message/1179
Stevia (stevioside) is safe: Prof. Jan M.C. Geuns: Murray 2005.07.06

http://groups.yahoo.com/group/aspartameNM/message/1084
26 stevia safety abstracts since 1993: aspartame vs stevia debate on
alt.support.diabetes, George Schmidt, OD: Murray 2004.05.25
____________________________________________________


"Of course, everyone chooses, as a natural priority, to enjoy
peace, joy, and love by helping to find, quickly share, and positively
act upon evidence about healthy and safe food, drink, and
environment."

Rich Murray, MA Room For All rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com  new primary archive

http://groups.yahoo.com/group/aspartameNM/messages
group with 127 members, 1,549 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1,124 members, 22,793 posts in a public archive
____________________________________________________


vinyl acetate, ethyl alcohol, or aspartame in womb increases later
cancers in adults with lifetime exposure in many studies,
M Soffritti et al, Ramazzini Foundation, Basic Clin. Pharm. Toxicol.
2008 Feb.: Murray 2008.02.01
http://rmforall.blogspot.com/2008_02_01_archive.htm
Friday, February 1, 2008
http://groups.yahoo.com/group/aspartameNM/message/1509

http://groups.yahoo.com/group/aspartameNM/message/1453
Souring on fake sugar (aspartame), Jennifer Couzin,
Science 2007.07.06: 4 page letter to FDA from 12 eminent
USA toxicologists re two Ramazzini Foundation cancer studies
2007.06.25: Murray 2007.07.18

http://groups.yahoo.com/group/aspartameNM/message/1503
Devra Lee Davis, U. Pittsburgh Cancer Institute, rejects aspartame
-- Luke Ravenstahl, Mayor, drinks 12 cans Diet Pepsi daily:
accurate warning by Ronald K. Frazer: Murray 2008.01.13
http://rmforall.blogspot.com/2008_01_01_archive.htm
Sunday, January 13, 2008

methanol impurity in alcohol drinks [ and aspartame ] is turned
into neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol
Syndrome, BM Kapur, DC Lehotay, PL Carlen at U. Toronto,
Alc Clin Exp Res 2007 Dec. plain text: detailed biochemistry,
CL Nie et al. 2007.07.18: Rich Murray 2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524

http://groups.yahoo.com/group/aspartameNM/message/1459
third study by expert Greek team of neurotoxicity in infant rats by
aspartame (or its parts, methanol, phenylalanine, aspartic acid), KH
Schulpis et al, Food Chem Toxicol 2007.06.16: Murray 2007.08.05

http://groups.yahoo.com/group/aspartameNM/message/782
Smith, Terpening, Schmidt, Gums: full text: aspartame, MSG,
fibromyalgia: Murray 2002.01.17
Jerry D Smith, Chris M Terpening,
Siegfried OF Schmidt, and John G Gums
Relief of Fibromyalgia Symptoms Following
Discontinuation of Dietary Excitotoxins.
The Annals of Pharmacotherapy 2001; 35(6): 702-706.
Malcolm Randall Veterans Affairs Medical Center,
Gainesville, FL, USA.
BACKGROUND: Fibromyalgia is a common rheumatologic
disorder that is often difficult to treat effectively.
CASE SUMMARY: Four patients diagnosed with fibromyalgia
syndrome for two to 17 years are described.
All had undergone multiple treatment modalities with limited success.
All had complete, or nearly complete, resolution of their symptoms
within months after eliminating monosodium glutamate (MSG)
or MSG plus aspartame from their diet.
All patients were women with multiple comorbidities prior to
elimination of MSG.
All have had recurrence of symptoms whenever MSG is ingested.

Siegfried O. Schmidt, MD Asst. Clinical Prof. siggy@...
Community Health and Family Medicine, U. Florida, Gainesville, FL
Shands Hospital West Oak Clinic Gainesville, FL 32608-3629
352-376-5071


Avoiding formaldehyde allergic reactions in children, aspartame,
vitamins, shampoo, conditioners, hair gel, baby wipes,
Sharon E Jacob, MD, Tace Steele, U. Miami, Pediatric Annals
2007 Jan.: eyelid contact dermatitis, AM Hill, DV Belsito,
2003 Nov.: Murray 2008.03.27
http://rmforall.blogspot.com/2008_03_01_archive.htm
Thursday, March 27, 2008
http://groups.yahoo.com/group/aspartameNM/message/1532

"It is generally recommended that exposure to products containing
formaldehyde, FRP's, and aspartame (NutraSweet) be avoided
in children."

"Through metabolism, aspartame is converted metabolically
in the liver to methanol,
which is in turn metabolized to formaldehyde. 8"

www.pediatricannalsonline.com/showPdf.asp?rID=21306

Avoiding formaldehyde allergic reactions in children
Pediatric Annals. 2007 Jan.; 36(1): 55-6. PMID: 17269284
Sharon E. Jacob, MD, Director, Contact Dermatitis Clinic,
Dept. of Dermatology and Cutaneous Surgery, U. of Miami,
1295 NW 14th St., Miami, FL 33125, fax 305-243-6191

formaldehyde from many sources, including aspartame, is major
cause of Allergic Contact Dermatitis, SE Jacob, T Steele,
G Rodriguez, Skin and Aging 2005 Dec.: Murray 2008.03.27
http://rmforall.blogspot.com/2008_03_01_archive.htm
Thursday, March 27, 2008
http://groups.yahoo.com/group/aspartameNM/message/1533

Sharon E. Jacob, MD
Assistant Professor of Medicine (Dermatology)
University of California, San Diego 200 W. Arbor Drive #8420
San Diego, CA 92103-8420
Tel: 858-552-8585 ×3504 Fax: 305-675-8317
sjacob@...;

"For example, diet soda and yogurt containing aspartame
(Nutrasweet), release formaldehyde in their natural biological
degradation.

One of aspartame's metabolites, aspartic acid methyl ester,
is converted to methanol in the body, which is oxidized to
formaldehyde in all organs, including the liver and eyes. 22

Patients with a contact dermatitis to formaldehyde have been seen
to improve once aspartame is avoided. 22

Notably, the case that Hill and Belsito reported had a 6-month
history of eyelid dermatitis that subsided after 1 week of avoiding
diet soda. 22"

"We present a case of a medical student who presented with
erythematous eczematoid plaques on her trunk and legs and
fine vesiculation of her scalp, 3 weeks after starting anatomy class.

Of note, she routinely washed her face and arms after leaving the
anatomy lab, but remained in her scrubs for the rest of the day.

Formaldehyde and Quaternium-15 positive reactions
in the same patient."

"Our patient underscores the importance of appropriate patch
testing and education.
Once we identified the allergy to formaldehyde and quaternium-15,
we provided patient education materials regarding the common and
not-so-common locations of these chemicals and cross-reactors.
We also gave the patient information on avoidance
and safe alternatives (see Table 5).

Fortunately, with technical advances, this student completed the
anatomy section via electronic learning tools.

By avoiding formaldehyde, including anatomy lab, FRP
in her shampoo and cosmetics,
and aspartame in her diet, this patient dramatically improved.

As with all contact dermatitides, the mainstay of treatment for
allergic contact dermatitis is avoidance."

http://www.skinandaging.com/article/5158
Allergen Focus:
Focus on T.R.U.E. Test Allergens #21, 13 and 18:
Formaldehyde and Formaldehyde-Releasing Preservatives
Skin & Aging, ISSN 1096-0120; 13(12) 2005 Dec.: 22-27.
Sharon E. Jacob, M.D.,
Tace Steele, B.A.,
and Georgette Rodriguez, M.D., M.P.H.   ]


two aspartame (methanol, formaldehyde, formic acid) toxicity
research studies by Resia Pretorius, U. Pretoria, South Africa,
debate with JD Fernstrom: Murray 2008.04.04 2008.05.22
http://rmforall.blogspot.com/2008_04_01_archive.htm
Friday, April 4, 2008
http://groups.yahoo.com/group/aspartameNM/message/1536

http://foodqualitynews.com/news/ng.asp?n=84424-aspartame-sweetener
recent news re E Pretorius aspartame and brain review

Direct and indirect cellular effects of aspartame on the brain.
Humphries P, Pretorius E, Naude H, U. Pretoria, South Africa,
Eur J Clin Nutr. 2007 Aug 8: Murray 2007.08.12
http://groups.yahoo.com/group/aspartameNM/message/1463

"The aim of this study was to discuss the direct and indirect
cellular effects of aspartame on the brain,
and we propose that excessive aspartame ingestion
might be involved in the pathogenesis
of certain mental disorders (DSM-IV-TR 2000)
and also in compromised learning and emotional functioning."

Eur J Clin Nutr. 2007 Aug 8; [Epub ahead of print]
Direct and indirect cellular effects of aspartame on the brain.
Humphries P,
Pretorius E, resia.pretorius@...;
Naude H.
[1] Department of Anatomy, University of Pretoria,
Pretoria, Gauteng, South Africa
[2] Department of Anatomy, University of the Limpopo,
South Africa.

The use of the artificial sweetener, aspartame, has long been
contemplated and studied by various researchers, and people are
concerned about its negative effects.

Aspartame is composed of phenylalanine (50%),
aspartic acid (40%) and methanol (10%).

Phenylalanine plays an important role in neurotransmitter regulation,
whereas aspartic acid is also thought to play a role as an excitatory
neurotransmitter in the central nervous system.

Glutamate, asparagines and glutamine are formed from their
precursor, aspartic acid.

Methanol, which forms 10% of the broken down product,
is converted in the body to formate,
which can either be excreted or can give rise to formaldehyde,
diketopiperazine (a carcinogen) and a number of other highly toxic
derivatives.

Previously, it has been reported that consumption of aspartame
could cause neurological and behavioural disturbances in sensitive
individuals.

Headaches, insomnia and seizures are also some of the neurological
effects that have been encountered, and these may be accredited to
changes in regional brain concentrations of catecholamines,
which include norepinephrine, epinephrine and dopamine.

The aim of this study was to discuss the direct and indirect
cellular effects of aspartame on the brain,
and we propose that excessive aspartame ingestion
might be involved in the pathogenesis
of certain mental disorders (DSM-IV-TR 2000)
and also in compromised learning and emotional functioning.

European Journal of Clinical Nutrition advance online publication,
8 August 2007; doi:10.1038/sj.ejcn.1602866.
PMID: 17684524

Keywords: astrocytes; aspartame; neurotransmitters; glutamate;
GABA; serotonin; dopamine; acetylcholine

Received 25 October 2006; revised 26 April 2007;
accepted 27 April 2007
Correspondence: Professor E Pretorius, Department of Anatomy,
University of Pretoria, BMW Building, Dr Savage Street,
PO Box 2034, Pretoria 0001,
Gauteng, South Africa.  E-mail: resia.pretorius@...

c 2007 Nature Publishing Group,
All rights reserved  0954-3007/07
$30.00  www.nature.com/ejcn


http://groups.yahoo.com/group/aspartameNMmessage/1452
phenylalanine and aspartic acid from low dose aspartame in rabbits
interfere with blood coagulation, Pretorius E and Humphries P,
U. of Pretoria, Ultrastruct Pathol 2007 March: Murray 2007.07.14

" The authors conclude by suggesting that aspartame usage
may interfere with the coagulation process
and might cause delayed fibrin breakup after clot formation.

They suggest this,
as the fibrin networks from aspartame-exposed rabbits
are more complex and dense,
due to the netlike appearance of the minor, thin fibers.

Aspartame usage should possibly be limited
by people on anti-clotting medicine
or those with prone to clot formation. "

Ultrastruct Pathol. 2007 Mar-Apr; 31(2): 77-83.
Ultrastructural changes to rabbit fibrin and platelets
due to aspartame.
Pretorius E,
Humphries P.
Department of Anatomy, Faculty of Medicine,
University of Pretoria, South Africa.
[ Humphries P also at
Department of Anatomy, University of Limpopo.
Medunsa Campus, Garankuwa. South Africa ]

email: E. Pretorius resia.pretorius@...
*Correspondence to E. Pretorius,
BMW Building, PO Box 2034,
Faculty of Health Sciences,
University of Pretoria, Pretoria 0001, South Africa

The coagulation process, including thrombin, fibrin,
as well as platelets,
plays an important role in hemostasis,
contributing to the general well-being of humans.

Fibrin formation and platelet activation are delicate processes
that are under the control of many small physiological events.

Any one of these many processes
may be influenced or changed by external factors,
including pharmaceutical or nutritional products, e.g.,
the sweetener aspartame (L-aspartyl-L-phenylalanine methyl ester).

It is known that phenylalanine is present at position P(9)
and aspartate at position P(10)
of the alpha-chain of human fibrinogen,
and plays an important role in the conversion of fibrinogen to fibrin
by the catalyst alpha-thrombin.

The authors investigate the effect of aspartame
on platelet and fibrin ultrastructure,
by using the rabbit animal model
and the scanning electron microscope.

Animals were exposed to 34 mg/kg of aspartame
26x during a 2-month period.

Aspartame-exposed fibrin networks appeared denser,
with a thick matted fine fiber network
covering thick major fibers.

Also, the platelet aggregates appeared more granular
than the globular control platelet aggregates.

The authors conclude by suggesting that aspartame usage
may interfere with the coagulation process
and might cause delayed fibrin breakup after clot formation.

They suggest this,
as the fibrin networks from aspartame-exposed rabbits
are more complex and dense,
due to the netlike appearance of the minor, thin fibers.

Aspartame usage should possibly be limited
by people on anti-clotting medicine
or those with prone to clot formation.
PMID: 17613990
____________________________________________________


http://groups.yahoo.com/group/aspartameNM/message/1426
ASDA (unit of Wal-Mart Stores WMT.N) and Marks & Spencer
will join Tesco and also Sainsbury to ban and limit aspartame,
MSG, artificial flavors dyes preservatives additives, trans fats, salt
"nasties" to protect kids from ADHD: leading UK media:
Murray 2007.05.15

http://groups.yahoo.com/group/aspartameNMmessage/1451
Artificial sweeteners (aspartame, sucralose) and coloring agents
will be banned from use in newly-born and baby foods,
the European Parliament decided: Latvia ban in schools 2006:
Murray 2007.07.12

http://groups.yahoo.com/group/aspartameNM/message/1341
Connecticut bans artificial sweeteners in schools, Nancy Barnes,
New Milford Times: Murray 2006.05.25
____________________________________________________


http://groups.yahoo.com/group/aspartameNM/message/1469
highly toxic formaldehyde, the cause of alcohol hangovers, is
made by the body from 100 mg doses of methanol from
dark wines and liquors, dimethyl dicarbonate, and aspartame:
Murray 2007.08.31

http://groups.yahoo.com/group/aspartameNM/message/1052
DMDC: Dimethyl dicarbonate 200mg/L in drinks adds
methanol 98 mg/L ( becomes formaldehyde in body ):
EU Scientific Committee on Foods 2001.07.12:
Murray 2004.01.22

http://europa.eu.int/comm/food/fs/sc/scf/out96_en.pdf

"...DMDC was evaluated by the SCF in 1990 and considered
acceptable for the cold sterilization of soft drinks and fruit juices
at levels of addition up to 250 mg/L (1)
...DMDC decomposes primarily to CO2 and methanol ...

[ Note: Sterilization of bacteria and fungi is a toxic process,
probably due to the inevitable conversion in the body of methanol
into highly toxic formaldehyde and then formic acid. ]

The use of 200 mg DMDC per liter would add 98 mg/L
of methanol to wine which
already contains an average of about 140 mg/L from natural sources.

http://groups.yahoo.com/group/aspartameNM/message/1286
methanol products (formaldehyde and formic acid) are main cause
of alcohol hangover symptoms [same as from similar amounts of
methanol, the 11% part of aspartame]: YS Woo et al, 2005 Dec:
Murray 2006.01.20

http://groups.yahoo.com/group/aspartameNM/message/1508
formaldehyde in FEMA trailers and other sources (aspartame,
dark wines and liquors, tobacco smoke): Murray 2008.01.30
http://rmforall.blogspot.com/2008_01_01_archive.htm
Wednesday, January 30, 2008

http://groups.yahoo.com/group/aspartameNM/message/1490
details on 6 epidemiological studies since 2004 on diet soda (mainly
aspartame) correlations, as well as 14 other mainstream studies
on aspartame toxicity since summer 2005: Murray 2007.11.27

http://groups.yahoo.com/group/aspartameNM/message/1340
aspartame groups and books:
updated research review of 2004.07.16: Murray 2006.05.11

http://groups.yahoo.com/group/aspartameNM/message/1143
methanol (formaldehyde, formic acid) disposition:
Bouchard M et al, full plain text, 2001:
substantial sources are degradation of fruit pectins,
liquors, aspartame, smoke: Murray 2005.04.02
____________________________________________________

Eat Your Heart Out, Felicity Lawrence expose on breakfast cereals and other
major junk food scams by global corporations, The Guardian, UK: Murray
2008.07.05
http://rmforall.blogspot.com/2008_07_01_archive.htm
Saturday, July 5, 2008
http://groups.yahoo.com/group/aspartameNM/message/1548
___________________________________________________


http://books.guardian.co.uk/extracts/story/0,,2285846,00.html

This is an edited extract from Eat Your Heart Out:
Why The Food Business Is Bad For The Planet And Your Health,
by Felicity Lawrence, to be published on June 26 by Penguin.
To order a copy for £ 8.99, with free UK p&p, call 0870 836 0875
or go to guardian.co.uk/bookshop

Drop that spoon!

Britain is one of the world's largest consumers of puffed, flaked and
sugared breakfast cereals. How did that happen when many were said to
contain less nutrition than the boxes they come in?

Felicity Lawrence investigates

Saturday June 14, 2008, The Guardian

Cornflakes in a bowl with a spoon
Cornflakes with spoon: J Garcia/Corbis [ photo ]

How did it all begin? It was one of those things that crept up on us and we
still can't quite believe happened. Looking back, we'd been in denial for
some time. Then a friend who hadn't seen the family for a while blurted out
the bald truth. "God, Dodi's got rather fat. In fact, you know, I think that
might count as obese."

Once said, it had to be admitted. If you looked at Dodi from behind when he
was sitting down, you could see a substantial spare tyre around his
13-year-old middle. It bulged out from his hips and flopped down like a
muffin rising out over its baking case. He had become quite lazy, too,
preferring to lounge in front of the fire rather than play in the garden as
he used to. His excess weight was slowing him down. His joints seemed stiff
as he climbed the stairs.

He had been hooked on a particular brand of instant meal for ages.
Guaranteed real tuna, the packaging said. Enriched with omega-3 and 6 fats!
What was inside, however, did not have much to do with tuna -- 10% minimum,
according to the small print.

It was largely rendered poultry meal mixed with corn gluten meal, ground
rice, soya oil and dried beet pulp.

Dodi is our cat, and we know cats do not normally eat carbohydrates such as
ground rice or sugar, nor corn, nor vegetable oils. Nevertheless, that's
what we had been feeding him. It said on the packet that it was
"scientifically formulated", after all.

The absurdity of feeding an animal something that it never evolved to eat
and that actually makes it fat and sick ought to be easy enough to see.

But we had not been alone in our blindness, apparently -- feline diabetes
has risen dramatically in the past few years in the UK.

Where the human diet is concerned, a similar myopia seems to have descended
upon the British. Instead of relying on a food culture developed over
centuries, we have come to defer to the pseudo-scientific instructions of
professionals.

Where did it all go wrong?

The rise of breakfast cereal makes a revealing case study of the
evolutionary process behind the modern diet. One of the earliest convenience
foods, processed cereals represent a triumph of marketing, packaging and US
economic policy. They are the epitome of cheap commodity converted by
manufacturing to higher-value goods; of agricultural surplus turned into
profitable export. Somehow, they have wormed into our confused consciousness
as intrinsically healthy, when, by and large, they are degraded foods that
have to have any goodness artificially restored.

When the first National Food Survey was conducted in 1863, it questioned 370
families of the "labouring poor" and found that breakfast consisted
variously of tea kettle broth (bread soaked in hot milk and salt), bread and
butter, bread and cheese, milk gruel, bread and water, and oatmeal and milk
porridge. Today, however, the British and the Irish are the largest eaters
of puffed, flaked, flavoured, shaped, sugared, salted and extruded cereals
in the world. We munch an average of 6.7kg of the dehydrated stuff per
person per year in the UK, and 8.4kg each in Ireland.

The Mediterraneans, generally credited with a healthy diet, have so far kept
this form of instant breakfast down to an average 1 kg per person per year.
The eastern Europeans, deprived of marketing until the fall of communism,
consume only a few grams each a year. Yet the British have succumbed almost
entirely to this American invention, with the result that 97% of households
today have at least one packet of cereal in their cupboards.

How can such a radical change have come about? Was there something
peculiarly susceptible about the British that led to it? To find out, I went
to the US, to the midwest states that are the heartland of industrial corn
production and to the home of the first cornflakes.

Prepackaged and ready-to-eat breakfast cereals began with the American
temperance movement in the 19th century. In the 1830s, the Reverend
Sylvester Graham preached the virtues of a vegetarian diet to his
congregation, and in particular the importance of wholemeal flour.
Meat-eating, he said, excited the carnal passions. Granula, considered the
first ready-to-eat breakfast cereal, was developed from his "Graham flour"
by one of his followers, James Caleb Jackson. It was a baked lump of
slow-cooked wheat and water that had to be soaked overnight to make it soft
enough to be edible. It was sold at 10 times the cost of its ingredients.
The business motive for proselytising by breakfast cereal was established.

After Jackson's invention, the Seventh-Day Adventists took up the mission. A
colony of them had set up in a small town called Battle Creek near the
American Great Lakes in Michigan. There, in 1866, they established the
Western Health Reform Institute to cure hog-guzzling Americans of their
dyspepsia and vices. John Harvey Kellogg turned it into the famous Battle
Creek Sanitarium, where he set about devising cures for what he believed
were the common ills of the day, in particular constipation and
masturbation. In Kellogg's mind, the two were closely linked, the common
cause being a lack of fibre, both dietary and moral.

Kellogg experimented in the sanitarium kitchen to produce an easily digested
form of cereal. Together with his wife and his younger brother, William
Keith, he came up with his own highly profitable Granula, but was promptly
sued by Jackson, the original maker of Granula, and had to change the name
to Granola.

Around the same time, an entrepreneur called Henry Perky had also invented a
way of passing steamed wheat through rollers to form strands that could be
pressed into biscuits to make the first shredded wheat. JH Kellogg
experimented further with his team, and eventually they found a way of
rolling cooked wheat to make flakes that could then be baked. Cornflakes
followed when the Kelloggs worked out how to use cheap American corn instead
of wheat, although initially they had problems keeping them crisp and
preventing them from going rancid. This great leap forward is of a piece
with other major developments in the industrialisation of our diets: it is
usually the combination of technological advances and the right economic
conditions that lead to major changes in what we eat.

It was a chronically dyspeptic businessman and former patient of Kellogg's
at the sanitarium who unleashed the power of marketing on breakfast. Charles
Post set up the rival La Vita Inn in Battle Creek and developed his own
versions of precooked cereals. "The sunshine that makes a business plant
grow is advertising," he declared, promoting his cereals with paid-for
testimonials from apparently genuine happy eaters. He also cheerfully
invented diseases that his products could cure. Grape Nuts were miraculously
marketed at the time both as "brain food" and also as a cure for consumption
and malaria. They were even, despite their enamel-cracking hardness, said to
be an antidote to loose teeth.

By 1903, Battle Creek had turned into a cereal Klondike. At one point there
were more than 100 cereal factories operating in the town, many making
fabulously exaggerated claims about the health benefits of their products.
The symbiotic relationship between sales, health claims and the promotion of
packaged breakfast cereals has continued ever since.

The Kelloggs had tried unsuccessfully to protect their flaking process with
patents. When William Keith saw how much others were making from the new
foods, he launched his own advertising campaign, giving away free samples
and putting ads in newspapers.

Global expansion quickly followed. Britain saw its first cornflakes in 1924,
when the company set up offices in London and used unemployed men and Scouts
to act as a sales force for the imported cereal. By 1936 UK sales topped £
1m, and Kellogg's was ready to open its first British manufacturing plant in
Manchester in 1938.

The technology used to make industrial quantities of breakfast cereal today
is essentially the same as that developed from the kitchen experiments of
those fundamentalist healers, although new ways have been found to add the
sugar, salt and flavourings. Flavour and vitamins lost in processing may be
put back during processing or sprayed on to the finished cereal product.

Worries about the nutritional value of such highly processed grains surfaced
early. Post's company was one of the first to begin the heavy-duty
presweetening of cereals with sugar coating in the late 40s. The sales were
enviable. The Kellogg company, however, held back. The charitable Kellogg
Foundation, which by then had been set up to promote children's health and
education, was a major shareholder and was, it is said, concerned that
flogging sugar coatings to the young may not be compatible with its purpose.

Many of the health benefits claimed for breakfast cereals depended on
fortification rather than on micronutrients from the raw ingredients, most
of which were either destroyed by the process or stripped away before it.
The earliest fortification was with vitamin D, the so-called sunshine
vitamin, and acted as a marketing tool. Today, a new wave of fortification
is coming.

Inulin, a form of fibre from plants, known to the food industry until
recently as a cheap bulking agent, thanks to its ability to retain water and
mimic the "mouthfeel" of fats, is now added as a "prebiotic". What this
means is that it resists digestion in the upper gastrointestinal tract and
reaches the large intestine almost intact, where it is fermented by
bacteria, encouraging the production of friendly microflora. The inulin, in
other words, does what the fibre naturally occurring in wholegrains would do
if it hadn't been stripped out by overprocessing.

Companies are also looking at adding omega-3 fatty acids such as DHA. There
are technical difficulties with this, however, not least that since the DHA
tends to come from fish, it makes things taste fishy.

All the technology at their disposal has not helped the manufacturers deal
with one serious problem, though.

Industrial cereal processing produces acrylamide, a chemical compound that
is known to cause cancer in animals and was classified as a probable human
carcinogen in 1994. The trade magazine Food Manufacture wrote nervously in
2006 that acrylamide could be "the next food scare round the corner". Since
then, further research has confirmed a link between acrylamide intake from
food and cancer.

Those eating 40 micrograms of acrylamide a day were twice as likely to get
cancer of the ovary or womb as those who had low intakes.

Some other processed foods contain much higher doses of acrylamide, but even
so, tests by the UK's Food Standards Agency a few years ago suggested that a
serving of breakfast cereal could contribute about nine micrograms.

The FSA's advice to consumers on processed foods was blandly reassuring --
no need to change their diet, the industry would be working to reduce the
formation of acrylamide. The European food and drink industry association,
the CIAA, has compiled a toolbox on acrylamide for manufacturers, and from
it you get a sense of the huge effort that is going into industrial pilots
to see how acrylamide levels could be reduced. But there are no easy
answers, and sometimes the toolbox makes clear that the ways of lowering
acrylamide may just be incompatible with making these types of products.

That processed cereals had become little more than sugary junk with milk and
vitamins added was an accusation made as long ago as 1970, when Robert
Choate, an adviser to President Nixon on nutrition, told a congressional
hearing into breakfast cereals that the majority "fatten but do little to
prevent malnutrition". Choate was outraged at the aggressive targeting of
children in breakfast cereal advertising. He analysed 60 well-known cereal
brands and concluded that two-thirds offered "empty calories, a term thus
far applied to alcohol and sugar".

Rats fed a diet of ground-up cereal boxes with sugar, milk and raisins were
healthier than rats fed the cereals themselves, he testified to senators.

Battle Creek today is a backwater in Michigan, three hours' drive from
Chicago. There is not much sign now of the cereal gold rush that changed the
British palate, and the flake factories have mostly gone. But the legacy
lives on. In their place alongside Kellogg airport and the Kellogg
Foundation is Kellogg's Cereal City. Built in the shape of an old grain
store, the museum is a testament to the power of marketing that so maddened
Choate. Walking through the collection, I was struck by how much our
breakfast today is the child of advertising.

One of my favourite sections was the cabinet of boxes and pamphlets
recording the original health claims that anticipate today's persuasive
messages. "Keeps the blood cool!" "Makes red blood redder!" Then there were
the cereals that echoed today's claims for prebiotics: "Will correct stomach
troubles!" or indeed mirrored claims made on my cat food: "The most
scientific food in the world!"

Getting children hooked, making them associate breakfast cereal with fun and
entertainment, were among the main aims of competing manufacturers from the
early days. Kellogg's sponsored a children's programme called The Singing
Lady. In 1931, the artist Vernon Grant heard the programme and was inspired
to draw the Kellogg's Rice Krispies ad characters Snap, Crackle and Pop. His
cartoon characters were used in ad campaigns that catapulted Rice Krispies
sales up into the league of the more established cornflakes brands.

Cereal advertising likewise helped shape early television. Using
"motivational research" to work out how to appeal to women and children with
different kinds of packaging, Kellogg's broadcast the first colour TV
programmes and commercials for children. The result was that by the mid-50s
the company had captured nearly half the US processed cereal market and was
in a prime position to build its empire in Europe.

The UK market for cereal was worth more than £ 1.27 bn in 2005. It, too, has
been created and maintained by advertising. Kellogg's has consistently been
the largest advertiser of cereal in this country, spending roughly £ 50 m a
year in recent years, about twice as much as its rival, Cereal Partners (a
joint venture with Nestlé). Without advertising, we might never know we
needed processed cereal and revert to porridge or bread instead. Or, as
Kellogg's European president Tim Mobsby put it to MPs conducting an inquiry
into obesity in 2004, "If we were not to have that capability [of TV
advertising], there is a probability that the consumption of cereals would
actually drop."

The following spring I was one of a handful of reporters flown in a private
jet by Kellogg's to its Old Trafford cornflakes factory, as part of its
campaign to protect its portfolio and its ability to market it, particularly
to children. The ostensible reason for the trip was that Kellogg's was
launching a new product in the UK -- Kashi, a brand of mixed-grain puffed
cereal free of all additives. But criticism of the food industry for selling
products high in fat, salt and sugar had reached a head, and the cereal
manufacturers were the subject of unwelcome attention.

Before touring the factory, we were ushered past a giant Tony the Tiger
cutout and into the strategic planning department for a presentation on
nutrition policy and labelling. Here, the company nutritionist explained
how, in response to pressure from the FSA, the Association of Cereal Food
Manufacturers had reduced salt by a quarter in five years. Cornflakes were
even tastier than before because you could taste the corn more now. So why
was there so much salt in the first place, we asked. The managing director
of Kellogg's Europe, Tony Palmer, confessed that "if we'd known you could
take out 25 % of the salt and make cornflakes taste even better, we would
have done it earlier. But it's also about the interaction with the sugar --
as you take the salt out, you've got to reduce the sugar because it starts
to taste sweeter."

But isn't the target to reduce sugar consumption, too? Why not just cut down
on salt and sugar, we wondered. Well, sugar helps keep the crispness and is
part of the bulk, so that would be difficult, we were told. Palmer's
eyebrows started working furiously as he answered: "And the risk is, if you
take the salt out, you might be better off eating the cardboard carton for
taste."

The public relations team moved us rapidly on from this unfortunate echo of
Senator Choate's observations about rats to a presentation on the Kashi Way.
"We hold the spirit of health in all we do," one of them explained, echoing
this time the quasi-religious marketing babble of the founding cereal
makers. Since this was a puffed cereal, what levels of acrylamide did it
contain, I wondered. No one was sure, but they'd come back to me, they said.
They never did. Perhaps they thought I had lost interest.

The industry is adamant that its products are a healthy way to start the
day, and has recruited Professor Tom Sanders, head of the nutrition
department at King's College London, to defend "breakfast cereals served
with semi-skimmed milk" as "low-energy meals that provide about one fifth of
the micronutrients of children".

However, Cereal Reoffenders, a survey published by the consumer watchdog
Which?, took a rather different view. When it analysed 275 big-name
breakfast cereals from leading manufacturers on sale in UK supermarkets in
2006, it found that 75% had high levels of sugar while almost a fifth had
high levels of salt, according to criteria drawn up by the Food Standards
Agency for its traffic-light nutritional labels. Several cereals making
claims to be good for you got a red light, too. All-Bran was high in salt;
Special K got a red for sugar and salt. Some high-fibre bran cereals were
giving you more salt per serving than a bag of crisps. Some products may
have been reformulated since the report to reduce salt and sugar.

Back at Battle Creek's museum, you can see Kellogg's vision for the future.
Before exiting the exhibition into the shop, where visitors enter into the
spirit by sporting strings of Fruit Loops as headbands, I passed a section
on "global expansion". As well as advertising in new markets, it revealed,
Kellogg's has been sponsoring school nutrition programmes and health
symposia for professionals. This activity is part of a "massive programme of
nutrition education directed at improving the world's eating habits".

With 90 % of breakfast cereal consumed in just a handful of countries, the
company that helped to transform the British diet "has rededicated itself to
reaching 1.5 billion new cereal customers around the world in the next
decade".

Improving the world's eating habits has the attraction, as the 19th-century
American entrepreneurs discovered, of being what economic analysts call a
"high-margin-to-cost business". The raw materials of breakfast cereals,
commodity grains, have been kept cheap for decades thanks to government
subsidies (although biofuels, a new focus for support, has changed the
equation recently).

US agricultural subsidies totalled $ 165 bn (£ 83.75 bn) in the years
between 1995 and 2005. Just five crops accounted for 90 % of the money -
corn, rice, wheat, soya beans and cotton. If you want to understand why all
those commodities, cotton aside, make it in to most of the processed foods,
this is where you have to start.

One of the biggest costs in cereal manufacture is not the value of the
ingredients nor the cost of production, but the marketing.

About a quarter of the money you spend on breakfast cereal goes on the cost
of persuading you to buy it.

That still leaves room for gross profit margins on processed cereals that
are 40 % to 45 %.

Start selling this kind of processed diet to new consumers in China and
India, and your profits -- and those of the country that has dominated grain
exports and trading, the US -- will soar.


http://books.guardian.co.uk/reviews/politicsphilosophyandsociety/0,,2289278,00.h\
tml

Fred Pearce is the author of Confessions of an Eco Sinner (Eden Project
Books).

Politics, philosophy and society

Fat cats in our kitchen

Fred Pearce gets a glimpse inside the secretive world of the global food
industry

Saturday July 5, 2008, The Guardian

Eat Your Heart Out, by Felicity Lawrence, 352 p, Penguin, £ 8.99

With her last book, Not on the Label, the investigative journalist Felicity
Lawrence turned our stomachs: many people haven't eaten the same since.

Now she wants to exercise our frontal lobes by taking us on a journey to
find out who decides what we eat, and how they manage to foist so much
rubbish on us in the name of choice, health and, increasingly, the
environment.

It is a restless snap-crackle-and-pop ride, jaunty in places, rarely
preachy, always engaging. Lawrence is a guide we can trust, whether she is
in the Amazon soya fields or grabbing organic tucker at the local farmers'
market.

Defying the conventional boundaries of her trade, she is both sensible and
readable on everything from your bodily functions to Britain's archipelago
of tax havens, from American industrial history to the living conditions of
Italy's migrant workers (Médecins sans Frontières says these conditions
wouldn't be allowed in African refugee camps).

British businesses such as Tate & Lyle and Unilever feature frequently.

But three American combines turn up in every chapter. Cargill, the world's
largest privately owned corporation, Archer Daniels Midland and Bunge sit
like giant spiders in a web, brokering grain, soya, animal feed, cocoa,
biofuel, palm oil and chickens -- not to mention fertiliser, seeds and
cotton.

They provide the feedstock for the human race, and quality control is not
their strong point. They have, for instance, transformed the fats we eat,
with results we are still guessing about. The chemistry of the nerve cells
in our brains -- our fattiest organ, apparently -- is being reconfigured by
these godfathers of our industrialised diet.

Lawrence offers some good history, too. We learn how John Harvey Kellogg's
evangelical obsessions with constipation and masturbation, combined with a
keen commercial eye and Uncle Sam's Marshall Plan, brought cornflakes to the
masses. How margarine began as an adjunct to the soap industry, moved on to
waste beef tallow, then whale blubber and the products of King Leopold's
genocidal tyranny in the Congo -- all thanks to the British and Dutch
companies that eventually combined to form Unilever.

Then there is the story of how Kurt Berger, a British food technologist who
once employed Margaret Thatcher as an ice-cream innovator, went on to
persuade food manufacturers to put palm oil into almost every product you
eat. Goodbye, southeast Asia's rainforests. Persuasion is the name of the
game. Lawrence's dissection of the marketing of "probiotic" yoghurt drinks
is superb, revealing as dodgy a wheeze for extracting maximum "added value"
from milk as anything dreamed up by Kellogg.

Why do we buy this rubbish? Are we forced to? The supermarkets and food
combines insist we have never had so much choice, but the trouble is that
our senses of smell and taste and sight -- which have evolved to allow us to
decide what we eat -- are being deliberately confused and titillated by
modern processing and packaging.

Lawrence gives us some great journalistic set pieces. She spends a day with
Cow 777, a 10,000-litres-a-year milk-making machine in the Cotswolds. She
joins Polish peasant farmers waking up to the fact that joining the EU means
having an American industrial pig farm in your backyard. She tours
Midwestern cornfields in the wake of combine harvesters yoked one minute to
the world breakfast cereal business and the next to biofuels -- but always
to the task of turning a cheap commodity into a high-value must-have
product. She meets African migrants queuing for work in the tomato fields of
southern Italy. And she joins campaigners against a giant soya shipping
terminal in the Amazon that is speeding the destruction of the jungle in
order to feed Europe's chickens.

I would have liked to hear more from the people in the fields of the world.
The people who feed us, like the fruit farmers of Chile or the bean-growers
of Kenya. Not least because one of the subtexts of a book like this is that
we should go back to eating simple and eating local -- and cutting these
people and their products out of our lives.

But there is much to feast on as Lawrence journeys from her own fat cat
(page one finds her musing on the girth of her moggy) to find the fat cats
of the food business, laying bare mind-boggling madnesses, such as the
global pandemic of addiction -- there is no other sensible world for it --
to sugar.

"The genius of globalised capitalism," Lawrence concludes, "is not just to
give consumers what they want, but to make them want what it has to sell."
If this book has a fault it is that it does not get close enough to this
genius. But sadly this is a reclusive world. Lawrence never got through the
doors of Cargill, which has its European headquarters at Cobham in Surrey.

We all of us eat the products supplied by such companies every day of our
lives. Most of the molecules in our bodies come from them, but they won't
even talk to us about it.


http://www.whale.to/a/sanders_h.html

Professor Tom Sanders

[ T. A. B.  Sanders BSc, PhD, DSc (London), Professor of Nutrition &
Dietetics, King's College London (University of London).

An 'expert' promoting aspartame.

This was in the end paragraph, called 'The Verdict',  to an article looking
at aspartame.  See: Dr Vincent Marks, who promotes sugar. ]

"The key point is that we can help people to live healthier lives if they
can reduce their calorie intake.  Sweeteners (aspartame) have a valuable
role to play in the fight against obesity." -- Prof Tom Sanders, head of
nutritional science at King's College, London (Daily Mail Oct 12, 2004).

A real expert:

"How silly of you to think that Nutrasweet replaced sugar --  it didn't. It
increased the craving for sugar and the percentage of people overweight also
has increased. That couldn't be Nutrasweet's fault, could it? -- BEATING THE
FOOD GIANTS by Paul A. Stitt

Artificial Sweeteners Once Again Linked to Weight Gain -- Ditching your diet
foods could be one of the best weight loss moves you make.
http://articles.mercola.com/sites/35570.aspx

http://www.whale.to/a/experts.html  list of corporate "experts"

http://www.whale.to/a/medical_industry.html
The Medical Industry (aka Big Pharma, Medical Industrial Complex)

http://www.whale.to/  [ one-sided, but informative, rather conspiracy
minded ]
scu23@...;

http://www.whale.to/v/stitt_b.html

BEATING THE FOOD GIANTS
by Paul A. Stitt, Natural Ovens Bakery
4300 County Highway CR, Manitowoc, WI 54220
920-758-2500 800-558-3535

ACKNOWLEDGEMENTS, FOREWORD & INTRODUCTION
1.  THE FIGHT BEGINS
2.  INSIDE A FOOD GIANT
3.  EXPERIMENT
4.  "CAN'T EAT JUST ONE" SYNDROME
5.  THE NATURAL REVOLUTION
6.  HELPING YOURSELF
7.  TEN EASY STEPS TO BETTER HEALTH.
8.  BEATING THE FOOD GIANTS
9.  RECIPES
APPENDIX 1
             Why all bakers should make bread like Natural Ovens
              Food, Teens & Behaviour
             Why George Should Eat Broccoli
             Why Calories Don't Count!
APPENDIX 2: [Media Oct 2005] Addiction Coke
APPENDIX 3: [Media Aug 2005] OREO. Craving the cookie

Ever wonder why you often don't feel good, can't think, can't remember,
can't sleep and don't feel like working either. If you want the answer, just
read "Beating the Food Giants." Paul Stitt gives a first hand account of the
inside workings of the giant food companies of America. He tells how they
program you to crave certain foods, to overeat every day, to make you feel
stuffed but hungry, and how this "mad energy" of the food industry is
destroying you and what you can do about it.

Stitt tells how you can feel 10 years younger, how you can restart your life
and slowly by example of his own life, how you might be able to start your
own business and help other people at the same time.

According to the Wall Street Journal (April 21. 1993), the president of
Coca-Cola makes $4,051,000 a year and the president of Pepsi-Cola makes
$11,136,000 by making a fool of you. Topping that, the president of Nabisco
makes $3,061,000 for making products like Oreo cookies that you can't stop
eating and Ritz Crackers (more fat per ounce than pork chops). The man who
gets the best grade of all in fooling people is the president of Budweiser.
He makes over $16,000,000 for making products that relieve your inhibitions,
then makes you fall asleep even while driving a car at high speeds. Do you
really want to keep these men living in the style in which they are
accustomed?  If not, read this book.

ABOUT THE AUTHOR

Paul A. Stitt was born on a farm near Verona, Illinois, Oct. 10, 1940, and
has devoted his entire life to human nutrition. From gathering eggs and
feeding pigs as a boy, to his four years as a food scientist for Tenneco
Corporation and the Quaker Oats Company, to his development of three
patented protein-synthesis techniques, and finally to the establishment of
his nationally recognized bakery, Natural Ovens of Manitowoc, Paul has been
working to produce better foods and to inform the world about the dangers of
our processed diets.

He received his undergraduate degree in chemistry at Beloit College in 1962,
and his Master of Science Degree in bio­chemistry from the University of
Wiscon­sin at Madison in 1968. From 1968 to 1970 he worked in protein
research for Tenneco. Paul then did exploratory re­search for Quaker until
he was fired for insubordination in 1972. As a food scientist he learned
that the American food industry was out to deceive the public. It was his
constant insistence that the Food Giants produce nutritious, non-addictive
foods that irritated his employer and led to his eventual termination.

Paul spent the following three and a half years in independent research, and
in 1976 founded Natural Ovens of Manitowoc Bakery to prove that commercial
production of nutritious foods is feasible. Today Natural Ovens is one of
the nation's largest and fastest growing distributors of whole-grain breads
and natural foods.

http://www.whale.to/v/stitt_h.html

http://www.naturalovens.com

Quotes
"I would drink chlorinated water only if the alternative was no water at
all."

"How silly of you to think that Nutrasweet replaced sugar -- it didn't. It
increased the craving for sugar and the percentage of people overweight also
has increased. That couldn't be Nutrasweet's fault, could it?" -- BEATING
THE FOOD GIANTS by Paul A. Stitt

The swelling ranks of diabetics can consider themselves victims of the Food
Giants. BEATING THE FOOD GIANTS by Paul A. Stitt

"There is a force in this country that's out to poison your food, to make it
addictive, to manipulate your very body chemistry.  This conspiracy wants to
keep you overfed but undernourished.  Who's behind this conspiracy?  The
food giants."-- Paul Stitt

The public knows very little about nutrition. Instead, it pays attention to
the advertisements of the Food Giants. People buy what the food
conglomerates make them want. More than 70 % of weekday food advertisements
time is spent in hawking garbage. To the Food Giants, sales are more
important than nutrition. Mean­while, the customers are being brainwashed --
lulled into thinking that because we have a Department of Health and Human
Services that approves these processed foods, they must be good to eat.
They're tragically mistaken. The time has come for people to start reading
labels and paying attention to what they put in their bodies. BEATING THE
FOOD GIANTS by Paul A. Stitt

In his fascinating book, "Paradox of Plenty," Harvey Wallenstein give a
detailed explanation of the philosophy and growth of the food industry from
1930 to 1990. He lays out in explicit detail the corrupt thinking and proves
with thousands of referenced articles how the American food industry has put
packaging, flavor, advertising gimmicks, clowns, etc., ahead of the all
important reason for eating food -- nutrition. "Paradox of Plenty" is a
scholarly work that fully indicates the food industry as the super cause of
American obesity and runaway sickness costs. I recommend it as a "must
read."  BEATING THE FOOD GIANTS by Paul A. Stitt

  We'd shown that protein could be made from natural gas, that it could be
done successfully on a large scale, and that it could be done cheaply (a
pound would cost about 11 cents to produce, and would provide eight people
with 100 % of their protein needs for a day). And we had done it in one
year -- half the time we'd been allotted for completion!    ......
     When we were called into the vice president's office on the afternoon of
New Year's Eve, we expected a raise and a pat on the back.  ......
"Gentlemen," he said nonchalantly, "the Board of Directors has decided to
terminate your project, effective immediately." ........They were actually
firing us! .......Finally, when I could stand it no longer, I marshalled my
courage and called the president of Tenneco. How could they do this
senseless thing?
     "Friend," he told me, "if I had a whole mountain of protein, I wouldn't
have the slightest idea what to do with it. Who's gonna buy something like
that?"
     I was dumb struck. What about the starving millions? Was the profit
motive all that counted for anything? I told myself that it could not be so,
that somewhere there must be a company which would embrace the project and
develop it to full potential. But I was still naive, and I still believed
that the best way to make money was to make things people really needed.
BEATING THE FOOD GIANTS by Paul A. Stitt

[2003] The Real Cause of Heart Disease Is Not Cholesterol by  Paul Stitt
http://www.realcauseofheartdisease.com/aboutbook.htm

http://www.cbn.com/700club/guests/bios/paul_stitt_062504.aspx

... Paul says that is possible because the American food industry
deliberately makes food that does not satisfy. "It's hollow food, food that
has no substance to it," he says. That's why one feels hungry soon after
eating it. In their processing, the food companies take out the nutrients,
and add artificial flavorings and lots of sugar. They add stimulants that
create cravings. In the film Paul says Morgan eats 5,000 calories per day!
People can eat that many calories per day and still be hungry soon after
because the food is specially designed to do that. That seems to be
shortsighted on the part of the industry. Paul says they think in terms of
making as much money as they can today, not thinking about the long-term
effects of what they are doing.

Paul knows this subject firsthand because he worked for several major food
companies years ago and became alarmed at what he saw as unhealthy food
practices. Scientifically, he knew this was not the best way to process
food. When he voiced his concerns, he was ignored at best, called a crazy
radical at worst. He says they tried to ban him from speaking in the media
and on TV, but they could not since there is free speech in America.

He started his own company in 1976. "I predicted this epidemic of obesity 25
years ago," he says. "Now that there is an epidemic of obesity, many call me
now to speak at their conferences."

TRIED AND TRUE

In his film Morgan crosses the country talking to fast food customers,
visiting schools, and interviewing many experts. Paul says he came to
Morgan's attention when Morgan did a Web search to find a healthy school
lunch program. He found only one, which was the one in Wisconsin's Appleton
School District. In the movie Morgan shows what happens when things are done
right. This bright spot is the Peak Performance school lunch program created
by Paul and his wife, Barbara, which is now in its sixth year. "I am
delighted to be part of Super Size Me," he says. "Morgan has humorously
depicted in 96 minutes what has taken me 20 years to research."

Morgan highlighted an Illinois school lunch program where a plate of french
fries or a slice of pizza are daily fare -- much like the rest of the
nation's. Contrast that to Paul's program where burgers and soda machines
are out and salad bars and energy drinks are in. After removing every
vending machine, the school hired two cooks to prepare meals based on fresh
produce, whole grains, and energy drinks. School officials noted a decided
change in the students' behavior -- they are able to better focus in class
and they feel better.

"Kids are bombarded with fast food -- even in school," Paul says, "but I've
proven if you give them healthy alternatives, they'll make the right choice
and life-changing results will follow." Parents and educators need to accept
responsibility for our exploding childhood obesity problem. "So many kids
are suffering because they are obese and unhealthy," he says. In 1997 the
Stitts underwrote the $100,000 five-year program in Appleton's Central
Alternative High School for students identified as at-risk or with
discipline problems. The school district has plans to expand the program to
its 25 schools that serve 15,000 students.

