Re: NOTMILK --  Dietary Protein Inhibits Bone Growth -- in five-year study
of 757 young girls in Beijing, China, British J of Nutrition 2010 March:
Robert Cohen: Rich Murray 2010.02.27
http://rmforall.blogspot.com/2010_02_01_archive.htm
Saturday, February 27, 2010
http://groups.yahoo.com/group/aspartameNM/message/1595
_____________________________________________________



----- Original Message -----
From: "cohensmilk1" <cohensmilk1@...>
To: <notmilk@yahoogroups.com>
Sent: Saturday, February 27, 2010 3:07 AM
Subject: NOTMILK -- Dietary Protein Inhibits Bone Growth


Dietary Protein Inhibits Bone Growth

If you are not a vegan, you are not a vegetarian.

Consumption of milk and dairy products represents
the consumption of liquid proteins from the most
abused of farm animals.

Every dairy cow in America suffers the pain of
being separated from her mother at birth.

Every dairy cow in America suffers the pain of
having her sensitive horn buds removed.

Most creatures receive no anaesthesia or post
surgical pain killers. Every cow being milked
in America suffers the ultimate indignity and
pain of slaughter.

The March, 2010 issue of the British Journal of
Nutrition (Mar;103(5):714-23) contains a study
which was designed to assess the association
between protein consumption and bone mass
accrual (BMC) in a 5-year study of 757 pre-pubescent
Chinese girls (average age = 10.1 years).

The authors conclude:

"When protein intake was considered according
to animal or plant food sources, protein from
animal foods, particularly meat, had significant
negative effects on BMC accrual..."

Robert Cohen
http://www.notmilk.com
notmilk-owner@yahoogroups.com;

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http://www.soytoy.com ... make your own grain and nut milks!

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To visit your group on the web, go to:
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_____________________________________________________


Br J Nutr. 2010 Mar;103(5):714-23. Epub 2009 Oct 9.
The association between dietary protein intake and bone mass
accretion in pubertal girls with low calcium intakes.
Zhang Q,
Ma G,
Greenfield H,
Zhu K,
Du X, Department of Food Science and Technology,
University of New South Wales, Sydney, Australia.
xdu@...
Foo LH,
Hu X,
Fraser DR.


Qian Zhang a1 c1,
Guansheng Ma a1, mags@...;
Heather Greenfield a2, heatherg@...;
http://www.vetsci.usyd.edu.au/about/staff/hgreenfield.shtml
Research Dairy products in human nutrition;
bone growth and development
(Supported by Dairy R&D Corporation, Nestle Foundation,
Murray Goulburn Cooperative Ltd)
www.vetsci.usyd.edu.au/research/bonehealth/index.shtml
Kun Zhu a2, kathyz@...;
http://www.vetsci.usyd.edu.au/about/staff/kzhu.shtml
Xueqin Du a2,  xdu@...;
PhD student with a project "Calcium and vitamin D status of female
adolescents in Beijing" funded by OPRS and DRDC (1994-1998)
Postdoctoral Research Fellow in the project entitled
"Promotion of bone health in Chinese schoolchildren"
funded by (1998-2001)
One of the Chief Investigators in the project entitled
"Genetic, pubertal and nutritional determinants of peak bone mass
accretion in adolescence" funded by Nestle Foundation (2002-2005)
Leng Huat Foo a2,
Xiaoqi Hu a1
and David R. Fraser a2 davidf@...;
http://www.vetsci.usyd.edu.au/about/staff/dfraser.shtml

a1 National Institute for Nutrition and Food Safety,
Chinese Centre for Disease Control and Prevention,
Beijing, China 100050
a2 Faculty of Veterinary Science, University of Sydney,
Sydney, Australia

To assess the association between protein intakes and bone mass
accrual in girls, data were analysed for 757 pre-pubertal girls
(mean age 10.1 years) in urban Beijing, China, who participated in a
5-year study including 2 years of milk supplementation
(intervention groups only) and 3 years of follow-up study.

At 0, 12, 24, 48 and 60 months from the baseline, bone mass of the
proximal or distal forearm (PF or DF) and total body (TB) was
measured with dual energy X-ray absorptiometry;
dietary intakes were assessed by a 3-d food record
(including two weekdays and one weekend day).

