*******************************************************

http://groups.yahoo.com/group/aspartameNM/message/1274
harm to fetus from formaldehyde from methanol from aspartame,
Woodrow C. Monte: Murray 2006.01.02

January 2, 2006

Governor Richardson and the Environmental Improvement Board:

I agree with the proposed ban of aspartame from New Mexico.

Simply put, I believe that aspartame is a poison because it turns into
poison when consumed. The gist of my objection to the sweetener
is that every molecule of it releases a molecule of methanol
which, in turn, is metabolized into formaldehyde.
Formaldehyde is a carcinogen (causes cancer)
and methanol a teratogen (causes birth defects).

Humans are more sensitive to methanol poisoning
than any other living thing. This sensitivity can be as high
as 100 times more than the average laboratory rat,
with tremendous individual variability.

There is a case where a human has died after consuming
2 teaspoons of methanol. As little as 10 ml of methanol
has been considered toxic in humans
(.09 gm/kg) [ = 90 mg/kg body weight ],
while it would take the human equivalent of over a quart
to kill the average laboratory rat (9 gm/kg),
and even the toxic dose for monkeys is 3-6 gm/kg.

Methanol, for all intents and purposes, is a poison only to humans.
What is important here is that this 100 times factor
(0.09 gm/kg versus 9 gm/kg) should have been used to extrapolate all
teratogenic and toxological data, before aspartame was allowed
into the food chain, just to be fair to those that are sensitive --
this has never been done.

There have now been two distinct historically significant eras
during which man's inordinate sensitivity to methanol consumption
have been vehemently denied, due primarily to economic consideration.
The first one was fought in the scientific journals of early 20th century.
It took until the 1940s and thousands of deaths before a Scandinavian
scientist named O. Roe wrote the definitive article that stopped
food companies from using methanol as an additive.
That battle was fought without any real interference
from pressure groups.
I am certain that without the present longstanding, egregious economic
pressure to declare methanol safe, we would by now
know the truth about this extraordinary human specific toxin.

There is an enzyme (catalase) that can be found in the livers of all other
animal species which has the ability to convert methanol directly into
formic acid, saving tissue from having to deal with formaldehyde.
[ Formic acid also is a serious, cumulative toxin. ]

Humans have a catalase but it is not capable of dealing with methanol.
We have no choice but to metabolize all of our methanol
to formaldehyde.
Complicating this scenario is that our designated enzyme (ADH)
is located inside many different cells in our body (not just our livers)
with tremendous individual variability in the location, distribution, and
concentration of these enzyme sites -- allowing the conversion of
methanol to formaldehyde almost anywhere in our bodies.
Why this is, we have no explanation, but it is one of the reasons
humans, and only humans, must consider methanol a poison.

[ 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 2005.01.28 rmforall

In the Stone Age, the human body may have evolved to use methanol
from fruits and formaldehyde from wood smoke as natural antibiotics to
limit contageous infections, which would be very prevelant in tribes
crowded into huts and caves. ]

The methanol controversy has persisted through 5 generations
of scientists. The first credible scientific reports of humans
being blinded or killed by small doses of methanol appeared
late in the 19th century. These compelling reports in medical journals
were considered nonsense and summarily dismissed
by the toxological community. The explanation for dismissing
the evidence was that the deaths must have been
"caused by some contaminant of the methanol", not the methanol itself.

Regretably, hundreds (perhaps thousands) of men, women, and children
were blinded or died at the turn of the century when methanol was first
intentionally used as a food additive. Industrial innovation made
available a tasteless, odorless, cheap form of methanol (wood alcohol).
To save money it was used to make such luxuries as vanilla extract
and food flavorings. As now, it was claimed that this would be "safe".

There was no conspiracy here -- the top scientists, legitimately,
considered methanol to be safer than ethanol (grain alcohol).
It had been know since the mid 1800's that laboratory animals
that were tested would die from ethanol long before methanol
would take them down. Rats, dogs, cats, birds, and monkeys all
could acutely consume large doses of methanol without effect --
there was absolutely no exception. Every animal tested acutely,
survived high doses of methanol. There were no animal models than,
or now, that duplicated what would be discovered, after much tragic
human suffering -- the exquisite human sensitivity to methanol.