VALUE

When asked if eating healthy costs too much, Paul puts this in perspective.
A loaf of whole grain bread averages $ 2.00 per loaf. Because this bread
feeds and satisfies the body, one slice per meal is enough. Three slices per
day (a loaf and a half) equals $ 3.00 per week, which totals $ 150 per year.
Whole grain bread provides 50 percent of all the nutrients you need. Add
some turnip greens, apples, bananas, chicken, or fish, and you have a
healthy, satisfying meal. Contrast that to spending at McDonald's (per the
movie) $ 27 per day on average -- that is $9 per meal -- and staying hungry.
That totals $ 850 per month. Paul says fast food gives you the perception of
being cheap, but it's not. To eat well you have to think ahead and plan. To
enjoy a healthy pot of beans, you have to start them the day before.

This is not high tech, he says, not gourmet, but just fresh fruits,
vegetables, and whole grains. Paul says the Lord put in food all we need to
stay healthy. We have to be wise in eating it.

Paul says he would like to encourage young people to start companies. Look
at the long-term benefits. All Natural Ovens' products are certified Kosher
Pareve by the Chicago Rabbinical Council Pas Yisroel.


http://clearingatkings.org/schools/biohealth/research/nutritional/staff/tsanders\
.html

Professor Tom AB Sanders BSc PhD DSc RPHNutr
Professor Tom Sanders Lecturer in Nutrition, Queen Elizabeth College/Kings
College London 1982- 1991
Reader in Nutrition, Kings College London 1991- 1994
Professor of Nutrition & Dietetics (established chair), Kings College London
October 1994-present

Head of the Department of Nutrition & Dietetics, Kings College London 1995-
2000
Head of Nutritional Sciences Division 2003-present
Tel: 44 (0)20 7848 4273, Fax: 44 (0)20 7848 4171,
E-mail: tom.sanders@...;
Franklin-Wilkins Building, 150 Stamford Street,
London SE1 9NH

Current Research Interests

The main focus of our research is on the mechanisms by which diet influences
risk of cardiovascular disease. Much of our research has been involved with
differentiating the effects of different types of fatty acids (trans fatty
acids, omega-6 and omega-3 polyunsaturated fatty acids, oleic acid, and
different chain length saturated fatty acids) as well as the relative
proportions of fat and type of carbohydrate on cardiovascular risk factors.

In addition to the work on dietary lipids and carbohydrates we have an
interest in the biologically active components in plant foods such as
isoflavones and flavonoids.

Wherever possible, we try to take a holistic view with regard to dietary
intake and are interested in the effects of overall dietary patterns.

We have a long-standing interest in comparing the health of vegans with
vegetarians, who consume milk and eggs, and omnivores, who eat meat/or fish
in addition to milk and eggs.

We also have an interest in the acute effects resulting from the consumption
of certain foods as well as the longer term effects.

Our group has specific expertise in the measurement of polyunsaturated fatty
acids and other lipids including eicosanoids.

Perhaps what differentiates the work of our group from other groups working
on dietary lipids is that we have tended to focus on the interaction between
the effects of dietary lipids and changes in haemostasis.

Our work was among the first to show that meals high in fat induce
activation of clotting factor VII and impair endothelial function.

Our most recent work in this area indicates that meals high in oleic acid
may have adverse effects on procoagulant activity and endothelial function
compared with meals containing stearic acid.

We endeavour to foster cross-disciplinary research and seek to work with
people with expertise that complements our own. We have much experience in
the design and execution of controlled dietary intervention trials.

Recently completed research includes OPTILIP which was a six-months dietary
intervention in 258 older men and women which compared the effects of
long-chain n-3 polyunsaturated fatty acids versus linolenic acid on
cardiovascular risk factors.

We also have an active programme of research investigating vegetarian
sources of long-chain n-3 polyunsaturated fatty acids derived from algae.

We are currently running two large dietary intervention trials. The RISCK
study is evaluating the effects of different levels of fat intake and
changes in the glycaemic index on insulin resistance and features of the
metabolic syndrome including vascular function.

DRFRUITNVEG study is a randomized controlled trial evaluating the effects of
increasing intakes of fruit and vegetable intake versus increased potassium
citrate intake on blood pressure and vascular function.

Most recent publications:

1. Sanders,T.A., Lewis,F., Slaughter,S., Griffin,B.A., Griffin,M.,
Davies,I., Millward,D.J., Cooper,J.A., & Miller,G.J. (2006)
Effect of varying the ratio of n-6 to n-3 fatty acids by increasing the
dietary intake of {alpha}-linolenic acid, eicosapentaenoic and
docosahexaenoic acid, or both on fibrinogen and clotting factors VII and XII
in persons aged 45-70 y: the OPTILIP Study.
Am J Clin Nutr, 84, 513-522.

2. Sanders,T.A., Gleason,K., Griffin,B., & Miller,G.J. (2006)
Influence of an algal triacylglycerol containing docosahexaenoic acid (22 :
6n-3) and docosapentaenoic acid (22 : 5n-6) on cardiovascular risk factors
in healthy men and women.
Br.J.Nutr., 95, 525-531.

3. Morkbak,A.L., Hvas,A.M., Lloyd-Wright,Z., Sanders,T.A., Bleie,O.,
Refsum,H., Nygaard,O.K., & Nexo,E. (2006)
Effect of vitamin B12 treatment on haptocorrin.
Clin Chem., 52, 1104-1111.

4. Sanders,T.A. & Berry,S.E. (2005)
Influence of stearic acid on postprandial lipemia and hemostatic function.
Lipids, 40, 1221-1227.

5. O'Neill,F.H., Sanders,T.A., & Thompson,G.R. (2005)
Comparison of efficacy of plant stanol ester and sterol ester: short-term
and longer-term studies.
Am J Cardiol., 96, 29D-36D

6. Rosell,M.S., Lloyd-Wright,Z., Appleby,P.N., Sanders,T.A., Allen,N.E., &
Key,T.J. (2005)
Long-chain n-3 polyunsaturated fatty acids in plasma in British meat-eating,
vegetarian, and vegan men.
Am.J.Clin.Nutr., 82, 327-334.
___________________________________________________



re "A Few too Many", Joan Acocella, The New Yorker,
long review of hangover research 2008.05.26 -- same levels of
formaldehyde and formic acid in FEMA trailers and other sources
(aspartame, dark wines and liquors, tobacco smoke):
Murray 2008.06.05
http://rmforall.blogspot.com/2008_06_01_archive.htm
Thursday, June 5, 2008
http://groups.yahoo.com/group/aspartameNM/message/1541

[ See also:
There really is no controversy, Adrienne Samuels PhD, letter re
evident toxicity of aspartame EJCN 2008.06.11:
Murray 2008.06.30
http://rmforall.blogspot.com/2008_06_01_archive.htm
Monday, June 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1546

former key Hillary Clinton staff Mark Penn and Patti Solis Doyle
use much neurotoxic aspartame Diet Coke -- also many other
politicians: Murray 2008.06.30
http://rmforall.blogspot.com/2008_06_01_archive.htm
Monday, June 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1545 ]


formaldehyde and formic acid in FEMA trailers and other sources
(aspartame, dark wines and liquors, tobacco smoke):
Murray 2008.01.30
http://rmforall.blogspot.com/2008_01_01_archive.htm
Wednesday, January 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1508

The FEMA trailers give about the same amount of formaldehyde
and formic acid daily as from a quart of dark wine or liquor,
or two quarts (6 12-oz cans) of aspartame diet soda,
from their over 1 tenth gram methanol impurity
(one part in 10,000), which the body quickly makes into
formaldehyde and then formic acid -- enough to be the major cause
of "morning after" alcohol hangovers.

Methanol and formaldehyde and formic acid also result from
many fruits and vegetables, tobacco and wood smoke, heater
and vehicle exhaust, household chemicals and cleaners, cosmetics,
and new cars, drapes, carpets, furniture, particleboard,
mobile homes, buildings, leather... so all these sources add up
and interact with many other toxic chemicals.

methanol impurity in alcohol drinks [ and aspartame ] is turned into
neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol
Syndrome, BM Kapur, DC Lehotay, PL Carlen at U. Toronto,
Alc Clin Exp Res 2007 Dec. plain text: detailed biochemistry,
CL Nie et al. 2007.07.18: Murray 2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524
___________________________________________________


"Of course, everyone chooses, as a natural priority, to enjoy peace,
joy, and love by helping to find, quickly share, and positively act
upon evidence about healthy and safe food, drink, and
environment."

Rich Murray, MA Room For All rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com  new primary archive

http://groups.yahoo.com/group/aspartameNM/messages
group with 126 members, 1,548 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1,121 members, 22,783 posts in public archive
___________________________________________________


http://www.newyorker.com/reporting/2008/05/26/080526fa_fact_acocella?currentPage\
=all

Annals Of Drinking
A Few Too Many
Is there any hope for the hung over?
by Joan Acocella May 26, 2008  themail@...

"Wayne Jones, of the Swedish National Laboratory
of Forensic Medicine"
[ http://groups.yahoo.com/group/aspartameNM/message/1469
highly toxic formaldehyde, the cause of alcohol hangovers, is
made by the body from 100 mg doses of methanol from
dark wines and liquors, dimethyl dicarbonate, and aspartame:
Murray 2007.08.31 ]

http://groups.yahoo.com/group/aspartameNM/message/1286
methanol products (formaldehyde and formic acid) are main cause
of alcohol hangover symptoms [same as from similar amounts of
methanol, the 11% part of aspartame]: YS Woo et al, 2005 Dec:
Murray 2006.01.20

Addict Biol. 2005 Dec;10(4): 351-5.
Concentration changes of methanol in blood samples during
an experimentally induced alcohol hangover state.
Woo YS, Yoon SJ, Lee HK, Lee CU, Chae JH, Lee CT, Kim DJ.
Chuncheon National Hospital, Department of Psychiatry,
The Catholic University of Korea, Seoul, Korea.
___________________________________________________

Artificial sweetener consumption and urinary tract tumors in Cordoba,
Argentina, MM Andreatta, SE Munoz, MJ Lantieri, AR Eynard, A Navarro, Prev.
Med. 2008.04.08: Murray 2008.07.01
http://rmforall.blogspot.com/2008_07_01_archive.htm
Tuesday, July 1, 2008
http://groups.yahoo.com/group/aspartameNM/message/1547
___________________________________________________


Prev Med. 2008 Jul; 47(1): 136-9. Epub 2008 Apr 8.
Artificial sweetener consumption and urinary tract tumors
in Cordoba, Argentina.
Andreatta MM,
Muñoz SE,
Lantieri MJ,
Eynard AR,  aeynard@...;
Navarro A.  anavarro@...;
Escuela de Nutrición, Facultad de Ciencias Médicas,
Universidad Nacional de Córdoba.

OBJECTIVE:
To determine the role of the habitual use of the most common
artificial sweeteners (AS) in the development
of urinary tract tumors (UTT) in Argentina.

METHODS:
Case-control study of 197 patients with histologically confirmed
UTT of transitional varieties, and 397 controls with
acute, non-neoplastic, and non-urinary tract diseases,
admitted to the same hospitals in Córdoba (Argentina)
between 1999 and 2006.

All subjects were interviewed about their use of AS and
their exposure to other known or suspected risk factors for UTT.

RESULTS:
Fifty-one UTT patients (26%) and 87 controls (22%) used AS.

The risk of UTT was significantly increased
in long-term (>/=10 years) AS users compared with none-AS users.

The OR (95% CI) for long-term consumers was 2.18 (1.22-3.89)
and for short-term users was 1.10 (0.61-2.00)
after adjustment for age, gender, BMI, social status,
and years of tobacco use.

CONCLUSION:
Regular use of AS for 10 years or more was positively associated
with UTT.  PMID: 18495230
___________________________________________________


Valerie B. Duffy <Valerie.Duffy@...>;
Hud Englehart <hud@...>;
webeditors@...;
Karen Springen <k-springen@...>;

http://www.newsweek.com/id/34923

Attack of the Diet Cokes
It's the one addiction people will admit to. But will Diet Coke --
now 25 years old -- be the same if it comes with vitamins?
By Jerry Adler | Newsweek Web Exclusive

"Mr. Englehart, meet Rich Underkofler,
a 47-year-old from Euclid, Ohio.
"I drink this stuff like crazy," Underkofler says.
"I don't even go to restaurants that don't serve Diet Coke."
Checking his refrigerator one night last week,
he found two 12-packs.
That would last him, he figured, a little more than a day.

With Matthew Philips, Anne Underwood, Karen Springen and
Joan Raymond"

Over 20 cans daily is a serious addiction and health hazard for this
middle aged man.

Likewise, a gallon is over 20 cans:

"Kristen Scaletta, a senior at Northwestern University
in Evanston, Ill., who recently cut back from
about a gallon of Diet Coke a day to three quarts,
drinks it only from cans, preferably at room temperature -- a taste
she formed as a child when she had to sneak it past her parents to
drink in her bedroom."

These are also probable, unnecessary tragedies:

"You might need to, if you're a Diet Coke fanatic like
Victoria Beckham, the former Posh Spice,
who drinks almost nothing else and claims to hate the taste of water.

Diet Coke is the one addiction that public figures willingly own up to.
It's the only beverage in the back of producer Harvey Weinstein's
limo, and makes up one half the diet of Florida State football coach
Bobby Bowden. The other half consists of peanuts."
___________________________________________________



re "A Few too Many", Joan Acocella, The New Yorker,
long review of hangover research 2008.05.26 -- same levels of
formaldehyde and formic acid in FEMA trailers and other sources
(aspartame, dark wines and liquors, tobacco smoke):
Murray 2008.06.05
http://rmforall.blogspot.com/2008_06_01_archive.htm
Thursday, June 5, 2008
http://groups.yahoo.com/group/aspartameNM/message/1541

[ See also:
There really is no controversy, Adrienne Samuels PhD, letter re
evident toxicity of aspartame EJCN 2008.06.11:
Murray 2008.06.30
http://rmforall.blogspot.com/2008_06_01_archive.htm
Monday, June 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1546

former key Hillary Clinton staff Mark Penn and Patti Solis Doyle
use much neurotoxic aspartame Diet Coke -- also many other
politicians: Murray 2008.06.30
http://rmforall.blogspot.com/2008_06_01_archive.htm
Monday, June 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1545 ]


formaldehyde and formic acid in FEMA trailers and other sources
(aspartame, dark wines and liquors, tobacco smoke):
Murray 2008.01.30
http://rmforall.blogspot.com/2008_01_01_archive.htm
Wednesday, January 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1508

The FEMA trailers give about the same amount of formaldehyde
and formic acid daily as from a quart of dark wine or liquor,
or two quarts (6 12-oz cans) of aspartame diet soda,
from their over 1 tenth gram methanol impurity
(one part in 10,000), which the body quickly makes into
formaldehyde and then formic acid -- enough to be the major cause
of "morning after" alcohol hangovers.

Methanol and formaldehyde and formic acid also result from
many fruits and vegetables, tobacco and wood smoke, heater
and vehicle exhaust, household chemicals and cleaners, cosmetics,
and new cars, drapes, carpets, furniture, particleboard,
mobile homes, buildings, leather... so all these sources add up
and interact with many other toxic chemicals.

methanol impurity in alcohol drinks [ and aspartame ] is turned into
neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol
Syndrome, BM Kapur, DC Lehotay, PL Carlen at U. Toronto,
Alc Clin Exp Res 2007 Dec. plain text: detailed biochemistry,
CL Nie et al. 2007.07.18: Murray 2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524
___________________________________________________


"Of course, everyone chooses, as a natural priority, to enjoy peace,
joy, and love by helping to find, quickly share, and positively act
upon evidence about healthy and safe food, drink, and
environment."

Rich Murray, MA Room For All rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com  new primary archive

http://groups.yahoo.com/group/aspartameNM/messages
group with 126 members, 1,547 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1,121 members, 22,780 posts in public archive
___________________________________________________


http://www.newyorker.com/reporting/2008/05/26/080526fa_fact_acocella?currentPage\
=all

Annals Of Drinking
A Few Too Many
Is there any hope for the hung over?
by Joan Acocella May 26, 2008  themail@...

"Wayne Jones, of the Swedish National Laboratory
of Forensic Medicine"
[ http://groups.yahoo.com/group/aspartameNM/message/1469
highly toxic formaldehyde, the cause of alcohol hangovers, is
made by the body from 100 mg doses of methanol from
dark wines and liquors, dimethyl dicarbonate, and aspartame:
Murray 2007.08.31 ]

http://groups.yahoo.com/group/aspartameNM/message/1286
methanol products (formaldehyde and formic acid) are main cause
of alcohol hangover symptoms [same as from similar amounts of
methanol, the 11% part of aspartame]: YS Woo et al, 2005 Dec:
Murray 2006.01.20

Addict Biol. 2005 Dec;10(4): 351-5.
Concentration changes of methanol in blood samples during
an experimentally induced alcohol hangover state.
Woo YS, Yoon SJ, Lee HK, Lee CU, Chae JH, Lee CT, Kim DJ.
Chuncheon National Hospital, Department of Psychiatry,
The Catholic University of Korea, Seoul, Korea.
___________________________________________________


Eur J Cancer Prev. 1998 Jun; 7(3): 207-13.
Alcohol, methylxanthine-containing beverages, and colorectal cancer
in Córdoba, Argentina.
Muñoz SE, Navarro A, Lantieri MJ, Fabro ME, Peyrano MG,
Ferraroni M, Decarli A, La Vecchia C, Eynard AR.
Instituto de Biologia Celular, Facultad de Ciencias Médicas,
Universidad Nacional de Córdoba, Argentina.

The relationship between social class indicators,
body mass index (BMI), selected life-style habits
(alcohol, coffee, maté and tea drinking) and colorectal cancer
was investigated in a case-control study conducted between
1993 and 1997 in Córdoba, Argentina,
a relatively high mortality area of colorectal cancer.

Cases were 190 patients below age 80 years with
incident, histologically confirmed colorectal adenocarcinomas,
and controls were 393 patients admitted to hospital
for a wide spectrum of acute, non-neoplastic disorders.

Higher social class, based on occupation of the head of the
household, was significantly associated with colorectal cancer risk:
the odds ratios (OR) and 95% confidence intervals (95% CI)
were 1.9 (1.2-2.9) for intermediate
and 2.0 (1.2-3.4) for the highest
as compared to the lowest social class individuals.

When compared with subjects whose BMI was < 25 kg/m2,
the OR was 1.1 (0.7-1.6) for those with BMI 25 to 29 kg/m2,
and 1.3 (0.7-2.3) for those > or = 30.

In comparison with alcohol abstainers,
the OR was 2.8 (1.6-5.1) for drinkers,
and there was a significant trend in risk with dose.

The association was observed with wine
(the most common alcoholic beverage in Argentina),
as well as for beer and spirits.

The consumption of coffee, maté and tea was
not significantly related to colorectal cancer,
but the ORs were below unity (0.9 (0.7-1.3) for coffee,
0.9 (0.6-1.2) for maté
and 0.8 (0.6-1.2) for tea drinkers).

The relationship between social class, alcohol drinking and
colorectal cancer were consistent across strata of sex and age.

This study confirms that colorectal cancer
has positive social class correlates.

The association with alcohol drinking is apparently stronger
than previously reported,
and may be due to the role of chance and/or peculiar correlates
of alcohol drinking in this Argentinean population.
PMID: 9696929
___________________________________________________

There really is no controversy, Adrienne Samuels PhD, letter re evident
toxicity of aspartame EJCN 2008.06.11: Murray 2008.06.30
http://rmforall.blogspot.com/2008_06_01_archive.htm
Monday, June 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1546
___________________________________________________



"Of course, everyone chooses, as a natural priority, to enjoy peace,
joy, and love by helping to find, quickly share, and positively act
upon evidence about healthy and safe food, drink, and
environment."

Rich Murray, MA Room For All rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com  new primary archive

http://groups.yahoo.com/group/aspartameNM/messages
group with 126 members, 1,546 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1,120 members, 22,777 posts in public archive
___________________________________________________



Letter to the Editor
European Journal of Clinical Nutrition advance online publication 11 June
2008; doi: 10.1038/ejcn.2008.38
There really is no controversy
A Samuels, Solana Beach, CA, USA

Correspondence: A Samuels, E-mail: adieonly@...;

It is noted in the excellent review by Humphries et al. (2008) that debate
[over safety] still continues 20 years after the FDA had approved the use of
aspartame.

Regarding that debate, the following comments are in order.

     "Aspartame has never been shown to be safe for human consumption."

     "Aspartame was discovered in 1965.
Required safety testing began in 1967.
To date, no research outside of the aspartame industry has found aspartame
to be safe for human consumption."

     "In June 1979, the US Food and Drug Administration (FDA) established a
Public Board of Inquiry (PBOI) to rule on aspartame safety issues.
The PBOI concluded that NutraSweet/aspartame should not be approved pending
further investigations of brain tumors in animals."

     "In 1981, Ronald Reagan became President of the United States; Arthur
Hull Hayes Jr was named FDA Commissioner; a Commissioner's panel was
established to review issues raised by the PBOI; the panel advised against
approval of aspartame; Hayes overruled the PBOI, ignored the recommendations
of his own internal FDA team and approved aspartame for use in dry
products."

    "The so-called aspartame-industry 'science' is flawed to the point of
being worthless."

     "Controversy about the safety of aspartame is a device used by those who
profit from production and sale of the product.
Industry sponsored studies referring to brain damage draw conclusions
without basis.
Illustrating this practice is a 1980 study which reads, in part, "On the
basis of blood absorption curves...[ it] is concluded that
(aspartame)...does not result in hypothalamic damage in the newborn monkey
(Reynolds et al., 1980)"."

     "Using techniques similar to those of the glutamate industry (Samuels,
1999), the aspartame industry, in studies of adverse reactions, has
manipulated subjects, procedures and statistics to enable researchers to
draw the conclusion that there is no significant difference in reactions
following ingestion of aspartame as opposed to ingestion of placebo.
The study of Geha et al., 1993 illustrates the point."

     "The FDA gives every appearance of cooperating with the aspartame
industry in promoting the 'safety' of aspartame."

     "Badly flawed industry sponsored studies have gone unchallenged."

     "Following the unwarranted approval of aspartame, the FDA Adverse
Reactions Monitoring System began receiving, and accepting, unsolicited
reports of reactions to aspartame.
A 26 June 1997 Memorandum from Technical Information Specialist (HFS-728) to
Health Hazard Evaluation Board reported that the FDA has received 7259
complaints of adverse reactions attributed to the use of aspartame."

     "The FDA has a history of minimizing the extent and severity of adverse
reactions to food.
Reports of debilitating or life-threatening reactions are not routinely
investigated, and reports of 'death,' for example, are listed as 'other.' "

     "In the late 1990s, the FDA stopped accepting reports of adverse
reactions to aspartame."

In conclusion, Humphries et al., 2008 suggested that 'serious further
testing and research be undertaken to eliminate any and all controversies
surrounding this product'.
It is suggested, rather, that with thoughtful analysis of the industry
sponsored studies, it will become abundantly clear that no legitimate
controversy about aspartame's toxic potential exists.

References

1. Geha R, Buckley CE, Greenberger P, Patterson R, Polmar S,
Saxon A et al. (1993).
Aspartame is no more likely than placebo to cause
urticaria/angioedema: results of a multicenter, randomized,
double-blind, placebo-controlled, crossover study.
J Allergy Clin Immunol 92, 513-520. Article  PubMed ChemPort

2. Humphries P, Pretorius E, Naude H (2008).
Direct and indirect cellular effects of aspartame on the brain.
Eur J Clin Nutr 62, 451-462. Article  PubMed ChemPort

3. Reynolds WA, Stegink LD, Filer Jr LJ, Renn E (1980).
Aspartame administration to the infant monkey:
hypothalamic morphology and plasma amino acid levels.
Nat Rec 198, 73-85. ChemPort|

4. Samuels A (1999). The toxicity/safety of processed
free glutamic acid (MSG): a study in suppression of information.
Account Res 6, 259-310.  PubMed
___________________________________________________


two aspartame toxicity research studies by Resia Pretorius,
U. Pretoria, South Africa, debate with JD Fernstrom:
Murray 2008.04.04
http://rmforall.blogspot.com/2008_04_01_archive.htm
Friday, April 4, 2008
http://groups.yahoo.com/group/aspartameNM/message/1536

two detailed critiques of industry affiliations and biased science in
99 page review with 415 references by BA Magnuson, GA
Burdock and 8 more, Critical Reviews in Toxicology, 2007 Sept.:
Mark D Gold 13 page: also Rich Murray 2007.09.15: 2008.03.24
http://rmforall.blogspot.com/2008_03_01_archive.htm
Monday, March 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1531

http://www.truthinlabeling.org/ Truth in Labeling Campaign [MSG]
Adrienne Samuels, PhD The toxicity/safety of processed
free glutamic acid (MSG): a study in suppression of information.
Accountability in Research 1999; 6: 259-310. 52-page review
adandjack@...; adieonly@...;

http://groups.yahoo.com/group/aspartameNM/message/857
www.dorway.com: original documents and long reviews of flaws in
aspartame toxicity research: Murray 2002.07.31

http://groups.yahoo.com/group/aspartameNM/message/858
Samuels: Strong: Roberts: Gold: flaws in double-blind studies re
aspartame and MSG toxicity: Murray 2002.08.01

http://www.dorway.com/upipart1.txt
http://groups.yahoo.com/group/aspartameNM/message/262
aspartame expose 96K Oct 1987 Part 1/3: Gregory Gordon,
UPI reporter: Murray 2000.07.10

http://www.dorway.com/enclosur.html
http://groups.yahoo.com/group/aspartameNM/message/53
aspartame history Part 1/4 1964-1976: Gold: Murray 1999.11.06

http://groups.yahoo.com/group/aspartameNM/message/928
revolving door, Monsanto, FDA, EPA: NGIN: Murray 2002.12.23

methanol impurity in alcohol drinks [ and aspartame ] is turned into
neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol
Syndrome, BM Kapur, DC Lehotay, PL Carlen at U. Toronto,
Alc Clin Exp Res 2007 Dec. plain text: detailed biochemistry,
CL Nie et al. 2007.07.18: Murray 2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524


re "A Few too Many", Joan Acocella, The New Yorker, long review
of hangover research 2008.05.26 -- same levels of formaldehyde
and formic acid in FEMA trailers and other sources (aspartame,
dark wines and liquors, tobacco smoke): Murray 2008.06.05
http://rmforall.blogspot.com/2008_06_01_archive.htm
Thursday, June 5, 2008
http://groups.yahoo.com/group/aspartameNM/message/1541

[ formaldehyde and formic acid in FEMA trailers and other sources
(aspartame, dark wines and liquors, tobacco smoke):
Murray 2008.01.30
http://rmforall.blogspot.com/2008_01_01_archive.htm
Wednesday, January 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1508

The FEMA trailers give about the same amount of formaldehyde
and formic acid daily as from a quart of dark wine or liquor, or two
quarts (6 12-oz cans) of aspartame diet soda, from their over 1
tenth gram methanol impurity (one part in 10,000), which the body
quickly makes into formaldehyde and then formic acid -- enough to
be the major cause of "morning after" alcohol hangovers.

Methanol and formaldehyde and formic acid also result from many
fruits and vegetables, tobacco and wood smoke, heater and vehicle
exhaust, household chemicals and cleaners, cosmetics, and new
cars, drapes, carpets, furniture, particleboard, mobile homes,
buildings, leather... so all these sources add up and interact
with many other toxic chemicals. ]

http://www.newyorker.com/reporting/2008/05/26/080526fa_fact_acocella?currentPage\
=all

Annals Of Drinking
A Few Too Many
Is there any hope for the hung over?
by Joan Acocella May 26, 2008  themail@...

"Wayne Jones, of the Swedish National Laboratory of Forensic
Medicine"
[ http://groups.yahoo.com/group/aspartameNM/message/1469
highly toxic formaldehyde, the cause of alcohol hangovers, is
made by the body from 100 mg doses of methanol from
dark wines and liquors, dimethyl dicarbonate, and aspartame:
Murray 2007.08.31 ]

http://groups.yahoo.com/group/aspartameNM/message/1286
methanol products (formaldehyde and formic acid) are main cause
of alcohol hangover symptoms [same as from similar amounts of
methanol, the 11% part of aspartame]: YS Woo et al, 2005 Dec:
Murray 2006.01.20

Addict Biol. 2005 Dec;10(4): 351-5.
Concentration changes of methanol in blood samples during
an experimentally induced alcohol hangover state.
Woo YS, Yoon SJ, Lee HK, Lee CU, Chae JH, Lee CT, Kim DJ.
Chuncheon National Hospital, Department of Psychiatry,
The Catholic University of Korea, Seoul, Korea.
___________________________________________________

former key Hillary Clinton staff Mark Penn and Patti Solis Doyle use much
neurotoxic aspartame Diet Coke -- also many other politicians: Murray 2008.06.30
http://rmforall.blogspot.com/2008_06_01_archive.htm
Monday, June 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1545
___________________________________________________


"Of course, everyone chooses, as a natural priority, to enjoy peace,
joy, and love by helping to find, quickly share, and positively act
upon evidence about healthy and safe food, drink, and
environment."

Rich Murray, MA Room For All rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com  new primary archive

http://groups.yahoo.com/group/aspartameNM/messages
group with 126 members, 1,546 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1,120 members, 22,778 posts in public archive
___________________________________________________


http://www.huffingtonpost.com/2008/04/21/clinton-camp-marred-by-di_n_97760.html?\
page=3

Clinton Camp Marred By Distrust, Lacks Leadership

The New Republic, Michelle Cottle, April 21, 2008 11:48 AM

By the time Hillary Clinton's campaign manager Patti Solis Doyle
finally packed up her lovely corner office with its fresh blue carpet
and mini-fridge full of Diet Coke, her exit must have come as a
relief -- even to many of her friends on Team Hillary...

http://www.nytimes.com/2007/09/02/magazine/02wwln-q4-t.html?_r=1&oref=slogin

Questions for Mark Penn

The Adviser

Interview by DEBORAH SOLOMON
Published: September 2, 2007

You're described on the jacket of your new book as the "chief
adviser" to Hillary Rodham Clinton's presidential campaign.
Are you really her chief adviser?

No. I'm the chief strategist and pollster...

You're also C.E.O. of Burson-Marsteller, which likes to call itself
the world's largest P.R. agency. When do you sleep?

I'm not into sleeping. I sleep about five hours a night, from 2 to 7.

How much coffee do you drink during the day?

None. I drink Diet Coke.
I drink between 5 to 10 cans of Diet Coke a day...


Joe Trippi, diabetic, still drinks Diet Pepsi -- now key staff for
John Edwards campaign -- John and Elizabeth Edwards, Bill
Clinton, Mitt Romney, Dick Cheney, George Bush, Tony Blair,
also use aspartame soda: Murray 2007.05.04
http://groups.yahoo.com/group/aspartameNM/message/1420

[ See also:

former NC Senator John Edwards gave up 8-12 cans daily Diet
Coke about January 2005, switching to caffeine free Diet Sprite
Zero with 27% of the aspartame per can: Murray 2006.12.28
http://groups.yahoo.com/group/aspartameNM/message/1392 ]


"It's a great business -- hurry up and wait," Trippi said, sipping a
Diet Pepsi between calls."

www.philly.com/inquirer/local/20070409_Tom_Knox__ready_on_the_set__is_rolling_on\
.html

The Philadelphia Inquirer   Posted on Mon, Apr. 09, 2007

Tom Knox, ready on the set, is rolling on
Behind the scenes with hired gun Joe Trippi, a media maven using
a candidate's millions to shape an image and lure votes.....

Contact staff writer Thomas Fitzgerald at 215-854-2718
or tfitzgerald@...


www.dailykos.com/story/2007/4/19/154849/379

Joe Trippi Joins Edwards for President
by philgoblue
Thu Apr 19, 2007 at 12:50:30 PM PDT

The press release from Edwards 2008:

     The John Edwards for President campaign announced today
that Joe Trippi will be joining the campaign as a key member
of the media team and senior advisor.

     Joe's Personal Website: http://www.joetrippi.com/

Wikipedia Entry on Joe Trippi

     Joe Trippi is a long-time American Democratic campaign
worker and consultant. A mainstay in presidential politics, Trippi
has worked on the presidential campaigns of Edward Kennedy,
Walter Mondale, Gary Hart, and Dick Gephardt. Most notably,
he served as campaign manager for presidential candidate and
former Vermont governor Howard Dean.

Also see Trippi's diary on MyDD, Transformational Politics --
Why the Dean Campaign was Different, from 26 December 2006.



http://popwatch.ew.com/popwatch/2007/04/the_food_bank_f.html

Bill Clinton's trip to The Edge and more
Apr 24, 2007, 06:32 PM | by Simon Vozick-Levinson

"Bill [ Clinton ] took occasional breaks from chatting to sip his Diet
Coke and enjoy speeches from chef Mario Batali, former SNL-er
Fallon (one of the night's two major honorees), and R.E.M.'s
Michael Stipe."


www.thesmokinggun.com/archive/0322061cheney1.html

Dick Cheney's Suite Demands
Veep's "rider" requires [Diet] Sprite, 68 degrees, TVs tuned to
Fox News

MARCH 23 2006 -- After posting the performance contracts of
artists like Bruce Springsteen, the Rolling Stones, and U2,
The Smoking Gun has finally obtained the backstage demands
of a real rock star. That's right, below you'll find a copy of Vice
President Dick Cheney's standard "tour" rider. The document is
provided to hotels where Cheney will be bunking and lists how the
Republican pol's "Downtime Suite" needs to be outfitted. While the
vice president's requests are pretty modest
(no extract-the-brown-M&M demands here), Cheney does like his
suite at a comfy 68 degrees. And, of course, all the televisions need
to be preset to the Fox News Channel (what, you thought he was a
Lifetime devotee?).

Decaf coffee should be ready upon his arrival along with four cans
of caffeine-free Diet Sprite......


http://news.scotsman.com/topics.cfm?tid=819&id=1288022003

2003.11.22  Best of mates go down the Dun Cow
ANDREW DENHOLM

"Mr Bush's Bitburger Drive non-alcoholic beer was £1.75.

Tony drank a Diet Coke (£1.50) and Mrs Blair had an Appletise
for the same price.

Mrs Bush was the only one to take an alcoholic drink -- a glass
of Australian Shiraz at £2.60"


www.telegraph.co.uk/news/main.jhtml?xml=/news/2006/07/18/wreaction118.xml

Slip-up reveals Bush and Blair's gossip secrets
By Alec Russell in St Petersburg
Last Updated: 3:05am BST 19/07/2006

"The recording also picks up Mr Bush speaking to other leaders,
bantering about his preference for Diet Coke, and making clear
his irritation at the formalities of summitry."


www.cnn.com/POLITICS/blogs/politicalticker/2006/10/cnn-political-ticker-am_10.ht\
ml
Tuesday, October 10, 2006  CNN Political Ticker AM

ROMNEY'S HURDLE: In seeking a presidential candidate for
2008, why would Republicans look further than the governor of
Massachusetts? Tall and urbane, Mitt Romney has a prime political
pedigree, an unblemished personal life and the cool confidence of a
CEO. He is a conservative Republican who won easy election in a
fiercely liberal state -- then streamlined Massachusetts' government
and enacted the country's most sweeping healthcare overhaul.
He is a passionate defender of states' rights and recently has
embraced strong views against stem cell research and abortion --
a reversal of earlier positions.

He never swears, and his sole vice is Diet Coke.

Not incidentally, the 59-year-old governor boasts Ivy League
credentials and movie-star looks. But Romney faces a potential
obstacle that has not confronted a presidential hopeful for almost
50 years. As a devout Mormon -- and a onetime bishop of the
Church of Jesus Christ of Latter-day Saints -- Romney adheres
to a faith that makes many Americans uncomfortable.
Los Angeles Times: Romney's 2008 Bid Faces Issue of Faith
Posted 10/10/2006 07:58:00 AM
___________________________________________________


http://groups.yahoo.com/group/aspartameNM/message/1101
John Edwards gives up Diet Coke: The Cult of Diet Coke,
Eric Gillin: Murray 2004.07.12 rmforall

http://groups.yahoo.com/group/aspartameNM/message/1102
John Edwards still drinks Diet Coke (aspartame): TIME Europe
July 19 issue: Murray 2004.07.12

http://groups.yahoo.com/group/aspartameNM/message/1065
politicians and celebrities hooked on diet sodas (aspartame):
Murray 2004.03.24

http://groups.yahoo.com/group/aspartameNM/message/1027
Senator John Edwards, avoid Diet Coke (aspartame toxicity):
Murray 2003.09.28

http://groups.yahoo.com/group/aspartameNM/message/1037
Joe Trippi, heavy user of Diet Pepsi (aspartame toxicity),
Dean's campaign manager: Murray 2003.11.16

http://groups.yahoo.com/group/aspartameNM/message/1016
President Bush & formaldehyde (aspartame) toxicity: Ramazzini
Foundation carcinogenicity results Dec 2002: Soffritti:
Murray 2003.08.03
___________________________________________________


methanol impurity in alcohol drinks [ and aspartame ] is turned into
neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol
Syndrome, BM Kapur, DC Lehotay, PL Carlen at U. Toronto,
Alc Clin Exp Res 2007 Dec. plain text: detailed biochemistry,
CL Nie et al. 2007.07.18: Murray 2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524


re "A Few too Many", Joan Acocella, The New Yorker, long review
of hangover research 2008.05.26 -- same levels of formaldehyde
and formic acid in FEMA trailers and other sources (aspartame,
dark wines and liquors, tobacco smoke): Murray 2008.06.05
http://rmforall.blogspot.com/2008_06_01_archive.htm
Thursday, June 5, 2008
http://groups.yahoo.com/group/aspartameNM/message/1541

[ formaldehyde and formic acid in FEMA trailers and other sources
(aspartame, dark wines and liquors, tobacco smoke):
Murray 2008.01.30
http://rmforall.blogspot.com/2008_01_01_archive.htm
Wednesday, January 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1508

The FEMA trailers give about the same amount of formaldehyde
and formic acid daily as from a quart of dark wine or liquor, or two
quarts (6 12-oz cans) of aspartame diet soda, from their over 1 tenth
gram methanol impurity (one part in 10,000), which the body quickly
makes into formaldehyde and then formic acid -- enough to be the
major cause of "morning after" alcohol hangovers.

Methanol and formaldehyde and formic acid also result from many
fruits and vegetables, tobacco and wood smoke, heater and vehicle
exhaust, household chemicals and cleaners, cosmetics, and new cars,
drapes, carpets, furniture, particleboard, mobile homes, buildings,
leather... so all these sources add up and interact with many other
toxic chemicals. ]

http://www.newyorker.com/reporting/2008/05/26/080526fa_fact_acocella?currentPage\
=all

Annals Of Drinking
A Few Too Many
Is there any hope for the hung over?
by Joan Acocella May 26, 2008  themail@...

"Wayne Jones, of the Swedish National Laboratory of Forensic
Medicine"
[ http://groups.yahoo.com/group/aspartameNM/message/1469
highly toxic formaldehyde, the cause of alcohol hangovers, is
made by the body from 100 mg doses of methanol from
dark wines and liquors, dimethyl dicarbonate, and aspartame:
Murray 2007.08.31 ]

http://groups.yahoo.com/group/aspartameNM/message/1286
methanol products (formaldehyde and formic acid) are main cause
of alcohol hangover symptoms [same as from similar amounts of
methanol, the 11% part of aspartame]: YS Woo et al, 2005 Dec:
Murray 2006.01.20

Addict Biol. 2005 Dec;10(4): 351-5.
Concentration changes of methanol in blood samples during
an experimentally induced alcohol hangover state.
Woo YS, Yoon SJ, Lee HK, Lee CU, Chae JH, Lee CT, Kim DJ.
Chuncheon National Hospital, Department of Psychiatry,
The Catholic University of Korea, Seoul, Korea.
___________________________________________________

Aspartame Induced Arrhythmias and Sudden Death, HJ Roberts 2004: Murray
2008.06.26
http://rmforall.blogspot.com/2008_06_01_archive.htm
Thursday, June 26, 2008
http://groups.yahoo.com/group/aspartameNM/message/1544
____________________________________________________


Aspartame Induced Arrhythmias and Sudden Death

By H. J. Roberts, M.D., F.A.C.P., F.C.C.P.
E-Mail:   HJrobertsmd@...
(c)2004 by H. J. Roberts, M.D.

A recent extensive review of sudden death in young athletes (1)
made no mention of aspartame as a primary cause or suspected
contributory factor, especially when demonstrable pathology was
absent.

This issue has assumed great public health importance because
"diet" products containing this chemical are being consumed by
over two-thirds of the population -- especially weight-conscious
persons.

I have repeatedly reported the serious cardiovascular,
'neuropsychiatric, metabolic and other adverse effects of
aspartame products. (2-4)

Among the first 1200 aspartame reactors in my data base,
193 (16%) had symptomatic arrhythmia,
85 (7%) atypical chest pain, and
64 (5%) recent or aggravated hypertension.

One hypertensive patient developed complete heart block within
hours after consuming his first diet cola.

Another had undergone unsuccessful radio frequency ablations in the
heart before awareness of having aspartame disease.

Pheochromocytoma was suspected in several aspartame reactors.

The issue of sudden death related to aspartame and its breakdown
products has been raised a number of times, particularly among
previously well individuals using such products... including pilots
and drivers, (3,4,6) and athletes.

I have detailed the release of norepinephrine, epinephrine, dopamine
and free methanol by aspartame; a host of pertinent-related
pathophysiologic conditions,
(e.g., cumulative formaldehyde adducts derived from aspartame in
tissue proteins and nucleic acids; excessive insulin release);
direct oropharyngeal absorption from gum, breath fresheners and
other products; and the increasing problem of aspartame addiction.
(4-7)

The likelihood of pulmonary hypertension induced by the
vasoconstrictive effects of aspartame products also has been
considered. (5)

It is relevant that unexplained dyspnea was experienced by 110
aspartame reactors, usually with prompt improvement after
abstinence.

Moreover, primary pulmonary hypertension was found at autopsy
in a 27 year old female aspartame reactor.

The lack of familiarity of most physicians and medical examiners
with the foregoing considerations can have serious legal
consequences.

A case in point is that of a young woman (also a Sunday School
teacher) who has been sentenced to serve 50 years in a Virginia
prison for allegedly poisoning her husband with methyl alcohol.
[ Diane and Charles Fleming ]

Elevated methanol blood concentrations were found postmortem in
this body builder/basketball player who drank ten diet drinks and
other aspartame products daily.

She remains incarcerated despite affidavits indicating that 10% of
aspartame becomes free methyl alcohol after consumption.

The need for clinicians and corporate-neutral investigators to
evaluate the contributory role of aspartame in cardiopulmonary
disorders and sudden death, and drug interactions with aspartame,
is underscored by the frequency of persons dying unexpectedly
being categorized as "death due to causes yet to be determined."

One interested resident of Orange county (California) found 192
persons listed in this category between July 11 and November 15,
2003 according to the Orange county Register.

References:

Maron BJ,
Sudden death in young athletes,
N Engl J Med 2003; 349: 1064-1075

Roberts HJ,
Reactions to aspartame containing products: 551 cases,
J Appl Nutr l988; 40: 86-94

Roberts HJ, Aspartame (NutraSweet): Is It Safe?
Philadelphia, The Charles Press, 1989.

Roberts HJ,
Aspartame Disease: An Ignored Epidemic.
West Palm Beach, Sunshine Sentinel Press, 2001

Roberts HJ,
Aspartame-induced dyspnea and pulmonary hypertension,
Townsend Letter for Doctors & Patients 2003; 237 (January): 64-65

Roberts HJ,
Ignored Health Hazards for Pilots and Drivers.
West Palm Beach, Sunshine Sentinel Press, 1998.

Roberts HJ, Aspartame (NutraSweet) addiction,
Townsend Letter for Doctors & Patients, 2000; 198 (January): 52-57

H. J. Roberts, MD, FACP, FCCP
Palm Beach Institute for Medical Research
P. O. Box 17799
West Palm Beach, Florida 33416 USA
____________________________________________________


http://www.dorway.com/tldaddic.html 5-page review
Roberts HJ Aspartame (NutraSweet) addiction.
Townsend Letter 2000 Jan; HJRobertsMD@...
http://www.sunsentpress.com/ sunsentpress@...
Sunshine Sentinel Press P.O.Box 17799 West Palm Beach, FL 33416
800-814-9800 561-588-7628 561-547-8008 fax

http://groups.yahoo.com/group/aspartameNM/message/669
1038-page medical text "Aspartame Disease: An Ignored Epidemic"
published May 30 2001 $ 60.00 postpaid data from 1200 cases
available at http://www.amazon.com
over 600 references from standard medical research

http://groups.yahoo.com/group/aspartameNM/message/790
Moseley: review Roberts "Aspartame Disease: An Ignored Epidemic":
Murray 2002.02.07

Roberts, Hyman J., 1924- ,
Useful insights for diagnosis, treatment and public heath: an updated
anthology of original research, 2002, 798 pages,
aspartame disease, pages 627-685, 778-780

http://groups.yahoo.com/group/aspartameNM/message/859
Roberts: the life work of a brilliant clinician: aspartame toxicity:
Murray 2002.08.02
____________________________________________________


re "A Few too Many", Joan Acocella, The New Yorker, long review of hangover
research 2008.05.26 -- same levels of formaldehyde and formic acid in FEMA
trailers and other sources (aspartame, dark wines and liquors, tobacco smoke):
Murray 2008.06.05
http://rmforall.blogspot.com/2008_06_01_archive.htm
Thursday, June 5, 2008
http://groups.yahoo.com/group/aspartameNM/message/1541


formaldehyde and formic acid in FEMA trailers and other sources (aspartame, dark
wines and liquors, tobacco smoke): Murray 2008.01.30
http://rmforall.blogspot.com/2008_01_01_archive.htm
Wednesday, January 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1508

The FEMA trailers give about the same amount of formaldehyde and formic acid
daily as from a quart of dark wine or liquor, or two quarts (6 12-oz cans) of
aspartame diet soda, from their over 1 tenth gram methanol impurity (one part in
10,000), which the body quickly makes into formaldehyde and then formic acid --
enough to be the major cause of "morning after" alcohol hangovers.

Methanol and formaldehyde and formic acid also result from many fruits and
vegetables, tobacco and wood smoke, heater and vehicle exhaust, household
chemicals and cleaners, cosmetics, and new cars, drapes, carpets, furniture,
particleboard, mobile homes, buildings, leather... so all these sources add up
and interact with many other toxic chemicals.

methanol impurity in alcohol drinks [ and aspartame ] is turned into
neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol Syndrome, BM
Kapur, DC Lehotay, PL Carlen at U. Toronto,  Alc Clin Exp Res 2007 Dec. plain
text: detailed biochemistry, CL Nie et al. 2007.07.18: Murray 2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524

"Of course, everyone chooses, as a natural priority, to enjoy peace, joy, and
love by helping to find, quickly share, and positively act upon evidence about
healthy and safe food, drink, and environment."

Rich Murray, MA Room For All rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com  new primary archive

http://groups.yahoo.com/group/aspartameNM/messages
group with 126 members, 1,544 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1,119 members, 22,762 posts in public archive

http://www.newyorker.com/reporting/2008/05/26/080526fa_fact_acocella?currentPage\
=all

Annals Of Drinking
A Few Too Many
Is there any hope for the hung over?
by Joan Acocella May 26, 2008  themail@...

"Wayne Jones, of the Swedish National Laboratory of Forensic Medicine"
[ http://groups.yahoo.com/group/aspartameNM/message/1469
highly toxic formaldehyde, the cause of alcohol hangovers, is
made by the body from 100 mg doses of methanol from
dark wines and liquors, dimethyl dicarbonate, and aspartame:
Murray 2007.08.31 ]

http://groups.yahoo.com/group/aspartameNM/message/1286
methanol products (formaldehyde and formic acid) are main cause
of alcohol hangover symptoms [same as from similar amounts of
methanol, the 11% part of aspartame]: YS Woo et al, 2005 Dec:
Murray 2006.01.20

Addict Biol. 2005 Dec;10(4): 351-5.
Concentration changes of methanol in blood samples during
an experimentally induced alcohol hangover state.
Woo YS, Yoon SJ, Lee HK, Lee CU, Chae JH, Lee CT, Kim DJ.
Chuncheon National Hospital, Department of Psychiatry,
The Catholic University of Korea, Seoul, Korea.
[ Han-Kyu Lee ]

A hangover is characterized by the unpleasant physical and mental
symptoms that occur between 8 and 16 hours after drinking alcohol.

After inducing experimental hangover in normal individuals,
we measured the methanol concentration prior to
and after alcohol consumption
and we assessed the association between the hangover condition
and the blood methanol level.