Linear mixed models were used
and continuous variables were logarithm transformed.

The mean longitudinal Ca intake (432-675 mg/d on average)
positively influenced bone mineral content (BMC) at TB, PF and DF
after controlling for baseline bone mass
and other possible confounders.

However, negative associations were observed between protein intake
(55.9-61.0 g/d on average) and BMC accrual at TB, PF or DF
(beta = - 1.92, - 10.2 or - 4.82, respectively, P < 0.01)
after adjustment.

When protein intake was considered according
to animal or plant food sources,
protein from animal foods, particularly meat,
had significant negative effects on BMC accrual at DF or PF
after adjustment.

It was concluded that higher protein intake,
especially from animal foods, appeared to have a negative effect on
bone mass accrual in Chinese pubertal girls with low Ca intakes.
PMID: 19814838

http://www.vetsci.usyd.edu.au/research/bonehealth/followup_project.shtml

FOLLOW UP PROJECT
A new project "Genetic, pubertal and nutritional determinants of
peak bone mass accretion in adolescence" has been funded by the
Nestle Foundation, 2002 - 2005.
This follow-up study is being conducted by the original team in
collaboration with the Institute of Nutrition and Food Safety in Beijing.
The Chinese team also receive funding from Danone-China for this
study.

This project will assess the growth and bone health of a random
sample of ~700 Chinese adolescent girls at ages 14 and 15.
These girls previously completed a milk supplementation trial
on schooldays when they were aged 10-12
(~450 supplemented, 250 unsupplemented controls),
and data are already available on growth and bone health measured at
baseline, mid-trial and end-trial, together with genetic information and
general and health information.
Measurements at ages 14 and 15 will be anthropometry, diet, physical
activity, UV exposure, bone mineral measurements, body composition,
pubertal stage.
At age 15 additional measurements will be bone age and biochemical
indicators.
The results will indicate how bone develops in adolescents consuming
a low calcium, plant-based diet (controls) especially the influences of
pubertal progression and genotype.
The results will also indicate whether the benefits to growth and bone
development of short-term milk supplementation commencing in early
puberty will be maintained throughout adolescence.
This information is needed to improve scientific understanding of
growth and bone mineral accretion in adolescent girls, and to make
recommendations about nutrition (including school milk programs)
to the responsible authorities in China.
The project will contribute to development of local nutrition scientists,
as well as school teachers and school health workers.

The follow-up study employs Dr Zhu Kun (Kathy) as Project Officer
and has two new PhD students:
Foo Leng Huat from Malaysia,
and Zhang Qian from Beijing.
_____________________________________________________


stevia approval due end of March by EFSA, Parma, (Europe) -- new
book "Stevia and steviol glycosides" Prof. Jan MC Geuns (Begium)
307p 70 euros: Rich Murray 2010.02.25
http://rmforall.blogspot.com/2010_02_01_archive.htm
Thursday, February 25, 2010
http://groups.yahoo.com/group/aspartameNM/message/1594
_____________________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298  rmforall@...

http://groups.yahoo.com/group/aspartameNM/messages
group with 145 members, 1,595 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1215 members, 24,020 posts in a public archive

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

http://groups.yahoo.com/group/rmforall/messages

http://groups.yahoo.com/group/AstroDeep/messages

participant, Santa Fe Complex www.sfcomplex.org

Arthur Hull Hayes Jr. 1933-2010 approved aspartame July 1981 -- NY Times
says, "...can sometimes cause cause incapacitating headaches and even
seizures.": Rich Murray 2010.03.01
http://rmforall.blogspot.com/2009_03_01_archive.htm
Monday, March 1, 2010
http://groups.yahoo.com/group/aspartameNM/message/1596
_____________________________________________________


http://www.nytimes.com/2010/03/01/health/policy/01hayes.html
http://www.nytimes.com/2010/03/01/health/policy/01hayes.html?pagewanted=print

March 1, 2010
Arthur Hayes Jr., Who Led F.D.A. in Tylenol Case, Is Dead at 76
By Dennis Hevesi

Arthur Hayes Jr., who while leading the Food and Drug
Administration during the Reagan administration helped calm
consumer fears after a Tylenol poisoning case and, amid some
controversy, approved the use of the artificial sweetener found
in Equal and Nutrasweet, died Feb. 11 in Danbury, Conn.
He was 76 and lived in Oxford, Conn.