Methanol is a chemical Trojan horse. Its metabolic fate in humans is to
become formaldehyde. Methanol (the smallest alcohol) is itself
not reactive and easily passes through every biological barrier.
Formaldehyde can not, by itself, get where the methanol molecule
can take it -- this is a toxological nightmare.

Formaldehyde is a very reactive substance, but dissolved in water,
it becomes a monster with the propensity to attach to every protein
molecule that it touches. Formaldehyde in the air causes cancers
in human nasal passages because it is so reactive, it attaches to the
first moist protein with which it makes contact. When we deal
with environmental (air pollution) formaldehyde it, is never found
in the bloodstream for this very reason -- it does not travel well
in the life spaces. We are only now discovering what dangers are
promulgated by formaldehyde produced inside the body.
What manner of biochemical horror evolves from the attachment of
formaldehyde to enzyme systems and other functional proteins
can only be extrapolated from our limited knowledge
of acute human aspartame toxicity.

We are told the lie that methanol is ubiquitous in the normal human diet.
I have studied this issue for quite some time, and I can say with certainty
as a trained food scientist that in the natural world methanol is consumed,
but only in small amounts. The average adult intake, before the
introduction of aspartame, would have been less than 10 mg a day
with most days approaching 2 mg or less. One liter of orange diet soda
contains over 90 mg of methanol. My attached article of 20 years ago
goes into this in great detail. There is no methanol found in
any red meat, bread, rice, fish, chicken or most anything normally
consumed in large amounts. Methanol is found in the following and,
except for barely measurable amounts, nowhere else.

The only significant sources of dietary methanol:

1. aspartame (Equal) sweetened foods, the worlds major source
of dietary methanol

2. high temperature canned fruits fruit juices and vegetables --
(liberated by the high temperature treatment of pectin)

3. tomato and black currant and some other juices
(please see my article)

4. smoking or second hand smoke

5. air pollution in areas using methanol as a fuel or fuel additive

6. gut breakdown of pectin (rare without ethanol co-production)

7. cooking of vegetables for very long periods
(much methanol is lost in steam)

8. alcohol beverages (ethanol protects here, since ethanol stops
methanol turning into formaldehyde)

In my article of 1984, Aspartame: Methanol And The Public Health,
I stated, "We know nothing of the mutagenic, teratogenic
or carcinogenic effect of methyl alcohol on man or mammal".

The year after my article was published in the
Journal of Applied Nutrition,
methanol was determined to cause birth defects (1985)*.

Methanol was classed as a teratogen capable
of causing neural tube birth defects**.

The list of teratogenic compounds is short, and the list of those that in
particular cause neural tube birth defects such as spina bifidia,
even shorter.

The incidence of the neural tube birth defect, spina bifida, in the United
States was significantly increasing from 1992 to 1995, to the point that
the US Food and Drug administration in 1996 mandated that
all enriched cereal grain products be fortified with folic acid
(a very unusual move, since up to that time folic acid was the
only vitamin the FDA limited consumption of).
The Center for Disease Control recommended that
all child bearing woman in the United States increase
their folic acid intake to 400 micrograms a day
in order to prevent "neural tube defects".

As I stated in my 1984 article, folic acid is primarily used by the body
to give some protection from methanol metabolites and little else.
Since folic acid fortification has been in effect it has been reported that
as much as 50% of the incidence of neural tube birth defects
have been prevented. How many more would have been prevented
by removing what is now the major source of the teratogen methanol
in food -- aspartame?

Methanol in the laboratory is always labeled as poisonous,
and we are warned that it "can not be made safe" and that
it is "not tolerated by fetal tissue" --- There are few poisons
as diabolical as formaldehyde yet there are those who, without qualm,
have encouraged these be fed to pregnant women and children,
the most vulnerable of our species.
It is true that methanol is found in nature, but then so is death.

The powers set against the truthful resolution of this methanol
controversy are far too great to trust the normal process
of earnest dialogue between scientists.
Methanol must be proved safe, if those imperious, remorseless
industries who would sell it for food or power are to have their way.
There is no worthy champion for the side of safety,
and the public protectors of caution have been warned to silence
by litigation. Those who were taught to "above else do no harm"
have been willing to turn their talents to trickery,
to please their doting keepers. It is time for someone to act in the public
interest. It is time for us to calculate our loses and learn from this
terrible, terrible mistake.