A total of 18 normal adult males participated in this study.

They did not have any previous histories of psychiatric
or medical disorders.

The blood ethanol concentration prior to the alcohol intake
(2.26+/-2.08) was not significantly different from that
13 hours after the alcohol consumption (3.12+/-2.38).

However, the difference of methanol concentration
between the day of experiment (prior to the alcohol intake)
and the next day (13 hours after the alcohol intake)
was significant (2.62+/-1.33/l vs. 3.88+/-2.10/l, respectively).

A significant positive correlation was observed
between the changes of blood methanol concentration
and hangover subjective scale score increment when covarying
for the changes of blood ethanol level (r=0.498, p<0.05).

This result suggests the possible correlation of methanol
as well as its toxic metabolite to hangover. PMID: 16318957

[ The toxic metabolite of methanol is formaldehyde, which in turn
partially becomes formic acid -- both potent cumulative toxins
that are the actual cause of the toxicity of methanol.]

This study by Jones AW (1987) found next-morning hangover
from red wine with 100 to 150 mg methanol
(9.5 % w/v ethanol, 100 mg/l methanol, 0.01 %).
Fully 11% of aspartame is methanol --
1,120 mg aspartame in 2 L diet soda,
almost six 12-oz cans, gives 123 mg methanol (wood alcohol).

Pharmacol Toxicol. 1987 Mar; 60(3): 217-20.
Elimination half-life of methanol during hangover.
Jones AW. wayne.jones@...;
Department of Forensic Toxicology,
University Hospital, SE-581 85 Linkoping, Sweden.

This paper reports the elimination half-life of methanol in human
volunteers.
Experiments were made during the morning after the subjects had
consumed 1000-1500 ml red wine
(9.5 % w/v ethanol, 100 mg/l methanol)
the previous evening. [ 100 to 150 mg methanol ]
The washout of methanol from the body
coincided with the onset of hangover.
The concentrations of ethanol and methanol in blood were
determined indirectly by analysis of end-expired alveolar air.
In the morning when blood-ethanol dropped
below the Km of liver alcohol dehydrogenase (ADH)
of about 100 mg/l (2.2 mM),
the disappearance half-life of ethanol was 21, 22, 18 and 15 min.
in 4 test subjects respectively.
The corresponding elimination half-lives of methanol
were 213, 110, 133 and 142 min. in these same individuals.
The experimental design outlined in this paper can be used
to obtain useful data on elimination kinetics of methanol
in human volunteers without undue ethical limitations.
Circumstantial evidence is presented to link methanol
or its toxic metabolic products, formaldehyde and formic acid,
with the pathogenesis of hangover. PMID: 3588516 ]
[ for more, see URL..... ]
____________________________________________________

M Soffritti of Ramazzini Foundation answers critique by Ajinomoto funded BA
Magnuson and GM Williams re aspartame (methanol) carcinogenicity,
Environmental Health Perspectives 2008 May: Murray 2008.06.24
http://rmforall.blogspot.com/2008_06_01_archive.htm
Tuesday, June 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1543
____________________________________________________


"Of course, everyone chooses, as a natural priority, to enjoy peace, joy,
and love by helping to find, quickly share, and positively act upon evidence
about healthy and safe food, drink, and environment."

Rich Murray, MA Room For All rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com  new primary archive

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http://www.ehponline.org/docs/2008/10881/letter.html

Environmental Health Perspectives (EHP) is a monthly journal of
peer-reviewed research and news on the impact of the environment on human
health.
EHP is published by the National Institute of Environmental Health Sciences
and its content is free online.
Print issues are available by paid subscription.

NIEHS  NIH  DHHS
Current Issue
Cover of Current Issue
Volume 116, Number 5  May 2008

Carcinogenicity of Aspartame in Rats Not Proven
     Magnuson B, et al. (More)

Correspondence-in-Press- Disclaimer - Full (PDF)

Correspondence

Letter: Magnuson B, Williams GM
Response: Soffritti M


[ two detailed critiques of industry affiliations and biased science in 99
page review with 415 references by BA Magnuson, GA Burdock
and 8 more, Critical Reviews in Toxicology, 2007 Sept.: Mark D
Gold 13 page: also Rich Murray 2007.09.15: 2008.03.24
http://rmforall.blogspot.com/2008_03_01_archive.htm
Monday, March 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1531

stevia herbal sweetener to be sold as Truvia (rebiana) by Cargill and
Coca-Cola, if blitz of 12 studies wins FDA approval in 30-90 days: Murray
2008.05.24
http://rmforall.blogspot.com/2008_05_01_archive.htm
Saturday, May 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1540
[ Extracts ]

Dr Ashley Roberts, Vice-President, Food and Nutrition Group, Cantox Health
Sciences International, of Mississauga, USA, www.cantox.com
Cantox  is the leading international scientific and regulatory consulting
firm with specialized expertise in the areas of Food &  Nutrition,
Pharmaceutical & Healthcare, Chemicals, and Agri, Biotech & Consumer
Products.

For the past 20 years, we have been helping clients resolve complex
scientific and toxicology issues, develop scientific and strategic
regulatory and compliance plans, and facilitate timely regulatory global
approvals. We optimize success and minimize client risk through broad
expertise and knowledge.

We are ideally equipped to help clients achieve success in a fast-paced,
changing global market with:

* Offices around the world
* Internationally recognized scientists, regulatory specialists, and
toxicologists
* More than 60 professionals dedicated to the interests of our clients.

Our lengthy track record of success speaks for itself and today, more than
70% of our projects come from existing clients or direct referrals.

Cantox -- Protecting Client Interests

We protect client interests while helping our clients achieve milestones and
bring products to market. Our clients benefit from successful outcomes,
reduced time to market, and decreased costs. That is why so many clients
return to Cantox when they have new challenges to overcome.

Our cost-effective, value-added service:

* Streamlines product development programs and eliminates unnecessary steps
* Addresses scientific issues prior to and during regulatory review
* Allows faster time to market and timely regulatory approvals

We focus on client success!

Cantox Health Sciences International  info@...;
1011 Route 22, West Bridgewater, NEW JERSEY 08807 U.S.A.
Telephone: (908) 429-9202  Fax: (908) 429-9260

http://www.cantox.com/staff.html

Scientific & Regulatory Consultants

Williams GM, GWilliams@...;

Bernadene Magnuson, Ph.D., Senior Scientific and Regulatory Consultant
BMagnuson@...;

Berna Magnuson brings to Cantox an exceptional broad range of skills and
knowledge in toxicology and food and nutritional sciences.
Her research on diet and cancer, and her work in food toxicology, has been
recognized internationally.
She is a pioneer in the developing field of food nanoscience, and is leading
efforts to address issues facing the food industry in the adoption of this
promising new technology.

Berna received her BSHEc with distinction in food science and nutrition.
After working in the food industry, she obtained her MSc in Toxicology from
the University of Saskatchewan, and her PhD in Food and Nutritional Sciences
from the University of Manitoba.
Her post-doctoral research focused on the pathology and biochemistry of
colon cancer.
As a university faculty member recently at the University of Maryland, Berna
led a competitive research program, mentored graduate students, and taught
courses for over 12 years.

She is now an adjunct professor in nutritional sciences at the University of
Toronto.

Her research has been published in over 40 peer-reviewed journal articles
and book chapters, and had led to several patents.
Recently, her work focused on safety assessments of various dietary
ingredients and supplements.
Berna has been elected to numerous leadership positions of the Institute of
Food Technologists and the Society of Toxicology, and she has been the
recipient of outstanding service awards from both the US FDA and IFT.
She is a member of the editorial board of the Journal of Food Protection and
an Associate Editor of Food Analytical Methods.
Berna is also a member of the American Association for Cancer Research, and
is a reviewer for many other toxicology, food science and cancer journals.

Berna is based in our Mississauga office as a Senior Scientific and
Regulatory Consultant.
Her expertise and knowledge in food science and toxicology will be a
valuable addition to our Food and Nutrition group.

http://www.utoronto.ca/nutrisci/faculty/Magnuson/
Bernadene A. Magnuson, Ph.D.
Adjunct Associate Professor, Department of Nutritional Sciences
Senior Scientific and Regulatory Consultant, Cantox Health Science
International
2233 Argentia Road, Suite 308, Mississauga, ON L5N 2X7
Tel: (905) 542 2900 Fax: (905) 542 1011 BMagnuson@...;
Research
My research interests have been in the area of diet and cancer and I am now
interested in the new and exciting area of nanotechnology and its role in
nutrition. ]

Carcinogenicity of Aspartame in Rats Not Proven

Environ Health Perspect. doi:10.1289/ehp.10881 available via
http://dx.doi.org [Online 27 May 2008]

Referencing: Life-Span Exposure to Low Doses of Aspartame Beginning during
Prenatal Life Increases Cancer Effects in Rats

In their article on lifetime exposure to aspartame in rats, Soffritti et al.
(2007) purported that their study demonstrated increased carcinogenic
effects in female rats as a result of exposure beginning during prenatal
life.

We believe that this article (Soffritti et al. 2007) has methodologic and
conceptual weaknesses that require exposition.

First, although the study was a toxicology study, the most important
element -- the reported doses -- are not correct. The doses are "estimates"
based on assuming constant food consumption of 20 g/day and constant body
weights of 400 g for each rat from in utero (fetal day 12) to death. These
assumptions are unrealistic and inaccurate. The doses during the early
growth phase of rats would be much higher because, as is well known, rats
consume more food per gram of body weight during the rapid growth phase.
Food consumption and body weight were reportedly measured throughout the
experiment; however, Soffritti et al. (2007) presented only data beginning
16 weeks postpartum, when rats reached adult body weight. Therefore the
authors' conclusions are built on the exposure period for which they provide
no data.

Second, for a study allegedly designed to assess prenatal exposure,
Soffritti et al. (2007) did not address important details, such as
a) pregnancy history and ages of breeders;
b) number of pregnant dams per dose group;
c) growth and food consumption of mothers during pregnancy and lactation;
d) pregnancy outcomes;
e) disposition of pups from all mothers and each litter;
f) the origin of the 70 pups;
and g) body weight of pups at birth and during lactation.
These details are typically required to allow other scientists to assess the
appropriateness of the study design and to repeat the study, if desired.

The findings are of questionable biological significance for a number of
reasons.

The lymphoma/leukemia incidences in the high-dose group, which were the only
significant differences from control, were within or near the reported
historical control ranges.

Similarly, the mammary gland carcinoma incidence in high-dose females
(again, the only significant difference from control) was similar to
historical controls.

In their article, Soffritti et al. (2007) stated that their study disproved
the conclusions of the European Food Safety Authority (EFSA 2006) that the
incidences of lymphomas/leukemias observed in the first report (Soffritti et
al. 2006) were "unrelated to aspartame given the high background incidence
of chronic inflammatory changes in the lungs ." (EFSA 2006).

The U.S. Food and Drug Administration (FDA 2007) agreed with the EFSA
assessment.

It is not clear to us how this study disproved the EFSA's conclusions.

Soffritti et al. (2007) indicated that the lung was often the site of
lymphoma again in this study, which is not surprising because they used the
same infected colony.

Studies in the 1960s demonstrated that the progression of chronic pneumonia
in rats resulted in lymphoid neoplasmas, and elimination of chronic
respiratory disease in rat colonies reduced the incidence of pulmonary
lymphoid neoplasias to near zero (Cotchin and Roe 1967).

Rats with pulmonary infections developed lesions in multiple sites earlier
than rats free from pulmonary disease (Cotchin and Roe 1967).

The establishment of pathogen-free animal suppliers for toxicity research
was impelled for this reason.

Therefore, we believe it is highly likely that the present findings are due
to infection and not aspartame consumption.

Data do not support the conclusions of Soffritti et al. (2007) that
aspartame has carcinogenic potential at doses near the human level of
exposure.

The authors observed no significant effects at the low-diet level, and the
actual dose is unknown.

Also, no data were provided on in utero exposure.

Aspartame is completely digested in the gastrointestinal tract into two
amino acids (phenylalanine and aspartic acid) and methanol, which is
subsequently metabolized to carbon dioxide and water.

In human clinical studies (reviewed by Stegink and Filer 1996), oral doses
equal to or exceeding the amount that would represent the 99th percentile of
aspartame intake did not increase plasma aspartate or phenylalanine levels
in adults or children, or in breast milk from lactating women beyond normal
postprandial concentrations.

Ratios of fetal/maternal plasma amino acids and transport across the
placental membrane were unchanged in pregnant rabbits that received 1,600 mg
aspartame/kg/day (Ranney et al. 1975).

Thus, a biologically plausible explanation is lacking for Soffritti et al.'s
(2007) contention that prenatal exposure to aspartame increases cancer risk.

In summary, considering that there are no significant differences in cancer
rates between high-dose groups and historical controls, plus the many
deficiencies in the experimental design and data, Soffritti et al. (2007)
failed to provide convincing evidence of aspartame carcinogenicity.

Given the effort expended by many government review agencies to document
shortcomings of the first article by this group (Soffritti et al. 2006), it
is disappointing that the editor and reviewers of this paper (Soffritti et
al. 2007) did not require the authors to address those problems that appear
again in this study.

Diligence is especially necessary on topics of great public interest and
relevance because the public is relying upon the scientific community to
assure that only high quality, well-documented, and controlled studies
appear in peer-reviewed journals.

The authors received payment from the Burdock Group during the preparation
of an expert review of the safety of aspartame.

The Burdock Group managed the independent review, which was financially
supported by Ajinomoto Company Inc., a producer of aspartame.

Bernadene Magnuson
Department of Nutrition and Food Science University of Maryland
College Park, Maryland
E-mail: bmagnuso@...;

Gary M. Williams
Department of Pathology
New York Medical College
Valhalla, New York

References

Cotchin E, Roe JFC. 1967.
Pathology of Laboratory Rats and Mice. Oxford,
UK:Blackwell Scientific Publications.

EFSA (European Food Safety Authority). 2006.
Opinion of the Scientific Panel on Food Additives, Flavourings, Processing
Aids and Materials in Contact with Food (AFC) on a Request from the
Commission Related to a New Long-term Carcinogenicity Study on Aspartame.
EFSA J 356:1-44. Available:
http://www.efsa.europa.eu/EFSA/Scientific_Opinion/afc_op_ej356_aspartame_en1,2.p\
df
[accessed 9 April 2008].

FDA (Food and Drug Administration). 2007.
FDA Statement on European Aspartame Study. Available:
http://www.cfsan.fda.gov/~lrd/fpaspar2.html [accessed 15 August 2007].

Ranney RE, Mares SE, Schroeder RE, Hutsell TC, Raczialowski FM. 1975.
The phenylalanine and tyrosine content of maternal and fetal body fluids
from rabbits fed aspartame.
Toxicol Appl Pharmacol 32:339-346.

Soffriti M, Belpoggi F, Degli Esposti D, Lambertini L, Tibaldi E, Rigano A.
2006.
First experimental demonstration of the multipotential carcinogenic effects
of aspartame administered in the feed to Sprague-Dawley rats.
Environ Health Perspect 114:379-385.

Soffritti M, Belpoggi F, Tibaldi E, Degli Esposti D, Lauriola M. 2007.
Life-span exposure to low doses of aspartame beginning during prenatal life
increases cancer effects in rats.
Environ Health Perspect 115:1293-1297.

Stegink LD, Filer LJ. 1996.
Effect of aspartame ingestion on plasma aspartate, phenylalanine, and
methanol concentrations in potentially sensitive populations.
In: The Clinical Evaluation of a Food Additive: Assessment of Aspartame
(Tschanz C, Butchko HH, Stargel WW, Kotsonis FN, eds).
Boca Raton, FL: CRC Press, 87-113.


Carcinogenicity of Aspartame: Soffritti Responds

Environ Health Perspect. doi:10.1289/ehp.10881R available via
http://dx.doi.org [Online 27 May 2008]

Magnuson and Williams's letter is substantially a repetition of the
arguments set forth in a recent article (Magnuson et al. 2007), which was a
"safety evaluation" sponsored entirely by Ajinomoto, the manufacturer of
aspartame.

Their article (Magnuson et al. 2007) and this letter contain numerous
erroneous statements about the long-term carcinogenesis studies on aspartame
conducted by the European Ramazzini Foundation (ERF).

First, Magnuson and Williams imply that our findings (Soffritti et al. 2007)
should be discounted because the incidence of lymphomas/leukemias in the
high-dose group "were within or near the reported historical control
ranges."

As reported in our study (Soffritti et al. 2007), the incidence of
lymphomas/leukemias observed in both sexes treated with 2,000 ppm aspartame
is nearly double the concurrent control (Soffritti et al. 2007).

The suggestion that concurrent control data should be ignored is contrary to
the widely accepted standard of good laboratory science.

Second, Magnuson and Williams attribute our findings (Soffritti et al. 2007)
to some kind of bias (i.e., infection) that would affect only treated
animals but not the controls.

We have responded in detail to this hypothesis in our article (Soffritti et
al. 2007) and in an earlier letter (Soffritti 2006).

To support their assertion, Magnuson and Williams mislead readers by stating
that "the lung was often the site of lymphoma again in this [second] study."

However, we actually reported that we observed the diffusion of neoplastic
tissue not only in the lung but also concurrently in various organs (liver,
spleen, mediastinal and other lymph nodes). (Soffritti et al. 2007)

Infection as a mode of action for induction of rat lymphoma has been
recently examined by a group of scientists at the National Center for
Environmental Assessment of the U.S. Environmental Protection Agency;

Caldwell et al. (2008) found that  a careful examination of available
information does not support the hypothesis that the observed
lymphomas/leukemias in the ERF bioassays are a general effect from
infection.

The reports of chemically-induced lymphomas/leukemias by the ERF seem to be
chemical specific.

Third, the idea that we must provide a "biologically plausible explanation"
for human or rodent carcinogens is a time-honored approach to postpone or
prevent the application of regulatory measures to minimize carcinogenic
risks.

The reality is that this explanation is quite often unknown, as is, in
general, the mode of action behind the carcinogenic process.

I regard the other questions raised by Magnuson and Williams as trivial.

For example, whatever the doses at various ages and weights, the finding of
any effect should be a cause for concern.

Likewise, the authors' observation that some methodologic details were
omitted from the publication certainly does not change the oncologic results
of this research.

Magnuson and Williams express disappointment that Environmental Health
Perspectives would publish original scientific research by the ERF after
regulatory agencies went through so much trouble to review our first
aspartame study (Soffritti 2006) only to disagree with our conclusions.

It is the obligation of the agencies responsible for food safety to review
any new scientific data available and to make their opinion available to the
public.

The Food and Drug Administration (FDA) did not make public the contents of
their review, but rather they issued a short press release a full year after
the European Food Safety Authority (EFSA) concluded its evaluation, and
coincidently, just days before I presented new aspartame data in a lecture
at the Mount Sinai School of Medicine in New York (FDA 2007).

I find it unfortunate that some scientists have such a low tolerance for
original, independent scientific research;
however, I welcome continued discussion and more importantly, additional
long-term experimental studies on aspartame and other artificial sweeteners.

We at the ERF stand behind our results, and we remain convinced that a
review of the current regulations governing the use of aspartame is
necessary to better protect public health.

The author declares he has no competing financial interests.

Morando Soffritti
European Foundation of Oncology and Environmental Sciences, "B. Ramazzini"
Cesare Maltoni Cancer Research Center, Bologna, Italy
E-mail: crcfr@...;

References

Caldwell J, Jinot J, DeVoney D, Gift JS. 2008.
Evaluation of evidence for infection as a mode of action for induction of
rat lymphoma.
Environ Mol Mutagen 49: 155-164.

FDA (Food and Drug Administration). 2007.
FDA Statement on European Aspartame Study. Available:
http://www.cfsan.fda.gov/~lrd/fpaspar2.html [accessed 12 January 2008].

Magnuson BA, Burdock GA, Doull J, Kroes RM, Marsh GM, Pariza MW, et al.
2007.
Aspartame: a safety evaluation based on current use levels, regulations, and
toxicological and epidemiological studies.
Crit Rev Toxicol 37: 629-727.

Soffritti M. 2006.
Acesulfame potassium: Soffritti responds [Letter].
Environ Health Perspect 114: A516-A519.

Soffritti M, Belpoggi F, Tibaldi E, Degli Esposti D, Lauriola M. 2007.
Life-span exposure to low doses of aspartame beginning during prenatal life
increases cancer effects in rats.
Environ Health Perspect 115:1293-1297.
____________________________________________________


JC Caldwell et al.  2007 refuted major, widely publicized criticisms of the
Ramazzini research by the European Food Safety Authority:
Environ Mol Mutagen. 2008 Mar; 49(2): 155-64.
Evaluation of evidence for infection as a mode of action for induction of
rat lymphoma.
Caldwell JC, Jinot J, DeVoney D, Gift JS.
National Center for Environmental Assessment, U.S. Environmental Protection
Agency, Washington, DC, USA. caldwell.jane@...;

The European Food Safety Authority (EFSA) released a 2006 report questioning
the relationship of aspartame exposure with increased incidence of
lymphomas/leukemias in a European Ramazzini Foundation (ERF) rat study.

The EFSA report suggested that the lymphoma/leukemia findings were most
likely explained by infection in the rat colony.

The ERF has also conducted the only available long-term oral study of methyl
tertiary-butyl ether (MTBE).

Thus, using the EFSA report as support, some have now raised questions about
the human relevance of MTBE-associated hemolymphoreticular tumors reported
by the ERF in female rats as well as whether their incidence was elevated
above background levels.

In this report, we discuss the hypothesized mode of action (MOA) of
infection-induced lymphoma and its relevance to MTBE-associated lymphomas.

We address the relationship of rat strain and study duration to lymphoma
susceptibility and review evidence of low background rates of this tumor in
control animals at the ERF, similar survival rates for female rats at the
ERF and National Toxicology Program (NTP), and chemical- and
gender-specificity of tumor induction for this type of tumor in studies at
the ERF.

We find that the background incidence of hemolymphoreticular tumors in
female rats in the MTBE study is consistent with contemporaneous studies at
the ERF and that there is an exposure-related effect, which is unlikely to
be due to infections.

We examine more recent tumor classification schemes for lymphomas, which
support the combination of lymphoblastic leukemias and lymphomas reported by
Belpoggi et al. ([1995] Toxicol Ind Health 11: 119-149; [1998]  Eur J Oncol
3: 201-206). Published 2007 Wiley-Liss, Inc.  PMID: 18095346
____________________________________________________


http://groups.yahoo.com/group/aspartameNM/message/1453
Souring on fake sugar (aspartame), Jennifer Couzin, Science 2007.07.06: 4
page letter to FDA from 12 eminent USA toxicologists re two Ramazzini
Foundation cancer studies 2007.06.25: Murray 2007.07.18

Dr. Kamal M. Abdo, PhD,
Carlos A. Camargo, Jr., MD, DrPH,
Devra Lee Davis, PhD, MPH,
David E. Egilman MD, MPH,
Samuel S. Epstein, MD,
John R. Froines, PhD,
Dale Hattis, PhD,
Kim Hooper, PhD,
James Huff, PhD,
Michael F. Jacobson, PhD,
Peter F. Infante, DDS, DrPH.
Letter to U.S. FDA commissioner. Questions about the safety of the
artificial sweetener aspartame.
Int J Occup Environ Health. 2007 Oct-Dec; 13(4): 449-50. No abstract
available. PMID: 18085059

" In light of the new aspartame study, which extends and corroborates the
finding from an earlier study, we urge the FDA to immediately commence a
careful review of the new study.

Considering how widely aspartame in consumed by young children, as well as
adults, in the United States and abroad, it is essential that this review be
done as expeditiously as possible.

If that review confirms that aspartame caused cancer in the laboratory
animals, the FDA must invoke the Delaney amendment and revoke its approval
for the artificial sweetener. 8 "

www.ramazzini.it/fondazione/pdfUpload/Science_06.07.2007.pdf

SCIENCE VOL 317 6 JULY 2007 page 31

Souring on Fake Sugar

Fearful it causes cancer, 12 U.S. environmental health experts last week
asked the U.S. Food and Drug Administration (FDA) to review the potential
health risks of the artificial sweetener aspartame, which appears in
everything from medicines to diet sodas.

A study published last month in Environmental Health Perspectives found
somewhat more leukemias and lymphomas in male rats receiving less aspartame
than the recommended maximum for humans;
at higher doses, the rats had a marked increase in cancers throughout the
body.

Pregnant rats were fed the sweetener, and animals received it once they'd
been weaned. The work, by scientists at the European Ramazzini Foundation of
Oncology and Environmental Sciences in Bologna, Italy, is "more sensitive
and more realistic" than earlier aspartame studies, says James Huff of the
National Institute of Environmental Health Sciences, who signed onto the FDA
letter drafted by the Washington, D.C.-based watchdog group
Center for Science in the Public Interest.

But because the study conflicts with earlier work, FDA spokesperson Michael
Herndon says that the agency finds the study unpersuasive and that
"aspartame is safe."

FDA's European counterpart has not responded publicly to the study.  --
Jennifer Couzin

www.cspinet.org/new/200706251.html
www.cspinet.org/new/200706251_print.html
http://cspinet.org/new/pdf/aspartame_letter_to_fda.pdf
____________________________________________________



(BA Magnuson et al, 2007)

4.1. Animal Studies

Studies in the 1970s by Opperman and coworkers (Oppermann et al., 1973b;
Ranney et al., 1976; Ranney and Oppermann, 1979; Oppermann and Ranney, 1979)
using radiolabeled aspartame demonstrated that aspartame was first
hydrolyzed to aspartylphenylalanine and methanol by intestinal esterases,
possibly chymotrypsin......

Methanol is not subject to metabolism within the enterocyte and rapidly
enters the portal circulation.

The methanol is oxidized in the liver to formaldehyde.

Enzymes involved depend on species: In the rat, the metabolism of methanol
to formaldehyde is mediated though a catalase-peroxidase system, whereas in
primates and humans, an alcohol dehydrogenase is responsible.

Formaldehyde is further oxidized to formic acid by formaldehyde
dehydrogenase.

This conversion is very rapid, with formaldehyde having a half-life of only
one to 2 min, so there is no accumulation of formaldehyde.

Formic acid is ultimately converted to CO2 and water, via the formation of
10-formyl tetrahydrofolate (Barceloux et al., 2002).


[ not cited in BA Magnuson et al, 2007]
Bull Mem Acad R Med Belg. 2006;161(6):425-34; discussion 434-6.Links
[Acute methanol intoxication: physiopathology, prognosis and treatment]
[Article in French]
Hantson PE.
Département des Soins Intensifs, Cliniques St-Luc-U.C.L.

Acute methanol poisoning is mainly the consequence of voluntary or
accidental ingestion.

The mortality and morbidity rates remain very high despite intensive care
therapy.

Methanol by itself is poorly toxic.

Methanol is transformed in the liver into formaldehyde and thereafter formic
acid.

Metabolic acidosis is the main biological feature of poisoning.

Acidosis is related to formic acid accumulation, and also to a less extent
to lactate production.

In contrast to rodents, primates are relatively deficient in
tetrahydrofolate reductase and therefore formic acid is usually the final
metabolite.

Formic acid is able to inhibit cytochrome oxidase activity in the
mitochondria, leading to histotoxic hypoxia.

The most sensitive organs to the effects of formic acid are the brain and
the visual pathway, while other organs may also be seriously damaged
according to the severity of metabolic acidosis.

Hemodialysis remains indicated for the removal of both methanol and formic
acid.

Fomepizole is a recently approved antidote.

It appears safe and effective.

Analysis of its cost-effectiveness ratio is still ongoing in methanol
poisoning.   PMID: 17288275


[ BA Magnuson et al, 2007]
6.9.2.1 "Formic acid accumulates in the blood because its half-life (t1/2 =
3.4-6 h) is very much longer than is that of formaldehyde (t1/2 = 1.5 min)
(Hantson et al., 2005).

Formic acid accumulation is considered the mechanism of toxicity of high
doses of methanol, which induces metabolic acidosis, ophthalmic toxicity and
central nervous system depression (Barceloux et al., 2002)."

[ Reference 133.
Hum Exp Toxicol. 2005 Feb; 24(2): 55-9.
Formate kinetics in methanol poisoning.
Hantson P, Haufroid V, Wallemacq P.
Department of Intensive Care, Cliniques St-Luc, Université catholique de
Louvain, Brussels, Belgium. hantson@...;

OBJECTIVE:
The objective is to describe the kinetics of formate, the main toxic
metabolite of methanol, in a series of consecutive patients treated in the
same intensive care unit for severe methanol poisoning.
METHODS:
The charts of the patients admitted between 1987 and 2001 were reviewed.
Inclusion criteria were: a history of deliberate methanol ingestion, with a
blood methanol concentration greater than 20 mg/dL (6.2 mmol/L) or a high
anion gap metabolic acidosis.
Indications for hemodialysis were: blood methanol concentration >50 mg/dL
(15.8 mmol/L), metabolic acidosis (bicarbonate <15 mmol/L, arterial pH
<7.30), visual toxicity.
Antidotal therapy included ethanol administration in 22 cases, and
fomepizole in three cases.
Serial blood measurements were obtained for pH, bicarbonate, methanol and
formate.
Endogenous and hemodialysis elimination half-lives were calculated as t1/2
=0.693/Ke.
Fick principle was applied for hemodialysis clearance calculation.
RESULTS:
The records of 25 methanol poisoned patients were analysed.
Among them, 18 patients had sufficient data to allow accurate determinations
of formate kinetics.
Formate half-life elimination during hemodialysis was 1.80+/-0.78 h, which
was statistically different from the values observed before or in the
absence of dialysis (6.04+/-3.26 h, P =0.004).
[ie, range about 2.78 - 9.30 h ]
The mean hemodialysis formate clearance rate calculated in eight cases was
176+/-43 mL/min.
A rebound in plasma formate concentration was observed in three patients
after the discontinuation of hemodialysis.
CONCLUSIONS:
In accordance with previous isolated case reports and in contrast with a
recent case series, our data document that hemodiaysis is effective in
reducing formate elimination half-life.
The impact on clinical outcome is still debatable.   PMID: 15850279 ]


[ not cited by BA Magnuson et al, 2007 ]
Kenneth E. McMartin, Gladys Martin-Amat, Patricia E. Noker and Thomas R.
Tephly
Lack of a role for formaldehyde in methanol poisoning in the monkey.
Biochemical Pharmcacology 1979: 28; 645-649.
The Toxicology Center, Dept. of Pharmacology,
University of Iowa, Iowa City, Iowa 52242
K.E. McMartin and T.R. Tephly, authors of many pro-aspartame studies, in
Biochemical Pharmacology (1979) remarked, "It is now generally accepted that
the toxicity of methanol is due to the formation of toxic metabolites,
either formaldehyde or formic acid."

"Methanol was administered [ by nasogastric tube ] either to untreated
cynomolgus monkeys [ 2-3.5 kg ] or to a folate-deficient cynomolgus monkey
which exhibits exceptional sensitivity to the toxic effects of methanol.

Marked formic acid accumulation in the blood and in body fluids and tissues
was observed."


Ernstgård L, Shibata E, Johanson G.
Uptake and disposition of inhaled methanol vapor in humans.
Toxicol Sci. 2005 Nov; 88(1): 30-8. Epub 2005 Aug 10.
Work Environment Toxicology, Institute of Environmental Medicine, Karolinska
Institutet, Stockholm, Sweden. Lena.Ernstgard@...
http://toxsci.oxfordjournals.org/cgi/content/full/88/1/30  free full text
Lena Ernstgård*,1, Eiji Shibata{dagger} and Gunnar Johanson{ddagger}

* Work Environment Toxicology, Institute of Environmental Medicine,
Karolinska Institutet, Stockholm, Sweden;
{dagger} Department of Health and Psycosocial Medicine, Aichi Medical
University School of Medicine, Nagakute-cho, Japan;
and {ddagger} Work Environment Toxicology, Institute of Environmental
Medicine, Karolinska Institutet, Stockholm, Sweden

1 To whom correspondence should be addressed at Work Environment Toxicology,
Institute of Environmental Medicine, Karolinska Institutet, SE-171 77
Stockholm, Sweden. Fax: +46 8 31 41 24. E-mail: Lena.Ernstgard@...;

"The absorbed dose of methanol ranged from 8.1 to 12.5 mmol in our
subjects."

Methanol is a widely used solvent and a potential fuel for motor vehicles.

Human kinetic data of methanol are sparse.

As a basis for biological exposure monitoring and risk assessment, we
studied the inhalation toxicokinetics of methanol vapor in four female and
four male human volunteers during light physical exercise (50 W) in an
exposure chamber.

The relative uptake of methanol was about 50% (range 47-53%).

Methanol in blood increased from a background level of about 20 to 116 and
244 microM/L after 2 h exposure at 0, 100 ppm (131 mg/m3), and 200 ppm (262
mg/m3), respectively.

Saliva showed substantially higher levels than blood immediately after
exposure.

This difference disappeared in a few minutes; thereafter the concentrations
and time courses in blood, urine, and saliva were similar, with half times
of 1.4, 1.7, and 1.3 h, respectively.

The postexposure decrease of methanol in exhaled air was faster, with a half
time of 0.8 h.

The methanol concentrations were approximately twice as high in all four
types of biological samples at 200 compared to 100 ppm.

No increase in urinary formic acid was seen in exposed subjects.

Our study indicates non-saturated, dose-proportional kinetics of methanol up
to 200 ppm for 2 h.

No gender differences were detected.

Similar, parallel patterns were seen with regard to the methanol time
courses in blood, urine, and saliva, whereas the concentration in exhaled
air decreased markedly faster.

Thus, apart from blood and urine, saliva also seems suitable for
biomonitoring of methanol exposure. PMID: 16093526

"Methanol is also a natural ingredient of various foods such as fresh
fruits, fruit juices, certain vegetables, and the artificial sweetener
aspartame (Kavet and Nauss, 1990; Lindinger et al., 1997; Taucher et al.,
1995)......The most common health effect of long-term exposure to low levels
of methanol vapor is CNS and ocular effects. Chronic occupational exposure
to methanol vapor concentrations of 365-3080 ppm has resulted in headache,
dizziness, nausea, and blurred vision (IPCS, 1997)."

"Two subjects at a time were exposed at three different times to 100 ppm
(131 mg/m3) or 200 ppm (262 mg/m3) methanol or to clean air for 2 h.

The subjects were exposed in different exposure orders, and exposure
sessions were separated by at least 2 weeks."

"Symptom ratings.

The subjects rated the level of perceived discomfort immediately before,
during (10, 50, 80, and 104 min), and after (126 and 210 min) each exposure
session.

Ten questions were answered, related to irritative symptoms
(eyes, nose, and throat or airways), the central nervous system
(headache, fatigue, nausea, dizziness, feeling of intoxication),
difficulty in breathing, and smell of solvent.

The ratings were performed using a 100-mm visual analogue scale
(Kjellberg et al., 1988Go) graded from "not at all" (corresponding to 0 mm)
through "hardly," "slightly," "fairly," "much," to "almost unbearable" (100
mm).

The same questionnaire has been used in several chamber inhalation studies
performed with organic solvent vapors in our laboratory (see for example,
Ernstgård et al., 1999Go, 2002Go; Järnberg et al., 1996Go; Nihlén et al.,
1998bGo)."

"Background levels of methanol were detected in all samples during control
exposure: blood range 9-76 µM/L, saliva 4-76 µM/L, urine 13-86 µM/L, and
exhaled air 0.0005-0.01 µM/L.
[Note the highest levels of background methanol, close to the mean level of
116 (94-144) microM/L after 2 h exposure at 100 ppm (131 mg/m3).]

For each individual and time point, the exposure-related methanol
concentrations were calculated as the difference between the concentrations
measured at methanol exposure and that measured at clean air exposure.

No difference between genders was seen with respect to background methanol
in blood.

Background methanol levels in urine were higher in men than in women (35.9
vs. 21.5 mcM/L, p = 0.03 in t-test).

Similar difference was seen for saliva (39.3 vs. 19.0 mcM/L, p = 0.008).

Methanol was rapidly absorbed by inhalation.

The relative uptake remained stable throughout the exposure and was
approximately 50% at both exposure levels (range 47-53%) (Table 1).

The blood methanol concentrations reached 116 (94-144) mcM/L after 2 h
exposure at 100 ppm and 244 (228-260) µM/L at 200 ppm methanol.

These levels are consistent with linear, nonsaturated metabolism of
methanol.

Linear (i.e., dose-proportional) kinetics is also indicated when comparing
the AUC (0-6 h) of blood methanol at the different exposure levels (Fig.
1A).

Blood methanol increased in a monoexponential fashion during exposure (Fig.
2A).

The postexposure decline was also monoexponential, considering the
background methanol.

According to the toxicokinetic model, the elimination half time in blood was
about 1.4 h, and the apparent total clearance 0.2-0.3 l/min.

The steady-state level of methanol at continuous exposure to methanol was
calculated to be 186 and 394 mcM at 100 and 200 ppm, respectively (Table 1),
again an indication of linear kinetics."


"The average rating of irritation and CNS symptoms during exposure to
methanol never exceeded that corresponding to "somewhat" (26 mm).

  There was no significant difference in symptoms ratings between methanol
exposure and control.

However, the women rated significantly higher than the men during exposure
to 200 ppm of methanol in three of the symptoms, namely irritation in throat
or airways (p = 0.047), fatigue (p = 0.014), and nausea (p = 0.045).

At the control condition the women rated significantly higher than men with
respect to irritation in the nose (p = 0.038)."

"We saw no increase in the symptom ratings after exposure to 100 or to 200
ppm of methanol compared to control exposure in our study.

This is in agreement with the findings of Muttray and colleagues (2001) who
found no differences in symptoms in 12 healthy volunteers exposed to 20 and
200 ppm methanol for 4 h.

However, it is noteworthy that women rated significantly higher than men for
three symptoms, namely headache, fatigue, and nausea, at 200 ppm methanol.

In addition, and in line with our previous experience (Ernstgård et al.,
2002), women rated significantly higher than men for irritation in the nose
at the control condition."


"The excretion of formic acid was seemingly not affected by exposure up to
200 ppm methanol

Similar findings have been reported by other investigators (Chuwers et al.,
1995; d'Alessandro et al., 1994; Lee et al., 1992; Osterloh et al., 1996).

The absorbed dose of methanol ranged from 8.1 to 12.5 mmol in our subjects.

Assuming complete conversion to formic acid and excretion in urine within 24
h, the same amount should be recovered in urine.

These amounts cannot be distinguished from the highly variable background
excretion of formic acid of 19-332 mmol.

In conclusion, formic acid is not a useful biomarker for low-dose methanol
exposure."


Int Arch Occup Environ Health. 2001 Jan; 74(1): 43-8.
Acute effects on the human EEG after an external exposure to 200 ppm
methanol.
Muttray A, Kürten R, Jung D, Schicketanz KH, Konietzko J.
Institut für Arbeits-, Sozial- und Umweltmedizin der Johannes
Gutenberg-Universität Mainz, Obere Zahlbacher Strasse 67, 55131 Mainz,
Germany. amuttray@...;

OBJECTIVES:
Even low concentrations of organic solvents may cause acute effects on the
human central nervous system.

The German MAK (threshold limit value) of methanol is 200 ppm.

The aim of this study was to investigate whether acute exposure to 200 ppm
methanol causes adverse effects, measured by EEG, and moreover, whether it
is possible to differentiate between sedative and excitatory effects with
this method.

METHODS:
Twelve healthy subjects were exposed for 4 h to 200 ppm and to 20 ppm
(control) in an exposure chamber in a cross-over design.

The EEG was recorded before (reference) and at the end of each exposure
with, the subject's eyes closed and opened and during a choice reaction test
(color word stress test).

Spectral power was calculated by fast Fourier transformation.

Subjective symptoms and effects of blinding with 20 ppm methanol were
assessed by questionnaires.

RESULTS:
The study was a single-blind one.

During subjects' exposure to 200 ppm, their scores for prenarcotic and
irritating symptoms were not different from controls.

In the closed-eye condition of subjects, the spectral power of the
theta-band and of some electrodes of the delta-band was significantly less
at the end of exposure to 200 ppm, than that of controls.

In the open-eye condition and during the color word stress test no
significant changes were found.

CONCLUSION:
The changes in the theta-band suggest a slight excitatory effect of 200 ppm
methanol.

The effect was weak, as scores of acute symptoms did not change.

With respect to our results, it is not necessary for the MAK value to be
decreased.  PMID: 11196080
____________________________________________________


http://groups.yahoo.com/group/aspartameNM/message/1143
methanol (formaldehyde, formic acid) disposition, Bouchard M et al, full
plain text, 2001 -- substantial sources are degradation of fruit pectins,
liquors, aspartame, smoke: Murray 2005.01.05

Michèle Bouchard *, #,1,  michele.bouchard@...;
Robert C. Brunet, # brunet@...;
Pierre-Olivier Droz, #
Gaétan Carrier* gaetan.carrier@...;
A Biologically Based Dynamic Model for Predicting the Disposition of
Methanol and Its Metabolites in Animals and Humans
Toxicological Sciences 64, 169-184 (2001)
http://www.toxsci.oupjournals.org/cgi/content/full/64/2/169  free full text

It is remarkable how little is known about the disposition of formaldehyde
and formic acid in human tissues, according to a sober review by Bouchard M,
2001:

"Exposure to methanol also results from the consumption of certain
foodstuffs (fruits, fruit juices, certain vegetables, aspartame sweetener,
roasted coffee, honey) and alcoholic beverages (Health Effects Institute,
1987; Jacobsen et al., 1988)."

"A biologically based dynamic model was developed to simulate the uptake and
disposition of methanol and its metabolites (formaldehyde, formate, CO2) in
animals and humans."

"Systemic methanol is extensively metabolized by liver alcohol dehydrogenase
and catalase-peroxidase enzymes to formaldehyde, which is in turn rapidly
oxidized to formic acid by formaldehyde dehydrogenase enzymes (Goodman and
Tephly, 1968; Heck et al., 1983; Røe, 1982; Tephly and McMartin, 1984)."

"Formaldehyde, as it is highly reactive, forms relatively stable adducts
with cellular constituents (Heck et al., 1983; Røe, 1982)."

"Thus, in monkeys and plausibly humans, a much larger fraction of body
formaldehyde is rapidly converted to unobserved forms rather than passed on
to formate and eventually CO2."

"Inversely, in monkeys and in humans, a larger fraction of body burden of
formaldehyde is rapidly transferred to a long-term component.
The latter represents the formaldehyde that (directly or after oxidation to
formate) binds to various endogenous molecules..."

"However, fits to the available data in rats and monkeys of Horton et al.
1992) and Dorman et al. (1994) show that, once formed, a substantial
fraction of formaldehyde is converted to unobserved forms.

This pathway contributes to a long-term unobserved compartment.

The latter, most plausibly, represents either the formaldehyde that
(directly or after oxidation to formate) binds to various endogenous
molecules (Heck et al., 1983; Røe, 1982)...

That substantial amounts of methanol metabolites or by-products are retained
for a long time is verified by Horton et al. (1992) who estimated that 18 h
following an iv injection of 100 mg/kg of 14C-methanol in male Fischer-344
rats, only 57% of the dose was eliminated from the body.

From the data of Dorman et al. (1994) and Medinsky et al. (1997), it can
further be calculated that 48 h following the start of a 2-h inhalation
exposure to 900 ppm of 14C-methanol vapors in female cynomolgus monkeys,
only 23% of the absorbed 14C-methanol was eliminated from the body.

These findings are corroborated by the data of Heck et al. (1983) showing
that 40% of a 14C-formaldehyde inhalation dose remained in the body 70 h
postexposure."
____________________________________________________


6.3.2 Lifetime Studies

[ The ASE review has devoted section 6.3.2 to many detailed criticisms of
the two Ramazzini lifetime cancer rat studies.

As a medical layman, never educated in biochemistry, I am not qualified to
address these matters, and I welcome comments pro and con, which I will put
on my aspartameNM group public archive:

aspartameNM@yahoogroups.com

I am qualified, however, to remind scientists that effective collaboration
between opposed viewpoints has to based on an ethic of going out of one's
way to present the best expressions by others of their evidence.

In fact, the Ramazzini Foundation has a large network of eminent supporters,
some of whom have taken an unusual public position in support of their two
cancer studies:

Abdo KM, Camargo CA Jr, Davis D, Egilman D, Epstein SS, Froines J, Hattis D,
Hooper K, Huff J, Infante PF, Jacobson MF, Teitelbaum DT, Tickner JA.
Letter to U.S. FDA commissioner. Questions about the safety of the
artificial sweetener aspartame.
Int J Occup Environ Health. 2007 Oct-Dec; 13(4): 449-50. No abstract
available.  PMID: 18085059

http://groups.yahoo.com/group/aspartameNM/message/1453
Souring on fake sugar (aspartame), Jennifer Couzin, Science 2007.07.06: 4
page letter to FDA from 12 eminent USA toxicologists re two Ramazzini
Foundation cancer studies 2007.06.25: Murray 2007.07.18


In addition, Ramazzini Foundation proved carcinogenity by similar studies in
Dec., 2002 for alcohol, aldehyde, methanol, and formaldehyde, and the
results are very compatible with their first aspartame cancer study, 2005,
and with their second aspartame study, 2007:

http://groups.yahoo.com/group/aspartameNM/message/1186
aspartame induces lymphomas and leukaemias in rats,
free full plain text, M Soffritti, F Belpoggi, DD Esposti, L Lambertini,
2005 April, 2005.07.14: main results agree with their previous methanol
and formaldehyde studies, Murray 2005.07.19

""Yellowing of the coat was observed in animals exposed to APM, mainly at
the highest concentrations.

This change was previously observed in our laboratory in rats exposed
to formaldehyde administered with drinking water 9."

http://groups.yahoo.com/group/aspartameNM/message/1441
Lifetime exposure to low doses of aspartame beginning during prenatal life
increases cancer effects in rats, Morando Soffritti et al, European
Ramazzini Foundation, USA EPA Environmental Health Perspectives 2007.06.13
free full text 24 pages: Murray 2007.06.16
www.ehponline.org/members/2007/10271/10271.pdf free full text 24 pages

Soffritti M, Belpoggi F, Lambertini L, Lauriola M.
Results of long-term experimental studies on the carcinogenicity of
formaldehyde and acetaldehyde in rats. In: Mehlman MA, Bingham E, Landrigan
PJ, et al.
Carcinogenesis bioassays and protecting public health.
Commemorating the lifework of Cesare Maltoni and colleagues.
Ann NY Acad Sci 2002; 982: 87-105.

Formaldehyde was administered for 104 weeks in drinking water supplied ad
libitum at concentrations of 1500, 1000, 500, 100, 50, 10, or 0 mg/L to
groups of 50 male and 50 female Sprague-Dawley rats beginning at seven weeks
of age.  Control animals (100 males and 100 females) received tap water
only.

Acetaldehyde was administered to 50 male and 50 female Sprague-Dawley rats
beginning at six weeks of age at concentrations of 2,500, 1,500, 500, 250,
50, or 0 mg/L.  Animals were kept under observation until spontaneous death.
Formaldehyde and acetaldehyde were found to produce an increase in total
malignant tumors in the treated groups and showed specific carcinogenic
effects on various organs and tissues. PMID: 12562630

Soffritti M, Belpoggi F, Cevolani D, Guarino M, Padovani M, Maltoni C.
Results of long-term experimental studies on the carcinogenicity of methyl
alcohol and ethyl alcohol in rats. In: Mehlman MA, Bingham E, Landrigan PJ,
et al.
Carcinogenesis bioassays and protecting public health.
Commemorating the lifework of Cesare Maltoni and colleagues.
Ann NY Acad Sci 2002; 982: 46-69.

Cancer Research Center, European Ramazzini Foundation for Oncology and
Environmental Sciences, Bologna, Italy. crcfr@...

Methyl alcohol was administered in drinking water supplied ad libitum at
doses of 20,000, 5,000, 500, or 0 ppm to groups of male and female
Sprague-Dawley rats 8 weeks old at the start of the experiment.
Animals were kept under observation until spontaneous death.
Ethyl alcohol was administered by ingestion in drinking water at a
concentration of 10% or 0% supplied ad libitum to groups of male and female
Sprague-Dawley rats; breeders and offspring were included in the experiment.
Treatment started at 39 weeks of age (breeders), 7 days before mating, or
from embryo life (offspring) and lasted until their spontaneous death.
Under tested experimental conditions, methyl alcohol and ethyl alcohol were
demonstrated to be carcinogenic for various organs and tissues.
They must also be considered multipotential carcinogenic agents.
In addition to causing other tumors, ethyl alcohol induced malignant tumors
of the oral cavity, tongue, and lips.
These sites have been shown to be target organs in man by epidemiologic
studies. Publication Types: Review Review, Tutorial PMID: 12562628


Here I have combined fairly equivalent data from their two aspartame, one
methanol, and one formaldehyde studies. Aspartame groups were 100-150 rats
each, methanol 100 rats each, and formaldehyde 50 rats each (formaldehyde
control groups 100 rats each).