The cause was leukemia, his son, Arthur III, said.

Dr. Hayes, a pharmacological researcher, was appointed
commissioner of the F.D.A. by President Ronald Reagan
in April 1981.
He served until August 1983.

The biggest crisis faced by the agency under Dr. Hayes was a
nationwide alarm in 1982 caused by the deaths of seven people in the
Chicago area who had taken Extra-Strength Tylenol capsules laced
with cyanide.
The case remains unsolved.
Under Dr. Hayes's leadership, the government and the drug industry
responded by developing the first federal regulations requiring
tamper-resistant packaging for all over-the-counter drugs.

In 1981, Dr. Hayes granted approval for the use of the sugar
substitute aspartame in dry foods and as a tabletop sweetener.
Research had found that aspartame was associated with high rates of
cancers in rats that had been given large doses, starting at what would
be the equivalent of four to five 20-ounce bottles of diet soda a day
for a 150-pound person.

Dr. Hayes insisted that there was no need for people to avoid the
sweetener.

Marketed as NutraSweet (when used as a food additive) and Equal
(the tabletop version), aspartame is now also used in products like
soft drinks, breakfast cereals, pudding mixes and gum.
Research done after Dr. Hayes's time as commissioner indicated that
aspartame can sometimes cause incapacitating headaches and even
seizures.

Arthur Hull Hayes Jr. was born in Highland Park, Mich.,
on July 18, 1933, one of four children of Arthur and Florence Gruber
Hayes.
His father was president of CBS Radio.

Dr. Hayes received his bachelor's degree in philosophy in 1955 from
Santa Clara University and then went to Oxford as a Rhodes scholar,
earning a degree in philosophy, politics and economics in 1957.
He returned to the United States to study medicine and graduated
from Cornell University Medical School in 1964.
He served in the Army Medical Corps from 1965 to 1967.

From 1967 to 1981, Dr. Hayes was an assistant professor of
medicine and pharmacology at Cornell.
He later became director of clinical pharmacology at the
Pennsylvania State University medical school.
After leaving the F.D.A., he was dean of New York Medical College
and, in 1986, was named president of E. M. Pharmaceuticals.

Besides his son, Arthur, he is survived by his wife of 49 years,
the former Barbara Anne Carey; two daughters, Lisa Hayes and
Kathy Saracino; two sisters, Mary Ann Kelley and Florence Hayes;
his brother, Joseph; and eight grandchildren.
_____________________________________________________


methanol (11% of aspartame), made by body into formaldehyde in
many vulnerable tissues, causes modern diseases of civilization,
summary of a century of research, Woodrow C Monte PhD,
Medical Hypotheses journal: Rich Murray 2009.11.15
http://rmforall.blogspot.com/2009_11_01_archive.htm
Sunday, November 15, 2009
http://groups.yahoo.com/group/aspartameNM/message/1589


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

[ This part of the Murray critique starts by quoting from the
  Magnuson review: ]

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 attorneys 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

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 ]
_____________________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298  rmforall@...

http://groups.yahoo.com/group/aspartameNM/messages
group with 145 members, 1,596 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1215 members, 24,031 posts in a public archive

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

http://groups.yahoo.com/group/rmforall/messages

http://groups.yahoo.com/group/AstroDeep/messages

participant, Santa Fe Complex www.sfcomplex.org
_____________________________________________________

formaldehyde from 11% methanol part of aspartame causes severe allergic
dermatitis in boy, JE Jacob et al, Pediatric Dermatology 2009 Nov: Rich
Murray 2010.03.30
http://rmforall.blogspot.com/2010_03_01_archive.htm
Tuesday, March 30, 2010
http://groups.yahoo.com/group/aspartameNM/message/1597
_______________________________________________


Pediatric  Dermatology. 2009 Nov-Dec;26(6):739-43.
Systematized contact dermatitis and montelukast in an atopic
boy.
Castanedo-Tardan MP,
González ME,
Connelly EA,
Giordano K,
Jacob SE.
University of Miami, Miller School of Medicine, Department
of Dermatology and Cutaneous Surgery, Miami, Florida,
USA.