Sincerely,

Woodrow C. Monte Ph.D.
Professor of Food Science (Retired)
6 Bates Street
Riverton, Southland 9654, New Zealand

[ color photo ]

This picture of a child who was soon to die without a functioning brain
was given to me long before we had any idea that methanol
could cause birth defects. Her tearful mother told me that she
had consumed, in the hot dry Arizona summer,
over two liters of diet soda a day for every day of her pregnancy.
She said that she "knew in her heart" that the culprit was in
that bottle. We will never know if her heart was right.

Teratological Articles of Interest*:


Fundam Appl Toxicol. 1985 Aug; 5(4): 727-36.
Teratological assessment of methanol and ethanol
at high inhalation levels in rats.
Nelson BK, Brightwell WS, MacKenzie DR, Khan A,
Burg JR, Weigel WW, Goad PT.

Alcohols are widely used as industrial solvents.
In spite of the fact that ethanol is a human teratogen,
there has not been systematic investigation of the potential
teratogenic effects of other alcohols,
particularly using the inhalation route of exposure,
as would be appropriate in assessing occupational
and environmental types of experience.
As part of a large teratological examination of industrial alcohols,
methanol and ethanol were administered by inhalation to groups of
approximately 15 pregnant Sprague-Dawley rats.
Methanol was administered at
20,000 ppm (20ME), 10,000 ppm (10ME), 5000 ppm (5ME),
and 0 ppm (MECO)
for 7 hr/day on Days 1-19 of gestation (Days 7-15 for 20ME).
Ethanol was administered at
20,000 ppm (20ET), 16,000 ppm (16ET), 10,000 ppm (10ET),
and 0 ppm (ETCO)
for 7 hr/day on Days 1-19 of gestation.
Dams were sacrificed on Day 20 (sperm = Day 0).
One-half of the fetuses were examined using the Wilson technique for
visceral defects, and the other half were examined for skeletal defects.
The highest concentration of methanol (20ME)
produced slight maternal toxicity
and a high incidence of congenital malformations (p less than 0.001),
predominantly extra or rudimentary cervical ribs
and urinary or cardiovascular defects.
Similar malformations were seen in the 10ME group,
but the incidence was not significantly different from controls.
No adverse effects were noted in the 5ME group.
Dams in the 20ET group were narcotized by the end of exposure,
and maternal weight gain and feed intake were decreased
during the first week of exposure.
The 16ET dams had slightly depressed weight gain (p less than 0.01)
during the first week of exposure,
but there were no significant effects on feed consumption.
There was no definite increase in malformations at any level of ethanol,
although the incidence in the 20ET group was of borderline significance.
PMID: 4043595
[ B.K. Nelson, National Institute of Occupational Safety and Health,
Cincinnati, Ohio 45226, USA. ]


Teratology. 1996 Oct; 54(4): 198-206.
Influence of maternal folate status on the developmental toxicity of
methanol in the CD-1 mouse.
Sakanashi TM, Rogers JM, Fu SS, Connelly LE, Keen CL.
Department of Nutrition, University of California, Davis 95616, USA.
[ rogers.john@...; Steven.Fu@... ;
clkeen@... ]