Aspartame and methanol are directly comparable, since the 11% methanol
component of aspartame upon ingestion is immediately and fully released into
the GI tract, and then much of that quickly turned into formaldehyde and
then formic acid, both of which account for the toxicity of methanol.

Comparison of two aspartame, one methanol, one formaldehyde studies:

Males
Females
Males + Females

Animals with lymphomas and leukaemias [hemolymphoreticular neoplasias] % of
each group of animals

Group
100 rats each
70 rats each 2nd cancer study 2007

aspartame dose ppm a
[400 ppm in 20 gm feed = 20 mg/kg rat body weight for 0.4 kg rats)

--------equivalent methanol dose (11% of aspartame)
----------------roughly equivalent formaldehyde dose (30% of methanol)

------------------------20,000-40.0
---------------------------------28.0 #^
-------------------------------- 34.0

I--100,000-29.0
-------------25.0**
-------------27.0

II--50,000--0.0--------5,000-36.0---1,500-46.0 **
-------------25.0**------------24.0------------20.0*
-------------22.5---------------30.0------------33.0

-------------------------------------------1,000-22.0*
---------------------------------------------------22.0*
---------------------------------------------------22.0

---------------------------------------------500-24.0*
--------------------------------------------------14.0
--------------------------------------------------19.0

III-10,000-15.0
-------------19.0*
-------------17.0

--------------------------500-35.0
--------------------------------24.0
--------------------------------29.5

---------------------------100-26.0**
---------------------------------16.0
---------------------------------21.0

---------------------------------------------50-20.0
-------------------------------------------------14.0
-------------------------------------------------17.0

IV---2,000-22.0
-------------18.7*
-------------20.3

------2,000-17.1 70 rats, 2nd study 2007
-------------31.4
-------------24.3


V------400-16.7
-------------20.0**
-------------18.3

--------400-15.7 70 rats, 2nd study 2007
-------------17.1
-------------16.4


---------------------------------------------10--8.0
-------------------------------------------------10.0
--------------------------------------------------9.0

----------------------------15-20.0 [-50 rats ]
--------------------------------10.0 [-50 rats ]
--------------------------------15.0 [100 rats ]

VI------80-15.3
-------------14.7
-------------15.0

VII-------0-20.7------------0-28.0--------0--8.0 [ control groups ]
---------------8.7--------------13.0------------7.0
--------------14.7--------------20.5-----------7.5

-----------0--9.5 2nd cancer study 2007 95 rats each control group
-------------12.6
-------------11.0 190 rats, combined male and female control groups

a ppm Considering the life-span average weight of a rat (male and female) as
400 g and the average consumption of food as 20 g per day

* aspartame, statistically significant p= 0.05;
** aspartame, statistically significant p= 0.01 using poly-k test (k = 3)

# methanol, p<0.05 using X2 test
^ methanol, p<0.05 using Cochrane-Armitage test for dose-response
relationship

* formaldemyde, p<0.05 using X2 test
** formaldehyde, p<0.01 using X2 test

The control groups vary widely, with the percentage of rats with these most
common cancers, present at natural death, ranging from 7.0% to 28.0%.

A layman can only speculate as to the possible causes in a uniform
population of rats in the same huge laboratory facility for decades, such as
various viruses, bacteria, or molds, or variable impurities in the tap
water.

Formaldehyde at 50 ppm shows a doubling of the percentage of rats with these
cancers, for groups of just 50 rats.

It is a safe bet that studies using groups of 100 to 200 rats would
establish significance at this 50 ppm level, which in turn would mandate the
reduction of the present USA EPA level (1999) from 1 ppm for lifetime
exposure to formaldehyde in drinking water to 0.05 ppm, since the human
limit is estimated by dividing the lowest harmful animal level by 1000.

The various standards for methanol and formaldehyde are not in harmony:

We can grasp the main picture by studying the results at a high level of
exposure:

II--50,000--0.0--------5,000-36.0----1,500-46.0 **
-------------25.0**------------24.0------------20.0*
-------------22.5---------------30.0------------33.0

The results amount to 1.3 to 5.75 times their control group levels.
Aspartame, methanol, and formaldehyde results broadly agree.
Unknown factors are causing differences between males and females.
____________________________________________________



http://groups.yahoo.com/group/aspartameNM/message/1475
19,000 people, the 4 % of users of aspartame who drink average 5 cans
daily, have more problems in NIH AARP study of 474,000 people: Murray
2007.09.21
http://RMForAll.blogspot.com September 21, 2007


Table 1. NIH-AARP Diet and Health Study aspartame intake levels from
beverages, 1995-2000 (N = 473,984)
[ adapted from article -- a 12-oz can diet soda has 200 mg aspartame ]

0 - under 100 - 100-200 - 200-400 - 400-600 - 600-1200 - over 1200 mg/d

cohort %
46 ------- 25 ------ 13 ------ 7 -------- 5 -- about 3 --- under 1


This is the first good data about the percentage of aspartame users
who use over 3 cans daily, averaging 5 cans daily at 200 mg per 12 oz
can diet soda.

About 4 % of 473,984 is 19,000 people, with a peak intake of 17 cans
daily, and average 5 cans daily.

It would be worthwhile to investigate a wide variety of symptoms for
the 0.1 % of highest level users, about 500 people.

For about 200 million USA aspartame users, this would be 200,000
people.
____________________________________________________


re "A Few too Many", Joan Acocella, The New Yorker, long review of hangover
research 2008.05.26 -- same levels of formaldehyde and formic acid in FEMA
trailers and other sources (aspartame, dark wines and liquors, tobacco
smoke): Murray 2008.06.05
http://rmforall.blogspot.com/2008_06_01_archive.htm
Thursday, June 5, 2008
http://groups.yahoo.com/group/aspartameNM/message/1541


formaldehyde and formic acid in FEMA trailers and other sources (aspartame,
dark wines and liquors, tobacco smoke): Murray 2008.01.30
http://rmforall.blogspot.com/2008_01_01_archive.htm
Wednesday, January 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1508

The FEMA trailers give about the same amount of formaldehyde and formic acid
daily as from a quart of dark wine or liquor, or two quarts (6 12-oz cans)
of aspartame diet soda, from their over 1 tenth gram methanol impurity (one
part in 10,000), which the body quickly makes into formaldehyde and then
formic acid -- enough to be the major cause of "morning after" alcohol
hangovers.

Methanol and formaldehyde and formic acid also result from many fruits and
vegetables, tobacco and wood smoke, heater and vehicle exhaust, household
chemicals and cleaners, cosmetics, and new cars, drapes, carpets, furniture,
particleboard, mobile homes, buildings, leather... so all these sources add
up and interact with many other toxic chemicals.
____________________________________________________


methanol impurity in alcohol drinks [ and aspartame ] is turned into
neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol Syndrome,
BM Kapur, DC Lehotay, PL Carlen at U. Toronto,  Alc Clin Exp Res 2007 Dec.
plain text: detailed biochemistry, CL Nie et al. 2007.07.18: Murray
2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524

http://www.newyorker.com/reporting/2008/05/26/080526fa_fact_acocella?currentPage\
=all

Annals Of Drinking
A Few Too Many
Is there any hope for the hung over?
by Joan Acocella May 26, 2008  themail@...;

"Wayne Jones, of the Swedish National Laboratory of Forensic Medicine"
[ http://groups.yahoo.com/group/aspartameNM/message/1469
highly toxic formaldehyde, the cause of alcohol hangovers, is
made by the body from 100 mg doses of methanol from
dark wines and liquors, dimethyl dicarbonate, and aspartame:
Murray 2007.08.31 ]

http://groups.yahoo.com/group/aspartameNM/message/1286
methanol products (formaldehyde and formic acid) are main cause
of alcohol hangover symptoms [same as from similar amounts of
methanol, the 11% part of aspartame]: YS Woo et al, 2005 Dec:
Murray 2006.01.20

Addict Biol. 2005 Dec;10(4): 351-5.
Concentration changes of methanol in blood samples during
an experimentally induced alcohol hangover state.
Woo YS, Yoon SJ, Lee HK, Lee CU, Chae JH, Lee CT, Kim DJ.
Chuncheon National Hospital, Department of Psychiatry,
The Catholic University of Korea, Seoul, Korea.
http://www.cuk.ac.kr/eng/ sysop@...
Songsin Campus: 02-740-9714 Songsim Campus: 02-2164-4116
Songeui Campus: 02-2164-4114
http://www.cuk.ac.kr/eng/sub055.htm eight hospitals

[ Han-Kyu Lee ]

A hangover is characterized by the unpleasant physical and mental
symptoms that occur between 8 and 16 hours after drinking alcohol.

After inducing experimental hangover in normal individuals,
we measured the methanol concentration prior to
and after alcohol consumption
and we assessed the association between the hangover condition
and the blood methanol level.

A total of 18 normal adult males participated in this study.

They did not have any previous histories of psychiatric
or medical disorders.

The blood ethanol concentration prior to the alcohol intake
(2.26+/-2.08) was not significantly different from that
13 hours after the alcohol consumption (3.12+/-2.38).

However, the difference of methanol concentration
between the day of experiment (prior to the alcohol intake)
and the next day (13 hours after the alcohol intake)
was significant (2.62+/-1.33/l vs. 3.88+/-2.10/l, respectively).

A significant positive correlation was observed
between the changes of blood methanol concentration
and hangover subjective scale score increment when covarying
for the changes of blood ethanol level (r=0.498, p<0.05).

This result suggests the possible correlation of methanol
as well as its toxic metabolite to hangover. PMID: 16318957

[ The toxic metabolite of methanol is formaldehyde, which in turn
partially becomes formic acid -- both potent cumulative toxins
that are the actual cause of the toxicity of methanol.]

This study by Jones AW (1987) found next-morning hangover
from red wine with 100 to 150 mg methanol
(9.5 % w/v ethanol, 100 mg/l methanol, 0.01 %).
Fully 11% of aspartame is methanol --
1,120 mg aspartame in 2 L diet soda,
almost six 12-oz cans, gives 123 mg methanol (wood alcohol).

Pharmacol Toxicol. 1987 Mar; 60(3): 217-20.
Elimination half-life of methanol during hangover.
Jones AW. wayne.jones@...;
Department of Forensic Toxicology,
University Hospital, SE-581 85 Linkoping, Sweden.

This paper reports the elimination half-life of methanol in human
volunteers.
Experiments were made during the morning after the subjects had
consumed 1000-1500 ml red wine
(9.5 % w/v ethanol, 100 mg/l methanol)
the previous evening. [ 100 to 150 mg methanol ]
The washout of methanol from the body
coincided with the onset of hangover.
The concentrations of ethanol and methanol in blood were
determined indirectly by analysis of end-expired alveolar air.
In the morning when blood-ethanol dropped
below the Km of liver alcohol dehydrogenase (ADH)
of about 100 mg/l (2.2 mM),
the disappearance half-life of ethanol was 21, 22, 18 and 15 min.
in 4 test subjects respectively.
The corresponding elimination half-lives of methanol
were 213, 110, 133 and 142 min. in these same individuals.
The experimental design outlined in this paper can be used
to obtain useful data on elimination kinetics of methanol
in human volunteers without undue ethical limitations.
Circumstantial evidence is presented to link methanol
or its toxic metabolic products, formaldehyde and formic acid,
with the pathogenesis of hangover. PMID: 3588516 ]
____________________________________________________

new stevia products -- Truvia (Cargill), rebiana (Coca-Cola), Stevia Plus
and Sweet Leaf (Wisdom Natural Brands), Zevia (Zevia), also one due from
Pepsi: WebTV: NPICenter.com:  Murray 2008.06.07
http://rmforall.blogspot.com/2008_06_01_archive.htm
Saturday, June 7, 2008
http://groups.yahoo.com/group/aspartameNM/message/1542


http://www.webmd.com/food-recipes/news/20080604/no-calorie-natural-sweetener-on-\
they-way

No-Calorie Natural Sweetener on the Way
Truvia, Made From Stevia, Expected to Debut This Year; Other Stevia Products
Step Up
By Miranda Hitti
WebMD Health News
Reviewed by Louise Chang, MD

June 5, 2008 -- Splenda. NutraSweet. Sweet'N Low. Equal. Those no-calorie
sweeteners may soon have new competition made from stevia, a shrub native to
South America.

Stevia isn't new. It's been used for centuries as a sweetener in South
America and is used Japan.

But in the U.S., stevia may only be sold as a dietary supplement -- not as a
sweetener or a food additive -- due to the FDA's safety concerns. But that
may be about to change.

Truvia, a new stevia product developed by Cargill and Coca-Cola, isn't
settling for supplement status. It's set to debut later this year as a
tabletop sweetener and ingredient in certain Coca-Cola products.

Truvia will have competition. Pepsi has its own stevia product in the works,
and stevia supplements may look to move into the mainstream. All that buzz
could spice up the competition for your sweet tooth.

But are the safety issues settled for good?\

Naturally Calorie-Free

There's no shortage of no-calorie sweeteners on the market. The FDA has
approved five artificial ones:

* Aspartame: Brand names include NutraSweet and Equal.
* Sucralose: Brand name is Splenda.
* Saccharin: Brand names include Sweet'N Low, Sweet Twin, and Necta Sweet.
* Acesulfame-K: Brand names include Sunett and Sweet One.
* Neotame: Approved for use as an ingredient in a wide variety of foods
including baked goods, soft drinks, chewing gum, jams, and syrups.

Truvia differs from those products because it's natural, and it differs from
current stevia products because it's backed by extensive safety studies,
notes Ann Tucker, Cargill's communications director.

Those studies, published in the advance online edition of Food and Chemical
Toxicology, show no signs of the possible health issues -- such as blood
pressure, blood sugar, and reproductive effects -- that have been noted in
some, but not all stevia studies done mainly on animals.

In the Cargill and Coca-Cola funded studies, Truvia didn't affect blood
pressure in healthy people or blood sugar in people with type 2 diabetes.
Further tests in rats show no effects on reproduction, fertility, or other
health problems.

When Will Truvia Debut?

"Is it a go? Yes, it's a go," Cargill spokeswoman Ann Tucker says of Truvia.
But she can't say exactly when Truvia will be available.

"That's the gazillion-dollar question," says Tucker, adding that Truvia will
get a "rigorous review" by the scientific community before it hits the
market.

The FDA says it will review Truvia's case to be considered "generally
recognized as safe," which would pave the way for it to become the first
stevia product allowed as a food additive in the U.S.

Perspective of a Watchdog Group

"No company was able to demonstrate its safety to FDA," David Schardt,
senior nutritionist at the nonprofit Center for Science in the Public
Interest (CSPI), tells WebMD. "Now maybe Cargill has done that. Maybe."

The CSPI hasn't been sweet on stevia because of possible safety issues.

"For good reason, FDA and a lot of other industrialized countries have not
allowed it to be used as a food additive until these safety questions have
been resolved. That's what Cargill thinks they've done ... at least with the
extract that they're selling," says Schardt.

"We've always told consumers you're not going to drop dead if you use it
[stevia] to sweeten your tea," says Schardt. "But there is concern about
using it as a food additive, putting it into a lot of products that are sold
to millions of people."

The CSPI's verdict on Truvia isn't in yet. But Schardt is cautiously
optimistic. "We hope that the stevia extract does prove to be safe."

Sweetness in Moderation

Nutritionist Elaine Magee, MPH, RD -- WebMD's "Recipe Doctor" and the author
of Food Synergy -- has blogged about her "wait and see" view of stevia.

"No matter what the alternative sweetener, including stevia, I would
recommend moderation," Magee writes in an email. "I think that it tricks our
body to taste sweetness and to not get the carbohydrates absorbed in the
bloodstream that the body then expects. For some people I suspect this can
bring on cravings or overeating later, perhaps."

That probably doesn't happen with "smaller amounts (like one diet soda a
day)," writes Magee. "But there are people who have many diet sodas a day.
This then also displaces more healthful beverages like green tea, water, or
nonfat or low-fat milk."

That theory hasn't been proven. But it has come up in past research on diet
sodas and weight gain. That research wasn't related to stevia.

Stevia Competition Heats Up

Pepsi plans to put its own highly purified, zero-calorie, all-natural stevia
sweetener -- which doesn't have a name yet -- in various new products after
it's approved by the FDA, PepsiCo spokesman David DeCecco tells WebMD in an
email.

Meanwhile, a Seattle company called Zevia is already marketing Zevia, a
carbonated dietary supplement containing stevia. The company touts its
product as "the world's only all natural sugar-free alternative to diet
soda." But Zevia hasn't bucked the "dietary supplement" label.

Zevia President and CEO Derek Newman tells WebMD in an email that the
company has perfected the stevia taste with Zevia.

"I would be shocked if Cargill's product is nearly as good," he writes.

In a statement emailed by Tucker, Zanna McFerson, business director for
Cargill Health and Nutrition, says, "There are many stevia blends available
as dietary supplements today. We cannot comment on all the variations and
only know that we consistently offer a safe, pure, and consistent product."

Truvia's research may not apply to other stevia products, notes Schardt.

"If you believe Cargill, the research establishing its safety is on a
particular extract, a pure extract [Truvia], and that it doesn't necessarily
apply to something else that's not quite the same. So that's an issue that I
guess FDA is going to have to address," says Schardt.

View Article Sources

SOURCES:

Ann Tucker, director of communications, Cargill. Ann_Tucker@...;

FDA.

David Schardt, senior nutritionist, Center for Science in the Public
Interest.
1875 Connecticut Avenue, NW, Suite 300, Washington, DC 20009
Phone 202-332-9110  Fax 202-265-4954  Email cspi@...;
www.cspinet.org/

Elaine Magee, MPH, RD, WebMD "Recipe Doctor"; author, Food Synergy.
http://recipedoctor.com/  elaine@...;

About Elaine

Elaine Magee is positively passionate about changing the way America
eats-one recipe at a time! Her national column, THE RECIPE DOCTOR, appears
in newspapers such as the Atlanta Journal-Constitution, Democrat and
Chronicle, Hartford Courant, Honolulu Advertiser, and magazines such as
Today's Health & Wellness. In the column-which she has been writing for the
past decade-she performs recipe "makeovers," in which she is able to bring
down the calories, fat, saturated fat, and sometimes sugar and sodium while
at the same time increasing fiber, phytochemicals, omega-3s, and
monounsaturated fat. Elaine "doctors" real recipes while retaining the
original good taste. And she keeps it easy. She believes that if there is a
shortcut in the kitchen, you should take it!

Elaine is the author of more than 25 books on nutrition and healthy cooking,
with her most recent book being FOOD SYNERGY (Rodale, March 2008). Elaine's
medical nutrition series includes TELL ME WHAT TO EAT IF I HAVE DIABETES,
TELL ME WHAT TO EAT IF I HAVE IRRITABLE BOWEL SYNDROME, TELL ME WHAT TO EAT
IF I HAVE ACID REFLUX. Hundreds of thousands of these books have been sold,
and they are now being distributed all over the world, including China,
Russia, Spain, Indonesia, and Arabic countries. New editions of these three
books in the series will be released October-December 2008.

Elaine is a nutrition expert/writer for WEBMD.com, SilverPlanet.com, and
magazines across the country, and she appears frequently on radio,
educational videos, and television shows. She has appeared on Eye on the Bay
in San Francisco, the Fine Living Network, the CBS Evening News, Mornings On
2 in San Francisco, and AM Northwest in Portland. She also conducted monthly
healthy cooking segments for the Saturday morning news on NBC-San Francisco
for two years. For two years before that, Elaine performed the "Light
Cooking" segment for the KSBW-TV (NBC) midday news in Salinas, California.
She was the writer and guest on a video with Teri Garr on multiple sclerosis
and with Shekhar Challa, M.D., on "The Heartburn Friendly Kitchen."

Elaine graduated as the Nutrition Science Department "Student of the Year"
from San Jose State University with a bachelor of science in nutrition and a
minor in chemistry. She also obtained her master's degree in public health
nutrition from UC-Berkeley and is a registered dietitian. She was a
nutrition instructor at Diablo Valley College for two years and the
nutrition marketing specialist (California Department of Health) for the now
national "5 a Day" health program for three years.

Other recent projects:
* Elaine is getting ready to launch her internet cooking show (stay tuned).
* Elaine was part of a satellite media tour in November 2007 on the topic of
heartburn and the holidays.
* Elaine was the recipe developer for Pfizer pharmaceuticals, providing
recipes to its website specific to three medical issues: high blood
pressure, high blood cholesterol, and diabetes.


WebMD Medical News: "Drink More Diet Soda, Gain More Weight?"

David DeCecco, spokesman, PepsiCo.

Derek A. Newman, president and CEO, Zevia.  DNewman@...;
http://www.zevia.com/  800.230.2221 zevia@...;
Zevia LLC, 505 Fifth Avenue South, Suite 610, Seattle, WA 98104
ian@...; jessica@...; michael@...; jeff@...;
stacey@...; brian@...; junior@...;


Email statement, Zanna McFerson, business director, Cargill Health and
Nutrition
Zanna_McFerson@...;

© 2008 WebMD, LLC. All rights reserved.

Miranda Hitti

Miranda Hitti is a medical writer for WebMD. Before joining WebMD full time,
she freelanced for WebMD and publications including Cooking Light, The
Atlanta Journal/Constitution, and Arthritis Today. She began her career by
working at CNN for five years.

Besides health, she has also covered topics including business, personal
finance, design, and architecture. Hitti's articles have appeared in This
Old House, Better Homes and Gardens, Fidelity Stages, Fidelity Focus, the
Atlanta Business Chronicle, and numerous other magazines, newspapers, and
web sites. She is the author of Life Lessons: A Guided Journal.

In 2004, Hitti received two Dalton Pen Communications Awards of Excellence
for articles written for Fidelity Stages, a personal finance magazine.

A graduate of Duke University, Hitti has a bachelor's degree in cultural
anthropology and a certificate in film and video.


Louise Chang, MD

Louise Chang, MD, is part of the WebMD medical editing team and is
responsible for reviewing WebMD news and feature stories to ensure their
medical accuracy. She has always considered herself a patient advocate and
educator at heart. She has had broad experience of both inpatient and
outpatient practice in urban and suburban settings. Dr. Chang shares the
WebMD mission to provide the most accurate and useful medical information
for people.

Dr. Chang completed her undergraduate degree at Stanford University and
attended medical school at New York Medical College. She completed her
internal medicine residency at Saint Vincent's Hospital in New York City,
where she also served as a chief resident from 2001-2002. Immediately prior
to joining WebMD, Dr. Chang worked as an attending physician and clinical
instructor at Grady Memorial Hospital as part of the Emory School of
Medicine in downtown Atlanta, seeing patients and working with and teaching
medical residents and students.

Dr. Chang is board-certified in internal medicine. She is a member of both
the American College of Physicians and the Society of General Internal
Medicine. Her prior research work has been published and presented at
regional and national conferences.

https://data.webmd.com/sdclive/SdcForm.aspx?FormId=magSupport
Contact WebMD, 1,000 character limit
____________________________________________________


http://www.npicenter.com/anm/templates/newsATemp.aspx?articleid=21381&zoneid=9

Sweet Success for Stevia.finally
2008-06-06 - Functional Ingredients magazine

By Kimberly Lord Stewart  editor@...;

After decades of controversy, two sweeteners, derived from the stevia plant,
may finally get their day in the consumer marketplace as something more than
a dietary supplement. On May 15, Cargill introduced TRUVIA, a branded
sweetener made from rebiana for use in foods and beverages. Within two weeks
of the Cargill announcement, Arizona based Wisdom Natural Brands, shipped
Sweet Leaf® sweetener, made from steviol glycosides, to grocers across the
country. Industry experts say with these two announcements, the race is on
to gain consumer acceptance and brand awareness.

The first test will be restaurants and coffee shops. "It will be a race to
who can own the tabletop market," says Kantha Shelke, Ph.D., industry
consultant from Corvus Blue. Shelke believes that consumers will form their
first impression of rebiana or stevia when they try it from the little
packets the coffee bar or restaurant table. It is a low-risk approach, she
says. "If it a pleasant experience, the taste will linger in consumer's food
memories and thus relieve any doubts." One of the drawbacks to previously
tested stevia dietary-supplement brands is an aftertaste reminiscent of
licorice. Rebiana and steviol glycosides contain no such aftertaste,
according to both company reports.

In as early as Feb. 1986, FDA issued import alerts for stevia, branding it
as an ingredient that should be detained if labeled as anything other than a
dietary supplement. Many saw the controversy as a political quarrel with the
end goal of quashing competition with the emerging artificial sweetener
market.

For now, TRUVIA and Sweet Leaf change all that. Why the attitude adjustment?
Even though the simultaneous release of Sweet Leaf and TRUVIA could easily
be compared to a David and Goliath corporate competition -- both companies
used the same sling shot -- a route called "self-determination of GRAS
status." This allows for the safety of the product to be decided by the
views of experts, as long as there are significant published, peer-reviewed
studies, available in the public domain. Wisdom Natural Brands and Cargill
both hired teams of stevia experts (with FDA experience) to garner enough
scientific support for each of their respective ingredients.

For Jim May, CEO of Wisdom Natural Brands, who introduced stevia to the US
marketplace from Paraguay in 1982, achieving self-determination GRAS status
was a hallmark moment. After decades of defending the safety of stevia, May
had enough proof in March of 2008 to move stevia up on the food chain, thus
allowing it to be sold on the sugar shelf, rather than relegated to the
dietary-supplement aisle. "No pun intended, but for me, this day is sweet
victory," May said.

For Cargill, the TRUVIA announcement was no less sweet. In partnership with
Coca-Cola, Cargill spent years evaluating the ingredient for safety and
perfecting ways to extract, what they consider, the best tasting component
of the stevia plant, called rebaudioside A. Research, funded by Cargill, and
published electronically on May 16, 2008, in the peer-reviewed scientific
journal, Food and Chemical Toxicology, demonstrated the safety of rebiana
for use in sweetened food and beverages.

"It is important to note that TRUVIA is rebiana, not stevia," says Steve
Snyder, VP Global Business Director, High Intensity Sweeteners, Cargill
Health & Nutrition. "Both stevia and rebiana come from the leaves of the
stevia plant. Stevia is a sweetener that exists in the marketplace today as
a dietary supplement. It is not a high-purity ingredient and its composition
can vary widely - impacting quality and taste. Rebiana is a high-purity,
fully-characterized extract that is consistently produced to a food-grade
specification by Cargill." See the sidebar below for more on the difference
between stevia, rebiana and steviol glycosides.

Industry experts believe both forms of the no-calorie sweetener open new
doors for the tabletop and beverage market, especially for consumers seeking
an alternative to artificial sweeteners. Cargill plans to introduce a
tabletop sweetener by end of year, though Coca-Cola has not announced the
exact release date of its new TRUVIA-based beverages, citing competitive
reasons. Wisdom Natural Brands began shipping their new Sweet Leaf sweetener
to stores on June 2. They currently serve 99% of all natural product stores
and thousands of grocery stores with their Stevia Plus brand.

The value of the alternative sweetener market is $915 million and continues
to grow, according to Freedonia Group, a global research firm. Earlier this
year the company said stevia (and agave) held the most hope for a widely
accepted alternative sweetener. The reasons are many. First, according to
recent research by the Department of Diabetes and Endocrinology, National
University in Paraguay, steviol glycosides have no ill effects on blood
sugar or blood pressure in patients with type I or type II diabetes.
Secondly, there is little argument about stevia being deemed a natural
ingredient, which is an ongoing debate between the sucralose and sugar
industry. And, since it is a non-GMO product, widespread acceptance in Asian
and European markets is another plus. According to the Stevia Association in
Paraguay, the product has applications in:

Beverages (low-calorie or no-sugar drinks) and milk drinks
Candy, ice cream, yogurt, jams
Canned and jarred fruits
Sweet and sour foods, sauces, pickles
Gums and candies
Table sweeteners
Toothpaste

[sidebar] Rebiana Refresher

Stevia typically refers to a crude preparation (powder or liquid) made from
the leaves of the stevia plant.  Such preparations contain a mixture of many
components, not just those that give a sweet taste to the leaf.  Because the
exact composition of the mixture is unknown, studies that have used "stevia"
are often difficult to interpret.

Steviol glycosides are the sweet components of the stevia leaf. There are
various kinds of steviol glycosides, but the two most abundant types are
stevioside and rebaudioside A.

Stevioside is the most abundant steviol glycoside in the stevia leaf, and
the most studied.

Rebaudioside A is the best-tasting steviol glycoside.  It is broken down by
the body into the same basic parts as stevioside.

Rebiana is a 97-percent pure extract of rebaudioside A. It is the first
high-purity, well-characterized form of rebaudioside A.

Steviol is the substance produced when the body breaks down steviol
glycosides in the colon.

Source: Cargill, Overview of the Rebiana Research Program, May 2008
____________________________________________________


stevia herbal sweetener to be sold as Truvia (rebiana) by Cargill and
Coca-Cola, if blitz of 12 studies wins FDA approval in 30-90 days: Murray
2008.05.24
http://rmforall.blogspot.com/2008_05_01_archive.htm
Saturday, May 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1540


re "A Few too Many", Joan Acocella, The New Yorker, long review of hangover
research 2008.05.26 -- same levels of formaldehyde and formic acid in FEMA
trailers and other sources (aspartame, dark wines and liquors, tobacco
smoke): Murray 2008.06.05
http://rmforall.blogspot.com/2008_06_01_archive.htm
Thursday, June 5, 2008
http://groups.yahoo.com/group/aspartameNM/message/1541

methanol impurity in alcohol drinks [ and aspartame ] is turned into
neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol Syndrome,
BM Kapur, DC Lehotay, PL Carlen at U. Toronto, Alc Clin Exp Res 2007 Dec.
plain text: detailed biochemistry, CL Nie et al. 2007.07.18: Murray
2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524

formaldehyde and formic acid in FEMA trailers and other sources (aspartame,
dark wines and liquors, tobacco smoke): Murray 2008.01.30
http://rmforall.blogspot.com/2008_01_01_archive.htm
Wednesday, January 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1508

The FEMA trailers give about the same amount of formaldehyde and formic acid
daily as from a quart of dark wine or liquor, or two quarts (6 12-oz cans)
of aspartame diet soda, from their over 1 tenth gram methanol impurity (one
part in 10,000), which the body quickly makes into formaldehyde and then
formic acid - enough to be the major cause of "morning after" alcohol
hangovers.

Methanol and formaldehyde and formic acid also result from many fruits and
vegetables, tobacco and wood smoke, heater and vehicle exhaust, household
chemicals and cleaners, cosmetics, and new cars, drapes, carpets, furniture,
particleboard, mobile homes, buildings, leather. so all these sources add up
and interact with many other toxic chemicals.

"Of course, everyone chooses, as a natural priority, to enjoy peace, joy,
and love by helping to find, quickly share, and positively act upon evidence
about healthy and safe food, drink, and environment."

Rich Murray, MA Room For All rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com new primary archive

http://groups.yahoo.com/group/aspartameNM/messages
group with 125 members, 1,542 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1,112 members, 22,714 posts in public archive

"Application of the hair of the dog may sound like nothing more than a way
of getting yourself drunk enough so that you don't notice you have a
hangover, but, according to Wayne Jones, of the Swedish National Laboratory
of Forensic Medicine, the biochemistry is probably more complicated than
that.

Jones's theory is that the liver, in processing alcohol, first addresses
itself to ethanol, which is the alcohol proper, and then moves on to
methanol, a secondary ingredient of many wines and spirits.
[ Just over 1 part in 10,000 = 100 mg methanol per liter -- the same level
of methanol as in 2 liters (6 12 oz cans) diet soda ]

Because methanol breaks down into formic acid, which is highly toxic, it is
during this second stage that the hangover is most crushing.

If at that point you pour in more alcohol, the body will switch back to
ethanol processing. This will not eliminate the hangover - the methanol
(indeed, more of it now) is still waiting for you round the bend - but it
delays the worst symptoms. It may also mitigate them somewhat. On the other
hand, you are drunk again, which may create difficulty about going to work."

http://www.newyorker.com/reporting/2008/05/26/080526fa_fact_acocella?currentPage\
=all

Annals Of Drinking
A Few Too Many
Is there any hope for the hung over?
by Joan Acocella May 26, 2008 themail@...;
[ more at initial URL ]
____________________________________________________

re "A Few too Many", Joan Acocella, The New Yorker, long review of hangover
research 2008.05.26 -- same levels of formaldehyde and formic acid in FEMA
trailers and other sources (aspartame, dark wines and liquors, tobacco
smoke): Murray 2008.06.05
http://rmforall.blogspot.com/2008_06_01_archive.htm
Thursday, June 5, 2008
http://groups.yahoo.com/group/aspartameNM/message/1541


formaldehyde and formic acid in FEMA trailers and other sources (aspartame,
dark wines and liquors, tobacco smoke): Murray 2008.01.30
http://rmforall.blogspot.com/2008_01_01_archive.htm
Wednesday, January 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1508

The FEMA trailers give about the same amount of formaldehyde and formic acid
daily as from a quart of dark wine or liquor, or two quarts (6 12-oz cans)
of aspartame diet soda, from their over 1 tenth gram methanol impurity (one
part in 10,000), which the body quickly makes into formaldehyde and then
formic acid -- enough to be the major cause of "morning after" alcohol
hangovers.

Methanol and formaldehyde and formic acid also result from many fruits and
vegetables, tobacco and wood smoke, heater and vehicle exhaust, household
chemicals and cleaners, cosmetics, and new cars, drapes, carpets, furniture,
particleboard, mobile homes, buildings, leather... so all these sources add
up and interact with many other toxic chemicals.

methanol impurity in alcohol drinks [ and aspartame ] is turned into
neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol Syndrome,
BM Kapur, DC Lehotay, PL Carlen at U. Toronto,  Alc Clin Exp Res 2007 Dec.
plain text: detailed biochemistry, CL Nie et al. 2007.07.18: Murray
2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524

"Of course, everyone chooses, as a natural priority, to enjoy peace, joy,
and love by helping to find, quickly share, and positively act upon evidence
about healthy and safe food, drink, and environment."

Rich Murray, MA Room For All rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com  new primary archive

http://groups.yahoo.com/group/aspartameNM/messages
group with 125 members, 1,541 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1,109 members, 22,714 posts in public archive

http://www.newyorker.com/reporting/2008/05/26/080526fa_fact_acocella?currentPage\
=all

Annals Of Drinking
A Few Too Many
Is there any hope for the hung over?
by Joan Acocella May 26, 2008  themail@...;

"Wayne Jones, of the Swedish National Laboratory of Forensic Medicine"
[ http://groups.yahoo.com/group/aspartameNM/message/1469
highly toxic formaldehyde, the cause of alcohol hangovers, is
made by the body from 100 mg doses of methanol from
dark wines and liquors, dimethyl dicarbonate, and aspartame:
Murray 2007.08.31 ]

http://groups.yahoo.com/group/aspartameNM/message/1286
methanol products (formaldehyde and formic acid) are main cause
of alcohol hangover symptoms [same as from similar amounts of
methanol, the 11% part of aspartame]: YS Woo et al, 2005 Dec:
Murray 2006.01.20

Addict Biol. 2005 Dec;10(4): 351-5.
Concentration changes of methanol in blood samples during
an experimentally induced alcohol hangover state.
Woo YS, Yoon SJ, Lee HK, Lee CU, Chae JH, Lee CT, Kim DJ.
Chuncheon National Hospital, Department of Psychiatry,
The Catholic University of Korea, Seoul, Korea.
http://www.cuk.ac.kr/eng/ sysop@...
Songsin Campus: 02-740-9714 Songsim Campus: 02-2164-4116
Songeui Campus: 02-2164-4114
http://www.cuk.ac.kr/eng/sub055.htm eight hospitals

[ Han-Kyu Lee ]

A hangover is characterized by the unpleasant physical and mental
symptoms that occur between 8 and 16 hours after drinking alcohol.

After inducing experimental hangover in normal individuals,
we measured the methanol concentration prior to
and after alcohol consumption
and we assessed the association between the hangover condition
and the blood methanol level.

A total of 18 normal adult males participated in this study.

They did not have any previous histories of psychiatric
or medical disorders.

The blood ethanol concentration prior to the alcohol intake
(2.26+/-2.08) was not significantly different from that
13 hours after the alcohol consumption (3.12+/-2.38).

However, the difference of methanol concentration
between the day of experiment (prior to the alcohol intake)
and the next day (13 hours after the alcohol intake)
was significant (2.62+/-1.33/l vs. 3.88+/-2.10/l, respectively).

A significant positive correlation was observed
between the changes of blood methanol concentration
and hangover subjective scale score increment when covarying
for the changes of blood ethanol level (r=0.498, p<0.05).

This result suggests the possible correlation of methanol
as well as its toxic metabolite to hangover. PMID: 16318957

[ The toxic metabolite of methanol is formaldehyde, which in turn
partially becomes formic acid -- both potent cumulative toxins
that are the actual cause of the toxicity of methanol.]

This study by Jones AW (1987) found next-morning hangover
from red wine with 100 to 150 mg methanol
(9.5 % w/v ethanol, 100 mg/l methanol, 0.01 %).
Fully 11% of aspartame is methanol --
1,120 mg aspartame in 2 L diet soda,
almost six 12-oz cans, gives 123 mg methanol (wood alcohol).

Pharmacol Toxicol. 1987 Mar; 60(3): 217-20.
Elimination half-life of methanol during hangover.
Jones AW. wayne.jones@...;
Department of Forensic Toxicology,
University Hospital, SE-581 85 Linkoping, Sweden.

This paper reports the elimination half-life of methanol in human
volunteers.
Experiments were made during the morning after the subjects had
consumed 1000-1500 ml red wine
(9.5 % w/v ethanol, 100 mg/l methanol)
the previous evening. [ 100 to 150 mg methanol ]
The washout of methanol from the body
coincided with the onset of hangover.
The concentrations of ethanol and methanol in blood were
determined indirectly by analysis of end-expired alveolar air.
In the morning when blood-ethanol dropped
below the Km of liver alcohol dehydrogenase (ADH)
of about 100 mg/l (2.2 mM),
the disappearance half-life of ethanol was 21, 22, 18 and 15 min.
in 4 test subjects respectively.
The corresponding elimination half-lives of methanol
were 213, 110, 133 and 142 min. in these same individuals.
The experimental design outlined in this paper can be used
to obtain useful data on elimination kinetics of methanol
in human volunteers without undue ethical limitations.
Circumstantial evidence is presented to link methanol
or its toxic metabolic products, formaldehyde and formic acid,
with the pathogenesis of hangover. PMID: 3588516 ]


"Maria Lucia Souza-Formigoni, a psychobiology researcher at the Federal
University of São Paolo"
[
http://www.newscientist.com/article/dn8901-energy-drink-mixers-give-a-false-sens\
e-of-sobriety.html

Energy drink mixers give a false sense of sobriety
16:52 27 March 2006 NewScientist.com news service,  Roxanne Khamsi

'Roseli Boerngen de Lacerda, who studies substance misuse at the Federal
University of Paraná in Curitiba, Brazil'
boerngen@...;

Alcohol Clin Exp Res. 2006 Apr; 30(4): 598-605.
Effects of energy drink ingestion on alcohol intoxication.
Ferreira SE, de Mello MT, Pompéia S, de Souza-Formigoni ML.
Department of Psychobiology, Federal University of Sao Paulo (UNIFESP), the
FAPESP fellowship, São Paulo-SP, Brasil.
PMID: 16573577
Sionaldo Eduardo Ferreira
Marco Túlio de Mello
Sabine Pompéia
Maria Lucia Oliveira de Souza-Formigoni, PhD  Department of Psychobiology,
Federal University of Sao Paulo (UNIFESP), Rua Botucatu n° 862 1° Andar,
Vila Clementino, São Paulo-SP, Brasil; Fax: +55-11-5572-5092; E-mail:
mlformig@...; ]


"Manuela Neuman, a Canadian researcher on alcohol-induced liver damage"
[ manuela@...;
Manuela Neuman, PhD
Division of Clinical Pharmacology, 2075 Bayview Ave E 242
Sunnybrook HSC, M4N 3M5 Toronto, Ont., Canada
Tel. +1 416 480 6100 ext. 3503, Fax +1 416 480 6025 ]

"Jeffrey Wiese, of Tulane University"
[ MD, Phone Number 504.988.1143  jwiese@... ]


"Emil Chiaberi, a co-founder of RU-21's manufacturer, Spirit Sciences, in
California"
[ http://www.spirit-sciences.com/
Mandy Barton, Director of Non-Profit Campaigns, at mb@...;
Spirit Sciences USA, Inc
9454 Wilshire Blvd, Suite 600
Beverly Hills, CA 90212
Telephone  310.568.1030   866.556.5577  Facsimile  310.861.5612
General  info@...;

http://www.ru21.com/
"Dr. Kenneth D Krull, Ph. D., Clinical Biochemist" (I found no leads via
Google )

http://en.wikipedia.org/wiki/RU-21
"Antipokhmelin is a Russian tablet that helps to prevent or overcome the
negative effects of alcohol consumption and hangover. The main ingredient is
succinic acid, also found in amber. It is marketed as RU-21 in the US and
UK. Claims of effectiveness are based primarily on anecdotal evidence, and
there have been no known placebo controlled double blind studies published
in peer reviewed scientific journals.

RU-21 was developed by Prof. Eugene Mayevski at the Institute of Theoretical
and Experimental Biophysics (division of the Russian Academy of Sciences),
where the product was also clinically tested. Further tests were conducted
at the Russian Ministry of Public Health. " ]


"Robert Lindsey, the president of the National Council on Alcoholism and
Drug Dependence"
[
http://www.hoovers.com/national-council-on-alcoholism-and-drug-dependence/--ID__\
130643,PID__13615899,target__company_executive--/free-co-samples-index.xhtml
Robert J. Lindsey
Mr. Lindsey has been in the forefront of the alcoholism and addiction
recovery services community for over 30 years as an employee assistance
professional, Director of Community Relations for the Betty Ford Center, and
Executive Director of a state and a local NCADD Affiliate.
Mr. Lindsey holds a B.A. in Psychology, a Masters of Science in Education
from St. Bonaventure University in New York, and is a Certified Employee
Assistance Professional (CEAP).....
http://www.canys.net/councils.htm
Robert Lindsey, President & CEO NCADD
20 Exchange Place, Suite 2902, New York , NY 10005-3201
Phone: (212) 269-7797   Fax: (212) 269-7510
www.ncadd.org   Email: president@...; ]


"Robert Swift, an alcohol researcher who teaches at Brown University"
[ http://groups.yahoo.com/group/aspartameNM/message/1047
Avoiding Hangover Hell 2003.12.31 Mark Sherman, AP writer:
Robert Swift, MD [ formaldehyde from methanol in aspartame ]:
Murray 2004.01.16

Robert_Swift_MD@...; joe.schwarcz@...; ]


"Genevieve Ames and her research team at the Prevention Research Center, in
Berkeley"
[ http://sph.berkeley.edu/faculty/ames.html
Genevieve Ames, Ph.D., Adjunct Professor of Medical Anthropology
PHONE: (510) 883-5726  FAX: (510) 644-0594
LOCATION:1995 University Ave., #450, Berkeley, CA 94704
E-MAIL: ames@...;
Research Interests
Anthropology of Health and Healing
Environmental approaches to prevention of substance abuse
Integrating Quantitative and Qualitative Methods
Workplace and alcohol problem prevention ]
____________________________________________________


methanol impurity in alcohol drinks [ and aspartame ] is turned into
neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol Syndrome,
BM Kapur, DC Lehotay, PL Carlen at U. Toronto,  Alc Clin Exp Res 2007 Dec.
plain text: detailed biochemistry, CL Nie et al. 2007.07.18: Murray
2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524

[ Rich Murray comments:  As a medical layman volunteer information
activist for aspartame and related toxicity issues since January 1999,
I note with appreciation the remarkable exponential progress on all
fronts, including a rapidly emerging consensus about the primary
importance of all toxicity challenges for our world.

This lengthy review features in detail two quite different, revolutionary
contributions, from Canada,  and England and China.

It is indicative of our times that the CL Nie et al. study, 2007
appears in a free, open access journal-- indeed,
as all life and death information must.

Following rather vigorously, indeed blindly, the imperatives of
single-minded, profit-driven capitalist competition -- manipulating
adroitly research, education, media, citizens, governments -- many
great global corporations have inevitably created results that
oppose the common good.  Alcohol and tobacco are well known.

Realistically, any further manipulations can only lead to inevitable
and even sudden corporate meltdowns, in the context of an
unfettered, cooperative, democratic global information forum,
the Internet.

Now, it is as easy and cheap to compose and instantly post a
30-page review as 3 pages a decade ago -- and such reviews
are archived forever in multiple collections, open via global search
engines to a billion Net citizens.

Perforce, and increasingly happily, all societal entities will have to
operate by high and shared voluntary universal standards
for the common good. ]


http://www.blackwell-synergy.com/doi/abs/10.1111/j.1530-0277.2007.00541.x

Alcoholism: Clinical and Experimental Research
Volume 31 Issue 12 Page 2114-2120, December 2007

Bhushan M. Kapur,  b.kapur@...;
Arthur C. Vandenbroucke, PhD, FCACB
Yana Adamchik,
Denis C. Lehotay,  dlehotay@...;
Peter L. Carlen  carlen@...;
(2007) Formic Acid, a Novel Metabolite of Chronic Ethanol
Abuse, Causes Neurotoxicity, Which Is Prevented by Folic Acid
Alcoholism: Clinical and Experimental Research 31 (12), 2114-2120.
doi:10.1111/j.1530-0277.2007.00541.x

Abstract

Background:
Methanol is endogenously formed in the brain and is present as a
congener in most alcoholic beverages.

Because ethanol is preferentially metabolized over methanol (MeOH)
by alcohol dehydrogenase, it is not surprising that MeOH
accumulates in the alcohol-abusing population.

This suggests that the alcohol-drinking population will have higher
levels of MeOH's neurotoxic metabolite, formic acid (FA).

FA elimination is mediated by folic acid.

Neurotoxicity is a common result of chronic alcoholism.

This study shows for the first time that FA,
found in chronic alcoholics, is neurotoxic
and this toxicity can be mitigated by folic acid administration.

Objective:
To determine if FA levels are higher in the alcohol-drinking
population and to assess its neurotoxicity in organotypic
hippocampal rat brain slice cultures.

Methods:
Serum and CSF FA was measured in samples from both ethanol
abusing and control patients, who presented to a hospital emergency
department.  [ CSF = Cerebral Spinal Fluid ]

FA's neurotoxicity and its reversibility by folic acid were assessed
using organotypic rat brain hippocampal slice cultures using clinically
relevant concentrations.

Results:
Serum FA levels in the alcoholics
(mean ± SE: 0.416 +- 0.093 mmol/l, n = 23)
were significantly higher than in controls
(mean ± SE: 0.154 +- 0.009 mmol/l, n = 82) (p < 0.0002).

FA was not detected in the controls' CSF (n = 20),
whereas it was >0.15 mmol/l in CSF of 3 of the 4 alcoholic cases.

Low doses of FA from 1 to 5 mmol/l added for 24, 48 or 72 hours
to the rat brain slice cultures caused neuronal death as measured by
propidium iodide staining.

When folic acid (1 umol/l) was added with the FA,
neuronal death was prevented. [ umol = micromole ]

Conclusions:
Formic acid may be a significant factor in the neurotoxicity of
ethanol abuse.

This neurotoxicity can be mitigated by folic acid administration
at a clinically relevant dose.

Key Words:
Formic Acid, Folic Acid, Methanol, Neurotoxicity, Alcoholism.

From the Department of Clinical Pathology (BMK),
Sunnybrook Health Science Centre,
Division of Clinical Pharmacology and Toxicology,
The Hospital for Sick Children, Toronto, Ontario, Canada;

St. Michael's Hospital (ACV), Toronto, Canada;

Department of Laboratory Medicine and Pathobiology
(BMK, ACV), Faculty of Medicine,
University of Toronto, Toronto, Ontario, Canada;

Departments of
Medicine (Neurology) and Physiology (YA, PLC),
Toronto Western Research Institute,
University of Toronto, Toronto, Ontario, Canada;

and University of Saskatchewan (DLC), Saskatchewan, Canada.

Received for publication May 1, 2007;
accepted September 24, 2007.

Reprint requests: Dr. Bhushan M. Kapur,
Department of Clinical Pathology,
Sunnybrook Health Science Centre,
2075 Bayview Ave, Toronto, Ontario, M4N 3M5, Canada;
Fax: 416-813-7562; E-mail: b.kapur@...;

Copyright  2007 by the Research Society on Alcoholism.
DOI: 10.1111/j.1530-0277.2007.00541.x
Alcoholism: Clinical and Experimental Research 2007 Dec.
Alcohol Clin Exp Res, Vol. 31, No 12, 2007: pp 2114-2120

NEUROTOXICITY AND BRAIN damage are common
concomitants findings of chronic alcoholism
(Carlen and Wilkinson, 1987; Carlen et al., 1981; Harper,
2007).