Upon ingestion, the artificial sweetener, aspartame is
metabolized to formaldehyde in the body and has been
reportedly associated with systemic contact dermatitis in
patients exquisitely sensitive to formaldehyde.

We present a case of a 9-year-old Caucasian boy with a
history of mild atopic dermatitis that experienced severe
systematized dermatitis after being started on montelukast
chewable tablets containing aspartame.

Patch testing revealed multiple chemical sensitivities which
included a positive reaction to formaldehyde.

Notably, resolution of his systemic dermatitis only occurred
with discontinuation of the montelukast chewables.
PMID: 20199453

four Murray AspartameNM reviews in SE Jacob & SA
Stechschulte debate with EG Abegaz & RG Bursey of
Ajinomoto re migraines from formaldehyde from aspartame,
Dermatitis 2009 May: TE Hugli -- folic acid with V-C
protects: Rich Murray 2009.08.12
http://rmforall.blogspot.com/2009_08_01_archive.htm
Wednesday, August 12, 2009
http://groups.yahoo.com/group/aspartameNM/message/1582
[ extracts ]

Formaldehyde, aspartame, migraines: a possible connection.
Abegaz EG, Bursey RG.
Dermatitis. 2009 May-Jun;20(3):176-7; author reply 177-9.
No abstract available. PMID: 19470307

Eyassu G. Abegaz *
Robert G. Bursey
Ajinomoto Corporate Services LLC, Scientific & Regulatory
Affairs, 1120 Connecticut Ave., N.W., Suite 1010,
Washington, DC 20036
* Corresponding author. Tel.: +1 202 457 0284;
fax: +1 202 457 0107.
abegazee@... (E.G. Abegaz),
burseyb@... (R.G. Bursey)

"For example, fruit juices, coffee, and alcoholic beverages
produce significantly greater quantities of formaldehyde than
aspartame-containing products. [6]"

"[6] Magnuson BA, Burdock GA, Doull J, et al. Aspartame:
a safety evaluation based on current use levels, regulations,
and toxicological and epidemiological studies.
Crit Rev Toxicol 2007;37:629-727"

[ 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." ]

http://www.medscape.com/viewarticle/579335

Dermatitis. 2008; 19(3): E10-E11.
© 2008  American Contact Dermatitis Society
Formaldehyde, Aspartame, and Migraines:
A Possible Connection
Sharon E. Jacob; Sarah Stechschulte
Published: 09/17/2008
[ Extract ]

Abstract

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.

Case Series

Six patients (ages 16 to 75 years) were referred for evaluation
of recalcitrant dermatitis. By history, five of the patients were
noted  to have developed migraines following aspartame
consumption; the sixth reported dermatitis flares associated
with diet cola consumption of >2 liters/day.

All six patients had current environmental exposures to
formaldehyde or formaldehyde-releasing preservatives in
their personal hygiene products and/or regular consumption
of "sugar-free food" artificially sweetened with aspartame.

Based on their histories and clinical presentations, these
patients were patch-tested with the North American Contact
Dermatitis Group 65-allergen Standard Screening Series and
selected chemicals from the University of Miami vehicle,
fragrance, bakery, and textile trays.

All six patients had positive reactions to formaldehyde, and
four had additional positive reactions to
formaldehyde-releasing preservatives (FRPs).
Expert counseling on allergen avoidance (including avoidance
of formaldehyde, FRPs, and aspartame) and alternative
product recommendations were provided to the patients.

At their follow-up appointments (between 8 and 12 weeks),
all the patients showed clearance of their dermatitis. Four
patients (two inadvertently) resumed their consumption of
aspartame and subsequently returned for an additional
follow-up visit. Three of the first five patients had recurrences
of both their migraines and their dermatitis; the sixth patient
(who had no migraines) had a positive rechallenge dermatitis.
These four patients were again counseled on avoidance
regimen.