Methanol, which is detoxified via a folic acid-dependent pathway,
has been shown to be teratogenic in mice.
Given recent observations that the level of dietary folic acid intake may
be inversely related to the occurrence of select birth defects in humans,
we tested the hypothesis that dietary folic acid intake would influence
the developmental toxicity of methanol.
Virgin female mice were fed one of three diets
containing 400 (low), 600 (marginal), or 1,200 (adequate) nmol
folic acid/kg diet for 5 weeks prior to and following mating.
On gestation days (GD) 6-15, dams were administered by gavage
either vehicle (distilled, deionized water)
or methanol at 2.0 or 2.5 g/kg body weight, twice daily.
On GD 18, mice were weighed and killed and the liver, kidneys,
and gravid uteri removed and weighed.
Implantation sites, live and dead fetuses, and resorptions
were counted;
fetuses were weighed individually
and examined for cleft palate and exencephaly.
One third of the fetuses in each litter
were examined for skeletal morphology.
Maternal liver folate concentrations were
approximately 40-50% lower in the low dietary folic acid groups
than in the marginal and adequate groups;
methanol did not affect maternal liver folate concentration at term.
Maternal net gestational weight gain was lowest
at the lowest dietary folate level
but was not affected by methanol.
Gravid uterus weights were
lowest in the low dietary folic acid groups
exposed to the high methanol dose and
the number of live fetuses per litter
was lowest in the low folic acid groups.
Fetal body weights were lowest in the low folic acid groups and
significantly lower in the methanol groups
relative to vehicle-treated animals.
Fetal crown-rump lengths were shorter in the methanol-treated groups;
this parameter was not affected by folic acid treatment.
Both methanol and low dietary folic acid
increased the incidence of cleft palate,
with the highest number of affected litters
in the low dietary folic acid group.
These results support the concept that maternal folate status
can modulate the developmental toxicity of methanol.
PMID: 9122889


Teratology. 1994 Jun; 49(6): 497-517.
Methanol-induced neural tube defects in mice: pathogenesis during
neurulation.
Bolon B, Welsch F, Morgan KT.
Department of Experimental Pathology and Toxicology,
Chemical Industry Institute of Toxicology,
Research Triangle Park, North Carolina 27709.
[ bradgempath@... ; Kevin.Morgan@... ]

A spectrum of cephalic neural tube defects was observed in near-term
(gestation day [GD] 17) mouse fetuses following maternal inhalation of
methanol at a high concentration (15,000 ppm) for 6 hr/day during
neurulation (GD 7-9).
Dysraphism, chiefly exencephaly, occurred in 15% of fetuses,
usually in association with reduction or absence of multiple bones in the
craniofacial skeleton and
ocular anomalies (prematurely open eyelids, cataracts, retinal folds).
Measurements of cerebrocortical width in grossly normal,
methanol-exposed fetuses revealed
significant semiquantitative differences in the thicknesses
of the frontal cortex and its constituent layers (neuroepithelium,
intermediate cortex/subventricular plate, and cortical layer 1)
as well as apparent increases in subventricular plate cellularity
relative to controls.
Subsequently, the early morphogenesis of these neural changes was
investigated in neurulating mouse embryos
to define tissue-specific patterns of methanol-induced damage
that lead to cephalic axial dysraphism.
Following daily 6-hr maternal inhalations
of 15,000 ppm methanol during GD 7-8,
the cephalic neural fold margins
were swollen, blunted, and poorly elevated on GD 8.5 and 9
relative to controls.
Histopathology of exposed GD 8.5 embryos revealed microcephaly
in association with reductions in the cell density and mitotic index
of at least 47% in the cranial mesoderm.
The mitotic index in the embryonic neuroepithelium
was also reduced by 55%,
and groups of neural crest cells were displaced
to the neural folds dorsal to the foregut
(relative to the more ventral location in the facial regions
of control embryos).
When examined on GD 9.5 and 10.5,
maternal methanol exposure (15,000 ppm for 6 hr/day)
during GD 7-9 resulted in stunting, delayed rotation, and
microcephaly in over 90% of the affected embryos.
Persistent patency
of the anterior neuropore and prosencephalichypoplasia
were seen in > 40% and up to 90% of embryos, respectively.
Shallow optic vesicles, stunted branchial arches, scoliosis,
and hydropericardium were also observed.
Many 10.5-day-old embryos were edematous.
Occult dysraphism, recognized grossly
by abnormally narrow cephalic conformation
and histopathologically by the absence of mesoderm in the
mesencephalon,
was present in at least 21% of methanol-exposed embryos
on GD 9.5 and 10.5.
Nile blue vital dye staining of methanol-exposed embryos
revealed no difference in dye accumulation between control
and treated embryos on GD 8.5, 9.0, or 9.5.
There were no apparent dysmorphogenic effects in
control embryos at any stage of development.
(ABSTRACT TRUNCATED AT 400 WORDS) PMID: 7747271