The cause of ethanol-induced neurotoxicity is still unclear.

We present here a novel hypothesis for neurotoxicity:
increased formic acid (FA) levels produced from methanol
(MeOH), whose catabolism is blocked by ethanol.

Axelrod and Daly (1965) demonstrated the endogenous formation
of MeOH from S-adenosylmethionine (SAM) in the pituitary
glands of humans and various other mammalian species.

Presence of MeOH in the breath of human subjects was
reported by Ericksen and Kulkarni (1963).

Most alcoholic beverages also have a small amount of MeOH
as a congener (Sprung et al., 1988).

As ethanol (EtOH) has a higher affinity for
alcohol dehydrogenase (ADH) than MeOH,
EtOH is preferentially metabolized (Mani et al., 1970).

As a result, MeOH accumulation from endogenously produced
MeOH, and/or, that consumed as part of an alcoholic beverage,
has been reported in concentrations up to 2 mmol/l in heavy
drinkers (Majchrowicz and Mendelson, 1971).

Toxicity resulting from MeOH consumption is extensively
documented in both humans and animals and has been
attributed to its metabolite, FA (Benton and Calhoun, 1952;
Roe, 1946, 1955; Wood, 1912; Wood and Buller, 1904).

The rate of formate oxidation and elimination is dependent on
adequate levels of hepatic folic acid, particularly hepatic
tetrahydrofolate (THF)
(Johlin et al., 1987; Tephly and McMartin, 1974).

Significantly higher formate levels were obtained when
folate-deficient animals were exposed to MeOH as compared
with folate-sufficient animals (Lee et al., 1994;
McMartin et al., 1975; Noker et al., 1980).

To understand ethanol's toxicity, one must consider FA
produced from MeOH, and its elimination mediated by folic acid.

We postulate that in the chronically drinking patient,
we will find higher levels of FA than in the nondrinking population,
and that formate is neurotoxic.

We also hypothesize that treatment with folic acid, which is a
critical factor in the catabolism of FA, can prevent or
diminish FA neurotoxicity.....

DISCUSSION

There are at least 2 sources of MeOH:
endogenous production of MeOH (Axelrod and Daly, 1965;
Ericksen and Kulkarni, 1963; Gilg et al., 1987;
Iffland and Staak, 1990; Jones and Lowinger, 1988;
Majchrowicz and Mendelson, 1971; Roine et al., 1989;
Sarkola and Eriksson, 2001; Sprung et al., 1988),

and its presence as a congener in most alcoholic beverages
(Sprung et al., 1988).

MeOH concentrations between 4 and 4500 mg/l can be
present in various alcoholic beverages (Sprung et al., 1988).

Majchrowicz and Mendelson (1971) in an elegant experiment,
showed a rise in MeOH levels in subjects
drinking MeOH-free alcohol, thus supporting
the previous findings of endogenous production of MeOH.

Endogenous production of MeOH was described again in
2001 by Sarkola and Eriksson (2001).

These authors gave 4-methyl pyrazole,
a competitive inhibitor of ADH,
to volunteers not exposed to EtOH and observed a significant
elevation in endogenous EtOH and MeOH plasma levels.

MeOH levels rose linearly from 20 ± 14 umol/l to 39 ± 22 umol/l.

It took 195 minutes for EtOH levels to reach their peak (from
<5 umol/l to 30 ± 20 umol/l) concentrations as compared
with 420 minutes for MeOH,
suggesting gradual accumulation of MeOH
and preferential elimination of EtOH.

Altered pharmacokinetic behavior of MeOH in the presence of
EtOH has been demonstrated by various authors
(Lesch et al., 1990; Martensson et al., 1988).

As a result of continuous drinking
and the preferential metabolism of EtOH,
MeOH levels will rise in chronic drinkers
(Gilg et al., 1987; Iffland and Staak, 1990;
Jones and Lowinger, 1988; Majchrowicz and Mendelson, 1971;
Roine et al., 1989; Sprung et al., 1988).

MeOH has even been suggested as a marker for alcohol abuse
(Iffland and Staak, 1990; Roine et al., 1989).

As MeOH is metabolized to FA, this would suggest
that there could be a steady increase in FA levels
to some concentration at which equilibrium is reached.

It has been suggested that the concentration of MeOH
remains almost constant until EtOH levels have decreased to
about 4 mmol/l (Martensson et al., 1988).

Our data do indeed show this pattern.

In the 4 patients in whom we had multiple samples,
initially there was equilibrium between MeOH and FA.

The frequency of sample collection in all our patients
was based on the attending physician's clinical reason.

As a result, in all the 4 patients and the patient represented in
Fig. 1, there is a large time gap between the last 2 samples.

Our patient data (Fig. 1) do suggest that there must have been
an exponential rise in FA as EtOH approached 4 mmol/l
(Table 2).

Our data suggest that in the plasma of an alcohol-drinking person,
there can be elevated levels of FA (Table 3).

Two nonfree radical pathways have been proposed for formate
conversion to carbon dioxide: oxidation through the
catalase-peroxidative system (Chance, 1950),
and one-carbon pool.

Formate enters the one-carbon pool by combining with
THF to form 10-formyl-THF, a reaction catalyzed
by 10-formyl-THF synthetase (Johlin et al., 1987).

This is followed by the oxidation of 10-formyl-THF
to carbon dioxide mediated
by 10-formyl THF dehydrogenase (10-FTHFDH).

Studies have shown that this is the major route of formate
metabolism (Chiao and Stokstad, 1977; Johlin et al., 1987;
Makar and Tephly, 1976; Palese and Tephly, 1975)

and the predominant one in primates (McMartin et al., 1977).

Formate oxidation to carbon dioxide is dependent upon folic acid
in rats, monkeys (McMartin et al., 1977; Noker et al., 1980),
and in humans (liver) (Johlin et al., 1989).

Although liver is the main source for folate,
Neymeyer and Tephly (1994) and Neymeyer et al. (1997))
showed the presence of folate and 10-FTHFDH in the
retina, optic nerve, and in the various regions of the rat brain.

Folate was found to be between 3% and 14%
of that found in the liver.

The presence of folate and 10-FTHFDH in brain suggests
that formate can be metabolized in these tissues.

Folic acid deficiency is a common finding in chronic alcoholics,
(Eells et al., 2000; Halsted et al., 2002b; Herbert, 1990).

Chronic alcohol ingestion reduces the intestinal absorption of
dietary folic acid leading to a decrease in the folate metabolic
pool (Halsted et al., 2002b).

A decrease in this pool prolongs the formate blood levels
by decreasing the rate at which formate combines with THF,
the first step in its metabolism to carbon dioxide
and leads to formate-mediated cytotoxicity
(McMartin et al., 1977).

Folate deficiency can lead to a decrease in SAM
(Miller et al., 1994).

The overall status of the one-carbon pathway is also dependent
on the levels of methionine and vitamin B6 and B12
(Bailey and Gregory,1999; Barak et al., 1991;
Barber et al., 1999; Halsted et al., 2002a; Lucock, 2000;
Scott et al., 1993).

In situation of poor folate status, S-adenosylhomocysteine (SAH)
concentration increases due to the impairment of methyl group
synthesis and homocysteine re-methylation.

Inhibition by the resulting product, SAH, suppresses many of the
(SAM)-dependent methyl transferase reactions
(Selhub and Miller, 1992; Sokoro, 2007).

A number of studies have shown that there is enzymatic
activity in the brain which can metabolize both ethanol and
acetaldehyde (Brzezinski et al., 1999; Kapoor et al., 2006;
Roberto et al., 2006; Sun and Sun, 2001; Upadhya et al.,
2000; Vasiliou et al., 2006; Yadav et al., 2006;
Zimatkin et al., 2006).

Vasiliou et al. (2006) suggested that "Although the
contribution and CYP2E1 and catalase in ethanol oxidation
may be of little significance, these enzymes appear to play a
significant role in ethanol metabolism in the brain."

Patients in whom we had a CSF samples,
FA was present in 3 of the 4 patient's CSF.

Formic acid was present in all the 4 corresponding serum samples.

The presence of FA in the CSF suggests that either FA crosses
the blood-brain barrier or is formed in situ from the metabolism
of water-soluble MeOH that must have crossed
the blood-brain barrier.

Carlen et al. (1980) showed profound CSF anion gap metabolic
acidosis in alcoholic patients.

Our data showing the presence of FA in CSF may indeed explain
(Holt and Karty, 2003) the observed acidosis.

Formate can cause oxidative stress by producing free radicals
through the Fenton-like reaction (Dikalova et al., 2001;
Walling, 2007).

In this reaction, a hydroxyl radical (OH) is
formed through the Fenton-like reaction, which in turn
oxidized formate (HCO2),
forming the carbon dioxide anion radical (CO2).

The carbon dioxide anion radical then reacts
with molecular oxygen forming carbon dioxide and
the cytotoxic reactive oxygen species (ROS)-  superoxide radical.


H2O2  +  Fe,2+  -->  *OH  +  Fe,3+  +  OH,-

HCO2,-  +  *OH  --> *CO2,-  +  H2O

*CO2,-  +  O2  --> CO2  +  *O2,-


Chance has shown that formate can be metabolized by the
catalase-peroxidative system (Chance, 1950).

When anti-oxidants are depleted, increased ROS are formed
(Treichel et al., 2004).

Formic acid-induced cell damage has been attributed
to the generation of the cytotoxic ROS species.

FA disrupts mitochondrial electron transport and energy production
by inhibiting cytochrome oxidase activity (Nicholls, 1975, 1976;
Sharpe et al., 1982)
and causes cell death by increased production of cytotoxic ROS
secondary to the blockade of the electron transport chain
(Reed and Savage, 1995).

Formyl group (CHO) is transferred to THF
resulting in the formation of carbon dioxide and water
Makar et al., 1990; Medinsky et al., 1997).

Our organotypic brain slice studies suggest that there is a
dose and time relationship between FA and neuronal cell death.

FA levels achieved in the blood of the alcohol drinking
population can cause neuronal cell death.

The FA concentrations we used in our studies are representative
and were achieved in 2 of the 4 patients in whom we had sequential
samples.

It is remarkable that neuronal cell death could be prevented
by folic acid, although the mechanism of this protection is unknown.

There is a large body of literature relating folic acid deficiency
to neural tube defect, but, there are no references
relating low levels of FA to neurotoxicity.

There are a few studies relating FA and mitochondrial inhibition,
with MeOH intoxication and retinal damage
(Seme et al., 1999, 2001).

Another study demonstrated toxic effects of high concentrations
of formate in dissociated primary mouse neural cell cultures
(Dorman et al., 1993).

The concentration of formate that resulted
in 50% lactate dehydrogenase leakage after an 8-hour incubation
was estimated to be 45 mmol/l.

The total intracellular ATP concentration was significantly
decreased following either 20 or 40 mmol/l FA
exposure for 8 hour.

This is consistent with the hypothesis that FA may inhibit
mitochondrial function resulting in decreased intracellular ATP
and formate-induced neurotoxicity.

Using organotypic hippocampal slices, which preserve neuronal
circuitry and are easily accessible for experimental manipulations
(Stoppini et al., 1991),
our group has previously shown that
free radical overproduction in hippocampal pyramidal neurons
during ischemia/reoxygenation
depended on the activation of glutamate receptors,
and was associated with elevations of intracellular calcium.

Mitochondria are thought to be the principal source of
glutamate-mediated, calcium-dependent free radical production
in cultured cortical neurons
(Dugan et al., 1995; Reynolds and Hastings, 1995).

Although we did not investigate FA levels below 1 mmol/l,
it is conceivable that a continuous exposure to low,
but, above normal levels (>0.15 mmol/l), may also be cytotoxic
and may be part of the pathology of alcohol-related
organ damage (Jiang et al., 2003)
including the fetal alcohol spectrum disorder.

CONCLUSION

Our studies, for the first time, have shown that MeOH from
endogenous sources and from congeners present in alcoholic
beverages can lead to FA concentrations that are neurotoxic.

Therapeutic intervention with folic acid could be a significant
treatment modality in preventing FA mediated cytotoxicity,
especially neurotoxicity, in alcoholics.

ACKNOWLEDGMENT

This study was supported by a grant from the CIHR.

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____________________________________________________



folic acid prevents neurotoxicity from formic acid, made by body
from methanol impurity in alcohol drinks [ also 11 % of aspartame ],
BM Kapur, PL Carlen, DC Lehotay, AC Vandenbroucke,
Y Adamchik, U. of Toronto, 2007 Dec., Alcoholism Cl. Exp. Res.:
Murray 2007.11.27
http://rmforall.blogspot.com/2007_11_01_archive.htm
Wednesday, November 27, 2007
http://groups.yahoo.com/group/aspartameNM/message/1495


http://www.faslink.org/Formic%20Acid%20Kapur.htm

Brief Summary:

Methanol in small amounts is present along with ethanol in beverage
alcohol.
[Murray: and about the same amounts from aspartame diet sodas]

The body's natural enzymes preferentially metabolize ethanol while
methanol breaks down into highly neurotoxic Formic Acid.

Use of high levels of Folic Acid was found to inhibit brain damage
caused by the methanol.

The use of Folic Acid during pregnancy has been recommended
for several years to prevent neural tube defects.

However, this study indicates that even higher levels of Folic Acid
can be very beneficial to the developing baby, particularly where
alcohol exposure is a factor.

Folic Acid is mandated as an additive to all flour sold in Canada.

The debate has begun on its required addition to all beverage
alcohol to help mitigate damage caused to both infants and adults.


Formic Acid in the Drinking patient and the expectant mother
Dr. Bhushan M. Kapur
Departments of Laboratory Medicine,
St. Michael's Hospital , Toronto, Ontario, Canada

Abstract

Methanol is produced endogenously in the pituitary glands of humans
and is present as a congener in almost all alcoholic beverages.

Ethanol and methanol are both bio-transformed by alcohol
dehydrogenase; however, ethanol has greater affinity for the enzyme.

Since ethanol is preferentially metabolized by the enzyme, it is not
surprising that trace amounts of methanol, most likely originating from
both sources, have been reported in the blood of people
who drink alcohol.

Toxicity resulting from methanol is very well documented
in both humans and animals and is attributed to its toxic metabolite
formic acid.

To understand ethanol toxicity
and Fetal Alcohol Spectrum Disorders, it is important to consider
methanol and its metabolite, formic acid, as
potential contributors to the toxic effects of alcohol.

Accumulation of methanol suggests that alcohol-drinking
population should have higher than baseline levels of formic acid.

Our preliminary studies do indeed show this.

Chronic low-level exposure to methanol has been suggested to
impair human visual functions.

Formic acid is known to be toxic to the optic nerve.

Ophthalmological abnormalities are a common finding in children
whose mothers used alcohol during pregnancy.

Formic acid, a low molecular weight substance, either crosses the
placenta or may be formed in-situ from the water soluble methanol
that crosses the placenta.

Embryo toxicity from formic acid has been reported
in an animal model.

To assess neurotoxicity we applied low doses of formic acid
to rat brain hippocampal slice cultures.

We observed neuronal death with a time and dose response.

Formic acid requires folic acid as a cofactor for its elimination.

Animal studies have shown that when folate levels are low, the
elimination of formic acid is slower and formate levels are elevated.

When folic acid was added along with the formic acid
to the brain slice cultures, neuronal death was prevented.

Therefore, folate deficient chronic drinkers may be at higher risk of
organ damage.

Women who are folic acid deficient and consume alcohol may have
higher levels of formic acid and should they become pregnant,
their fetus may be at risk.

To our knowledge low level chronic exposure to formic acid and its
relationship to folic acid in men or women who drink alcohol has
never been studied.

Our hypothesis is that the continuous exposure to low levels of
formic acid is toxic to the fetus and may be part of the etiology of
Fetal Alcohol Spectrum Disorders.
____________________________________________________


http://www.come-over.to/FAS/

The incidence of Fetal Alcohol Syndrome in America
is 1.9 cases per 1,000 births (1/500).

Incidence of babies with disabilities
resulting from prenatal alcohol exposure: 1/100!
____________________________________________________


http://groups.yahoo.com/group/aspartameNM/message/1067
eyelid contact dermatitis by formaldehyde from aspartame,
AM Hill & DV Belsito, Nov 2003: Murray 4.4.4 rmforall [150 KB]

[ Extracts ]

McMartin, KE et al 1979, put 3,000 mg/kg methanol in the
stomachs of small monkeys and, 18 hours later found accumulation
of formate in liver, kidney, optic nerve, cerebrum, and midbrain
in 2 of three monkeys.

Biochemical Pharmcacology 1979: 28; 645-649.
Lack of a role for formaldehyde in methanol poisoning in the monkey.
Kenneth E. McMartin, Gladys Martin-Amat, Patricia E. Noker
and Thomas R. Tephly  kmcmar@...;
The Toxicology Center, Dept. of Pharmacology,
University of Iowa, Iowa City, Iowa 52242

K.E. McMartin and T.R. Tephly, authors of many pro-aspartame
studies, in Biochemical Pharmacology (1979) remarked,
"It is now generally accepted
that the toxicity of methanol is due to the formation of toxic
metabolites, either formaldehyde or formic acid."

They put damage doses of methanol into the stomachs
of three monkeys,
and, using insensitive tests, found no formaldehyde in many tissues --
except for a single datum in the midbrain,
1.5 times their detection limit.

They did report widespread accumulation of formic acid
in five tissues.

The use of inadequate tests is common in industry research that is
funded to claim the safety of profitable toxins.

Since then, industry scientists have been very wary of doing studies
on primates, which all too easily show the dangers to humans.

"Abstract [ not given in PubMed ]:
[ My briefer comments are in square brackets. ]

Methanol was administered [ by nasogastric tube ] either to untreated
cynomolgus monkeys [ 2-3.5 kg ] or to a folate-deficient cynomolgus
monkey which exhibits exceptional sensitivity to the toxic effects of
methanol.

Marked formic acid accumulation in the blood and in body fluids and
tissues was observed.

No formaldehyde accumulation was observed in the blood and no
formaldehyde was detected in the urine, cerebrospinal fluid, vitreous
humor, liver, kidney, optic nerve, and brain in these monkeys at a
time when marked metabolic acidosis and other characteristics of
methanol poisoning were observed.

Following intravenous infusion into the monkey, formaldehyde was
rapidly eliminated from the blood with a half-life of about 1.5 min
and formic acid levels promptly increased in the blood.

Since formic acid accumulation accounted for the metabolic acidosis
and since ocular toxicity essentially identical to that produced in
methanol poisoning has been described after formate treatment,
the predominant role of formic acid as the major metabolic agent
for methanol toxicity is certified.

Also, results suggest that formaldehyde is not a major factor in the
toxic syndrome produced by methanol in the monkey."

"It is now generally accepted that the toxicity of methanol is due to
the formation of toxic metabolites (1,2),
either formaldehyde or  formic acid."

So, this is an acute toxicity study, with little relevance for chronic
long-term, low-level exposure.

Monkeys, like people, are susceptible to methanol toxicity.

This team cites their six previous methanol in monkey studies,
from 1975 to 1977.

The report is difficult to understand, since the three monkeys were
treated differently, and different assays were used.

For the methanol sensitive, folate-deficient monkey A, the assay
used was the chromatropic acid method,
with a detection limit of .025 mmol/L.

None of the five tissues showed any formaldehyde with this assay,
except the midbrain, 0.14 mmol/kg wet weight tissue
[ units converted from their 0.14 micromole/gm -- just
1.5 times the detection limit of .09 mmol/kg wet tissue weight
(given on p. 648).
[ Since 1 kg of water is 1 L, 1 mmol/kg is equivalent to 1 mmol/L. ]

Meanwhile, in the methanol sensitive, folate-deficient monkey A,
the blood formate level rose by 18 hours from 0.18 to 10.02 mEq/L.
[ I assume that a mEq is equivalent to a mmol -- let me know
if I'm wrong. ]

The formate detection limits for the assays were not given
in this report.

The formate level in the vitreous humor of the eye of monkey A
was 7.90 mEq/L.

It is well known that formate is extremely damaging to the eye.

For unexplained reasons, formate levels in the five tissues and
cerebrospinal fluid were not measured in the methanol sensitive,
folate-deficient monkey A.,
in the cerebrospinal fluid of monkey B,
or in the optic nerve of monkey C.

Formaldehyde was not measured in the optic nerve of Monkey A.

The kidney formate level for monkey B was 6.33
and for C was only 0.44,
with no comment or explanation given.

The experiment seems arbitrary, capricious, and erratic.

For monkey A, after 18 hours, the urine formaldehyde level was
below detection level, while urine formate was 115.80 mEq/L -- so
much of the formaldehyde had been converted into formic acid,
another cumulative, potent toxin.

"In the presence of high formate values and definitive evidence of
toxicity in methanol-poisoned monkeys, no measurable formaldehyde
was found in the body tissues that were tested."

It is reasonable to surmise that more sensitive assays would have found
formaldehyde and formate bound to and reacted with a variety of cellular
substances in all tissues -- just as the 1998 Trocho study confirmed.
(Appendix E)

Monkeys B and C were normal, not extra vulnerable to methanol,
and were given 3,000 mg/kg methanol, and samples taken at 18 hr.

Formaldehyde was detected only in the blood of Monkey B,
while formate was found in 8 and 10, respectively,
of the 10 fluid and tissue samples in Monkeys B and C.

For instance, the lowest value of formate, except for zero-time blood,
for each monkey was in the midbrain, 2.16 mmol/kg for Monkey B
(24 times the detection limit for the chromatropic acid method)
and 1.02 mmol/kg (1.3 times the detection for the dimedon method)
for Monkey C.

This shows accumulation of formate in liver, kidney, optic nerve,
cerebrum, and midbrain.

"Thus, whereas one can associate formate intimately with ocular
toxicity in the monkey, no association of formaldehyde with ocular
toxicity can be made at this time.

It is not possible to completely eliminate formaldehyde as a toxic
intermediate because formaldehyde could be formed slowly within
cells and interfere with normal cellular function without ever obtaining
levels that were detectable in body fluids..."

"Acknowledgements-- This research was supported by
NIH grant GM 19420
and GM 12675." [not funded by the industry]


Life Sci 1991; 48(11): 1031-41.
The toxicity of methanol.
Tephly TR.
Department of Pharmacology, University of Iowa, Iowa City 52242.

"Abstract:
Methanol toxicity in humans and monkeys is characterized by a latent
period of many hours followed by a metabolic acidosis
and ocular toxicity.

This is not observed in most lower animals.

The metabolic acidosis and blindness is apparently due to
formic acid accumulation in humans and monkeys,
a feature not seen in lower animals.

The accumulation of formate is due to a deficiency in formate
metabolism which is, in turn, related, in part,
to low hepatic tetrahydrofolate (H4 folate).

An excellent correlation between hepatic H4 folate and
formate oxidation rates has been shown within and across species.

Thus, humans and monkeys possess low hepatic H4 folate levels,
low rates of formate oxidation and accumulation of formate
after methanol.

Formate, itself, produces blindness in monkeys in the absence of
metabolic acidosis.

In addition to low hepatic H4 folate concentrations, monkeys and
humans also have low hepatic 10-formyl H4 folate dehydrogenase
levels, the enzyme which is the ultimate catalyst for conversion of
formate to carbon dioxide.

This review presents the basis for the role of folic acid-dependent
reactions in the regulation of methanol toxicity.
Publication Types: Review Review, Academic PMID: 1997785"

p. 1035 "In the past, formaldehyde has often been suggested as the
methanol metabolite which produces toxicity (34,35).

Today, a great deal of information is available concerning its lack of
such a role.

The presence of elevated formaldehyde levels in body fluids or
tissues following methanol administration has not been observed.

No formaldehyde has been detected in blood, urine or tissues
obtained from methanol-treated animals (36,37) and,
in methanol-poisoned humans, formaldehyde increases
have not been observed....

About 85% of a low dose of 14C-formaldehyde [radioactive label]
is excreted as pulmonary 14CO2 (49,50)....."

[ This suggests that 15% of the formaldehyde is indeed retained in
the body, a very significant result, considering its extreme
and complex toxicity. ]

49. W.B. Neely, Biochem. Pharmacol. 13: 1137-1142 (1964).

50. Xenobiotica 1982 Feb; 12(2): 119-24.
Formaldehyde metabolism by the rat: a re-appraisal.
Mashford PM, Jones AR.
1. The metabolism of [14C]formaldehyde has been investigated
in the male Sprague-Dawley rat.
It is extensively oxidized to CO2 and formate,
which is excreted in the urine.
2. Two radioactive compounds isolated from the urine of rats dosed
with [14C] formaldehyde have been identified as
N-(hydroxymethyl)urea and
N,N'-bis-(hydroxymethyl)urea, and shown to be urinary artefacts.
3. Previous studies of the metabolism of formaldehyde by rats have
been re-appraised.
Differences in the rate of oxidation of formaldehyde in various strains
of rats result in the excretion of different urinary metabolites and, in
some cases, formaldehyde.
Excretion of formaldehyde leads to the formation of several artefacts
depending on the components present in the urine. PMID: 6806997
____________________________________________________


new details on how formaldehyde and formic acid from methanol are
neurotoxic: Chun Lai Nie, Rong Giao He, et al, PLoS ONE 2(7):
e629 2007.07.18 Chinese Academy of Sciences, Beijing:
Murray 2007.09.01
http://groups.yahoo.com/group/aspartameNM/message/1470

" Recent studies have shown that neurodegeneration
is closely related to misfolding and aggregation of neuronal tau. "

" The significant protein tau aggregation induced by formaldehyde
and the severe toxicity of the aggregated tau to neural cells may
suggest that toxicity of methanol and formaldehyde ingestion
is related to tau misfolding and aggregation. "

" Neuronal tau is an important protein in promoting and stabilizing
the microtubule system involved in cellular transport and neuronal
morphogenesis. "

" Both formaldehyde and acetaldehyde can go through the
blood-brain barrier and cause some lesions to CNS,
especially our visual system [38].

Clinically, the lethal dose of formaldehyde for human beings is
about 0.08% in the circulation [39].

We have shown in the present study that formaldehyde can
significantly induce tau aggregation and polymerization at
concentrations even lower than 0.08%,
the clinical dose of toxicosis. "

" Formaldehyde exposure leads to formation of DNA/protein
crosslinks, a major mechanism of DNA damage.

The DNA/protein crosslinks have been used as a measure
of dose in drug delivery [20].

Formaldehyde, as a crosslinking agent, also reacts with
thiol and amino groups, leading to protein polymerization [21], [22].

Furthermore, methanol ingestion is an important public health
concern because of the selective actions of its toxic metabolites,
formaldehyde and formic acid, on the retina, the optic nerves
and the central nervous system (CNS) [23].

Illicit consumption of industrial methylated spirits can cause severe
and even fatal illness [24].

In the liver and retina, methanol is oxidized by alcohol
dehydrogenase, resulting in formaldehyde.

In semicarbazide-sensitive amine oxidase (SSAO)-mediated
pathogenesis of Alzheimer's disease, formaldehyde interacts
with B-amyloids and produces irreversibly cross-linked neurotoxic
amyloid-like complexes [21], [22], [25].

We have examined the role of formaldehyde in misfolding
of protein tau [26].

In particular, we investigated the toxicity of formaldehyde-induced
tau aggregates on human neuroblastoma cells (SH-SY5Y cell line)
and rat hippocampal cells [27].

The results showed that low concentrations (0.01 - 0.1%) of
formaldehyde are sufficient to induce formation of amyloid-like tau
aggregates, which can induce apoptosis of both SH-SY5Y
and hippocampal cells.

This may be significant to understand the mechanism of chronic
damage caused by methanol toxicity
and formaldehyde stress [18], [28].

However, we have still not known the mechanism of protein tau
aggregation in the presence of formaldehyde at low concentrations.

The present study concerns the characteristic of misfolding and
polymerization of extracellular and intracellular neuronal tau induced
by formaldehyde at low concentrations. "

http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=1763784\
4
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0000629
free full text

Formaldehyde at Low Concentration Induces Protein Tau
into Globular Amyloid-Like Aggregates In Vitro and In Vivo
PLoS ONE. 2007 Jul 18; 2(7): e629.
doi:10.1371/journal.pone.0000629
Chun Lai Nie 1,
Yan Wei 1,
Xinyong Chen 2,
Yan Ying Liu 1,
Wen Dui 1,
Ying Liu 1,
Martyn C. Davies 2, Martyn.Davies@...;
Saul J.B. Tendler 2, Saul.Tendler@...;
Rong Giao He 1* herq@...;

1 State Key Laboratory of Brain and Cognitive Science,
Institute of Biophysics, Graduate School,
Chinese Academy of Sciences, Chaoyang District, Beijing, China,

2 Laboratory of Biophysics and Surface Analysis,
School of Pharmacy, The University of Nottingham,
Nottingham, United Kingdom

Received: March 5, 2007; Accepted: June 13, 2007;
Published: July 18, 2007

Copyright: © 2007 Nie et al.
This is an open-access article distributed under
the terms of the Creative Commons Attribution License, which
permits unrestricted use, distribution, and reproduction in any
medium, provided the original author and source are credited.

* To whom correspondence should be addressed.
E-mail: herq@...;

Abstract

Recent studies have shown that neurodegeneration is closely
related to misfolding and aggregation of neuronal tau.

Our previous results show that neuronal tau aggregates in
formaldehyde solution and that aggregated tau induces apoptosis
of SH-SY5Y and hippocampal cells.

In the present study, based on atomic force microscopy (AFM)
observation, we have found that formaldehyde at low concentrations
induces tau polymerization whilst acetaldehyde does not.

Neuronal tau misfolds and aggregates into globular-like polymers
in 0.01 - 0.1% formaldehyde solutions.

Apart from globular-like aggregation, no fibril-like polymerization
was observed when the protein was incubated with formaldehyde
for 15 days.

SDS-PAGE results also exhibit tau polymerizing in the presence
of formaldehyde.

Under the same experimental conditions, polymerization of bovine
serum albumin (BSA) or a-synuclein was not markedly detected.

Kinetic study shows that tau significantly misfolds and polymerizes
in 60 minutes in 0.1% formaldehyde solution.

However, presence of 10% methanol prevents protein tau from
polymerization.

This suggests that formaldehyde polymerization is involved in tau
aggregation.

Such aggregation process is probably linked to the tau's special
"worm-like" structure, which leaves the e-amino groups of Lys
and thiol groups of Cys exposed to the exterior.

Such a structure can easily bond to formaldehyde molecules
in vitro and in vivo.

Polymerizing of formaldehyde itself results in aggregation of
protein tau.

Immunocytochemistry and thioflavin S staining of both endogenous
and exogenous tau in the presence of formaldehyde at low
concentrations in the cell culture have shown that formaldehyde can
induce tau into amyloid-like aggregates in vivo during apoptosis.

The significant protein tau aggregation induced by formaldehyde
and the severe toxicity of the aggregated tau to neural cells may
suggest that toxicity of methanol and formaldehyde ingestion is
related to tau misfolding and aggregation.

Funding: This project was supported by NSFB (06J11),
the NSFC (Nos. 90206041, 30570536 and 30621004)
and 973-Project (2006CB500703 and 2006CB911003).

Competing interests: The authors have declared that no competing
interests exist.

Academic Editor: Christophe Herman, Baylor College of Medicine,
United States of America

Introduction

Neuronal tau is an important protein in promoting and stabilizing the
microtubule system involved in cellular transport
and neuronal morphogenesis.

The tau molecule can be subdivided into an amino-terminal domain
that projects from the microtubule surface and a carboxy-terminal
microtubule-binding domain.

The discovery that incubation of bacterially expressed human tau
with sulphated glycosaminoglycans leads to bulk assembly of tau
filaments [1], making it possible to obtain structural information [2].

By using circular dichroism measurement, Schweer et al. have found
that protein tau lacks secondary structures and is considered in a
"worm-like" conformation with a high flexibility [3].

Therefore, the side-chains of amino acids such as Lys, Cys, Thr
and Ser are mostly exposed and vulnerable to chemical modification.

Recently, many laboratories have found that misfolding and
aggregation of protein tau are involved in neurodegeneration
[2], [4] - [6].

Protein tau has been found as the major component of paired
helical filaments in neurofibrillary tangles in the brains of Alzheimer's
patients, where abnormal hyper-phosphorylation induces tau to
misfold and form the paired helical filaments,
depositing in the cytoplasm of neurons [7] - [10].

Recently, a great deal of evidence has demonstrated that oxidation
and glycation stresses are key causal factors of neuronal degenerative
diseases [11] - [13].

Both of them inevitably produce a variety of unsaturated carbonyls
as intermediates, like malondialdehyde and 4-hydroxynonenal,
which usually cause carbonyl-amino crosslinking and lead to
accumulation of irreversible changes (like lipofuscin) related to
various neurodegenerative diseases in particular [14] - [16].

Such carbonyl stress-related reactions (carbonylation) can form
unstable and reversible 1:1 amino-carbonyl (Shiff's base)
compounds at an early stage of protein modification [16], [17].

Carbonylation binds and blocks a-/e- amino groups,
and results in changes in charge and conformation of a protein.

In order to investigate the relationship between carbonylation and
protein tau misfolding, the basic and simplest carbonyl compound
formaldehyde [18] has come into our attention.

Formaldehyde is a common environmental agent found in paint, cloth,
exhaust gas and many other medicinal and industrial products [19].

Formaldehyde exposure leads to formation of DNA/protein
crosslinks, a major mechanism of DNA damage.

The DNA/protein crosslinks have been used as a measure of dose
in drug delivery [20].

Formaldehyde, as a crosslinking agent, also reacts with thiol and
amino groups, leading to protein polymerization [21], [22].

Furthermore, methanol ingestion is an important public health
concern because of the selective actions of its toxic metabolites,
formaldehyde and formic acid, on the retina, the optic nerves
and the central nervous system (CNS) [23].

Illicit consumption of industrial methylated spirits can cause severe
and even fatal illness [24].

In the liver and retina, methanol is oxidized by alcohol
dehydrogenase, resulting in formaldehyde.

In semicarbazide-sensitive amine oxidase (SSAO)-mediated
pathogenesis of Alzheimer's disease, formaldehyde interacts
with B-amyloids and produces irreversibly cross-linked neurotoxic
amyloid-like complexes [21], [22], [25].

We have examined the role of formaldehyde
in misfolding of protein tau [26].

In particular, we investigated the toxicity of formaldehyde-induced
tau aggregates on human neuroblastoma cells (SH-SY5Y cell line)
and rat hippocampal cells [27].

The results showed that low concentrations (0.01 - 0.1%) of
formaldehyde are sufficient to induce formation of amyloid-like tau
aggregates, which can induce apoptosis of both SH-SY5Y
and hippocampal cells.

This may be significant to understand the mechanism of chronic
damage caused by methanol toxicity
and formaldehyde stress [18], [28].

However, we have still not known the mechanism of protein tau
aggregation in the presence of formaldehyde at low concentrations.

The present study concerns the characteristic of misfolding and
polymerization of extracellular and intracellular neuronal tau induced
by formaldehyde at low concentrations.....

Discussion

Clinical lethal dose of formaldehyde

Why did we investigate tau misfolding in the presence of
formaldehyde at low concentrations (0.01 - 0.1%)?

Methanol and ethanol are metabolized to formaldehyde and
acetaldehyde respectively in our hepatocytes
and some neural cells [36], [37].

Both formaldehyde and acetaldehyde can go through the
blood-brain barrier and cause some lesions to CNS,
especially our visual system [38].

Clinically, the lethal dose of formaldehyde for human beings is
about 0.08% in the circulation [39].

We have shown in the present study that formaldehyde can
significantly induce tau aggregation and polymerization at
concentrations even lower than 0.08%,
the clinical dose of toxicosis.

The same low concentration of formaldehyde did not induce
polymerization of BSA though theoretically it will cause any
protein to polymerize if the concentration is high enough.

On the other hand, although it is known that acetaldehyde is
acutely toxic and would covalently bind to proteins and other
macromolecules [40], in our AFM and SDS-PAGE studies
we did not observe tau polymerization caused by acetaldehyde at
the concentration range that we studied (0.1 - 1%)......

Tau aggregation relating to methanol and formaldehyde toxicity

Methanol is an ocular toxicant, which causes visual dysfunction and
often leads to blindness after acute exposure.

However, physiological and biochemical changes responsible
for the toxicity have not yet been well understood [28].

According to a recent report, humans are uniquely sensitive to the
toxicity of methanol, as they have limited capacity to oxidize and
detoxify formic acid.

Thus, the toxicity of methanol in humans is characterized by formic
acidaemia, metabolic acidosis, blindness or serious visual impairment,
mild central nervous system depression
and even death [23], [27], [28].

However, methanol toxicosis induces progressive complications
to CNS.

It is hard to explain the progressively chronic damage by local
accumulation of formic acid alone.

Therefore, the potential effect of formaldehyde on protein
misfolding may be significant, although formaldehyde remains
in the human body for only a short time.

In semicarbazide-sensitive amine oxidase (SSAO)-mediate
pathogenesis of Alzheimer's disease, formaldehyde interacts with
B-amyloids and produces irreversibly cross-linked neurotoxic
amyloid-like complexes [21], [22], [25].

Our studies showed that formaldehyde induced neuronal tau
to aggregate.

The amyloid-like tau induces apoptosis of SY5Y
and hippocampal cells [27].

In fact, chemically, formaldehyde reacts with thiol and
amino groups instantly,
resulting in subsequent misfolding of neuronal tau (Figure 11).

This suggests that amyloid-like tau is involved in methanol toxicosis,
especially the damage of neurons and the resulted complications
after exposure to formaldehyde.

Although there have been many studies on methanol and
formaldehyde intoxication [23], [24], none of them has addressed
the contribution of protein misfolding to the pathological mechanism,
in particular the effect of formaldehyde on protein conformation
and polymerization.

Interestingly, neurofibrillary tangles have been found in brains of
chronic alcoholics possessing neuropathological signs
of thiamine-deficiency [40], [47].

This suggests that tau misfolding may be involved in the
alcohol-induced pathological pathway.

Khlistunova and his colleagues found that neuronal tau repeat domain
could aggregate in vivo and was toxic to neuronal cells.

The degree of tau aggregation and toxicity depends on the propensity
of the B-structure [2], [48].

In the present study, we have demonstrated that amyloid-like
intracellular tau aggregates could induce cell apoptosis, a similar result
as that obtained for extracellular amyloid or a-synuclein [49] -- [51].

This suggests that an enriched B-sheet structure is important to
amyloid-like protein aggregation and neurotoxicity.

In our experiments, a low concentration of formaldehyde induced
both extracellular and intracellular tau proteins to aggregate into
cell-toxic amyloid-like granular aggregates [27].

It appears to provide a new mechanism for triggers of tauopathies
in the formaldehyde toxicosis.....

Acknowledgments

We thank Ms. Ya-Qun Zhang for technical assistance
and Dr. Ya-Jie Xu for providing the clone of HA-tau40.

Author Contributions

Conceived and designed the experiments: RH.
Performed the experiments: CN YW YL WD.
Analyzed the data: CN.
Wrote the paper: CN RH YL XC MD ST.

References.....

#19 Quievryn G, Zhitkovich A. (2000)
Loss of DNA-protein crosslinks from formaldehyde-exposed cells
occurs through spontaneous hydrolysis and an active repair process
linked to proteosome function.
Carcinogenesis 21: 1573 - 1580.

#20 Heck H, Casanova M. (1999)
Pharmacodynamics of formaldehyde: applications of a model for the
arrest of DNA replication by DNA-protein cross-links.
Toxicol Appl Pharmacol 160: 86 - 100.

#21 Yu PH, Lu LX, Fan H, Kazachkov M, Jiang ZJ, et al. (2006)
Involvement of semicarbazide-sensitive amine oxidase-mediated
deamination in lipopolysaccharide-induced
pulmonary inflammation.
Am J Pathol 168: 718 - 726.

#22 Yu PH. (2001)
Involvement of cerebrovascular semicarbazide-sensitive amine
oxidase in the pathogenesis

#23 Eells JT, Henry MM, Lewandowski MF, Seme MT,
Murray TG. (2000)
Development and characterization of a rodent model of
methanol-induced retinal and optic nerve toxicity.
Neurotoxicology 21: 321 - 330.

#24 Dayan AD, Paine AJ. (2001)
Mechanisms of chromium toxicity, carcinogenicity
and allergenicity: review of the literature from 1985 to 2000.
Hum Exp Toxicol 20: 439 - 451.

#25 Gubisne-Haberle D, Hill W, Kazachkov M,
Richardson JS, Yu PH. (2004)
Protein cross-linkage induced by formaldehyde derived from
semicarbazide-sensitive amine oxidase-mediated deamination
of methylamine.
J Pharmacol Exp Ther 310: 1125 - 1132.

#26 Nie CL, Zhang W, Zhang D, He RQ. (2005)
Changes in conformation of human neuronal tau during
denaturation in formaldehyde solution.
Protein Pept Lett 12: 75 - 78.

#27 Nie CL, Wang XS, Liu Y, Perrett S, He RQ. (2007)
Amyloid-like aggregates of neuronal tau induced by formaldehyde
promote apoptosis of neuronal cells.
BMC Neurosci 8: 9.

#28 Garner CD, Lee EW, Louis-Ferdinand RT. (1995)
Muller cell involvement in methanol-induced retinal toxicity.
Toxicol Appl Pharmacol 130: 101 - 107.

#32 Pomerantz M, Bittner S, Khader SB. (1982)
"Formaldehyde semicarbazone."�
J Org Chem 47: 2217 - 2218.

#36 Barceloux DG, Bond GR, Krenzelok EP,
Cooper H, Vale JA. (2002)
American Academy of Clinical Toxicology practice guidelines
on the treatment of methanol poisoning.
J Toxicol Clin Toxicol 40: 415 - 446.

#37 Valentine WM. (1990)
Toxicology of selected pesticides, drugs, and chemicals.
Short-chain alcohols.
Vet. Clin. North Am. Small Anim. Pract 20: 515 - 523.

#38 Shcherbakova LN, Tel'pukhov VI, Trenin SO,
Bashilov IA, Lapkina TI. (1986)
[Permeability of the blood-brain barrier
to intra-arterial formaldehyde].
Biull Eksp Biol Med 102: 573 - 575.

[  Biull Eksp Biol Med. 1986 Nov; 102(11): 573-5.
[Permeability of the blood-brain barrier to intra-arterial
formaldehyde]
[Article in Russian]
Shcherbakova LN, Tel'pukhov VI, Trenin SO,
Bashilov IA, Lapkina TI.

Formaldehyde concentration was assessed in the brain,
cerebrospinal liquor, arterial and venous blood of intact animals
and following its intraarterial injections.

It is concluded that formaldehyde is capable of penetrating
through the blood-brain barrier, with the degree of permeability
depending on blood formaldehyde concentration.

The distribution of formaldehyde in the blood-brain-cerebrospinal
liquor system suggests the presence of both protein-bound
and unbound formaldehyde forms in the organism.
PMID: 3779084  ]

#39 Erkrath KD, Adebahr G, Kloppel A. (1981)
[Lethal intoxication by formalin during dialysis (author's transl)].
Z Rechtsmed 87: 233 - 236.

#40 Niemela O. (1999)
Aldehyde-protein adducts in the liver as a result of
ethanol-induced oxidative stress.
Front Biosci 4: D506 - D513.

#45 Jiang W, Schwendeman SP. (2000)
Formaldehyde-mediated aggregation of protein antigens:
comparison of untreated and formalinized model antigens.
Biotechnol Bioeng 70: 507 - 517.

#46 Rait VK, O'Leary TJ, Mason JT. (2004)
Modeling formalin fixation and antigen retrieval with
bovine pancreatic ribonuclease A:
I-structural and functional alterations.
Lab Invest 84: 292 - 299.

#47 Cullen KM, Halliday GM. (1995)
Neurofibrillary tangles in chronic alcoholics.
Neuropathol Appl Neurobiol 21: 312 - 318.
____________________________________________________



Note: many recent aspartame bans.....

http://groups.yahoo.com/group/aspartameNM/message/1426
ASDA (unit of Wal-Mart Stores WMT.N) and Marks & Spencer
will join Tesco and also Sainsbury to ban and limit aspartame,
MSG, artificial flavors dyes preservatives additives, trans fats, salt
"nasties" to protect kids from ADHD: leading UK media:
Murray 2007.05.15

http://groups.yahoo.com/group/aspartameNMmessage/1451
Artificial sweeteners (aspartame, sucralose) and coloring agents
will be banned from use in newly-born and baby foods,
the European Parliament decided: Latvia ban in schools 2006:
Murray 2007.07.12

http://groups.yahoo.com/group/aspartameNM/message/1341
Connecticut bans artificial sweeteners in schools, Nancy Barnes,
New Milford Times: Murray 2006.05.25

http://groups.yahoo.com/group/aspartameNM/message/1369
Bristol, Connecticut, schools join state program to limit artificial
sweeteners, sugar, fats for 8800 students, Johnny J Burnham,
The Bristol Press: Murray 2006.09.22

British Columbia guidelines against "any drinks with artificial sweeteners"
in January 2008 in school vending machines, stores, cafeterias or
fundraisers -- also recently in Ontario and Quebec, Janet Steffenhagen
2007.12.28 Vancouver Sun:  Murray 2008.04.10
http://rmforall.blogspot.com/2008_04_01_archive.htm
Thursday, April 10, 2008
http://groups.yahoo.com/group/aspartameNM/message/1537

stevia herbal sweetener to be sold as Truvia (rebiana) by Cargill and
Coca-Cola, if blitz of 12 studies wins FDA approval in 30-90 days: Murray
2008.05.24
http://rmforall.blogspot.com/2008_05_01_archive.htm
Saturday, May 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1540
____________________________________________________


http://groups.yahoo.com/group/aspartameNM/message/1513
metabolic syndrome is tied to diet soda, PL Lutsey, LM Steffen,
J Stevens, Circulation 2008.01.22: role of formaldehyde and
formic acid from methanol in wines, liquors, or aspartame?:
Murray 2008.02.21

"But the one-third who ate the most fried food increased their risk
by 25 percent, compared with the one-third who ate the least, and
surprisingly, the risk of developing metabolic syndrome was 34
percent higher among those who drank one can of diet soda a day
compared with those who drank none.

"This is interesting," said Lyn M. Steffen, an associate professor of
epidemiology at the University of Minnesota and a co-author of the
paper, which was posted online in the journal Circulation on Jan. 22.
"Why is it happening?  Is it some kind of chemical in the diet soda,
or something about the behavior of diet soda drinkers?""

"The diet soda association was not hypothesized
and deserves further study."
____________________________________________________


Avoiding formaldehyde allergic reactions in children, aspartame, vitamins,
shampoo, conditioners, hair gel, baby wipes, Sharon E Jacob, MD, Tace
Steele, U. Miami, Pediatric Annals 2007 Jan.: eyelid contact dermatitis, AM
Hill, DV Belsito, 2003 Nov.: Murray 2008.03.27
http://rmforall.blogspot.com/2008_03_01_archive.htm
Thursday, March 27, 2008
http://groups.yahoo.com/group/aspartameNM/message/1532

"It is generally recommended that exposure to products containing
formaldehyde, FRP's, and aspartame (NutraSweet) be avoided
in children."

"Through metabolism, aspartame is converted metabolically
in the liver to methanol,
which is in turn metabolized to formaldehyde. 8"

www.pediatricannalsonline.com/showPdf.asp?rID=21306

Avoiding formaldehyde allergic reactions in children
Pediatric Annals. 2007 Jan.; 36(1): 55-6. PMID: 17269284
Sharon E. Jacob, MD, Director, Contact Dermatitis Clinic,
Dept. of Dermatology and Cutaneous Surgery, U. of Miami,
1295 NW 14th St., Miami, FL 33125, fax 305-243-6191

formaldehyde from many sources, including aspartame, is major cause of
Allergic Contact Dermatitis, SE Jacob, T Steele, G Rodriguez, Skin and Aging
2005 Dec.: Murray 2008.03.27
http://rmforall.blogspot.com/2008_03_01_archive.htm
Thursday, March 27, 2008
http://groups.yahoo.com/group/aspartameNM/message/1533

Sharon E. Jacob, MD
Assistant Professor of Medicine (Dermatology)
University of California, San Diego 200 W. Arbor Drive #8420
San Diego, CA 92103-8420
Tel: 858-552-8585 ×3504 Fax: 305-675-8317
sjacob@...;

"For example, diet soda and yogurt containing aspartame
(Nutrasweet), release formaldehyde in their natural biological
degradation.

One of aspartame's metabolites, aspartic acid methyl ester,
is converted to methanol in the body, which is oxidized to
formaldehyde in all organs, including the liver and eyes. 22

Patients with a contact dermatitis to formaldehyde have been seen
to improve once aspartame is avoided. 22

Notably, the case that Hill and Belsito reported had a 6-month
history of eyelid dermatitis that subsided after 1 week of avoiding
diet soda. 22"

"We present a case of a medical student who presented with
erythematous eczematoid plaques on her trunk and legs and
fine vesiculation of her scalp, 3 weeks after starting anatomy class.

Of note, she routinely washed her face and arms after leaving the
anatomy lab, but remained in her scrubs for the rest of the day.

Formaldehyde and Quaternium-15 positive reactions
in the same patient."

"Our patient underscores the importance of appropriate patch
testing and education.
Once we identified the allergy to formaldehyde and quaternium-15,
we provided patient education materials regarding the common and
not-so-common locations of these chemicals and cross-reactors.
We also gave the patient information on avoidance
and safe alternatives (see Table 5).

Fortunately, with technical advances, this student completed the
anatomy section via electronic learning tools.

By avoiding formaldehyde, including anatomy lab, FRP
in her shampoo and cosmetics,
and aspartame in her diet, this patient dramatically improved.

As with all contact dermatitides, the mainstay of treatment for
allergic contact dermatitis is avoidance."

http://www.skinandaging.com/article/5158
Allergen Focus:
Focus on T.R.U.E. Test Allergens #21, 13 and 18:
Formaldehyde and Formaldehyde-Releasing Preservatives
Skin & Aging, ISSN 1096-0120; 13(12) 2005 Dec.: 22-27.
Sharon E. Jacob, M.D.,
Tace Steele, B.A.,
and Georgette Rodriguez, M.D., M.P.H.   ]
____________________________________________________


two aspartame (methanol, formaldehyde, formic acid) toxicity research
studies by Resia Pretorius, U. Pretoria, South Africa, debate with JD
Fernstrom: Murray 2008.04.04 2008.05.29
http://rmforall.blogspot.com/2008_04_01_archive.htm
Friday, April 4, 2008
http://groups.yahoo.com/group/aspartameNM/message/1536

http://foodqualitynews.com/news/ng.asp?n=84424-aspartame-sweetener
recent news re E Pretorius aspartame and brain review

Direct and indirect cellular effects of aspartame on the brain.
Humphries P, Pretorius E, Naude H, U. Pretoria, South Africa,
Eur J Clin Nutr. 2007 Aug 8: Murray 2007.08.12
http://groups.yahoo.com/group/aspartameNM/message/1463

"The aim of this study was to discuss the direct and indirect
cellular effects of aspartame on the brain,
and we propose that excessive aspartame ingestion
might be involved in the pathogenesis
of certain mental disorders (DSM-IV-TR 2000)
and also in compromised learning and emotional functioning."

Eur J Clin Nutr. 2007 Aug 8; [Epub ahead of print]
Direct and indirect cellular effects of aspartame on the brain.
Humphries P,
Pretorius E, resia.pretorius@...;
Naude H.
[1] Department of Anatomy, University of Pretoria,
Pretoria, Gauteng, South Africa
[2] Department of Anatomy, University of the Limpopo,
South Africa.

The use of the artificial sweetener, aspartame, has long been
contemplated and studied by various researchers, and people are
concerned about its negative effects.

Aspartame is composed of phenylalanine (50%),
aspartic acid (40%) and methanol (10%).

Phenylalanine plays an important role in neurotransmitter regulation,
whereas aspartic acid is also thought to play a role as an excitatory
neurotransmitter in the central nervous system.

Glutamate, asparagines and glutamine are formed from their
precursor, aspartic acid.

Methanol, which forms 10% of the broken down product,
is converted in the body to formate,
which can either be excreted or can give rise to formaldehyde,
diketopiperazine (a carcinogen) and a number of other highly toxic
derivatives.

Previously, it has been reported that consumption of aspartame
could cause neurological and behavioural disturbances in sensitive
individuals.

Headaches, insomnia and seizures are also some of the neurological
effects that have been encountered, and these may be accredited to
changes in regional brain concentrations of catecholamines,
which include norepinephrine, epinephrine and dopamine.

The aim of this study was to discuss the direct and indirect
cellular effects of aspartame on the brain,
and we propose that excessive aspartame ingestion
might be involved in the pathogenesis
of certain mental disorders (DSM-IV-TR 2000)
and also in compromised learning and emotional functioning.

European Journal of Clinical Nutrition advance online publication,
8 August 2007; doi:10.1038/sj.ejcn.1602866.
PMID: 17684524

Keywords: astrocytes; aspartame; neurotransmitters; glutamate;
GABA; serotonin; dopamine; acetylcholine

Received 25 October 2006; revised 26 April 2007;
accepted 27 April 2007
Correspondence: Professor E Pretorius, Department of Anatomy,
University of Pretoria, BMW Building, Dr Savage Street,
PO Box 2034, Pretoria 0001,
Gauteng, South Africa.  E-mail: resia.pretorius@...

c 2007 Nature Publishing Group,
All rights reserved  0954-3007/07
$30.00  www.nature.com/ejcn


http://groups.yahoo.com/group/aspartameNMmessage/1452
phenylalanine and aspartic acid from low dose aspartame in rabbits
interfere with blood coagulation, Pretorius E and Humphries P,
U. of Pretoria, Ultrastruct Pathol 2007 March: Murray 2007.07.14

" The authors conclude by suggesting that aspartame usage
may interfere with the coagulation process
and might cause delayed fibrin breakup after clot formation.

They suggest this,
as the fibrin networks from aspartame-exposed rabbits
are more complex and dense,
due to the netlike appearance of the minor, thin fibers.

Aspartame usage should possibly be limited
by people on anti-clotting medicine
or those with prone to clot formation. "

Ultrastruct Pathol. 2007 Mar-Apr; 31(2): 77-83.
Ultrastructural changes to rabbit fibrin and platelets
due to aspartame.
Pretorius E,
Humphries P.
Department of Anatomy, Faculty of Medicine,
University of Pretoria, South Africa.
[ Humphries P also at
Department of Anatomy, University of Limpopo.
Medunsa Campus, Garankuwa. South Africa ]

email: E. Pretorius resia.pretorius@...
*Correspondence to E. Pretorius,
BMW Building, PO Box 2034,
Faculty of Health Sciences,
University of Pretoria, Pretoria 0001, South Africa

The coagulation process, including thrombin, fibrin,
as well as platelets,
plays an important role in hemostasis,
contributing to the general well-being of humans.

Fibrin formation and platelet activation are delicate processes
that are under the control of many small physiological events.

Any one of these many processes
may be influenced or changed by external factors,
including pharmaceutical or nutritional products, e.g.,
the sweetener aspartame (L-aspartyl-L-phenylalanine methyl ester).

It is known that phenylalanine is present at position P(9)
and aspartate at position P(10)
of the alpha-chain of human fibrinogen,
and plays an important role in the conversion of fibrinogen to fibrin
by the catalyst alpha-thrombin.

The authors investigate the effect of aspartame
on platelet and fibrin ultrastructure,
by using the rabbit animal model
and the scanning electron microscope.

Animals were exposed to 34 mg/kg of aspartame
26x during a 2-month period.

Aspartame-exposed fibrin networks appeared denser,
with a thick matted fine fiber network
covering thick major fibers.

Also, the platelet aggregates appeared more granular
than the globular control platelet aggregates.

The authors conclude by suggesting that aspartame usage
may interfere with the coagulation process
and might cause delayed fibrin breakup after clot formation.

They suggest this,
as the fibrin networks from aspartame-exposed rabbits
are more complex and dense,
due to the netlike appearance of the minor, thin fibers.

Aspartame usage should possibly be limited
by people on anti-clotting medicine
or those with prone to clot formation.
PMID: 17613990
____________________________________________________


http://groups.yahoo.com/group/aspartameNM/message/1459
third study by expert Greek team of neurotoxicity in infant rats by
aspartame (or its parts, methanol, phenylalanine, aspartic acid), KH
Schulpis et al, Food Chem Toxicol 2007.06.16: Murray 2007.08.05

http://groups.yahoo.com/group/aspartameNMmessage/1447
second study by expert Greek team of neurotoxicity in infant rats by
aspartame (or its parts, methanol, phenylalanine, aspartic acid), KH
Schulpis et al, Toxicology 2007.05.18: Murray 2007.07.04

http://groups.yahoo.com/group/aspartameNMmessage/1444
expert Greek group finds aspartame (or its parts, methanol,
phenylalanine, aspartic acid) harm infant rat brain enzyme activity,
KH Schulpis et al, Pharmacol. Res. 2007.05.13:
Murray 2007.06.23

http://groups.yahoo.com/group/aspartameNM/message/939
aspartame (aspartic acid, phenylalanine) binding to DNA:
Karikas July 1998: Murray 2003.01.05 rmforall
Karikas GA, Schulpis KH, Reclos GJ, Kokotos G
Measurement of molecular interaction of aspartame and
its metabolites with DNA. Clin Biochem 1998 Jul; 31(5): 405-7.
Dept. of Chemistry, University of Athens, Greece
http://www.chem.uoa.gr gkokotos@...
K.H. Schulpis inchildh@... ; G.J. Reclos reklos@...

5 recent aspartame reports by S Tsakiris, KH Schulpis, I Simintzi,
with responses to critiques by AG Renwick and
by EB Abegaz, RG Bursey, 2005-2008 2008.03.05

Pharmacological Research 57 (2008) 89-90
Letter to the Editor
Answer to Letter sent to the Editor by
Drs. E. Abegaz and R. Bursey
(Ajinomoto Corporate Services LLC, Washington, USA)
related to Simintzi et al. report published in
Pharmacol Res 2007; 56: 155-9
Letter to the Editor / Pharmacological Research 57 (2008) 89-90

Stylianos Tsakiris a,?  stsakir@...;
Kleopatra H. Schulpis b inchildh@...;
a Department of Experimental Physiology, Medical School,
Athens University, P.O. Box 65257, GR-15401 Athens, Greece

b Inborn Errors of Metabolism Department, Institute of Child
Health, Research Center, Greece
? Corresponding author.
E-mail addresses:
S. Tsakiris  stsakir@...;
K.H. Schulpis  inchildh@...;

Pharmacological Research 57 (2008) 87-88
Response to "The effect of aspartame on the acetylcholinesterase
activity in hippocampal homogenates of suckling rats"
by Simintzi et al.

Eyassu G. Abegaz ?
Robert G. Bursey
Ajinomoto Corporate Services LLC,
Scientific & Regulatory Affairs,
1120 Connecticut Ave., N.W., Suite 1010,
Washington, DC 20036, United States

? Corresponding author. Tel.: +1 202 457 0284;
fax: +1 202 457 0107.
E-mail addresses: abegazee@...; (E.G. Abegaz),
burseyb@...; (R.G. Bursey)

Keywords:
Aspartame; Aspartate; Phenylalanine; Methanol; AChE activity

Tsakiris S, Schulpis KH.
Answer to letter sent by Professor A.G. Renwick
(University of Southampton, UK)
related to Simintzi et al. report published in Food and Chemical
Toxicology 2007; 45(12): 2397-401.
Food Chem Toxicol. 2008 Mar; 46(3): 1208-9.
Epub 2007 Oct 25. No abstract available. PMID: 18054419
doi:10.1016/j.fct.2007.10.016
Copyright © 2007 Elsevier Ltd All rights reserved.

Renwick AG.
The effect of aspartame metabolites on the suckling rat frontal cortex
acetylcholinesterase. An in vitro study. By I. Simintzi, K.H. Schulpis,
P. Angelogianni, C. Liapi and S. Tsakiris.
Food Chem Toxicol. 2008 Mar; 46(3): 1206-7.
Epub 2007 Oct 26. No abstract available. PMID: 18061330

1: Simintzi I, Schulpis KH, Angelogianni P, Liapi C, Tsakiris S.
The effect of aspartame metabolites on the suckling rat frontal cortex
acetylcholinesterase. An in vitro study.
Food Chem Toxicol. 2007 Dec;45(12):2397-401.
Epub 2007 Jun 16. PMID: 17673349

2: Simintzi I, Schulpis KH, Angelogianni P, Liapi C, Tsakiris S.
L-Cysteine and glutathione restore the reduction of rat
hippocampal Na+, K+-ATPase activity
induced by aspartame metabolites.
Toxicology. 2007 Jul 31;237(1-3):177-83.
Epub 2007 May 18. PMID: 17602817

3: Simintzi I, Schulpis KH, Angelogianni P, Liapi C, Tsakiris S.
The effect of aspartame on acetylcholinesterase activity in
hippocampal homogenates of suckling rats.
Pharmacol Res. 2007 Aug;56(2):155-9.
Epub 2007 May 13. PMID: 17580119

4: Schulpis KH, Papassotiriou I, Parthimos T, Tsakiris T, Tsakiris S.
The effect of L-cysteine and glutathione
on inhibition of Na+, K+-ATPase activity by aspartame metabolites
in human erythrocyte membrane.
Eur J Clin Nutr. 2006 May;60(5):593-7. PMID: 16391576

5: Tsakiris S, Giannoulia-Karantana A, Simintzi I, Schulpis KH.
The effect of aspartame metabolites on human erythrocyte
membrane acetylcholinesterase activity.
Pharmacol Res. 2006 Jan;53(1):1-5.
Epub 2005 Aug 29. PMID: 16129618
____________________________________________________



http://groups.yahoo.com/group/aspartameNM/message/1143
methanol (formaldehyde, formic acid) disposition:
Bouchard M et al, full plain text, 2001:
substantial sources are degradation
of fruit pectins, liquors, aspartame, smoke:
Murray 2005.04.02

http://groups.yahoo.com/group/aspartameNM/message/1511
vinyl acetate, ethyl alcohol, or aspartame in womb increases later
cancers in adults with lifetime exposure in many studies, M Soffritti
et al, Ramazzini Foundation, Basic Clin. Pharm. Toxicol. 2008 Feb.:
Rich Murray 2008.02.07

http://groups.yahoo.com/group/aspartameNM/message/1016
President Bush & formaldehyde (aspartame) toxicity:
Ramazzini Foundation carcinogenicity results Dec 2002:
Soffritti: Murray 2003.08.03 rmforall

p. 88 "The sweetening agent aspartame hydrolyzes in the
gastrointestinal tract to become free methyl alcohol,
which is metabolized in the liver
to formaldehyde, formic acid, and CO2. (11)"
Medinsky MA & Dorman DC. 1994;
Assessing risks of low-level methanol exposure.
CIIT Act. 14: 1-7.

http://groups.yahoo.com/group/aspartameNM/message/1453
Souring on fake sugar (aspartame), Jennifer Couzin,
Science 2007.07.06: 4 page letter to FDA from 12 eminent
USA toxicologists re two Ramazzini Foundation cancer studies
2007.06.25: Murray 2007.07.18

30 female pet store rats drinking lifelong 13.5 mg aspartame,
1/3 packet of Equal, had 33% with obvious tumors -- also bulging,
sick, and missing eyes, paralysis, obesity, skin sores -- agrees with
Ramazzini Foundation results, Victoria Inness-Brown:
Murray 2008.02.15
http://rmforall.blogspot.com/2008_02_01_archive.htm
Friday, February 15, 2008
http://groups.yahoo.com/group/aspartameNM/message/1521
____________________________________________________


http://groups.yahoo.com/group/aspartameNM/message/1490
details on 6 epidemiological studies since 2004 on diet soda (mainly
aspartame) correlations, as well as 14 other mainstream studies
on aspartame toxicity since summer 2005: Murray 2007.11.27

http://groups.yahoo.com/group/aspartameNM/message/1340
aspartame groups and books:
updated research review of 2004.07.16: Murray 2006.05.11
____________________________________________________


old tiger roars -- Woodrow C Monte, PhD -- aspartame causes
many breast cancers, as ADH enzyme in breasts makes methanol
from diet soda into carcinogenic formaldehyde -- same in dark
wines and liquors, Fitness Life 2008 Jan.: Murray 2008.02.11
http://rmforall.blogspot.com/2008_02_01_archive.htm
Monday, February 11, 2008
http://groups.yahoo.com/group/aspartameNM/message/1517

"Alcohol dehydrogenase ADH is required for the conversion of
methanol to formaldehyde (112).

ADH is not a common enzyme in the human body -- not many cells
in the human body contain this enzyme.

The human breast is one of the few organs in the body with a high
concentration of ADH (190b), and it is found there exclusively in the
mammary epithelial cells, the very cells known to transform into
adenocarcinoma (190c) (breast cancer).

The most recent breast cancer scientific literature implicates ADH
as perhaps having a pivotal role in the formation of breast cancer,
indicating a greater incidence of the disease in those
with higher levels of ADH activity in their breasts (190a)."

role of formaldehyde, made by body from methanol from foods
and aspartame, in steep increases in fetal alcohol syndrome, autism,
multiple sclerosis, lupus, teen suicide, breast cancer, Nutrition
Prof. Woodrow C. Monte, retired, Arizona State U., two reviews,
190 references supplied, Fitness Life, New Zealand
2007 Nov, Dec: Murray 2007.12.26
http://rmforall.blogspot.com/2007_12_01_archive.htm
Wednesday, December 26 2007
http://groups.yahoo.com/group/aspartameNM/message/1498
____________________________________________________


two detailed critiques of industry affiliations and biased science in 99
page review with 415 references by BA Magnuson, GA Burdock
and 8 more, Critical Reviews in Toxicology, 2007 Sept.: Mark D
Gold 13 page: also Rich Murray 2007.09.15: 2008.03.24
http://rmforall.blogspot.com/2008_03_01_archive.htm
Monday, March 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1531


"Nearly every section of the Magnuson (2007) review has research
that is misrepresented
and/or crucial pieces of information are left out.

In addition to the misrepresentation of the research,
readers (including medical professionals) are often not told that
this review was funded by the aspartame manufacturer, Ajinomoto,
and the reviewers had enormous conflicts of interest."
____________________________________________________


MSG and Aspartame -- A Personal Story, TV health reporter
Dick Allgire (vegetarian) healed of migraines and panic attacks:
Murray 2008.02.12
http://rmforall.blogspot.com/2008_02_01_archive.htm
Tuesday, February 12, 2008
http://groups.yahoo.com/group/aspartameNM/message/1520
____________________________________________________

stevia herbal sweetener to be sold as Truvia (rebiana) by Cargill and Coca-Cola,
if blitz of 12 studies wins FDA approval in 30-90 days: Murray 2008.05.24
http://rmforall.blogspot.com/2008_05_01_archive.htm
Saturday, May 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1540
____________________________________________________


As a volunteer medical layman information activist for aspartame toxicity and
related issues for nine years, during the last 5 years I have reviewed over two
dozen quality positive abstracts on stevia safety, and daily use about 1 tsp
green stevia powder myself, with no problems.

Reports of symptoms by users are extremely rare on the Net, while some reject
the taste.

Years ago, I encouraged the use of sucralose, only to find that its safety has
never been confirmed by adequate studies on humans, a substantial fraction of
its complex metabolites remains in the body, and there are increasing reports on
the Net of alarming symptoms.

Are these dozen studies science or yet another consummate industry propaganda
blitz, as has been the case for aspartame, neotame, sucralose, and Acesulfame-K?

If science, then financing has to be explicit, the authors, their resumes, and
full contact details listed, and, all texts put for free in the public domain.

All evidence and research re aspartame, stevia, and other sweetener toxicity
should be made fully and conveniently available for free.

The huge corporations and government agencies responsible for the major public
health debacle and cover up re aspartame rightfully should set up a hundred
billion dollar fund for compensation of injured citizens.

The evidence shows that stevia affects blood pressure and glucose.  Therefore,
this is a drug.  Few drugs indeed have no bad effects for some or many users.

All toxicity research has to be subject to fierce, reason and evidence based
public scrutiny and debate, open to all citizens, fully archived and searchable,
along with a perpetual record of all citizen and expert negative reports.

The authors of the dozen studies have strong conflicts of interest:

AG Renwick, AR Boobis, and GW Williams are defenders of aspartame, while many of
these authors work for Coca-Cola, Cargill, and Cantox, a dedicated industry
consultancy.

DJ Brusic ( an "independent toxicologist" ) and GW Williams are authors, both
members of Cantox and  on the International Editorial Board of Food and Chemical
Toxicology.

AR Boobis is editor of Food Chemical Toxicology.

BA Magnuson and GW Williams of Cantox were authors of a massive, spurious review
in 2007, financed by Ajinomoto, that exonerated aspartame:

two detailed critiques of industry affiliations and biased science in 99
page review with 415 references by BA Magnuson, GA Burdock
and 8 more, Critical Reviews in Toxicology, 2007 Sept.: Mark D
Gold 13 page: also Rich Murray 2007.09.15: 2008.03.24
http://rmforall.blogspot.com/2008_03_01_archive.htm
Monday, March 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1531

"Nearly every section of the Magnuson (2007) review has research
that is misrepresented
and/or crucial pieces of information are left out.

In addition to the misrepresentation of the research,
readers (including medical professionals) are often not told that
this review was funded by the aspartame manufacturer, Ajinomoto,
and the reviewers had enormous conflicts of interest."
____________________________________________________



www.foodweek.com.au/main-features-page.aspx?articleType=ArticleView&articleId=19\
43

New artificial sweetener to go global
4:17 PM : 0 Comments :

Global agribusiness and ingredients giant Cargill is set to shake up the
artificial sweeteners sector with a new product made from the leaves of the
stevia plant.

The sweetener will be called Rebiana and marketed under the brand name Truvia.

It has been developed in partnership with Coca-Cola which has exclusive global
rights to use it in beverages.

It will be marketed as a natural alternative to artificial sweeteners such as
Equal, Nutrasweet and Splenda and sold through natural foods retailers as a
tabletop sugar alternative, the president of Cargill's health and nutrition
unit, Marcelo Montero told Reuters.

Formal approval has yet to be received from the US FDA to date, although
applications have been lodged and it can be sold in the meantime as a dietary
supplement.

It has been approved as a food additive by about a dozen countries including
Japan, China and Brazil.

Meanwhile, the company is already in talks with a number of unnamed food
manufacturers to use the product as a substitute for sugar or artificial
sweeteners in processed food products.

Coke has yet to announce when its first Rebiana-sweetened products will hit
supermarket shelves.

The stevia plant is native to Paraguay and Cargill is overseeing commercial
cropping to ensure ongoing supply.

“This new, natural sweetener leverages Cargill’s expertise in specialty food
ingredients, agronomy, food science and safety as well as consumer insight and
marketing capabilities,” said Steve Snyder, vice president, Cargill Health &
Nutrition. “The company is positioned to manage the development of this new
sweetener from the first plantings in the field to formulation for foods and
beverages, all the way to the product that will sweeten your morning coffee.”

Scientific Studies Supporting Truvia Natural Sweetener

Research published electronically today in the peer-reviewed, scientific journal
Food and Chemical Toxicology clearly establishes the safety of rebiana for use
as a natural, zero-calorie sweetener in food and beverages.
A rigorous safety evaluation program -- the first of its kind to evaluate
rebiana -- addressed unresolved questions and verified the safety of the product
for use as a general purpose sweetener.
The research program included metabolism, safety, intake, stability and human
studies that complement the body of previously published research on purified
steviol glycosides, the sweet components of the stevia leaf.

Background on Stevia

The stevia plant has been grown, harvested and used in South America to sweeten
foods and beverages for more than 200 years.
The plant was discovered by the Guarani natives of Paraguay who used its leaves
to sweeten drinks.
In 1931, two French food-researchers isolated the sweet components of the stevia
leaf.

Consumers in Japan have been using stevia commercially for more than three
decades, and today, stevia represents 40 percent of the country’s low- or
zero-calorie sweetener market.

Because rebiana begins with a leaf, supply is contingent upon the strength of
the stevia crop.
Over many years, Cargill has built a strong and consistent stevia supply chain
in anticipation of launching TRUVIA natural sweetener, and has a dedicated staff
on the ground and partner companies in key regions around the world supervising
production and ensuring good stewardship of land and water.
Today, one stevia plant yields enough rebiana for 30 six-ounce cups of coffee.

About TRUVIA Natural Sweetener

TRUVIA natural sweetener is a great-tasting, natural, zero-calorie product, made
from rebiana, the best-tasting part of the stevia leaf.

For more information, visit
www.allaboutrebiana.com
or www.TRUVIA.com

About Cargill

Headquartered in Minneapolis, Minn., Cargill is a privately held international
provider of food, agricultural and risk management products and services.
As a global leader in nourishing people, Cargill offers a wide range of
sweetness solutions based on consumer demand and tastes.
With 158,000 employees in 66 countries, the company is committed to using its
knowledge and experience to collaborate with customers to help them succeed.

© 2007 Cargill, Incorporated. All Rights Reserved
Cargill, Inc., PO Box 9300, Minneapolis, MN 55440-9300
800-227-4455
Ann Tucker  952-742-4057  ann_tucker@...


www.twincities.com/ci_9275122?IADID=Search-www.twincities.com-www.twincities.com

Stevia a sweet bet for Cargill
Sugar substitute shows promise
By Tom Webb  twebb@...;
Tom Webb can be reached at 651-228-5428.
Article Launched: 05/16/2008 12:01:00 AM CDT

Finding a no-calorie sweetener that's safe, natural and appetizing has been
dubbed the holy grail of the food industry.
On Thursday, Cargill Inc. moved a big step closer to unlocking the secret.

The Wayzata-based food giant announced publication of 12 peer-reviewed
scientific studies that affirmed the safety of rebiana, a refined extract of a
South American herb called stevia, which it hopes someday will be used widely in
food and beverages.

Cargill said it has christened the sweetener "Truvia," and revealed plans to
introduce it to consumers later this year.

Coca-Cola Co. has an exclusive partnership with Cargill to use Truvia in
beverages.

The substance is about 200 times as sweet as sugar, contains no calories and has
some advantages to the food industry because it doesn't degrade when heated or
when mixed with other foods.

Stevia is commonly used in Japan and parts of South America, but it's rare in
this country outside of health-food circles.

The scientific studies -- four years in the making -- are a major step because
the U.S. Food and Drug Administration does not now recognize stevia as a safe
food additive.

In 1991, FDA restricted its importation based on a handful of previous studies
suggesting possible liver damage and other problems.

The new studies were funded by Cargill, reviewed by independent scientists and
published Thursday in the journal Food and Chemical Toxicology.

They found that a high-purity extract of the stevia leaf -- different from what
was tested earlier -- does not affect organ function, reproductive health, blood
pressure or general health.

Leslie Curry, director of regulatory and scientific affairs for Cargill's food
ingredients unit, noted the role independent experts played in the process.

"What this group does, individually and collectively, is evaluate the full
dossier of old studies and newer works, with the aim of understanding whether
the ingredient is acceptable for its intended use. ... Their conclusion is that
rebiana is safe for use in food and beverages."

Cargill formally notified the FDA on Thursday of the findings, but company
officials were reluctant to discuss what route to acceptance they're seeking
from the agency.

Ted Labuza, professor of food science and engineering at the University of
Minnesota, said that under a newer and expedited process, companies are able to
assemble their own panel of experts to analyze data.

"But they still have to go to FDA, and the FDA may address it within 30 to 90
days," Labuza said. "And because it's Coca-Cola and Cargill, which are big,
they'll probably be pushed to move faster on this."

Ann Tucker, a Cargill spokeswoman, said Truvia will make its debut in "tabletop
and beverage applications, over a period of time."
Precisely when, she wouldn't say, citing competitive issues.

But Cargill has big dreams for Truvia. The company, which has reported earnings
of $2.9 billion for the first nine months of its current fiscal year, is now
ramping up production of the natural herb in South America and China.
Someday, it hopes to see it in ice cream, cereals, cookies and other many
products.


Dr. Ted Labuza tplabuza@...;
Prof. of Food Science Dept. of Food Science & Nutrition
136 ABLMS U of Minn St Paul, MN 55108
Voice 612-624-9701 Fax 612-625-5272 home fax 651-483-3302
cellemail 6126697885@...
http://fscn.che.umn.edu/Ted_Labuza/tpl.html


Apparent lack of pharmacological effect of steviol glycosides used as sweeteners
in humans.
A pilot study of repeated exposures in some normotensive and hypotensive
individuals and in Type 1 and Type 2 diabetics.
Regul Toxicol Pharmacol. 2008 Jun; 51(1): 37-41.  Epub 2008 Mar 5.
Luis A. Barriocanal a, Corresponding Author
Mafalda Palacios a,
Gilda Benitez a,
Sussam Benitez a,
Jorge T. Jimenez a,
Nora Jimenez b
and Vicenta Rojas
Department of Diabetes and Endocrinology, 3rd Internal Medicine Unit, Faculty of
Medicine, Clinical Hospital, National University Asunción, Mayor Bullo 315,
Asuncion, Paraguay.

Abstract

Steviol glycosides, isolated from the plant Stevia rebaudiana (Bertoni) Bertoni,
have been used as safe sweetening agents for more than 30 years.

Beneficial effects of high doses of steviol glycosides on hyperglycemia and
hypertension have been previously described when these abnormalities are
present.

This study was designed to evaluate the effects of steviol glycosides on blood
glucose and on blood pressure (BP) in 3 groups of individuals.

This was a randomized, double-blind, placebo-controlled, long-term study in
three groups of patients:
Group 1: subjects with Type 1 diabetes;
Group 2: subjects with Type 2 diabetes;
and Group 3: subjects without diabetes and with normal/low-normal BP levels.

The subjects in each group were randomly allocated to active treatment (the
steviol glycoside stevioside: 250mgt.d.s.) or to placebo treatment and
followed-up for 3 months.

Post-treatment systolic BP, diastolic BP, glucose and glycated hemoglobin
(HbA(1c)) were not significantly different from baseline measurements, except
for the placebo Type 1 diabetics group where a significant difference was
observed for systolic BP and glucose.

No side effects were observed in the two treatment groups.

This study shows that oral steviol glycosides, taken as sweetener are well
tolerated and have no pharmacological effect. PMID: 18397817
Keywords: Steviol glycosides; Hypotension; Type 1 diabetes mellitus; Type 2
diabetes mellitus
doi:10.1016/j.yrtph.2008.02.006
Copyright © 2008 Elsevier Inc. All rights reserved.


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Food and Chemical Toxicology, Article in Press, Accepted Manuscript - Note to
users
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Related Articles in ScienceDirect

Microbial hydrolysis of steviol glycosides
Food and Chemical Toxicology,
In Press, Accepted Manuscript, Available online 16 May 2008
A.G. Renwick,
S.M. Tarka
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Pharmacokinetics of rebaudioside A and stevioside after single oral doses in
healthy men
Food and Chemical Toxicology
In Press, Accepted Manuscript, Available online 16 May 2008
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Mandarino
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The hemodynamic effects of rebaudioside A in healthy adults with normal and
low-normal blood pressure
Food and Chemical Toxicology,
In Press, Accepted Manuscript, Available online 16 May 2008
K.C. Maki, L.L. Curry, M.C. Carakostas, S.M. Tarka, M.S. Reeves, M.V. Farmer,
J.M. McKenney, P.D. Toth, S.L. Schwartz, B.C. Lubin, M.R. Dicklin, A.C. Boileau,
J.D. Bisognano
Purchase PDF (314 K)  Leslie_Curry@...;

doi:10.1016/j.fct.2008.05.003  Copyright © 2008 Published by Elsevier Ltd.

Overview: the history, technical function and safety of rebaudioside A, a
naturally occurring steviol glycoside, for use in food and beverages
M.C. Carakostas a, Corresponding Author
L.L. Curry b,  Leslie_Curry@...;
A.C. Boileau b
and D.J. Brusick c
a The Coca-Cola Company, Atlanta, GA
b Cargill, Incorporated, Wayzata, MN
c Independent toxicologist, Bumpass, VA
[ D. J. Brusick, B. C. Myhr, D. G. Stetka, J. 0. Rundell, Genetic and
Transforming Activity of. Formaldehyde (Litton. Bionetics. Report,. Litton,...]
Received 6 May 2008; accepted 6 May 2008. Available online 16 May 2008.
Corresponding Author:  Tel.: +001 404 676 4234; fax: +001 404 598 4234.

[ http://groups.yahoo.com/group/aspartameNM/message/1018
aspartame toxicity coverup increases danger of corporate meltdown:
Michael C. Carakostas of Coca-Cola: Murray 2003.08.11 rmforall
http://www.isrtp.org/new_members/members1.htm
The International Society of Regulatory Toxicology and Pharmacology
Carakostas, Michael C., DVM, PhD Director/Scientific & Regulatory
Affairs The Coca-Cola Company PO Drawer 1734 Atlanta, GA 30301
T. 404/676-4234 F. 404/676-7166 E-mail: mcarakostas@...;
http://www2.coca-cola.com/ourcompany/columns_aspartame.html [ no longer on the
Net ]
[photo] Aspartame: The world agrees it's safe
By Michael Carakostas, DVM, PhD
Director, Scientific and Regulatory Affairs, Coca-Cola

It is commendable that Carakostas mentions the core problem, albeit
disparagingly, and overlaid with multiple untruths: "During digestion,
aspartame yields a very small amount of methanol-- as do many other
food substances. The body converts this methanol to formaldehyde,
which is instantly converted to formate.
Formate is quickly eliminated as carbon dioxide and water."

Carakostas deceptively make claims, unsupported by research,
that the amount of methanol from aspartame is "very small",
and that little of the inevitable formaldehyde or formic acid toxic
products accumulate in body tissues. This executive, with a PhD
in veterinary science, is deceiving people
about very serious multiple toxicities.

Thus, there is evidence here cited from 1973 to 2004 that research
and reviews by immense vested interests about aspartame must
be scrutinized with the greatest skepticism.
The greatest Internet myth about aspartame is this:
"Aspartame is the most thoroughly tested food additive in history."

http://groups.yahoo.com/group/aspartameNM/message/857
www.dorway.com: original documents and long reviews of flaws in
aspartame toxicity research: Murray 2002.07.31

http://groups.yahoo.com/group/aspartameNM/message/858
Samuels: Strong: Roberts: Gold: flaws in double-blind studies re
aspartame and MSG toxicity: Murray 2002.08.01

"Survey of aspartame studies: correlation of outcome and funding
sources," 1998, unpublished: http://www.dorway.com/peerrev.html
Walton found 166 separate published studies in the peer reviewed
medical literature, which had relevance for questions of human safety.
The 74 studies funded by industry all (100 %) attested to aspartame's
safety, whereas of the 92 non-industry funded studies, 84 (91 %)
identified a problem. Six of the seven non-industry funded studies
that were favorable to aspartame safety were from the FDA, which
has a public record that shows a strong pro-industry bias.
Ralph G. Walton, MD, Prof. of Clinical Psychology, Northeastern Ohio
Universities, College of Medicine, Dept. of Psychiatry, Youngstown,
OH 44501, Chairman, The Center for Behavioral Medicine,
Northside Medical Center, 500 Gypsy Lane, P.O. Box 240
Youngstown, OH 44501 330-740-3621 rwalton193@...
http://www.neoucom.edu/DEPTS/Psychiatry/walton.htm

http://groups.yahoo.com/group/aspartameNM/message/622
Gold: Koehler: Walton: Van Den Eeden: Leon:
aspartame toxicity: Murray 2001.06.04 four double-blind studies ]


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_ob=ArticleListURL&_method=list&_ArticleListID=744319304&_sort=v&_st=17&view=c&_\
acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=9a474db4552e5e6f4532c2ef\
c3120c5d

1. Microbial hydrolysis of steviol glycosides
Food and Chemical Toxicology, In Press, Accepted Manuscript, Available online 16
May 2008
A.G. Renwick,
S.M. Tarka
Purchase PDF (243 K)
[ Nature. 2002 Jul 18; 418(6895): 289-90.
Cacao usage by the earliest Maya civilization.
Hurst WJ, Tarka SM Jr, Powis TG, Valdez F Jr, Hester TR.
Hershey Foods Technical Center, PO Box 805, Hershey, Pennsylvania 17033, USA.
whurst@...;

Food Chem Toxicol. 1991 Jan; 29(1): 7-19.
Chronic toxicity/carcinogenicity studies of cocoa powder in rats.
Tarka SM Jr, Morrissey RB, Apgar JL, Hostetler KA, Shively CA.
Hershey Foods Corporation Technical Center, PA 17033-0805. ]


2. Pharmacokinetics of rebaudioside A and stevioside after single oral doses in
healthy men
FCT, Available online 16 May 2008
A. Wheeler, A.C. Boileau, P.C. Winkler, J.C. Compton, I. Prakash, X. Jiang, D.A.
Mandarino
Purchase PDF (296 K)
[ Experimental Biology and Medicine 227: 914-919 (2002)
© 2002 Society for Experimental Biology and Medicine
SYMPOSIA
Bioavailability of all-trans and cis-Isomers of Lycopene
Thomas W.-M. Boileau*,
Amy C. Boileau{dagger}
and John W. Erdman, Jr{ddagger},1  jwerdman@...;
* Department of Human Nutrition and Food Management, The Ohio State University,
Columbus, Ohio 43210;
{dagger} Ross Products Division, Abbott Laboratories, Inc., Columbus, Ohio
43215; and
{dagger} Division of Nutritional Sciences, University of Illinois,
Urbana-Champaign, Illinois 61801 ]


3. The hemodynamic effects of rebaudioside A in healthy adults with normal and
low-normal blood pressure
FCT, Available online 16 May 2008
K.C. Maki, L.L. Curry, M.C. Carakostas, S.M. Tarka, M.S. Reeves, M.V. Farmer,
J.M. McKenney, P.D. Toth, S.L. Schwartz, B.C. Lubin, M.R. Dicklin, A.C. Boileau,
J.D. Bisognano
Purchase PDF (314 K)
[ Journal of the American College of Nutrition, Vol 16, Issue 6 578-583,
Copyright © 1997 by American College of Nutrition
JOURNAL ARTICLE
Age-dependence of the relationship between adiposity and serum low density
lipoprotein cholesterol in men
K. C. Maki, K. Kritsch, S. Foley, I. Soneru and M. H. Davidson
Chicago Center for Clinical Research, Illinois 60610, USA.
[ www.jacn.org/cgi/content/full/19/1/23
Journal of the American College of Nutrition, Vol. 19, No. 1, 23-30 (2000)
Published by the American College of Nutrition
Original Research
Low-Density Lipoprotein Subclass Distribution Pattern and Adiposity-Associated
Dyslipidemia in Postmenopausal Women
Kevin C. Maki, PhD, Michael H. Davidson, MD, Mary Sue Cyrowski, RD, Ann C. Maki,
MS, RD and Phyllis Marx, MD
Chicago Center for Clinical Research, Chicago, Illinois
Kevin C. Maki, PhD, Chicago Center for Clinical Research, 515 North State
Street, 27th Floor, Chicago, Illinois 60610

http://www.providentcrc.com/
http://www.providentcrc.com/newsletter.php
Provident has a team of research professionals with extensive experience in the
design and conduct of clinical trials to evaluate pharmaceuticals, medical and
functional foods, dietary supplements and medical devices.
For more information, visit our web site: http://www.providentcrc.com.
Kevin C. Maki, PhD, President/Chief Science Officer  kmaki@...;
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ACADEMIC & PROFESSIONAL EXPERIENCE:
2004-Present President & Chief Science Officer
Provident Clinical Research, a division of Provident Clinical Research &
Consulting, Inc.
Glen Ellyn, Illinois & Bloomington, Indiana

"Dr Maki’s continued consulting work as a GLG SCHOLAR for the Gerson Lehrman
Group has helped investment firms, corporations and non-profit organizations to
better understand products, services, companies, issues, and industries, scoring
in the top quintile."

"Toth PP, Maki KC. Practical Lipid Management: London: John Wiley & Sons, (in
press). Expected release date July, 2008.
The book Therapeutic Lipidology, edited by Drs. Michael H. Davidson, Peter P.
Toth and Kevin C. Maki, is available for purchase at Amazon.com."

Provident Perspective Back Issues
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Indiana: 1000 West 1st Street; Bloomington, IN 47403
Phone: (630) 858-4400  Fax: (630) 858-4490

http://www.providentcrc.com/media/kmaki_cv.pdf
PUBLICATIONS (peer reviewed journals):
1. Maki KC, Curry LL, Carakostas MC, Tarka SM, Reeves MS, Farmer MV, McKenney
JM, Toth PD, Schwartz SL, Lubin BC, Dicklin MR, Boileau AC, Bisognano JD. The
hemodynamic effects of rebaudioside A in healthy adults with normal and
low-normal blood pressure. Food and Chemical Toxicology, 2008 (in press)

2. Maki KC, Curry LL, Reeves MS, Toth PD, McKenney JM, Farmer MV, Schwartz SL,
Lubin BC, Boileau AC, Dicklin MR, Carakostas MC, Tarka SM. Chronic consumption
of rebaudioside A, a steviol glycoside, in men and women with type 2 diabetes
mellitus. Food and Chemical Toxicology, 2008 (in press).

3. Voss AC, Maki KC, Carvey TW, Hustead DS, Alish C, Fix B, Mustad VA. Effect of
two carbohydrate-modified tube-feeding formulas on metabolic responses in
patients with type 2 diabetes. Nutrition, 2008 (in press).

4. Maki KC, McKenney JM, Reeves MS, Lubin BC, Dicklin MR. Effects of adding
prescription omega-3 fatty acid ethyl esters to simvastatin (20 mg/day) on
lipids and lipoprotein particles in men and women with mixed dyslipidemia. Am J
Cardiol, 2008 (in press).

5. Maki KC, Carson ML, Miller MP, Turowski M, Bell M, Wilder D, Rains TM, Reeves
MS. High-viscosity hydroxypropylmethylcellulose lowers postprandial insulin
levels. J Nutr. 2008; 138:292-296.

6. Davidson MH, Stein EA, Bays H, Maki KC, Doyle R, Shalwitz RA, Ballantyne CM,
Ginsberg HN. Efficacy and tolerability of adding prescription omega-3 fatty
acids to simvastatin 40mg/d in hypertriglyceridemic patients: An 8-week,
randomized, double-blind, placebo-controlled study – The COMBOS Trial. Clin
Ther. 2007;29:1354-1367.

7. Maki KC, Carson ML, Miller MP, Turowski M, Wilder D, Reeves MS, Bell M.
High-viscosity hydroxypropylmethylcellulose blunts postprandial glucose and
insulin responses. Diabetes Care. 2007;30:1039-1043.

8. Izumi R, Hurt J, Maki KC, Bell M, Zavras AI, McCamish M. Clinical predictors
of glycosylated hemoglobin responses to thiazolidinedione therapy. Diabetes
Technol Ther. 2007;9:553-561.

9. Maki KC, Davidson MH, Witchger MS, Dicklin MR, Subbaiah PV. Effects of
high-fiber oat and wheat cereals on postprandial glucose and lipid responses.
Int J Vitam Nutr Res. 2007;77:347-356.

10. Maki KC, Rains TM, Kaden VN, Raneri KR, Davidson MH. Effects of a reduced
glycemic load diet on body weight, body composition and cardiovascular risk
markers in overweight and obese men and women. Am J Clin Nutr. 2007;85:724-734.

11. Davidson MH, Bays HE, Stein E, Maki KC, Shalwitz RA, Doyle R. Effects of
fenofibrate on atherogenic dyslipidemia in hypertriglyceridemic subjects. Clin
Cardiol. 2006;29:268-273.

12. Ansell BJ, Fonarow GC, Maki KC, Dicklin MR, Bell M, Davidson MH. Reduced
treatment success in lipid management among women with coronary heart disease or
risk equivalents: results of a national survey. Am Heart J.
2006;152:976-981...... ]


4. Chronic consumption of rebaudioside A, a steviol glycoside, in men and women
with type 2 diabetes mellitus
FCT, Available online 16 May 2008
K.C. Maki, L.L. Curry, M.S. Reeves, P.D. Toth, J.M. McKenney, M.V. Farmer, S.L.
Schwartz, B.C. Lubin, A.C. Boileau, M.R. Dicklin, M.C. Carakostas, S.M. Tarka
Purchase PDF (306 K)

5. Rebaudioside A: two-generation reproductive toxicity study in rats
FCT, Available online 16 May 2008
Leslie L. Curry, Ashley Roberts, Nigel Brown
Purchase PDF (367 K)

[ Dr Ashley Roberts, Vice-President, Food and Nutrition Group, Cantox Health
Sciences International, of Mississauga, USA, www.cantox.com
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Use of hydrogen peroxide-based tooth whitening products and its relationship to
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Berna Magnuson brings to Cantox an exceptional broad range of skills and
knowledge in toxicology and food and nutritional sciences.
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recognized internationally.
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efforts to address issues facing the food industry in the adoption of this
promising new technology.

Berna received her BSHEc with distinction in food science and nutrition.
After working in the food industry, she obtained her MSc in Toxicology from the
University of Saskatchewan, and her PhD in Food and Nutritional Sciences from
the University of Manitoba.
Her post-doctoral research focused on the pathology and biochemistry of colon
cancer.
As a university faculty member recently at the University of Maryland, Berna led
a competitive research program, mentored graduate students, and taught courses
for over 12 years.

She is now an adjunct professor in nutritional sciences at the University of
Toronto.

Her research has been published in over 40 peer-reviewed journal articles and
book chapters, and had led to several patents.
Recently, her work focused on safety assessments of various dietary ingredients
and supplements.
Berna has been elected to numerous leadership positions of the Institute of Food
Technologists and the Society of Toxicology, and she has been the recipient of
outstanding service awards from both the US FDA and IFT.
She is a member of the editorial board of the Journal of Food Protection and an
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Berna is also a member of the American Association for Cancer Research, and is a
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http://www.utm.utoronto.ca/
University of Toronto Mississauga, 3359 Mississauga Rd N., Mississauga, ON L5L
1C6

http://www.utoronto.ca/nutrisci/faculty/Magnuson/
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Senior Scientific and Regulatory Consultant, Cantox Health Science International
2233 Argentia Road, Suite 308, Mississauga, ON L5N 2X7
Tel: (905) 542 2900 Fax: (905) 542 1011 BMagnuson@...;
Research
My research interests have been in the area of diet and cancer and I am now
interested in the new and exciting area of nanotechnology and its role in
nutrition.  ]


6. Development of rebiana, a natural, non-caloric sweetener
FCT, Available online 16 May 2008
I. Prakash, G.E. DuBois, J.F. Clos, K.L. Wilkens, L.E. Fosdick
Purchase PDF (398 K)

7. A critical review of the genetic toxicity of steviol and steviol glycosides
FCT, Available online 16 May 2008
D.J. Brusick
Purchase PDF (496 K)

8. Subchronic toxicity of rebaudioside A
FCT, Available online 16 May 2008
Leslie L. Curry, Ashley Roberts
Purchase PDF (369 K)

9. Comparative toxicokinetics and metabolism of rebaudioside A, stevioside, and
steviol in rats
FCT, Available online 16 May 2008
A. Roberts, A.G. Renwick
Purchase PDF (362 K)

10. Steviol glycoside biosynthesis
Phytochemistry, Volume 68, Issue 14, July 2007, Pages 1855-1863
J.E. Brandle, P.G. Telmer
Purchase PDF (529 K)
Graphical abstract [ image ]
Steviol glycosides are found in high concentrations in the leaves of the
Paraguayan perennial herb Stevia rebaudiana, their intense sweetness and high
concentration in Stevia leaf tissue has made them the subject of research
interest for over 100 years.
The convergence of genomics and plant biochemistry has led to the rapid
elucidation of the genes coding for the various enzymes in the biosynthetic
pathway.