Fundam Appl Toxicol. 1993 Nov; 21(4): 508-16.
Phase-specific developmental toxicity in mice
following maternal methanol inhalation.
Bolon B, Dorman DC, Janszen D, Morgan KT, Welsch F.
Chemical Industry Institute of Toxicology,
Research Triangle Park, North Carolina 27709.
[ dorman@... ; welsch@... ]

Methanol is toxic to embryos of mice and rats
when inhaled by dams at high concentrations.
The present studies examined methanol-induced
developmental toxicity following inhalation exposure (6 hr/day)
of pregnant CD-1 mice to 5000, 10,000 or 15,000 ppm
either throughout organogenesis (GD 6-15),
during the period of neural tube development and closure (GD 7-9),
or during a time of potential neural tube reopening (GD 9-11).
Transient neurologic signs and reduced body weights were observed
in up to 20% of dams exposed to 15,000 ppm.
Examination of near-term fetuses revealed embryotoxicity
(increased resorptions, reduced fetal weights, and/or
fetal malformations) at 10,000 and 15,000 ppm,
while 3-day exposures at 5000 ppm
yielded no observable adverse effects.
Terata included neural and ocular defects, cleft palate,
hydronephrosis, deformed tails, and limb (paw and digit) anomalies.
Neural tube defects and ocular lesions occurred
after methanol inhalation between GD 7-9,
while limb anomalies were induced only during GD 9-11;
cleft palate and hydronephrosis were observed
after exposure during either period.
These findings were consistent with prior reports
that maternal methanol inhalation at high levels
induces developmental toxicity in a concentration-dependent manner.
Furthermore, our data indicate that the spectrum of teratogenic effects
depended upon both the timing (i.e., stage of embryonic development)
and the number of methanol exposures. PMID: 8253303
*******************************************************

CRC Crit Rev Toxicol. 1982 Oct; 10(4): 275-86.
Species differences in methanol poisoning.
Roe O.
Publication Types: Review PMID: 6756793

Trans Ophthalmol Soc U K. 1970; 89: 235-42.
Past, present and future fight against methanol blindness and death.
Roe O.
PMID: 5276655

Pharmacol Rev. 1955 Sep; 7(3): 399-412.
The metabolism and toxicity of methanol.
ROE O.
PMID: 13266515
*******************************************************

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@...
The methanol from 2 L of diet soda, 5.6 12-oz cans, 20 mg/can, is
112 mg, 11% 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)."
********************************************************

January 2, 2006

Any unsuspected source of methanol, which the body always quickly
and largely turns into formaldehyde and then formic acid, must be
monitored, especially for high responsibility occupations, often with
night shifts, such as pilots and nuclear reactor operators.

In particular, the next review gives many recent mainstream
peer-reviewed studies that show formaldehyde,
always inevitably derived in the body from any methanol source,
including aspartame, causes endothelial injury,
ie, diabetic neuropathy -- among the most serious and complex
complications of diabetes.

http://groups.yahoo.com/group/aspartameNM/message/1263
many studies on endothelial injury (diabetic neuropathy) by adducts of
formaldehyde derived from methylamine from many of the same sources
as also supply methanol (formaldehyde), including aspartame:
PH Yu et al: DJ Conklin et al: Murray 2005.12.04

http://groups.yahoo.com/group/aspartameNM/message/1237
ubiquitous potent uncontrolled co-factors in nutrition research are
formaldehyde from wood and tobacco smoke and many sources,
including from methanol in dark wines and liquors, in pectins
in fruits and vegetables, and in aspartame: Murray 2006.01.01

http://groups.yahoo.com/group/aspartameNM/message/925
aspartame puts formaldehyde adducts into tissues, Part 1/2
full text Trocho & Alemany 1998.06.26
Universitat Autònoma de Barcelona : Murray 2002.12.22

http://groups.yahoo.com/group/aspartameNM/message/1250
aspartame causes cancer in rats at levels approved for humans,
Morando Soffritti et al, Ramazzini Foundation, Italy &
National Toxicology Program
of National Institute of Environmental Health Sciences
2005.11.17 Env. Health Pers. 35 pages: Murray

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

As a medical layman, I suggest that evidence mandates immediate
exploration of the role of these ubiquitious, potent formaldehyde
sources as co-factors in epidemiology, research, diagnosis,
and treatment in a wide variety of disorders.