11. Apparent lack of pharmacological effect of steviol glycosides used as
sweeteners in humans. A pilot study of repeated exposures in some normotensive
and hypotensive individuals and in Type 1 and Type 2 diabetics
Regulatory Toxicology and Pharmacology, Volume 51, Issue 1, June 2008, Pages
37-41
Luis A. Barriocanal, Mafalda Palacios, Gilda Benitez, Sussam Benitez, Jorge T.
Jimenez, Nora Jimenez, Vicenta Rojas
Purchase PDF (181 K)

12. Enzymatic modification of stevioside by cell-free extract of Gibberella
fujikuroi
Journal of Biotechnology, Volume 131, Issue 1, 1 August 2007, Pages 92-96
Brás H. de Oliveira, Janaina F. Packer, Márcio Chimelli, Daniel A. de Jesus
Purchase PDF (425 K)

13. Simultaneous determination of stevioside, rebaudioside A and C and dulcoside
A in foods by high-performance liquid chromatography
Journal of Chromatography A, Volume 474, Issue 2, 1989, Pages 447-451
Yoshimi Kitada, Michiko Sasaki, Yutaka Yamazoe, Hiroyuki Nakazawa
Purchase PDF (288 K)

14.Letter to the Editor
Food and Chemical Toxicology, Volume 45, Issue 12, December 2007, Pages
2597-2598
Gary M. Williams  Gary_Williams@...;
Purchase PDF (71 K)
[ Eur J Cancer Prev. 2007 Dec; 16(6): 528-34.
Inhibition by acetaminophen of neoplastic initiation elicited in rat liver by
the DNA-reactive hepatocarcinogen N-acetyl-2-aminofluorene.
Williams GM, Iatropoulos MJ, Jeffrey AM, Duan JD, Perrone CE.
Department of Pathology, New York Medical College, Valhalla, New York, USA.
Gary_Williams@...;

15. Postscript
FCT, Available online 16 May 2008
David J. Brusick
Purchase PDF (129 K)

16. Validated high-performance thin-layer chromatography method for steviol
glycosides in Stevia rebaudiana
Journal of Pharmaceutical and Biomedical Analysis, In Press, Corrected Proof,
Available online 28 March 2008
Vikas Jaitak, A.P. Gupta, V.K. Kaul, P.S. Ahuja
Purchase PDF (250 K)

17. Risk assessment of dietary exposures to compounds that are genotoxic and
carcinogenic -- an overview
Toxicology Letters, In Press, Accepted Manuscript, Available online 23 May 2008
E. Dybing, J. O’Brien, A.G. Renwick, T. Sanner
Purchase PDF (269 K)

18. Safety assessment of dietary administered paprika color in combined chronic
toxicity and carcinogenicity studies using F344 rats
Food and Chemical Toxicology, In Press, Accepted Manuscript, Available online 3
May 2008
T. Inoue, T. Umemura, M. Maeda, Y. Ishii, T. Okamura, M. Tasaki, A. Nishikawa
Purchase PDF (327 K)

Note to users: The section "Articles in Press" contains peer reviewed accepted
articles to be published in this journal.
When the final article is assigned to an issue of the journal, the "Article in
Press" version will be removed from this section and will appear in the
associated published journal issue.
The date it was first made available online will be carried over.
Please be aware that although "Articles in Press" do not have all bibliographic
details available yet, they can already be cited using the year of online
publication and the DOI as follows:
Author(s), Article Title, Journal (Year), DOI.
Please consult the journal's reference style for the exact appearance of these
elements, abbreviation of journal names and the use of punctuation.
There are three types of "Articles in Press":

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accepted for publication by the Editorial Board.
The articles have not yet been copy edited and/or formatted in the journal house
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yet finalized and that will be corrected by the authors.
Therefore the text could change before final publication.
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may, or may not yet have specific issue and page numbers assigned.

28. The Threshold of Toxicological Concern (TTC) in risk assessment
Toxicology Letters, In Press, Accepted Manuscript, Available online 22 May 2008
I.C. Munro, A.G. Renwick, B. Danielewska-Nikiel    imunro@...;
Purchase PDF (313 K)

77. Use of non-mammalian alternative models for neurotoxicological study
NeuroToxicology, In Press, Accepted Manuscript, Available online 25 April 2008
Randall T. Peterson, Richard Nass, Windy A. Boyd, Jonathan H. Freedman, Ke Dong,
Toshio Narahashi
Purchase PDF (600 K)

88. The use of a sweetener substitution method to predict dietary exposures for
the intense sweetener rebaudioside A
Food and Chemical Toxicology, In Press, Accepted Manuscript, Available online 16
May 2008
A.G. Renwick
Purchase PDF (340 K)

95. Comments to the paper by Nunes et al. (2007), Analysis of genotoxic
potentiality of stevioside by comet assay, Food and Chemical Toxicology 45
(2007) 662-666
Food and Chemical Toxicology, Volume 45, Issue 12, December 2007, Pages
2601-2602
Jan M.C. Geuns
Purchase PDF (65 K)

135. Evaluation of the ability of a battery of three in vitro genotoxicity tests
to discriminate rodent carcinogens and non-carcinogens. III. Appropriate
follow-up testing in vivo
Mutation Research/Genetic Toxicology and Environmental Mutagenesis, Available
online 16 May 2008
David Kirkland, Günter Speit
Purchase PDF (446 K)

143. Approaches to the risk assessment of genotoxic carcinogens in food: A
critical appraisal
Food and Chemical Toxicology, Volume 44, Issue 10, October 2006, Pages 1613-1635
J. O’Brien, A.G. Renwick, A. Constable, E. Dybing, D.J.G. Müller, J. Schlatter,
W. Slob, W. Tueting, J. van Benthem, G.M. Williams, A. Wolfreys
Purchase PDF (354 K)


Int J Toxicol. 2008 Jan-Feb; 27(1): 65-80.
A 90-day oral (dietary) toxicity study of rebaudioside A in Sprague-Dawley rats.
Nikiforov AI, anikiforov@...;
Eapen AK.
Toxicology Regulatory Services, Inc., Charlottesville, Virginia 22911, USA.

Rebaudioside A is one of several glycosides found in the leaves of Stevia
rebaudiana (Bertoni) Bertoni (Compositae) stevia that has been identified as a
potential sweetener.
The present study (initiated in April 2006 and completed in October 2006)
evaluated the safety of this sweetener when administered as a dietary admix at
target exposure levels of 500, 1000, and 2000 mg/kg/day to Sprague-Dawley rats
for 90 days.
There were no treatment-related effects on the general condition and behavior of
the animals as determined by clinical observations, functional observational
battery, and locomotor activity assessments.
Evaluation of clinical pathology parameters revealed no toxicologically
relevant, treatment-related effects on hematology, serum chemistry, or
urinalysis.
Macroscopic and microscopic findings revealed no treatment-related effects on
any organ evaluated.
Lower mean body weight gains were noted in males in the 2000 mg/kg/day group
throughout the study, which was considered to be test article related; however,
given the small magnitude of the difference as compared to controls, this effect
was not considered to be adverse.
Results of this study clearly demonstrate that dietary administration of high
concentrations of rebaudioside A for 90 consecutive days to Sprague-Dawley rats
was not associated with any signs of toxicity.
PMID: 18293214


J Agric Food Chem. 2007 Dec 26; 55(26): 10962-7. Epub 2007 Nov 27.
Oxidative DNA damage preventive activity and antioxidant potential of Stevia
rebaudiana (Bertoni) Bertoni, a natural sweetener.
Ghanta S, Banerjee A, Poddar A, Chattopadhyay S.
Drug Development/Diagnositcs and Biotechnology Division, Indian Institute of
Chemical Biology, Kolkata, India.

At 0.1 mg/mL, the ethyl acetate extract (EAE) of the crude 85% methanolic
extract (CAE) of Stevia rebaudiana leaves exhibited preventive activity against
DNA strand scission by *OH generated in Fenton's reaction on pBluescript II SK
(-) DNA.
Its efficacy is better than that of quercetin.
The radical scavenging capacity of CAE was evaluated by the DPPH test
(IC50=47.66+/-1.04 microg/mL).
EAE was derived from CAE scavenged DPPH (IC50=9.26+/-0.04 microg/mL), ABTS+
(IC50=3.04+/-0.22 microg/mL) and *OH (IC50=3.08+/-0.19 microg/mL).
Additionally, inhibition of lipid peroxidation induced with 25 mM FeSO 4 on rat
liver homogenate as a lipid source was noted with CAE (IC50=2.1+/-1.07 mg/mL).
The total polyphenols and total flavonoids of EAE were 0.86 mg gallic acid
equivalents/mg and 0.83 mg of quercetin equivalents/mg, respectively.
Flavonoids, isolated from EAE, were characterized as quercetin-3-O-arabinoside,
quercitrin, apigenin, apigenin-4-O-glucoside, luteolin, and
kaempferol-3-O-rhamnoside by LC-MS and NMR analysis. These results indicate that
Stevia rebaudiana may be useful as a potential source of natural antioxidants. 
PMID: 18038982


http://groups.yahoo.com/group/aspartameNM/message/1491
industry scientists praise aspartame safety and benefits in Paris on
2006.05.30, Herve Nordmann, Andrew G. Renwick,
Carlo La Vecchia, Tommy Visscher, Jaap Seidell, France Bellisle,
Adam Drewnowski, Margaret Ashwell, Anne de la Hunty,
Sigrid A. Gibson, Alan R. Boobis: Murray 2007.11.18


http://www.elsevier.com/wps/find/journaldescription.cws_home/237/description#des\
cription

Food and Chemical Toxicology
Description

Food and Chemical Toxicology publishes original research reports and occasional
interpretative reviews on the toxic effects, in animals or humans, of natural or
synthetic chemicals occurring in the human environment.
In addition to studies relating to food, water and other consumer products,
papers on industrial and agricultural chemicals and pharmaceuticals are
encouraged.
Furthermore new areas such as safety evaluation of novel foods and
biotechnologically derived products and inter-relationships between nutrition
and toxicology are welcomed.
The studies may address the physiological, biochemical or pathological changes
induced by specific substances, techniques for assessing potential toxicity,
including molecular biology or the mechanisms underlying toxic phenomena.
All aspects of in vivo toxicology are covered, including systemic effects on
specific organ systems, immune functions, carcinogenesis and teratogenesis.
Papers reporting the toxicological examination of specific chemicals or consumer
products are published irrespective of the positive or negative nature of the
results, provided the tests and reporting meet current standards of adequacy.
The Journal's editorial policy reflects the need for high-quality science in
support of health and safety decisions.
FCT is willing to consider papers of a more regulatory nature, provided they are
part of a more general scientific analysis.
On acceptance these papers will be published in a Regulatory Toxicology section.
We recommend that before submitting a regulatory paper one of the editors of the
journal is contacted.

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ISSN: 0278-6915
Imprint: PERGAMON
Commenced publication 1963

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Managing Editors:
Joseph F. Borzelleca
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Imperial College, London, United Kingdom,  a.boobis@...;

Review Editors:
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Harrington House, 8 Harrington Road, Brighton, East Sussex, BN1 6RE, UK

Founding Editor:
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http://groups.yahoo.com/group/aspartameNMmessage/1488
Coca-Cola, Cargill Inc., PureCircle global operations market stevia
for foods and drinks: Murray 2007.11.12

http://groups.yahoo.com/group/aspartameNM/message/1438
Coca-Cola and Cargill Inc., after years of development,
with 24 patents, will soon sell rebiana (stevia)
in drinks and foods: Murray 2007.05.31
[ gives links to reviews of previous stevia studies ]

http://groups.yahoo.com/group/aspartameNMmessage/1437
stevia to be approved and cyclamates limited by Food Standards
Australia New Zealand: JMC Geuns critiques of two recent stevia
studies by Nunes: Murray 2007.05.29

http://groups.yahoo.com/group/aspartameNM/message/1436
FDA's corrupt war against safe herbal sweetener stevia,
Mary Nash Stoddard, 2006 January,
Aspartame Consumer Safety Network: Murray 2007.05.24

http://groups.yahoo.com/group/aspartameNM/message/1430
stevia, balanced factual detailed review in Wikipedia: Murray
2007.05.19
http://en.wikipedia.org/wiki/Stevia

http://groups.yahoo.com/group/aspartameNM/message/1419
two recent warning studies on stevia toxicity on rats and bacteria, AP
Nunes et al, 2007 April, 2006 Dec, links to 18 positive abstracts from
2000 February to 2004 January: Murray 2007.05.03

At the end of this post, I link to my 5 previous reviews in 2005
August that give 18 full abstacts in PubMed on stevia toxicity from
2000 February to 2004 January, which do not find that stevia is
practically toxic to humans in ordinary use -- and give an opposite
positive abstract using the Comet assay in 2002 December, and then
share the conclusion from the full text of another study on
mutagenicity, T Terai et al 2002 July. ]

Planta Med. 2001 Dec; 67(9): 796-9.
Inhibitory effect of stevioside on calcium influx to produce
antihypertension.
Lee CN, Wong KL, Liu JC, Chen YJ, Cheng JT, Chan P.
Department of Medicine, Taipei Medical University-Wan Fang Hospital,
Wen Shan, Taipei, Taiwan.

Antiviral Res. 2001 Jan; 49(1): 15-24.
Analysis of anti-rotavirus activity of extract from Stevia rebaudiana.
Takahashi K, Matsuda M, Ohashi K, Taniguchi K, Nakagomi O, Abe Y,
Mori S, Sato N, Okutani K, Shigeta S.
Department of Microbiology, School of Medicine, Fukushima Medical
University, 1 Hikarigaoka, Fukushima-shi 960-1295, Japan.
k-t...@...

Metabolism. 2000 Feb; 49(2): 208-14.
Stevioside acts directly on pancreatic beta cells to secrete insulin:
actions independent of cyclic adenosine monophosphate and
adenosine triphosphate-sensitive K+-channel activity.
Jeppesen PB, Gregersen S, Poulsen CR, Hermansen K.
Department of Endocrinology and Metabolism, Aarhus University
Hospital, Denmark.

http://groups.yahoo.com/group/aspartameNM/message/1201
here's three more stevia abstracts: lowers blood pressure, Lee CN 2001
Dec: antiviral, Takashashi K 2001 Jan: antihyperglycemic, Jeppesen PB,
2000 Feb: Murray 2005.08.07

http://groups.yahoo.com/group/aspartameNM/message/1199
yet three more stevia abstracts: mutagenic in bacteria, Terai T, 2002
July: lowers blood pressure in rats, Hsu YH, 2002 Jan:
antihyperglycaemic, insulinotropic and glucagonostatic benefits in
rats, Jeppesen PB 2002 Jan; Murray 2005.08.07

http://groups.yahoo.com/group/aspartameNM/message/1198
three more stevia abstracts: no genotoxicity in mice, Sekihashi K,
Saitoh H, Sasaki Y 2002 Dec: lowers blood pressure in dogs,
Liu JC 2003 Jan: inhibits tumors in mice, Yasukawa K 2002 Nov:
Murray 2005.08.05

http://groups.yahoo.com/group/aspartameNM/message/1197
three abstracts on expert stevia research: hypertension, Chan P
2000 Sept; microflora, Gardana C 2003.10.22; helps blood pressure
and glucose level, Jeppesen PB 2003 Mar: Murray 2005.08.05

http://groups.yahoo.com/group/aspartameNM/message/1196
Alan in alt.support.diabetes re Stevia and Glycemic and Hypertension
Control 2004.05.14: 2 year large scale blood pressure study,
Hsieh MH, 2003 Nov: insulin in muscles, Lailerd N 2004 Jan:
glucose in diabetics, Gregersen S 2004 Jan: Murray 2005.08.04

http://groups.yahoo.com/group/aspartameNM/message/1179
Stevia (stevioside) is safe: Prof. Jan M.C. Geuns: Murray 2005.07.06

http://groups.yahoo.com/group/aspartameNM/message/1084
26 stevia safety abstracts since 1993: aspartame vs stevia debate on
alt.support.diabetes, George Schmidt, OD: Murray 2004.05.25
____________________________________________________


"Of course, everyone chooses, as a natural priority, to enjoy
peace, joy, and love by helping to find, quickly share, and positively
act upon evidence about healthy and safe food, drink, and
environment."

Rich Murray, MA Room For All rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com  new primary archive

http://groups.yahoo.com/group/aspartameNM/messages
group with 125 members, 1,540 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1,107 members, 22,690 posts in a public archive
____________________________________________________


vinyl acetate, ethyl alcohol, or aspartame in womb increases later cancers
in adults with lifetime exposure in many studies, M Soffritti et al,
Ramazzini Foundation, Basic Clin. Pharm. Toxicol. 2008 Feb.: Murray
2008.02.01
http://rmforall.blogspot.com/2008_02_01_archive.htm
Friday, February 1, 2008
http://groups.yahoo.com/group/aspartameNM/message/1509

http://groups.yahoo.com/group/aspartameNM/message/1453
Souring on fake sugar (aspartame), Jennifer Couzin,
Science 2007.07.06: 4 page letter to FDA from 12 eminent
USA toxicologists re two Ramazzini Foundation cancer studies
2007.06.25: Murray 2007.07.18

http://groups.yahoo.com/group/aspartameNM/message/1503
Devra Lee Davis, U. Pittsburgh Cancer Institute, rejects aspartame -- Luke
Ravenstahl, Mayor, drinks 12 cans Diet Pepsi daily: accurate warning
by Ronald K. Frazer: Murray 2008.01.13
http://rmforall.blogspot.com/2008_01_01_archive.htm
Sunday, January 13, 2008

methanol impurity in alcohol drinks [ and aspartame ] is turned
into neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol
Syndrome, BM Kapur, DC Lehotay, PL Carlen at U. Toronto,
Alc Clin Exp Res 2007 Dec. plain text: detailed biochemistry,
CL Nie et al. 2007.07.18: Rich Murray 2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524

http://groups.yahoo.com/group/aspartameNM/message/1459
third study by expert Greek team of neurotoxicity in infant rats by
aspartame (or its parts, methanol, phenylalanine, aspartic acid), KH
Schulpis et al, Food Chem Toxicol 2007.06.16: Murray 2007.08.05

http://groups.yahoo.com/group/aspartameNM/message/782
Smith, Terpening, Schmidt, Gums: full text: aspartame, MSG, fibromyalgia:
Murray 2002.01.17
Jerry D Smith, Chris M Terpening,
Siegfried OF Schmidt, and John G Gums
Relief of Fibromyalgia Symptoms Following
Discontinuation of Dietary Excitotoxins.
The Annals of Pharmacotherapy 2001; 35(6): 702-706.
Malcolm Randall Veterans Affairs Medical Center,
Gainesville, FL, USA.
BACKGROUND: Fibromyalgia is a common rheumatologic
disorder that is often difficult to treat effectively.
CASE SUMMARY: Four patients diagnosed with fibromyalgia
syndrome for two to 17 years are described.
All had undergone multiple treatment modalities with limited success.
All had complete, or nearly complete,
resolution of their symptoms within months after eliminating
monosodium glutamate (MSG) or MSG plus aspartame from their diet.
All patients were women with multiple comorbidities
prior to elimination of MSG.
All have had recurrence of symptoms whenever MSG is ingested.

Siegfried O. Schmidt, MD Asst. Clinical Prof. siggy@...
Community Health and Family Medicine, U. Florida, Gainesville, FL
Shands Hospital West Oak Clinic Gainesville, FL 32608-3629
352-376-5071


Avoiding formaldehyde allergic reactions in children, aspartame, vitamins,
shampoo, conditioners, hair gel, baby wipes, Sharon E Jacob, MD, Tace
Steele, U. Miami, Pediatric Annals 2007 Jan.: eyelid contact dermatitis, AM
Hill, DV Belsito, 2003 Nov.: Murray 2008.03.27
http://rmforall.blogspot.com/2008_03_01_archive.htm
Thursday, March 27, 2008
http://groups.yahoo.com/group/aspartameNM/message/1532

"It is generally recommended that exposure to products containing
formaldehyde, FRP's, and aspartame (NutraSweet) be avoided
in children."

"Through metabolism, aspartame is converted metabolically
in the liver to methanol,
which is in turn metabolized to formaldehyde. 8"

www.pediatricannalsonline.com/showPdf.asp?rID=21306

Avoiding formaldehyde allergic reactions in children
Pediatric Annals. 2007 Jan.; 36(1): 55-6. PMID: 17269284
Sharon E. Jacob, MD, Director, Contact Dermatitis Clinic,
Dept. of Dermatology and Cutaneous Surgery, U. of Miami,
1295 NW 14th St., Miami, FL 33125, fax 305-243-6191

formaldehyde from many sources, including aspartame, is major cause of
Allergic Contact Dermatitis, SE Jacob, T Steele, G Rodriguez, Skin and Aging
2005 Dec.: Murray 2008.03.27
http://rmforall.blogspot.com/2008_03_01_archive.htm
Thursday, March 27, 2008
http://groups.yahoo.com/group/aspartameNM/message/1533

Sharon E. Jacob, MD
Assistant Professor of Medicine (Dermatology)
University of California, San Diego 200 W. Arbor Drive #8420
San Diego, CA 92103-8420
Tel: 858-552-8585 ×3504 Fax: 305-675-8317
sjacob@...;

"For example, diet soda and yogurt containing aspartame
(Nutrasweet), release formaldehyde in their natural biological
degradation.

One of aspartame's metabolites, aspartic acid methyl ester,
is converted to methanol in the body, which is oxidized to
formaldehyde in all organs, including the liver and eyes. 22

Patients with a contact dermatitis to formaldehyde have been seen
to improve once aspartame is avoided. 22

Notably, the case that Hill and Belsito reported had a 6-month
history of eyelid dermatitis that subsided after 1 week of avoiding
diet soda. 22"

"We present a case of a medical student who presented with
erythematous eczematoid plaques on her trunk and legs and
fine vesiculation of her scalp, 3 weeks after starting anatomy class.

Of note, she routinely washed her face and arms after leaving the
anatomy lab, but remained in her scrubs for the rest of the day.

Formaldehyde and Quaternium-15 positive reactions
in the same patient."

"Our patient underscores the importance of appropriate patch
testing and education.
Once we identified the allergy to formaldehyde and quaternium-15,
we provided patient education materials regarding the common and
not-so-common locations of these chemicals and cross-reactors.
We also gave the patient information on avoidance
and safe alternatives (see Table 5).

Fortunately, with technical advances, this student completed the
anatomy section via electronic learning tools.

By avoiding formaldehyde, including anatomy lab, FRP
in her shampoo and cosmetics,
and aspartame in her diet, this patient dramatically improved.

As with all contact dermatitides, the mainstay of treatment for
allergic contact dermatitis is avoidance."

http://www.skinandaging.com/article/5158
Allergen Focus:
Focus on T.R.U.E. Test Allergens #21, 13 and 18:
Formaldehyde and Formaldehyde-Releasing Preservatives
Skin & Aging, ISSN 1096-0120; 13(12) 2005 Dec.: 22-27.
Sharon E. Jacob, M.D.,
Tace Steele, B.A.,
and Georgette Rodriguez, M.D., M.P.H.   ]


two aspartame (methanol, formaldehyde, formic acid) toxicity research
studies by Resia Pretorius, U. Pretoria, South Africa, debate with JD
Fernstrom: Murray 2008.04.04 2008.05.22
http://rmforall.blogspot.com/2008_04_01_archive.htm
Friday, April 4, 2008
http://groups.yahoo.com/group/aspartameNM/message/1536

http://foodqualitynews.com/news/ng.asp?n=84424-aspartame-sweetener
recent news re E Pretorius aspartame and brain review

Direct and indirect cellular effects of aspartame on the brain.
Humphries P, Pretorius E, Naude H, U. Pretoria, South Africa,
Eur J Clin Nutr. 2007 Aug 8: Murray 2007.08.12
http://groups.yahoo.com/group/aspartameNM/message/1463

"The aim of this study was to discuss the direct and indirect
cellular effects of aspartame on the brain,
and we propose that excessive aspartame ingestion
might be involved in the pathogenesis
of certain mental disorders (DSM-IV-TR 2000)
and also in compromised learning and emotional functioning."

Eur J Clin Nutr. 2007 Aug 8; [Epub ahead of print]
Direct and indirect cellular effects of aspartame on the brain.
Humphries P,
Pretorius E, resia.pretorius@...;
Naude H.
[1] Department of Anatomy, University of Pretoria,
Pretoria, Gauteng, South Africa
[2] Department of Anatomy, University of the Limpopo,
South Africa.

The use of the artificial sweetener, aspartame, has long been
contemplated and studied by various researchers, and people are
concerned about its negative effects.

Aspartame is composed of phenylalanine (50%),
aspartic acid (40%) and methanol (10%).

Phenylalanine plays an important role in neurotransmitter regulation,
whereas aspartic acid is also thought to play a role as an excitatory
neurotransmitter in the central nervous system.

Glutamate, asparagines and glutamine are formed from their
precursor, aspartic acid.

Methanol, which forms 10% of the broken down product,
is converted in the body to formate,
which can either be excreted or can give rise to formaldehyde,
diketopiperazine (a carcinogen) and a number of other highly toxic
derivatives.

Previously, it has been reported that consumption of aspartame
could cause neurological and behavioural disturbances in sensitive
individuals.

Headaches, insomnia and seizures are also some of the neurological
effects that have been encountered, and these may be accredited to
changes in regional brain concentrations of catecholamines,
which include norepinephrine, epinephrine and dopamine.

The aim of this study was to discuss the direct and indirect
cellular effects of aspartame on the brain,
and we propose that excessive aspartame ingestion
might be involved in the pathogenesis
of certain mental disorders (DSM-IV-TR 2000)
and also in compromised learning and emotional functioning.

European Journal of Clinical Nutrition advance online publication,
8 August 2007; doi:10.1038/sj.ejcn.1602866.
PMID: 17684524

Keywords: astrocytes; aspartame; neurotransmitters; glutamate;
GABA; serotonin; dopamine; acetylcholine

Received 25 October 2006; revised 26 April 2007;
accepted 27 April 2007
Correspondence: Professor E Pretorius, Department of Anatomy,
University of Pretoria, BMW Building, Dr Savage Street,
PO Box 2034, Pretoria 0001,
Gauteng, South Africa.  E-mail: resia.pretorius@...

c 2007 Nature Publishing Group,
All rights reserved  0954-3007/07
$30.00  www.nature.com/ejcn


http://groups.yahoo.com/group/aspartameNMmessage/1452
phenylalanine and aspartic acid from low dose aspartame in rabbits
interfere with blood coagulation, Pretorius E and Humphries P,
U. of Pretoria, Ultrastruct Pathol 2007 March: Murray 2007.07.14

" The authors conclude by suggesting that aspartame usage
may interfere with the coagulation process
and might cause delayed fibrin breakup after clot formation.

They suggest this,
as the fibrin networks from aspartame-exposed rabbits
are more complex and dense,
due to the netlike appearance of the minor, thin fibers.

Aspartame usage should possibly be limited
by people on anti-clotting medicine
or those with prone to clot formation. "

Ultrastruct Pathol. 2007 Mar-Apr; 31(2): 77-83.
Ultrastructural changes to rabbit fibrin and platelets
due to aspartame.
Pretorius E,
Humphries P.
Department of Anatomy, Faculty of Medicine,
University of Pretoria, South Africa.
[ Humphries P also at
Department of Anatomy, University of Limpopo.
Medunsa Campus, Garankuwa. South Africa ]

email: E. Pretorius resia.pretorius@...
*Correspondence to E. Pretorius,
BMW Building, PO Box 2034,
Faculty of Health Sciences,
University of Pretoria, Pretoria 0001, South Africa

The coagulation process, including thrombin, fibrin,
as well as platelets,
plays an important role in hemostasis,
contributing to the general well-being of humans.

Fibrin formation and platelet activation are delicate processes
that are under the control of many small physiological events.

Any one of these many processes
may be influenced or changed by external factors,
including pharmaceutical or nutritional products, e.g.,
the sweetener aspartame (L-aspartyl-L-phenylalanine methyl ester).

It is known that phenylalanine is present at position P(9)
and aspartate at position P(10)
of the alpha-chain of human fibrinogen,
and plays an important role in the conversion of fibrinogen to fibrin
by the catalyst alpha-thrombin.

The authors investigate the effect of aspartame
on platelet and fibrin ultrastructure,
by using the rabbit animal model
and the scanning electron microscope.

Animals were exposed to 34 mg/kg of aspartame
26x during a 2-month period.

Aspartame-exposed fibrin networks appeared denser,
with a thick matted fine fiber network
covering thick major fibers.

Also, the platelet aggregates appeared more granular
than the globular control platelet aggregates.

The authors conclude by suggesting that aspartame usage
may interfere with the coagulation process
and might cause delayed fibrin breakup after clot formation.

They suggest this,
as the fibrin networks from aspartame-exposed rabbits
are more complex and dense,
due to the netlike appearance of the minor, thin fibers.

Aspartame usage should possibly be limited
by people on anti-clotting medicine
or those with prone to clot formation.
PMID: 17613990
____________________________________________________


http://groups.yahoo.com/group/aspartameNM/message/1426
ASDA (unit of Wal-Mart Stores WMT.N) and Marks & Spencer
will join Tesco and also Sainsbury to ban and limit aspartame,
MSG, artificial flavors dyes preservatives additives, trans fats, salt
"nasties" to protect kids from ADHD: leading UK media:
Murray 2007.05.15

http://groups.yahoo.com/group/aspartameNMmessage/1451
Artificial sweeteners (aspartame, sucralose) and coloring agents
will be banned from use in newly-born and baby foods,
the European Parliament decided: Latvia ban in schools 2006:
Murray 2007.07.12

http://groups.yahoo.com/group/aspartameNM/message/1341
Connecticut bans artificial sweeteners in schools, Nancy Barnes,
New Milford Times: Murray 2006.05.25
____________________________________________________


http://groups.yahoo.com/group/aspartameNM/message/1469
highly toxic formaldehyde, the cause of alcohol hangovers, is
made by the body from 100 mg doses of methanol from
dark wines and liquors, dimethyl dicarbonate, and aspartame:
Murray 2007.08.31

http://groups.yahoo.com/group/aspartameNM/message/1052
DMDC: Dimethyl dicarbonate 200mg/L in drinks adds
methanol 98 mg/L ( becomes formaldehyde in body ):
EU Scientific Committee on Foods 2001.07.12:
Murray 2004.01.22

http://europa.eu.int/comm/food/fs/sc/scf/out96_en.pdf

"...DMDC was evaluated by the SCF in 1990 and considered
acceptable for the cold sterilization of soft drinks and fruit juices
at levels of addition up to 250 mg/L (1)
...DMDC decomposes primarily to CO2 and methanol ...

[ Note: Sterilization of bacteria and fungi is a toxic process,
probably due to the inevitable conversion in the body of methanol
into highly toxic formaldehyde and then formic acid. ]

The use of 200 mg DMDC per liter would add 98 mg/L
of methanol to wine which
already contains an average of about 140 mg/L from natural sources.

http://groups.yahoo.com/group/aspartameNM/message/1286
methanol products (formaldehyde and formic acid) are main cause
of alcohol hangover symptoms [same as from similar amounts of
methanol, the 11% part of aspartame]: YS Woo et al, 2005 Dec:
Murray 2006.01.20

http://groups.yahoo.com/group/aspartameNM/message/1508
formaldehyde in FEMA trailers and other sources (aspartame,
dark wines and liquors, tobacco smoke): Murray 2008.01.30
http://rmforall.blogspot.com/2008_01_01_archive.htm
Wednesday, January 30, 2008

http://groups.yahoo.com/group/aspartameNM/message/1490
details on 6 epidemiological studies since 2004 on diet soda (mainly
aspartame) correlations, as well as 14 other mainstream studies
on aspartame toxicity since summer 2005: Murray 2007.11.27

http://groups.yahoo.com/group/aspartameNM/message/1340
aspartame groups and books:
updated research review of 2004.07.16: Murray 2006.05.11

http://groups.yahoo.com/group/aspartameNM/message/1143
methanol (formaldehyde, formic acid) disposition:
Bouchard M et al, full plain text, 2001:
substantial sources are degradation of fruit pectins,
liquors, aspartame, smoke: Murray 2005.04.02
____________________________________________________

Are a few persons extremely sensitive to a few food additives? Yes.: Charles
Thomas Wild 2008.05.06   Tartrazine_and_ADHD-owner@yahoogroups.com
http://groups.yahoo.com/group/aspartameNM/message/1539

Are a few persons (not everyone) extremely chemically sensitive to a
few food additives (not all food additives)?  Yes.

There are a small number of food additives to which I am quite
sensitive to.  The way I deal with them is to avoid the ones which I do
not care for.  I believe in the idea of full disclosure ingredient
labeling so persons can choose the foods they want.  Sorry, I
personally do not promote the idea of banning every single food
additive in the world or threatening to burn at the stake every
business which may use food additives.  That, to me, is an extremist
political approach which I do not support.

With full disclosure ingredient labeling, persons can choose what they
want to eat and can consume fresh, healthy, whole, additive-free foods
it seems to me.

Here's my extensive website about food additives which mirrors the
above non-extremist point-of-view.  Thank you.

http://health.groups.yahoo.com/group/Tartrazine_and_ADHD/

for 500,000 kids in YMCA Childcare Centers: Expel Junk Food petition, MeMe
Roth, CHC, President, National Action Against Obesity: aspartame toxicity
research, Rich Murray 2008.04.15

http://rmforall.blogspot.com/2008_04_01_archive.htm
Tuesday, April 15, 2008
http://groups.yahoo.com/group/aspartameNM/message/1538


http://www.petitiononline.com/YMCAFood/petition.html

YMCA Childcare Centers: Expel Junk Food

View Current Signatures
Sign the Petition  http://www.petitiononline.com/YMCAFood/petition-sign.html

To:  YMCA of the USA

April 11, 2008 (Petition Active until Junk Food is Expelled from all YMCA
Childcare Centers)

Mr. Neil Nicoll,  President and CEO,  YMCA of the USA,  101 N. Wacker Drive,
Chicago. IL 60606
http://www.ymca.net/   Telephone  (800) 872-9622  Email
fulfillment@...;Dear Mr. Neil Nicoll and the YMCA of the USA,

     Thank you to the YMCA of the USA for the many great things you do for
children, in every U.S. community and across all socio-economic strata. We
applaud your efforts to provide safe and healthy environments where families
and children can gather and participate in life-enriching events.

     Given the YMCA's leadership role as America's largest provider of
childcare--serving 500,000 children across 10,000 centers--we parents,
advocates, healthcare professionals and concerned citizens urge the YMCA of
the USA to make 2 commitments in 2008:

     1-- End the YMCA of the USA's partnership with PepsiCo upon its
expiration in 2010. While the YMCA's "Health Kids Day" and "Activate
  America" campaigns are worthy initiatives, having one the world's largest
suppliers of soft drinks and foods of low nutritional value fund the events
introduces a conflict of interest.

     2 -- Commit to the long-term elimination of "junk food" at all YMCA
childcare centers including food offered from on-site kitchens, vending
machines and meal programs. Reversing America's obesity crisis will take a
multitude of compromises and new considerations. Of particular emphasis will
be America's youngest children ages 0-5, as their body composition, eating
patterns and exercise habits are not yet set. Promoting and serving fried
food, refined rather than whole grains and those foods containing substances
potentially harmful to health (including partially hydrogenated oil, high
concentrations of sugar and high fructose corn syrup, high sodium content,
nitrites, MSG, synthetic hormones, antibiotics, artificial colors, and
artificial sweeteners), undermines the health of the very children entrusted
to the YMCA's care and contradicts the YMCA of the USA's own mission
statement.

     The means and timing to effect the necessary changes are solely up to
the YMCA of the USA including its 1,000+ boards of directors and 2,663
individual centers. However, we strongly urge there be no delay in making
the 2 commitments immediately.

     Just as New York City is considered the "domino" city, where public
health improvement strategies by the Department of Health and Mental Hygiene
are suggested, passed, and then emulated across the country, so too is it
our belief that the YMCA's leadership role in eliminating junk food from its
childcare centers will begin a cascading effect across all of America's
childcare facilities. The YMCA of the USA will earn credit for being the
catalyst for fostering a new generation of healthy children, Gen-H.

Respectfully,

MeMe Roth, CHC, Nutrition Counselor; President, National Action Against
Obesity  www.ActionAgainstObesity.com  www.MeMeRoth.net
info@...

Dr. Barry Popkin, Ph.D., Professor, Department of Nutrition; Director, UNC
Interdisciplinary Obesity Center (IDOC); Fellow, Carolina Population Center;
Director: The Nutrition Transition Research Program  www.nutrans.org

Dr. Walter Willett, M.D., Dr.P.H., Professor of Epidemiology and Nutrition;
Chairman, Department of Nutrition, Harvard School of Public Health;
Professor of Medicine, Harvard Medical School;
Co-Investigator, Nurses Health Study I; Principal Investigator, Nurses
Health Study II; Author, "The Fertility Diet"
http://www.amazon.com/Fertility-Diet-Jorge-Chavarro/dp/0071494790

Dr. David L. Katz, M.D., M.P.H., F.A.C.P.M., F.A..C.P; Director, Prevention
Research Center; Yale University School of Medicine
http://www.davidkatzmd.com/nutritiondetectives.aspx

Chevy Chase, Actor, Writer; Co-Founder, Center for Environmental Education;
Child Nutrition Advocate  http://www.youtube.com/watch?v=sZ-1O4HdYes
Jayni Chase, Co-Founder;  Center for Environmental Education; Child
Nutrition Advocate; Environment, Health, Education, Safety Advocate and
Author  http://www.ceeonline.org/about/about.aspx
Center for Environmental Education at Unity College, 90 Quaker Hill Road,
Unity, Maine 04988   Office: (207) 948 - 3131 ext 308
Cynthia Thomashow,  Executive Director cthomashow@...  Rob Beranek,
Managing Director  rberanek@...

Dr. Melissa E. Glassman, M.D., Asst. Attending Pediatrician, Columbia
University Medical Center;  Morgan-Stanley Children's Hospital of NewYork --
Presbyterian; Co-author of studies examining early childhood obesity risk
factors in ages 1-5.
http://www.cumc.columbia.edu/news/press_releases/Melissa_Glassman-Obese_Children\
.html
+1 212 305 6227

Dr. Ruby Natale, Ph.D, Psy.D., Asst. Professor of Clinical Pediatrics;
University of Miami School of Medicine; Mailman Center for Child
Development; Co-author of studies examining early childhood obesity risk
factors in childcare centers for children ages 2-5.
http://www.rwjf.org/programareas/features/digest.jsp?id=7425&pid=1138
http://americanheart.mediaroom.com/index.php?s=43&item=361
305-243-6624

Dr. Susan Linn, Ed.D., Associate Director, Media Center, Judge Baker
Children Center; Director, Campaign for a Commercial-Free Childhood; Author,
"Consuming Kids"  www.commercialfreechildhood.org   617-278-4172  Fax:
617-232-7343  ccfc@...  Judge Baker Children's Center, 53
Parker Hill Ave., Boston, MA  02120

Dr. Michael F. Roizen, M.D.; Co-Founder of RealAge; Co-Author, "You on a
Diet; Chief Wellness Officer, Cleveland Clinic  www.realage.com
http://www.realage.com/company_info/roizen_bio.aspx
http://www.clevelandclinic.org/  info@...;

Dr. Neal D. Barnard, M.D., Nutrition Researcher, Author, Health Advocate;
Adjunct Associate Professor, George Washington University School of
Medicine; Founder, Physicians Committee for Responsible Medicine
www.pcrm.org   5100 Wisconsin Ave., N.W., Ste. 400, Washington, DC 20016
202-686-2210  pcrm@...

Chef Ann Cooper, Director of Nutrition Services, Berkeley, CA Unified School
District; Renegade LunchLady; Author, "Lunch Lessons"  www.lunchlessons.org
www.chefann.com/blog/
ann@...  362 Vermont Avenue, Moss Beach, CA 94038

Joshua Rosenthal, Founder, Institute for Integrative Nutrition; Author,
"Integrative Nutrition";
http://www.amazon.com/Integrative-Nutrition-Joshua-Rosenthal/dp/097952640X
www.integrativenutrition.com  (212) 730 5433  (877) 730 5444  Mon - Thurs 9
AM - 7 PM  Fri 9 AM - 5:30 PM  admissions@...

Dr. Jennifer L. Ashton, M.D., F.A.C.O.G.; National Medical Contributor, FOX
News Channel  www.drjenniferashton.com  (201) 399-2812  One Engle Street,
Englewood, NJ
Consulting Staff, Department of Obstetrics and Gynecology, Englewood
Hospital Medical Center, All-Women Ob-Gyn Associates, LLC

Kate Adamick, JD, Chef, School Food Expert; Food Systems Solutions, LLC;
Consultant, The Orfalea Fund  www.sCoolFood.org  Orfalea Fund, 1283 Coast
Village Circle, Santa Barbara, CA 93108 USA   805.565.7550  Fax:
805.565.7554   info@...

Stephen Joseph, CEO, BanTransFat.com, Inc.  www.bantransfat.com  "On April
21, 2007, this website passed the one million visitors mark."
bantf@...

Amy Kalafa, Holistic Health and Nutrition Counselor; Award-Winning Producer
"Two Angry Moms" www.angrymoms.org

Dr. Susan Rubin, D.M.D, H.H.C., Holistic Health Counselor; Featured in film
"Two Angry Moms"; Founder, Better School Food  www.betterschoolfood.org  487
E. Main Street, Mount Kisco, NY 10549
(914) 864-1293 info@...  Mary Ann Petrilena, President of
BSF  (914) 671-1373  maryann@...

Ann W. Armstrong, Ed.D, Executive Director, The Center for Educational
Outreach & Innovation; President, Teachers College Innovations, Columbia
University  http://continuingeducation.tc.columbia.edu/
525 West 120th Street, Box 132, New York, NY  10027  1.800.209.1245 or
1.212.678.3987  FAX: 1.212.678.8417 ceoi_mail@...

MaryRose Barranco Morris, Ed.D., Director, Continuing Education & Outreach
Programs and the New Teacher Academy; The Center for Educational Outreach
and Innovation, Teachers College
Columbia University

Bryan Young, Producer, Shinebox Media "Killer at Large"
http://www.killeratlarge.com/  801.806.9494  contact@...

Joel Christian McEwen, Director, Wolf & Moon Productions "American Dream"
www.americandreamthemovie.com  pr@...

Dr. Lisa R. Young, Ph.D, R.D., Author "The Portion Teller Plan"
www.portionteller.com  Nutrition, Food Studies, & Public Health, The
Steinhardt School of Culture, Education, and Human Development

Josh Golin, Associate Director, Campaign for a Commercial-Free Childhood
www.commercialfreechildhood.org

Julia Havey, Author, Motivational Speaker www.vicebustingdiet.com  The
Health & Wellness Institute, DC PC Weight Loss by Julia 1-800-908-3001

Cathy Sorbo, Comedian, Columnist, Social Satirist www.CathySorbo.com

Dr. Gary Huber, D.O., Executive Director, Whole Lunches Program; School Food
Expert

Dena Smith Givens, Health Counselor; Founder, Publisher, Executive Editor,
Primal Parenting Magazine  www.primalparentingmagazine.com  Rebecca Hecking,
Managing Editor, Primal Parenting Magazine
PO Box 1461, Hermitage, PA 16148  +1 (724) 383-3043  fax: +1 (413) 714-8550
editor@...;

Patrick Wright, Documentary Films Director; Chair, Video Department,
Maryland Institute College of Art

Felicia Brodzky, Founder, Integration Health; Personal Integrative Health
Counselor  www.integrationhealth.com

Yvette Berman Executive Director, Whole Lunches Program, School Food Expert

Katy Attebery, Women's Heart Disease Expert;  Co-Founder,  Queen of Hearts
Foundation   www.qohf.org

Phyllis McCarthy, Integrative Nutrition Expert, Certified Health Counselor

Amy Groh, YMCA IGNITE Instructor, Northern Neck Family YMCA, Kilmarnock, VA

Holly L. Halvorson, M.A., Ed.S., School Psychologist, Children's Librarian,
YMCA Member

Karen Fletcher, Pre-K Teacher, CDA Certified

Charlotte Schoenke, Preschool Teacher

Jo Wehage. Certified Wellness Consultant

Sincerely,

The Undersigned

View Current Signatures

     The YMCA Childcare Centers: Expel Junk Food Petition to YMCA of the USA
was created by National Action Against Obesity and written by MeMe Roth
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"Of course, everyone chooses, as a natural priority, to enjoy
peace, joy, and love by helping to find, quickly share, and positively
act upon evidence about healthy and safe food, drink, and
environment."

Rich Murray, MA Room For All rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com  new primary archive

http://groups.yahoo.com/group/aspartameNM/messages
group with 121 members, 1,538 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1,093 members, 22,565 posts in a public archive


two aspartame toxicity research studies by Resia Pretorius, U. Pretoria,
South Africa, debate with JD Fernstrom: Murray 2008.04.04
http://rmforall.blogspot.com/2008_04_01_archive.htm
Friday, April 4, 2008
http://groups.yahoo.com/group/aspartameNM/message/1536

[ See also:
methanol impurity in alcohol drinks [ and aspartame ] is turned
into neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol
Syndrome, BM Kapur, DC Lehotay, PL Carlen at U. Toronto,
Alc Clin Exp Res 2007 Dec. plain text: detailed biochemistry,
CL Nie et al. 2007.07.18: Rich Murray 2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524 ]

http://foodqualitynews.com/news/ng.asp?n=84424-aspartame-sweetener
recent news re E Pretorius aspartame and brain review

Direct and indirect cellular effects of aspartame on the brain.
Humphries P, Pretorius E, Naude H, U. Pretoria, South Africa,
Eur J Clin Nutr. 2007 Aug 8: Murray 2007.08.12
http://groups.yahoo.com/group/aspartameNM/message/1463

"The aim of this study was to discuss the direct and indirect
cellular effects of aspartame on the brain,
and we propose that excessive aspartame ingestion
might be involved in the pathogenesis
of certain mental disorders (DSM-IV-TR 2000)
and also in compromised learning and emotional functioning."

Eur J Clin Nutr. 2007 Aug 8; [Epub ahead of print]
Direct and indirect cellular effects of aspartame on the brain.
Humphries P,
Pretorius E, resia.pretorius@...;
Naude H.
[1] Department of Anatomy, University of Pretoria,
Pretoria, Gauteng, South Africa
[2] Department of Anatomy, University of the Limpopo,
South Africa.

The use of the artificial sweetener, aspartame, has long been
contemplated and studied by various researchers, and people are
concerned about its negative effects.

Aspartame is composed of phenylalanine (50%),
aspartic acid (40%) and methanol (10%).

Phenylalanine plays an important role in neurotransmitter regulation,
whereas aspartic acid is also thought to play a role as an excitatory
neurotransmitter in the central nervous system.

Glutamate, asparagines and glutamine are formed from their
precursor, aspartic acid.

Methanol, which forms 10% of the broken down product,
is converted in the body to formate,
which can either be excreted or can give rise to formaldehyde,
diketopiperazine (a carcinogen) and a number of other highly toxic
derivatives.

Previously, it has been reported that consumption of aspartame
could cause neurological and behavioural disturbances in sensitive
individuals.

Headaches, insomnia and seizures are also some of the neurological
effects that have been encountered, and these may be accredited to
changes in regional brain concentrations of catecholamines,
which include norepinephrine, epinephrine and dopamine.

The aim of this study was to discuss the direct and indirect
cellular effects of aspartame on the brain,
and we propose that excessive aspartame ingestion
might be involved in the pathogenesis
of certain mental disorders (DSM-IV-TR 2000)
and also in compromised learning and emotional functioning.

European Journal of Clinical Nutrition advance online publication,
8 August 2007; doi:10.1038/sj.ejcn.1602866.
PMID: 17684524

Keywords: astrocytes; aspartame; neurotransmitters; glutamate;
GABA; serotonin; dopamine; acetylcholine

Received 25 October 2006; revised 26 April 2007;
accepted 27 April 2007
Correspondence: Professor E Pretorius, Department of Anatomy,
University of Pretoria, BMW Building, Dr Savage Street,
PO Box 2034, Pretoria 0001,
Gauteng, South Africa.  E-mail: resia.pretorius@...

c 2007 Nature Publishing Group,
All rights reserved  0954-3007/07
$30.00  www.nature.com/ejcn
____________________________________________________


two detailed critiques of industry affiliations and biased science in 99
page review with 415 references by BA Magnuson, GA Burdock
and 8 more, Critical Reviews in Toxicology, 2007 Sept.: Mark D
Gold 13 page: also Rich Murray 2007.09.15: 2008.03.24
http://rmforall.blogspot.com/2008_03_01_archive.htm
Monday, March 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1531


"Nearly every section of the Magnuson (2007) review has research
that is misrepresented
and/or crucial pieces of information are left out.

In addition to the misrepresentation of the research,
readers (including medical professionals) are often not told that
this review was funded by the aspartame manufacturer, Ajinomoto,
and the reviewers had enormous conflicts of interest."