Folic acid, from fruits and vegetables, plays a role by powerfully
protecting against methanol (formaldehyde) toxicity.

Many common drugs, such as aspirin, interfere with folic acid,
as do some mutations in relevant enzymes.

The majority of aspartame reactors are female.

In mutual service, Rich Murray
*******************************************************

"Of course, everyone chooses, as a natural priority,
to actively find, quickly share, and act upon the facts
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://groups.yahoo.com/group/aspartameNM/messages
group with 149 members, 1,274 posts in a public, searchable archive
http://RoomForAll.blogspot.com http://AspartameNM.blogspot.com

Dark wines and liquors, as well as aspartame, provide
similar levels of methanol, above 100 mg daily, for
long-term heavy users, 2 L daily, about 6 cans.

Methanol is inevitably largely turned into formaldehyde,
and thence largely into formic acid.
It is the major cause of the dreaded symptoms of "next
morning" hangover.

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 18.5 times the USA EPA limit for daily formaldehyde in
drinking water, 2.0 mg in 2 L average daily drinking water.

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

http://groups.yahoo.com/group/aspartameNM/message/835
ATSDR: EPA limit 1 ppm formaldehyde in drinking water July
1999: Murray 2002.05.30 rmforall

Aspartame is made of phenylalanine (50% by weight) and
aspartic acid (39%), both ordinary amino acids, bound
loosely together by methanol (wood alcohol, 11%).
The readily released methanol from aspartame is within hours
turned by the liver into formaldehyde and then formic acid,
both potent, cumulative toxins.

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
[ Any scientist can get access to this data for free by submitting a proper
research proposal.
No one has admitted mining the extensive data on diet soda use
and many symptoms for decades for about 100,000 nurses. ]

http://groups.yahoo.com/group/aspartameNM/message/1213
aspartame (methanol, phenylalanine, aspartic acid) effects, detailed
expert studies in 2005 Aug and 1998 July, Tsakiris S, Schulpis KH,
Karikas GA, Kokotos G, Reclos RJ, et al,
Aghia Sophia Children's Hospital, Athens, Greece: Murray 2005.09.09

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@...

http://groups.yahoo.com/group/aspartameNM/message/1088
Murray, full plain text & critique: chronic aspartame in rats affects
memory, brain cholinergic receptors, and brain chemistry, Christian B,
McConnaughey M et al, 2004 May: 2004.06.05

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

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.
http://www.drthrasher.org/formaldehyde_embryo_toxicity.html full text

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://groups.yahoo.com/group/aspartameNM/message/925
aspartame puts formaldehyde adducts into tissues, Part 1/2
full text Trocho & Alemany 1998.06.26
Universitat Autònoma de Barcelona: Murray 2002.12.22

http://groups.yahoo.com/group/aspartameNM/message/1224
Aspartame disease: an FDA-approved epidemic, H. J. Roberts,
MD 2004: Murray 2005.09.30

http://groups.yahoo.com/group/aspartameNM/message/1233
Aspartame -- the shocking story, The Ecologist, 2005 Sept.,
p. 35-51, full text: Murray 2005.09.30: the correct author,
Pat Thomas, What Doctors Don't Tell You www.wddty.co.uk :
2005.10.11

http://groups.yahoo.com/group/aspartameNM/message/1131
genotoxicity of aspartame in human lymphocytes 2004.07.29
full plain text, Rencuzogullari E et al, Cukurova University,
Adana, Turkey 2004 Aug: Murray 2004.11.06

http://groups.yahoo.com/group/aspartameNM/message/1237
ubiquitous potent uncontrolled co-factors in nutrition research are
formaldehyde from wood and tobacco smoke and many sources,
including from methanol in dark wines and liquors, in pectins
in fruits and vegetables, and in aspartame: Murray 2005.12.16

http://groups.yahoo.com/group/aspartameNM/message/1264
fructose in rats increases uric acid, obesity, insulin resistance,
endothelial damage -- RJ Johnson et al, U. Florida: Murray 2005.12.07
*******************************************************

http://groups.yahoo.com/group/aspartameNM/message/1106
hangover research relevant to toxicity of 11% methanol in
aspartame (formaldehyde, formic acid): Calder I (full text):
Jones AW: Murray 2004.08.05 2005.09.28

Since no adaquate 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.