[ See also:

http://groups.yahoo.com/group/aspartameNM/message/1453
Souring on fake sugar (aspartame), Jennifer Couzin,
Science 2007.07.06: 4 page letter to FDA from 12 eminent
USA toxicologists re two Ramazzini Foundation cancer studies
2007.06.25: Murray 2007.07.18


http://groups.yahoo.com/group/aspartameNM/message/957
safety of aspartame Part 1/2 12.4.2: EC HCPD-G SCF:
Murray 2003.01.12 EU Scientific Committee on Food, a whitewash

http://groups.yahoo.com/group/aspartameNM/message/1045
http://www.holisticmed.com/aspartame/scf2002-response.htm
Mark Gold exhaustively critiques European Commission Scientific
Committee on Food re aspartame ( 2002.12.04 ):
59 pages, 230 references

bias, omissions, incuriosity = opportunity, aspartame safety
evaluation, Magnuson BA, Burdock GA, Williams GM, 7 more,
2007 Sept, Ajinomoto funded 98 pages html [ $ 32 pdf ]:
Murray 2007.09.15
http://rmforall.blogspot.com/2007_09_01_archive.htm
Saturday, September 15, 2007 ]


Hawaii Senate Health Committee will consider resolution SCR191
by Sen. Suzanne Chun Oakland, and 10 other of 25 Senators,
to have FDA ban aspartame
and for National Academy of Sciences to review research:
Murray 2008.03.14
http://rmforall.blogspot.com/2008_03_01_archive.htm
Friday, March 14, 2008
http://groups.yahoo.com/group/aspartameNM/message/1527

http://groups.yahoo.com/group/aspartameNM/message/1525
House Concurrent Resolution #132 for Health Department panel
to decide aspartame ban by early 2010,
Hawaii Rep. Josh Green MD, Health Committee Chair:
Murray 2008.03.12
http://rmforall.blogspot.com/2008_03_01_archive.htm
Wednesday, March 12, 2008
____________________________________________________



British Columbia guidelines against "any drinks with artificial sweeteners"
in January 2008 in school vending machines, stores, cafeterias or
fundraisers -- also recently in Ontario and Quebec, Janet Steffenhagen
2007.12.28 Vancouver Sun:  Murray 2008.04.10
http://rmforall.blogspot.com/2008_04_01_archive.htm
Thursday, April 10, 2008
http://groups.yahoo.com/group/aspartameNM/message/1537

http://groups.yahoo.com/group/aspartameNM/message/1426
ASDA (unit of Wal-Mart Stores WMT.N) and Marks & Spencer
will join Tesco and also Sainsbury to ban and limit aspartame,
MSG, artificial flavors dyes preservatives additives, trans fats, salt
"nasties" to protect kids from ADHD: leading UK media:
Murray 2007.05.15

http://groups.yahoo.com/group/aspartameNMmessage/1451
Artificial sweeteners (aspartame, sucralose) and coloring agents
will be banned from use in newly-born and baby foods,
the European Parliament decided: Latvia ban in schools 2006:
Murray 2007.07.12

http://groups.yahoo.com/group/aspartameNM/message/1341
Connecticut bans artificial sweeteners in schools, Nancy Barnes,
New Milford Times: Murray 2006.05.25

http://groups.yahoo.com/group/aspartameNM/message/1369
Bristol, Connecticut, schools join state program to limit artificial
sweeteners, sugar, fats for 8800 students, Johnny J Burnham,
The Bristol Press: Murray 2006.09.22


bias, omissions, incuriosity = opportunity, aspartame safety
evaluation, Magnuson BA, Burdock GA, Williams GM, 7 more,
2007 Sept, Ajinomoto funded 98 pages html [ $ 32 pdf ]:
Murray 2007.09.15
http://rmforall.blogspot.com/2007_09_01_archive.htm
Saturday, September 15, 2007

http://groups.yahoo.com/group/aspartameNM/message/1491
industry scientists praise aspartame safety and benefits in Paris on
2006.05.30, Herve Nordmann, Andrew G. Renwick,
Carlo La Vecchia, Tommy Visscher, Jaap Seidell, France Bellisle,
Adam Drewnowski, Margaret Ashwell, Anne de la Hunty,
Sigrid A. Gibson, Alan R. Boobis: Murray 2007.11.18

http://groups.yahoo.com/group/aspartameNM/message/1070
critique of aspartame review, French Food Safety Agency AFSSA
2002.05.07 aspartamgb.pdf (18 pages, in English), Martin Hirsch:
Murray 2004.04.13

http://groups.yahoo.com/group/aspartameNM/message/957
safety of aspartame Part 1/2 12.4.2: EC HCPD-G SCF:
Murray 2003.01.12 EU Scientific Committee on Food, a whitewash

http://groups.yahoo.com/group/aspartameNM/message/1045
http://www.holisticmed.com/aspartame/scf2002-response.htm
Mark Gold exhaustively critiques European Commission Scientific
Committee on Food re aspartame ( 2002.12.04 ):
59 pages, 230 references

http://www.eatright.org/Nutritive(1).pdf
J Am Diet Assoc. 2004 Feb; 104(2): 255-75.
Position of the American Dietetic Association: use of nutritive and
nonnutritive sweeteners. American Dietetic Association.

http://groups.yahoo.com/group/aspartameNM/message/1068
critique of aspartame review
by American Dietetic Association Feb 2004,
Valerie B. Duffy & Madeleine J. Sigman-Grant: Murray 2004.05.14



http://www.dorway.com/upipart1.txt
http://groups.yahoo.com/group/aspartameNM/message/262
aspartame expose 96K Oct 1987 Part 1/3: Gregory Gordon,
UPI reporter: Murray 2000.07.10

http://www.dorway.com/enclosur.html
http://groups.yahoo.com/group/aspartameNM/message/53
aspartame history Part 1/4 1964-1976: Gold: Murray 1999.11.06

http://groups.yahoo.com/group/aspartameNM/message/927
Donald Rumsfeld, 1977 head of Searle Corp.,
got aspartame FDA approval: Turner: Murray 2002.12.23

http://groups.yahoo.com/group/aspartameNM/message/1483
Donald Rumsfeld CEO 1977-85 G.D. Searle & Co., got new
President Reagan to prohibit FDA opposition to aspartame
1981.01.25, history by lawyer James S. Turner:
Murray 2007.10.29

http://groups.yahoo.com/group/aspartameNM/message/928
revolving door, Monsanto, FDA, EPA: NGIN: Murray 2002.12.23

http://groups.yahoo.com/group/aspartameNM/message/858
Samuels: Strong: Roberts: Gold: flaws in double-blind studies re
aspartame and MSG toxicity: Murray 2002.08.01

"Survey of aspartame studies: correlation of outcome and funding
sources," 1998, unpublished: http://www.dorway.com/peerrev.html
Walton found 166 separate published studies in the peer reviewed
medical literature, which had relevance for questions of human
safety.
The 74 studies funded by industry all (100 %) attested to
aspartame's safety, whereas of the 92 non-industry funded studies,
84 (91 %) identified a problem.
Six of the seven non-industry funded studies
that were favorable to aspartame safety were from the FDA,
which has a public record that shows a strong pro-industry bias.

Ralph G. Walton, MD, Prof. of Clinical Psychology, Northeastern
Ohio Universities, College of Medicine, Dept. of Psychiatry,
Youngstown, OH 44501,
Chairman, The Center for Behavioral Medicine,
Northside Medical Center, 500 Gypsy Lane, P.O. Box 240
Youngstown, OH 44501 330-740-3621 rwalton193@...
http://www.neoucom.edu/DEPTS/Psychiatry/walton.htm


http://groups.yahoo.com/group/aspartameNM/message/1395
Aspartame Controversy, in Wikipedia democratic
encyclopedia, 72 references (including AspartameNM # 864
and 1173 by Murray, brief fair summary of much more research:
Murray 2007.01.01


methanol impurity in alcohol drinks [ and aspartame ] is turned
into neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol
Syndrome, BM Kapur, DC Lehotay, PL Carlen at U. Toronto,
Alc Clin Exp Res 2007 Dec. plain text: detailed biochemistry,
CL Nie et al. 2007.07.18: Rich Murray 2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524


http://groups.yahoo.com/group/aspartameNM/message/1513
metabolic syndrome is tied to diet soda, PL Lutsey, LM Steffen,
J Stevens, Circulation 2008.01.22: role of formaldehyde and
formic acid from methanol in wines, liquors, or aspartame?:
Murray 2008.02.21

"But the one-third who ate the most fried food increased their risk
by 25 percent, compared with the one-third who ate the least, and
surprisingly, the risk of developing metabolic syndrome was 34
percent higher among those who drank one can of diet soda a day
compared with those who drank none.

"This is interesting," said Lyn M. Steffen, an associate professor of
epidemiology at the University of Minnesota and a co-author of the
paper, which was posted online in the journal Circulation on Jan. 22.
"Why is it happening?  Is it some kind of chemical in the diet soda,
or something about the behavior of diet soda drinkers?""

"The diet soda association was not hypothesized
and deserves further study."


http://groups.yahoo.com/group/aspartameNM/message/1143
methanol (formaldehyde, formic acid) disposition:
Bouchard M et al, full plain text, 2001:
substantial sources are degradation
of fruit pectins, liquors, aspartame, smoke:
Murray 2005.04.02


http://groups.yahoo.com/group/aspartameNM/message/1511
vinyl acetate, ethyl alcohol, or aspartame in womb increases later
cancers in adults with lifetime exposure in many studies, M Soffritti
et al, Ramazzini Foundation, Basic Clin. Pharm. Toxicol. 2008 Feb.:
Rich Murray 2008.02.07

http://groups.yahoo.com/group/aspartameNM/message/1016
President Bush & formaldehyde (aspartame) toxicity:
Ramazzini Foundation carcinogenicity results Dec 2002:
Soffritti: Murray 2003.08.03 rmforall

p. 88 "The sweetening agent aspartame hydrolyzes in the
gastrointestinal tract to become free methyl alcohol,
which is metabolized in the liver
to formaldehyde, formic acid, and CO2. (11)"
Medinsky MA & Dorman DC. 1994;
Assessing risks of low-level methanol exposure.
CIIT Act. 14: 1-7.

http://groups.yahoo.com/group/aspartameNM/message/1453
Souring on fake sugar (aspartame), Jennifer Couzin,
Science 2007.07.06: 4 page letter to FDA from 12 eminent
USA toxicologists re two Ramazzini Foundation cancer studies
2007.06.25: Murray 2007.07.18


Avoiding formaldehyde allergic reactions in children, aspartame, vitamins,
shampoo, conditioners, hair gel, baby wipes, Sharon E Jacob, MD, Tace
Steele, U. Miami, Pediatric Annals 2007 Jan.: eyelid contact dermatitis, AM
Hill, DV Belsito, 2003 Nov.: Murray 2008.03.27
http://rmforall.blogspot.com/2008_03_01_archive.htm
Thursday, March 27, 2008
http://groups.yahoo.com/group/aspartameNM/message/1532

"It is generally recommended that exposure to products containing
formaldehyde, FRP's, and aspartame (NutraSweet) be avoided
in children."

"Through metabolism, aspartame is converted metabolically
in the liver to methanol,
which is in turn metabolized to formaldehyde. 8"

www.pediatricannalsonline.com/showPdf.asp?rID=21306

Avoiding formaldehyde allergic reactions in children
Pediatric Annals. 2007 Jan.; 36(1): 55-6. PMID: 17269284
Sharon E. Jacob, MD, Director, Contact Dermatitis Clinic,
Dept. of Dermatology and Cutaneous Surgery, U. of Miami,
1295 NW 14th St., Miami, FL 33125, fax 305-243-6191

formaldehyde from many sources, including aspartame, is major cause of
Allergic Contact Dermatitis, SE Jacob, T Steele, G Rodriguez, Skin and Aging
2005 Dec.: Murray 2008.03.27
http://rmforall.blogspot.com/2008_03_01_archive.htm
Thursday, March 27, 2008
http://groups.yahoo.com/group/aspartameNM/message/1533

"For example, diet soda and yogurt containing aspartame
(Nutrasweet), release formaldehyde in their natural biological
degradation.

One of aspartame's metabolites, aspartic acid methyl ester,
is converted to methanol in the body, which is oxidized to
formaldehyde in all organs, including the liver and eyes. 22

Patients with a contact dermatitis to formaldehyde have been seen
to improve once aspartame is avoided. 22

Notably, the case that Hill and Belsito reported had a 6-month
history of eyelid dermatitis that subsided after 1 week of avoiding
diet soda. 22"

"We present a case of a medical student who presented with
erythematous eczematoid plaques on her trunk and legs and
fine vesiculation of her scalp, 3 weeks after starting anatomy class.

Of note, she routinely washed her face and arms after leaving the
anatomy lab, but remained in her scrubs for the rest of the day.

Formaldehyde and Quaternium-15 positive reactions
in the same patient."

"Our patient underscores the importance of appropriate patch
testing and education.
Once we identified the allergy to formaldehyde and quaternium-15,
we provided patient education materials regarding the common and
not-so-common locations of these chemicals and cross-reactors.
We also gave the patient information on avoidance
and safe alternatives (see Table 5).

Fortunately, with technical advances, this student completed the
anatomy section via electronic learning tools.

By avoiding formaldehyde, including anatomy lab, FRP
in her shampoo and cosmetics,
and aspartame in her diet, this patient dramatically improved.

As with all contact dermatitides, the mainstay of treatment for
allergic contact dermatitis is avoidance."

http://www.skinandaging.com/article/5158
Allergen Focus:
Focus on T.R.U.E. Test Allergens #21, 13 and 18:
Formaldehyde and Formaldehyde-Releasing Preservatives
Skin & Aging, ISSN 1096-0120; 13(12) 2005 Dec.: 22-27.
Sharon E. Jacob, M.D.,
Tace Steele, B.A.,
and Georgette Rodriguez, M.D., M.P.H.


30 female pet store rats drinking lifelong 13.5 mg aspartame,
1/3 packet of Equal, had 33% with obvious tumors -- also bulging,
sick, and missing eyes, paralysis, obesity, skin sores -- agrees with
Ramazzini Foundation results, Victoria Inness-Brown:
Murray 2008.02.15
http://rmforall.blogspot.com/2008_02_01_archive.htm
Friday, February 15, 2008
http://groups.yahoo.com/group/aspartameNM/message/1521


http://groups.yahoo.com/group/aspartameNM/message/1490
details on 6 epidemiological studies since 2004 on diet soda (mainly
aspartame) correlations, as well as 14 other mainstream studies
on aspartame toxicity since summer 2005: Murray 2007.11.27

http://groups.yahoo.com/group/aspartameNM/message/1340
aspartame groups and books:
updated research review of 2004.07.16: Murray 2006.05.11


old tiger roars -- Woodrow C Monte, PhD -- aspartame causes
many breast cancers, as ADH enzyme in breasts makes methanol
from diet soda into carcinogenic formaldehyde -- same in dark
wines and liquors, Fitness Life 2008 Jan.: Murray 2008.02.11
http://rmforall.blogspot.com/2008_02_01_archive.htm
Monday, February 11, 2008
http://groups.yahoo.com/group/aspartameNM/message/1517

"Alcohol dehydrogenase ADH is required for the conversion of
methanol to formaldehyde (112).

ADH is not a common enzyme in the human body -- not many cells
in the human body contain this enzyme.

The human breast is one of the few organs in the body with a high
concentration of ADH (190b), and it is found there exclusively in the
mammary epithelial cells, the very cells known to transform into
adenocarcinoma (190c) (breast cancer).

The most recent breast cancer scientific literature implicates ADH
as perhaps having a pivotal role in the formation of breast cancer,
indicating a greater incidence of the disease in those
with higher levels of ADH activity in their breasts (190a)."

role of formaldehyde, made by body from methanol from foods
and aspartame, in steep increases in fetal alcohol syndrome, autism,
multiple sclerosis, lupus, teen suicide, breast cancer, Nutrition
Prof. Woodrow C. Monte, retired, Arizona State U., two reviews,
190 references supplied, Fitness Life, New Zealand
2007 Nov, Dec: Murray 2007.12.26
http://rmforall.blogspot.com/2007_12_01_archive.htm
Wednesday, December 26 2007
http://groups.yahoo.com/group/aspartameNM/message/1498


Since no adequate data has ever been published on the
exact disposition of toxic metabolites in specific tissues in humans
of the 11 % methanol component of aspartame,
the many studies on morning-after hangover from the methanol
impurity in alcohol drinks are the main available resource to date.

http://groups.yahoo.com/group/aspartameNM/message/1469
highly toxic formaldehyde, the cause of alcohol hangovers, is
made by the body from 100 mg doses of methanol from
dark wines and liquors, dimethyl dicarbonate, and aspartame:
Murray 2007.08.31

http://groups.yahoo.com/group/aspartameNM/message/1052
DMDC: Dimethyl dicarbonate 200mg/L in drinks adds
methanol 98 mg/L ( becomes formaldehyde in body ):
EU Scientific Committee on Foods 2001.07.12:
Murray 2004.01.22

http://europa.eu.int/comm/food/fs/sc/scf/out96_en.pdf

"...DMDC was evaluated by the SCF in 1990 and considered
acceptable for the cold sterilization of soft drinks and fruit juices
at levels of addition up to 250 mg/L (1)
...DMDC decomposes primarily to CO2 and methanol ...

[ Note: Sterilization of bacteria and fungi is a toxic process,
probably due to the inevitable conversion in the body of methanol
into highly toxic formaldehyde and then formic acid. ]

The use of 200 mg DMDC per liter would add 98 mg/L
of methanol to wine which
already contains an average of about 140 mg/L from natural sources.

http://groups.yahoo.com/group/aspartameNM/message/1286
methanol products (formaldehyde and formic acid) are main cause
of alcohol hangover symptoms [same as from similar amounts of
methanol, the 11% part of aspartame]: YS Woo et al, 2005 Dec:
Murray 2006.01.20

Addict Biol. 2005 Dec;10(4): 351-5.
Concentration changes of methanol in blood samples during
an experimentally induced alcohol hangover state.
Woo YS, Yoon SJ, Lee HK, Lee CU, Chae JH, Lee CT, Kim DJ.
Chuncheon National Hospital, Department of Psychiatry,
The Catholic University of Korea, Seoul, Korea.
http://www.cuk.ac.kr/eng/ sysop@...
Songsin Campus: 02-740-9714 Songsim Campus: 02-2164-4116
Songeui Campus: 02-2164-4114
http://www.cuk.ac.kr/eng/sub055.htm eight hospitals

[ Han-Kyu Lee ]

A hangover is characterized by the unpleasant physical and mental
symptoms that occur between 8 and 16 hours after drinking alcohol.

After inducing experimental hangover in normal individuals,
we measured the methanol concentration prior to
and after alcohol consumption
and we assessed the association between the hangover condition
and the blood methanol level.

A total of 18 normal adult males participated in this study.

They did not have any previous histories of psychiatric
or medical disorders.

The blood ethanol concentration prior to the alcohol intake
(2.26+/-2.08) was not significantly different from that
13 hours after the alcohol consumption (3.12+/-2.38).

However, the difference of methanol concentration
between the day of experiment (prior to the alcohol intake)
and the next day (13 hours after the alcohol intake)
was significant (2.62+/-1.33/l vs. 3.88+/-2.10/l, respectively).

A significant positive correlation was observed
between the changes of blood methanol concentration
and hangover subjective scale score increment when covarying
for the changes of blood ethanol level (r=0.498, p<0.05).

This result suggests the possible correlation of methanol
as well as its toxic metabolite to hangover. PMID: 16318957

[ The toxic metabolite of methanol is formaldehyde, which in turn
partially becomes formic acid -- both potent cumulative toxins
that are the actual cause of the toxicity of methanol.]

This study by Jones AW (1987) found next-morning hangover
from red wine with 100 to 150 mg methanol
(9.5 % w/v ethanol, 100 mg/l methanol, 0.01 %).
Fully 11% of aspartame is methanol --
1,120 mg aspartame in 2 L diet soda,
almost six 12-oz cans, gives 123 mg methanol (wood alcohol).

Pharmacol Toxicol. 1987 Mar; 60(3): 217-20.
Elimination half-life of methanol during hangover.
Jones AW. wayne.jones@...
Department of Forensic Toxicology,
University Hospital, SE-581 85 Linkoping, Sweden.

This paper reports the elimination half-life of methanol in human
volunteers.
Experiments were made during the morning after the subjects had
consumed 1000-1500 ml red wine
(9.5 % w/v ethanol, 100 mg/l methanol)
the previous evening. [ 100 to 150 mg methanol ]
The washout of methanol from the body
coincided with the onset of hangover.
The concentrations of ethanol and methanol in blood were
determined indirectly by analysis of end-expired alveolar air.
In the morning when blood-ethanol dropped
below the Km of liver alcohol dehydrogenase (ADH)
of about 100 mg/l (2.2 mM),
the disappearance half-life of ethanol was 21, 22, 18 and 15 min.
in 4 test subjects respectively.
The corresponding elimination half-lives of methanol
were 213, 110, 133 and 142 min. in these same individuals.
The experimental design outlined in this paper can be used
to obtain useful data on elimination kinetics of methanol
in human volunteers without undue ethical limitations.
Circumstantial evidence is presented to link methanol
or its toxic metabolic products, formaldehyde and formic acid,
with the pathogenesis of hangover. PMID: 3588516

http://groups.yahoo.com/group/aspartameNM/message/1047
Avoiding Hangover Hell 2003.12.31 Mark Sherman, AP writer:
Robert Swift, MD [ formaldehyde from methanol in aspartame ]:
Murray 2004.01.16

http://groups.yahoo.com/group/aspartameNM/message/1048
hangovers from formaldehyde from methanol (aspartame?):
Schwarcz: Linsley: Murray 2004.01.18


Thrasher (2001): "The major difference is that the Japanese
demonstrated the incorporation of FA and its metabolites
into the placenta and fetus.
The quantity of radioactivity remaining in maternal and fetal tissues
at 48 hours was 26.9 % of the administered dose." [ Ref. 14-16 ]

Arch Environ Health 2001 Jul-Aug; 56(4): 300-11.
Embryo toxicity and teratogenicity of formaldehyde. [100 references]
Thrasher JD, Kilburn KH. toxicology@...
Sam-1 Trust, Alto, New Mexico, USA.
www.drthrasher.org/formaldehyde_embryo_toxicity.html full text

http://www.drthrasher.org/formaldehyde_1990.html full text
Jack Dwayne Thrasher, Alan Broughton, Roberta Madison.
Immune activation and autoantibodies in humans
with long-term inhalation exposure to formaldehyde.
Archives of Environmental Health. 1990; 45: 217-223.
"Immune activation, autoantibodies,
and anti-HCHO-HSA antibodies
are associated with long-term formaldehyde inhalation."
PMID: 2400243


formaldehyde in FEMA trailers and other sources (aspartame,
dark wines and liquors, tobacco smoke): Murray 2008.01.30
http://rmforall.blogspot.com/2008_01_01_archive.htm
Wednesday, January 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1508

The FEMA trailers give about the same amount of formaldehyde
daily as from a quart of dark wine or liquor, or two quarts
(6 12-oz cans) of aspartame diet soda, from their over 1 tenth gram
methanol impurity (one part in 10,000),
which the body quickly makes into formaldehyde -- enough
to be the major cause of "morning after" alcohol hangovers.

Methanol and formaldehyde also result from many fruits and
vegetables, tobacco and wood smoke, heater and vehicle exhaust,
household chemicals and cleaners, cosmetics, and new cars, drapes,
carpets, furniture, particleboard, mobile homes, buildings, leather ...
so all these sources add up and interact
with many other toxic chemicals.

BN Ames and LS Gold, 1998, have presented detailed information
that there is no increase in recent decades for most cancers,
and that common carcinogens do not result in significant exposures
to the average human population.

However, individuals are not average -- each person has a unique
genetic makeup, resulting in a huge range of variation of vulnerability
to specific chemicals, as is well evidenced in the case of methanol,
formaldehyde, and formic acid, especially with regard
to behavioral effects.

Each is subject to very wide ranges of exposure levels.

Many are in especially vulnerable groups, depending on diet, obesity,
sex, exercise, life stress, age from conception to very old, unusually
severe toxic exposures, injuries, and diseases.

It is clear that a variety of multiple chemical sensitivity syndromes do
exist, often with remarkable hypersensitivity.

Methanol, formaldehyde, and formic acid toxicity are unusual, in that
humans are far more vulnerable than any other mammal, as much as
ten to sixty-fold, which complicates the utility of animal data.

The unusally long human life span also increases the role of long-term
chronic low-level exposure.

http://groups.yahoo.com/group/aspartameNM/message/1455
FEMA slow to safety test Katrina toxic trailers, Charles Babington,
Associated Press -- 1 ppm formaldehyde in air is about half the daily
dose from 3 cans aspartame diet soda and ten times the 1999 EPA
alarm level for drinking water: Murray 2007.07.23



http://groups.yahoo.com/group/aspartameNM/message/1277
50% UK baby food is now organic - aspartame or MSG
with food dyes harm nerve cells, CV Howard 3 year study
funded by Lizzy Vann, CEO, Organix Brands,
Children's Food Advisory Service: Murray 2006.01.13

http://groups.yahoo.com/group/aspartameNM/message/1271
combining aspartame and quinoline yellow, or MSG and
brilliant blue, harms nerve cells, eminent
C. Vyvyan Howard et al, 2005 education.guardian.co.uk,
Felicity Lawrence: Murray 2005.12.21


http://groups.yahoo.com/group/aspartameNM/message/1373
aspartame rat brain toxicity re cytochrome P450 enzymes,
especially CYP2E1, Vences-Mejia A, Espinosa-Aguirre JJ et al,
2006 Aug, Hum Exp Toxicol: relevant abstracts re formaldehyde
from methanol in alcohol drinks: Murray 2006.09.29


http://groups.yahoo.com/group/aspartameNM/message/1463
Direct and indirect cellular effects of aspartame on the brain,
Humphries P, Pretorius E, Naude H, U. Pretoria, South Africa,
Eur J Clin Nutr. 2007 Aug 8: Murray 2007.08.12

http://groups.yahoo.com/group/aspartameNMmessage/1452
phenylalanine and aspartic acid from low dose aspartame
in rabbits interfere with blood coagulation,
Pretorius E and Humphries P, U. of Pretoria,
Ultrastruct Pathol 2007 March: Murray 2007.07.14


http://groups.yahoo.com/group/aspartameNM/message/1459
third study by expert Greek team of neurotoxicity in infant rats by
aspartame (or its parts, methanol, phenylalanine, aspartic acid), KH
Schulpis et al, Food Chem Toxicol 2007.06.16: Murray 2007.08.05

http://groups.yahoo.com/group/aspartameNMmessage/1447
second study by expert Greek team of neurotoxicity in infant rats by
aspartame (or its parts, methanol, phenylalanine, aspartic acid), KH
Schulpis et al, Toxicology 2007.05.18: Murray 2007.07.04

http://groups.yahoo.com/group/aspartameNMmessage/1444
expert Greek group finds aspartame (or its parts, methanol,
phenylalanine, aspartic acid) harm infant rat brain enzyme activity,
KH Schulpis et al, Pharmacol. Res. 2007.05.13:
Murray 2007.06.23

http://groups.yahoo.com/group/aspartameNM/message/939
aspartame (aspartic acid, phenylalanine) binding to DNA:
Karikas July 1998: Murray 2003.01.05 rmforall
Karikas GA, Schulpis KH, Reclos GJ, Kokotos G
Measurement of molecular interaction of aspartame and
its metabolites with DNA. Clin Biochem 1998 Jul; 31(5): 405-7.
Dept. of Chemistry, University of Athens, Greece
http://www.chem.uoa.gr gkokotos@...
K.H. Schulpis inchildh@... ; G.J. Reclos reklos@...

5 recent aspartame reports by S Tsakiris, KH Schulpis, I Simintzi,
with responses to critiques by AG Renwick and
by EB Abegaz, RG Bursey, 2005-2008 2008.03.05

Pharmacological Research 57 (2008) 89-90
Letter to the Editor
Answer to Letter sent to the Editor by
Drs. E. Abegaz and R. Bursey
(Ajinomoto Corporate Services LLC, Washington, USA)
related to Simintzi et al. report published in
Pharmacol Res 2007; 56: 155-9
Letter to the Editor / Pharmacological Research 57 (2008) 89-90

Stylianos Tsakiris a,?  stsakir@...;
Kleopatra H. Schulpis b inchildh@...;
a Department of Experimental Physiology, Medical School,
Athens University, P.O. Box 65257, GR-15401 Athens, Greece

b Inborn Errors of Metabolism Department, Institute of Child
Health, Research Center, Greece
? Corresponding author.
E-mail addresses:
S. Tsakiris  stsakir@...;
K.H. Schulpis  inchildh@...;

Pharmacological Research 57 (2008) 87-88
Response to "The effect of aspartame on the acetylcholinesterase
activity in hippocampal homogenates of suckling rats"
by Simintzi et al.

Eyassu G. Abegaz ?
Robert G. Bursey
Ajinomoto Corporate Services LLC,
Scientific & Regulatory Affairs,
1120 Connecticut Ave., N.W., Suite 1010,
Washington, DC 20036, United States

? Corresponding author. Tel.: +1 202 457 0284;
fax: +1 202 457 0107.
E-mail addresses: abegazee@...; (E.G. Abegaz),
burseyb@...; (R.G. Bursey)

Keywords:
Aspartame; Aspartate; Phenylalanine; Methanol; AChE activity

Tsakiris S, Schulpis KH.
Answer to letter sent by Professor A.G. Renwick
(University of Southampton, UK)
related to Simintzi et al. report published in Food and Chemical
Toxicology 2007; 45(12): 2397-401.
Food Chem Toxicol. 2008 Mar; 46(3): 1208-9.
Epub 2007 Oct 25. No abstract available. PMID: 18054419
doi:10.1016/j.fct.2007.10.016
Copyright © 2007 Elsevier Ltd All rights reserved.

Renwick AG.
The effect of aspartame metabolites on the suckling rat frontal cortex
acetylcholinesterase. An in vitro study. By I. Simintzi, K.H. Schulpis,
P. Angelogianni, C. Liapi and S. Tsakiris.
Food Chem Toxicol. 2008 Mar; 46(3): 1206-7.
Epub 2007 Oct 26. No abstract available. PMID: 18061330

1: Simintzi I, Schulpis KH, Angelogianni P, Liapi C, Tsakiris S.
The effect of aspartame metabolites on the suckling rat frontal cortex
acetylcholinesterase. An in vitro study.
Food Chem Toxicol. 2007 Dec;45(12):2397-401.
Epub 2007 Jun 16. PMID: 17673349

2: Simintzi I, Schulpis KH, Angelogianni P, Liapi C, Tsakiris S.
L-Cysteine and glutathione restore the reduction of rat
hippocampal Na+, K+-ATPase activity
induced by aspartame metabolites.
Toxicology. 2007 Jul 31;237(1-3):177-83.
Epub 2007 May 18. PMID: 17602817

3: Simintzi I, Schulpis KH, Angelogianni P, Liapi C, Tsakiris S.
The effect of aspartame on acetylcholinesterase activity in
hippocampal homogenates of suckling rats.
Pharmacol Res. 2007 Aug;56(2):155-9.
Epub 2007 May 13. PMID: 17580119

4: Schulpis KH, Papassotiriou I, Parthimos T, Tsakiris T, Tsakiris S.
The effect of L-cysteine and glutathione
on inhibition of Na+, K+-ATPase activity by aspartame metabolites
in human erythrocyte membrane.
Eur J Clin Nutr. 2006 May;60(5):593-7. PMID: 16391576

5: Tsakiris S, Giannoulia-Karantana A, Simintzi I, Schulpis KH.
The effect of aspartame metabolites on human erythrocyte
membrane acetylcholinesterase activity.
Pharmacol Res. 2006 Jan;53(1):1-5.
Epub 2005 Aug 29. PMID: 16129618



C. Trocho (1998):
"In all, the rats retained, 6 hours after administration, about 5 %
of the label, half of it in the liver."

They used a very low level of aspartame ingestion, 10 mg/kg,
for rats, which have a much greater tolerance for aspartame
than humans.
So, the corresponding level for humans would be
about 1 or 2 mg/kg.
Many headache studies in humans used doses of
about 30 mg/kg daily.

http://groups.yahoo.com/group/aspartameNM/message/925
aspartame puts formaldehyde adducts into tissues, Part 1/2
full text, Trocho & Alemany 1998.06.26: Murray 2002.12.22

http://ww.presidiotex.com/barcelona/index.html full text
Formaldehyde derived from dietary aspartame
binds to tissue components in vivo.
Life Sci June 26 1998; 63(5): 337-49.
Departament de Bioquimica i Biologia Molecular,
Facultat de Biologia, Universitat de Barcelona, Spain.
http://www.bq.ub.es/cindex.html Línies de Recerca: Toxicitat de
l'aspartame http://www.bq.ub.es/grupno/grup-no.html
Sra. Carme Trocho, Sra. Rosario Pardo, Dra. Immaculada Rafecas,
Sr. Jordi Virgili, Dr. Xavier Remesar, Dr. Jose Antonio
Fernandez-Lopez, Dr. Marià Alemany [male]
Fac. Biologia Tel.: (93)4021521, FAX: (93)4021559
Sra. Carme Trocho "Trok-ho" Fac. Biologia Tel.: (93)4021544,
FAX: (93)4021559 alemany@...;
bioq@...

Abstract:
Adult male rats were given an oral dose of 10 mg/kg aspartame,
14C-labeled in the methanol carbon.
At timed intervals of up to 6 hours, the radioactivity in plasma
and several organs was investigated.
Most of the radioactivity found (>98 % in plasma, >75 % in liver)
was bound to protein.
Label present in liver, plasma and kidney was in the range
of 1-2 % of total radioactivity administered per g or mL,
changing little with time.
Other organs (brown and white adipose tissues, muscle, brain,
cornea and retina) contained levels of label
in the range of 1/12th to 1/10th of that of liver.
In all, the rats retained, 6 hours after administration,
about 5 % of the label, half of it in the liver.

The specific radioactivity of tissue protein, RNA and DNA
was quite uniform.
The protein label was concentrated in amino acids,
different from methionine, and largely coincident
with the result of protein exposure to labeled formaldehyde.
DNA radioactivity was essentially in a single different adduct base,
different from the normal bases present in DNA.
The nature of the tissue label accumulated was, thus,
a direct consequence of formaldehyde binding to tissue structures.

The administration of labeled aspartame to a group of cirrhotic rats
resulted in comparable label retention by tissue components,
which suggests that liver function (or its defect) has little effect
on formaldehyde formation from aspartame
and binding to biological components.

The chronic treatment of a series of rats with 200 mg/kg of
non-labeled aspartame during 10 days results in the accumulation
of even more label when given the radioactive bolus,
suggesting that the amount of formaldehyde adducts
coming from aspartame in tissue proteins and nucleic acids
may be cumulative.

It is concluded that aspartame consumption may constitute
a hazard because of its contribution
to the formation of formaldehyde adducts. PMID: 9714421

[ Extracts ]
"The high label presence in plasma and liver is in agreement with the
carriage of the label from the intestine to the liver via the portal vein.
The high label levels in kidney and, to a minor extent, in brown
adipose tissue and brain are probably a consequence
of their high blood flows (45).
Even in white adipose tissue, the levels of radioactivity found 6 hours
after oral administration were 1/25th those of liver.
Cornea and retina, both tissues known to metabolize actively
methanol (21,28) showed low levels of retained label.
In any case, the binding of methanol-derived carbon to tissue
proteins was widespread, affecting all systems,
fully reaching even sensitive targets such as the brain and retina....

The amount of label recovered in tissue components was quite high
in all the groups, but especially in the NA rats.
In them, the liver alone retained, for a long time, more than 2 % of
the methanol carbon given in a single oral dose of aspartame,
and the rest of the body stored an additional 2 % or more.
These are indeed extremely high levels for adducts of formaldehyde,
a substance responsible of chronic deleterious effects (33),
that has also been considered carcinogenic (34,47).
The repeated occurrence of claims that aspartame
produces headache and other neurological and psychological
secondary effects --
more often than not challenged by careful analysis --
(5, 9, 10, 15, 48)
may eventually find at least a partial explanation in the permanence
of the formaldehyde label,
since formaldehyde intoxication can induce similar effects (49).

The cumulative effects derived from the incorporation of label in the
chronic administration model suggests that regular intake of
aspartame may result in the progressive accumulation
of formaldehyde adducts.
It may be further speculated that the formation of adducts can help to
explain the chronic effects aspartame consumption may induce on
sensitive tissues such as brain (6, 9, 19, 50).
In any case, the possible negative effects that the accumulation of
formaldehyde adducts can induce is, obviously, long-term.
The alteration of protein integrity and function may needs some time
to induce substantial effects.
The damage to nucleic acids, mainly to DNA,
may eventually induce cell death and/or mutations.
The results presented suggest that the conversion of aspartame
methanol into formaldehyde adducts in significant amounts in vivo
should to be taken into account because of the widespread utilization
of this sweetener.
Further epidemiological and long-term studies are needed to
determine the extent of the hazard that aspartame consumption
poses for humans."



Many scientific studies and case histories report: * headaches
* many body and joint pains (or burning, tingling, tremors, twitching,
spasms, cramps, stiffness, numbness, difficulty swallowing)
* fever, fatigue, swollen glands * "mind fog", "feel unreal",
poor memory, confusion, anxiety, irritability, depression, mania,
insomnia, dizziness, slurred speech, sexual problems,
poor vision, hearing (deafness, tinnitus), or taste
* red face, itching, rashes, allergic dermatitis, hair loss,
burning eyes or throat, dry eyes or mouth, mouth sores,
burning tongue * obesity, bloating, edema, anorexia,
poor appetite or excessive hunger or thirst
* breathing problems, shortness of breath
* nausea, diarrhea or constipation * coldness * sweating
* racing heart, low or high blood pressure, erratic blood sugar levels
* hypothryroidism or hyperthyroidism * seizures * birth defects
* brain cancers * addiction * aggrivates diabetes, autism, allergies,
lupus, ADHD, fibromyalgia, chronic fatigue syndrome,
multiple chemical sensitivity, multiple sclerosis, pseudotumor cerebri
and interstitial cystitis (bladder pain).


http://groups.yahoo.com/group/aspartameNM/message/870
Aspartame: Methanol and the Public Interest 1984: Monte:
Murray 2002.09.23 rmforall

Dr. Woodrow C. Monte
Aspartame: methanol, and the public health.
Journal of Applied Nutrition 1984; 36 (1): 42-54.
(62 references) Professsor of Food Science [retired 1992]
Arizona State University, Tempe, Arizona 85287
woodymonte@...; woodymonte@...;
The methanol from 2 L of diet soda, 5.6 12-oz cans, 20 mg/can, is
112 mg, 10% of the aspartame.
The EPA limit for water is 7.8 mg daily for methanol
(wood alcohol), a deadly cumulative poison.
Many users drink 1-2 L daily.
The reported symptoms are entirely consistent with chronic methanol
toxicity. (Fresh orange juice has 34 mg/L, but, like all juices, has 16
times more ethanol, which strongly protects against methanol.)

"The greater toxicity of methanol to man is deeply rooted in the
limited biochemical pathways available to humans for detoxification.
The loss of uricase (EC 1.7.3.3.),
formyl-tetrahydrofolate synthetase (EC 6.3.4.3.) (42)
and other enzymes (18) during evolution sets man apart from all
laboratory animals including the monkey (42).

There is no generally accepted animal model
for methanol toxicity (42, 59).

Humans suffer "toxic syndrome" (54) at a minimum lethal dose
of <1 gm/kg, much less than that of monkeys, 3-6 g/kg (42, 59).

The minimum lethal dose of methanol in the
rat, rabbit, and dog is 9.5, 7.0 , and 8.0 g/kg, respectively (43);
ethyl alcohol is more toxic than methanol to these test animals (43)."

Recent research [see links at end of post] supports his focus on the
methanol to formaldehyde toxic process:

"The United States Environmental Protection Agency in their
Multimedia Environmental Goals for Environmental Assessment
recommends a minimum acute toxicity concentration
of methanol in drinking water at 3.9 parts per million,
with a recommended limit of consumption below 7.8 mg/day (8).

This report clearly indicates that methanol:

"...is considered a cumulative poison due to the low rate of excretion
once it is absorbed. In the body, methanol is oxidized to
formaldehyde and formic acid; both of these metabolites
are toxic." (8)...

Recently the toxic role of formaldehyde (in methanol toxicity)
has been questioned (34).
No skeptic can overlook the fact that, metabolically, formaldehyde
must be formed as an intermediate to formic acid production (54).

Formaldehyde has a high reactivity,
which may be why it has not been found in humans or other primates
during methanol poisoning (59)....

If formaldehyde is produced from methanol and does have a
reasonable half life within certain cells in the poisoned organism
he chronic toxicological ramifications could be grave.

Formaldehyde is a known carcinogen (57) producing squanous-cell
carcinomas by inhalation exposure in experimental animals (22).
The available epidemiological studies do not provide adequate data
for assessing the carcinogenicity of formaldehyde in man
(22, 24, 57).

However, reaction of formaldehyde with deoxyribonucleic acid
(DNA) has resulted in irreversible denaturation that could interfere
with DNA replication and result in mutation (37)..."



It is certain that high levels of aspartame use,
above 2 liters daily for months and years,
must lead to chronic formaldehyde-formic acid toxicity.

Fully 11 % of aspartame is methanol -- 1,120 mg aspartame
in 2 L diet soda, almost six 12-oz cans, gives 123 mg methanol
(wood alcohol). The methanol is immediately released
into the body after drinking .
Within hours, the liver turns much of the methanol into formaldehyde,
and then much of that into formic acid, both of which in time
are partially eliminated as carbon dioxide and water.

However, about 30 % of the methanol remains in the body
as cumulative durable toxic metabolites of formaldehyde
and formic acid -- 37 mg daily,
a gram every month, accumulating in and affecting every tissue.

If only 10 % of the methanol is retained daily as formaldehyde,
that would give 12 mg daily formaldehyde accumulation -- about
60 times more than the 0.2 mg from 10 % retention
of the 2 mg EPA daily limit for formaldehyde in drinking water.

Bear in mind that the EPA limit for formaldehyde in drinking water is
1 ppm, or 2 mg daily for a typical daily consumption of 2 L of water.

http://groups.yahoo.com/group/aspartameNM/message/835
ATSDR: EPA limit 1 ppm formaldehyde in drinking water July 1999:
Murray 2002.05.30

This long-term low-level chronic toxic exposure leads to typical
patterns of increasingly severe complex symptoms,
starting with headache, fatigue, joint pain, irritability, memory loss,
rashes, and leading to vision and eye problems, and even seizures.
In many cases there is addiction. Probably there are immune system
disorders, with a hypersensitivity to these toxins and other chemicals.

J. Nutrition 1973 Oct; 103(10): 1454-1459.
Metabolism of aspartame in monkeys.
Oppermann JA, Muldoon E, Ranney RE.
Dept. of Biochemistry, Searle Laboratories,
Division of G.D. Searle and Co. Box 5110, Chicago, IL 60680
They found that about 70 % of the radioactive methanol in aspartame
put into the stomachs of 3 to 7 kg monkeys
was eliminated within 8 hours, with little additional elimination,
as carbon dioxide in exhaled air and as water in the urine.
They did not mention that this meant that about 30 % of the methanol
must transform into formaldehyde and then into formic acid,
both of which must remain as toxic products in all parts of the body.
They did not report any studies on the distribution of radioactivity
in body tissues, except that blood plasma proteins after 4 days
held 4 % of the initial methanol.
This study did not monitor long-term use of aspartame.

The low oral dose of aspartame and for methanol
was 0.068 mmol/kg, about 1 part per million [ppm]
of the acute toxicity level of 2,000 mg/kg, 67,000
mmol/kg, used by McMartin (1979).
Two L daily use of diet soda provides 123 mg methanol,
2 mg/kg for a 60 kg person, a dose of 67 mmole/kg,
a thousand times more than the dose in this study.
By eight hours excretion of the dose in air and urine had leveled off at
67.1 +-2.1 % as CO2 in the exhaled air
and 1.57+-0.32 % in the urine, so 68.7 % was excreted,
and 31.3 % was retained.
This data is the average of 4 monkeys.
"...the 14C in the feces was negligible."

"That fraction not so excreted (about 31%) was converted to body
constituents through the one-carbon metabolic pool."
"All radioactivity measurements were counted to +-1 % accuracy..."
This indicates that the results could not be claimed to have a
precision of a tenth of a percent. OK, so this is a nit-pick -- but I
believe espousing spurious accuracy is a sign of scientific insecurity.

The abstract ends, "It was concluded that aspartame was digested to
its three constituents that were then absorbed
as natural constituents of the diet.
Thus, the concept is very subtly insinuated that methanol, as a
constituent of aspartame, is absorbed as a natural constituent
of the diet.
Nowhere in this report are mentioned the dread words,
"formaldehyde" and "formic acid".

Of course, methanol and formaldehyde toxicity studies are highly
relevant to the issue of aspartame toxicity.
[ Aspartame has to be turned into its toxic products,
formaldehyde and formic acid, in the body, before it is toxic,
so some pro-aspartame reseach studies test aspartame outside the
body, and then proclaim that they have proved that it is not toxic. ]



http://www.dorway.com/tldaddic.html 5-page review
Roberts HJ Aspartame (NutraSweet) addiction.
Townsend Letter 2000 Jan; HJRobertsMD@...
http://www.sunsentpress.com/ sunsentpress@...
Sunshine Sentinel Press P.O.Box 17799
West Palm Beach, FL 33416
800-814-9800 561-588-7628 561-547-8008 fax

http://groups.yahoo.com/group/aspartameNM/message/669
1038-page medical text "Aspartame Disease: An Ignored Epidemic"
published May 30 2001 $ 60.00 postpaid data from 1200 cases
available at http://www.amazon.com
over 600 references from standard medical research

http://groups.yahoo.com/group/aspartameNM/message/790
Moseley: review Roberts
"Aspartame Disease: An Ignored Epidemic":
Murray 2002.02.07 rmforall

Roberts, Hyman J., 1924- ,
Useful insights for diagnosis, treatment and public heath: an updated
anthology of original research, 2002, 798 pages,
aspartame disease, pages 627-685, 778-780

http://groups.yahoo.com/group/aspartameNM/message/859
Roberts: the life work of a brilliant clinician: aspartame toxicity:
Murray 2002.08.02 rmforall



Russell L. Blaylock, MD 601-982-1175 Madison, Mississippi
"Excitotoxins: The Taste that Kills", 1977, 298 p., 493 references.
"Health and Nutrition Secrets that can save your life", 2002, 459 p.,
558 + 30 references, $ 30 http://www.russellblaylockmd.com/

http://groups.yahoo.com/group/aspartameNM/message/1090
aspartame, MSG, excitotoxins, NMDA glutamate receptors,
multiple sclerosis: Blaylock: Murray 2004.06.09

http://groups.yahoo.com/group/aspartameNM/message/97
Lancet website aspartame letter 1999.07.29:
Excitotoxins 1999 Part 1/3 Blaylock: Murray 2000.01.14
The Medical Sentinel Journal 1999 Fall; (95 references)
http://www.dorway.com/blayenn.html



http://groups.yahoo.com/group/aspartameNM/message/935
Comet assay finds DNA damage from sucralose, cyclamate,
saccharin in mice: Sasaki YF & Tsuda S Aug 2002:
Murray 2003.01.01
[ Also borderline evidence, in this pilot study of 39 food additives,
using test groups of 4 mice, for DNA damage from for stomach,
colon, liver, bladder, and lung 3 hr after oral dose of 2000 mg/kg
aspartame -- a very high dose. Methanol is the only component of
aspartame that can lead to DNA damage. ]

http://groups.yahoo.com/group/aspartameNM/message/961
genotoxins, Comet assay in mice: Ace-K, stevia fine;
aspartame poor; sucralose, cyclamate, saccharin bad:
Y.F. Sasaki Aug 2002: Murray 2003.01.27
[A detailed look at the data] ]


MSG and Aspartame -- A Personal Story, TV health reporter
Dick Allgire (vegetarian) healed of migraines and panic attacks:
Murray 2008.02.12
http://rmforall.blogspot.com/2008_02_01_archive.htm
Tuesday, February 12, 2008
http://groups.yahoo.com/group/aspartameNM/message/1520



http://groups.yahoo.com/group/aspartame/messages
group with 1,080 members, 22,439 posts in a public archive
E. Bryant Holman bryanth@...
Carol Guilford CarolGuilford@...
http://www.presidiotex.com/aspartame/
aspartame@...
http://www.presidiotex.com/aspartame/Links/links.html

http://www.HolisticMed.com/aspartame mgold@...
Aspartame Toxicity Information Center Mark D. Gold
12 East Side Drive #2-18 Concord, NH 03301 603-225-2100
http://www.holisticmed.com/aspartame/abuse/methanol.html
"Scientific Abuse in Aspartame Research"

http://health.groups.yahoo.com/group/GFCFKids/  excellent group
Gluten Free Casein Free Kids
This list is unmoderated and unrestricted.
The principle aim of this list is to provide a discussion forum for
parents of children on the autism spectrum who are avoiding gluten
and casein and other substances in their children's diets.
9,108 members, 234,968 posts in public archive since Dec. 1998
http://health.groups.yahoo.com/group/GFCFKids/links

A very detailed, highly credible account of the dubious approval
process for aspartame in July, 1981 is part of the just released
two-hour documentary "Sweet Misery, A Poisoned World:
An Industry Case Study of a Food Supply In Crisis"
by Cori Brackett:  cori@...