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%, one part in ten thousand).

http://groups.yahoo.com/group/aspartameNM/message/1182
Joining together: short review: research on aspartame
methanol, formaldehyde, formic acid) toxicity: Murray
2005.07.08 rmforall

http://groups.yahoo.com/group/aspartameNM/message/1071
research on aspartame (methanol, formaldehyde, formic acid)
toxicity: Murray2004.04.29 rmforall

http://groups.yahoo.com/group/aspartameNM/message/1250
aspartame causes cancer in rats at levels approved for humans,
Morando Soffritti et al, Ramazzini Foundation, Italy &
National Toxicology Program
of National Institute of Environmental Health Sciences
2005.11.17 Env. Health Pers. 35 pages: Murray

http://groups.yahoo.com/group/aspartameNM/message/1226
USA National Institutes of Health National Toxicology
Program aids eminent Ramazzini Foundation, Bologna, Italy,
in more results on cancers in rats from lifetime low levels
of aspartame (methanol, formaldehyde), Felicity Lawrence,
www.guardian.co.uk: Murray 2005.09.30

http://groups.yahoo.com/group/aspartameNM/message/1186
aspartame induces lymphomas and leukaemias in rats, full plain text,
M Soffritti, F Belpoggi, DD Esposti, L Lambertini: Ramazzini
Foundation study 2005.07.14: main results agree with their previous
methanol and formaldehyde studies: Murray 2005.09.03

http://groups.yahoo.com/group/aspartameNM/message/1189
Michael F Jacobson of CSPI now and in 1985 re aspartame
toxicity, letter to FDA Commissioner Lester Crawford;
California OEHHA aspartame critique 2004.03.12; Center for
Consumer Freedom denounces CSPI: Murray 2005.07.27

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
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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,
EU Scientific Committee on Food, a whitewash; Murray 2003.01.12

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.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"

Gold points out that industry methanol assays were too insensitive to
properly measure blood methanol levels. ]

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

"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/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.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
P.O. Box 2532 Darien, Illinois 60561
858-481-9333 adandjack@...

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

http://groups.yahoo.com/group/aspartameNM/message/927
Donald Rumsfeld, 1977 head of Searle Corp., got aspartame FDA
approval: Turner: Murray 2002.12.23 rmforall
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http://groups.yahoo.com/group/aspartameNM/message/1273
citizens against aspartame (methanol, formaldehyde), made by
Ajinomoto, at Jan 3 hearing of NM EIB in Santa Fe: Lehrman:
Murray 2006.01.01

http://groups.yahoo.com/group/aspartameNM/message/1272
New Mexico Gov. Bill Richardson endorses Nutrition Council,
mercury ban, aspartame hearings: Lehrman, Fox, Stoller:
Murray 2005.12.27

http://groups.yahoo.com/group/aspartameNM/message/1248
Aspartame and Thimerosal getting banned in New Mexico
by the Pharmacy Board? with notes by Rich Murray: 2005.11.15

http://groups.yahoo.com/group/aspartameNM/message/1247
Aspartame quagmire quickly deepens, methanol (formaldehyde, formic
acid) toxicity facts spreading at the grassroots level,
3 items in The New Mexican,
and long article in Vanity Fair by Rich Cohen: Murray 2005.11.15

http://groups.yahoo.com/group/aspartameNM/message/1245
Fox, Stoller, Murray to give Citizen's Petition
to ban aspartame (methanol, formaldehyde) and mercury
in children's medicines and vitamins: New Mexico Board of Pharmacy,
2:45-3:45 pm Monday Nov. 14, Albuquerque: Murray 2005.11.13

http://groups.yahoo.com/group/aspartameNM/message/1228
NM EIB votes 4-2 for 5-day aspartame toxicity hearing July,
2006, requesting a Hearing Officer and a medical expert from
Environmental Dept. and legal advice from NM Attorney
General: Murray 2005.10.04
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