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

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@...;
Sarah A. Stechschulte, BA  sstechschulte@...

methanol (11% of aspartame), made by body into
formaldehyde in many vulnerable tissues, causes modern
diseases of civilization, summary of a century of research,
Woodrow C Monte PhD, Medical Hypotheses journal:
Rich Murray 2009.11.15
http://rmforall.blogspot.com/2009_11_01_archive.htm
Sunday, November 15, 2009
http://groups.yahoo.com/group/aspartameNM/message/1589
_______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298  rmforall@...

http://groups.yahoo.com/group/AstroDeep/messages

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 145 members, 1,597 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1217 members, 24,053 posts in a public archive

http://groups.yahoo.com/group/rmforall/messages

participant, Santa Fe Complex www.sfcomplex.org
_______________________________________________

recent aspartame (methanol, formaldehyde, formic acid) symptoms in English
professor: Kristi Siegel: Rich Murray 2010.04.17
http://rmforall.blogspot.com/2010_04_01_archive.htm
Saturday, April 17, 2010
http://groups.yahoo.com/group/aspartameNM/message/1599
_______________________________________________


Other sources include alcohol drinks and tobacco smoke,
while adequate folic acid levels protect most people.


Case History: [ sent to Betty Martini ]

[ I changed layout to individual sentences to add clarity. ]

Kristi Siegel, Ph.D., Professor of English
59 y.o. [ born ~1951 ]

Relevant medical background:

* Hypertension diagnosed (idiopathic) -- 1977 (have taken
spironolactone for past 33 years)

* Bilateral retinal detachment -- January 1979;
scleral buckles on both eyes and repair of retinal tears

* Radial Keratotomy (both eyes) -- July 1992

In mid-January 2010, in an effort to drink more fluids,
I started using Crystal Light.
In the past, with the exception of Sweet & Low, which I use
in my coffee in the morning, I rarely used any artificial
sweeteners as I don't like the taste of diet drinks and
artificially sweetened food.
Given that I was trying to drink the recommended 8 glasses
of water a day, I was drinking that equivalent flavored with
Crystal Light.

[ 8 8-oz glasses = 64 oz = 5.3 12 oz cans of diet drinks,
which at 200 mg aspartame each give 1,060 mg aspartame,
releasing in the body their 11% methanol as 117 mg,
of which about 30% becomes cumulative retained
formaldehyde and formic acid toxic products,
about 34 mg daily, mostly in
retina, brain, liver, and kidneys. ]

Due to the eye surgeries noted above, my vision has
worsened over the past five years.
Doctors are finding that many patients who've had radial
keratotomy (which was approved prior to Lasix surgery)
start to develop "unstable cornea" about 10 years
post-surgery.
To see if anything could be done, I'd made an
appointment with an ophthalmologist on January 22, 2010.
Given my medical history, she did a thorough workup
including a complete examination of my retinas, which she
said were in good health.
She had few suggestions to remedy my problem and
advised that I see a cornea specialist.

Shortly after seeing the ophthalmologist and about two
weeks or so into my Crystal Light regimen, I had my first
episode of vision loss. [ last week of January ]
This incident was completely different in degree and kind
than the normal visual problems (increased far-sightedness
and visual lability) I had been experiencing.
Rather abruptly, I lost the visual field of the left hemisphere
of my left eye.
The vision loss lasted for about 20 or 30 minutes and after
approximately 15 minutes, I started to develop a crushing
headache which lasted for hours.
I've never had a history of headaches, so the intensity and
duration of this headache was unusual.
My husband wanted me to go to the emergency room right
away, but I pointed out that I had an appointment scheduled
with a cornea specialist on February 11.
Prior to seeing the second eye doctor, I had a couple more
incidents of vision loss and bilateral, crushing headaches that
lasted several hours, and included abdominal bloating, reflux,
and a lot of ambient noise (not really ringing in my ears, just
more of a rushing noise).
Each episode left me feeling weak and tired for days.

The cornea specialist, after hearing about the vision loss,
dilated my eyes again, and also pronounced my retinas
perfectly healthy.
However, he felt it was important to rule out strokes or
heart-related problems.
Over the next few weeks -- and I continued to have
episodes during this time -- I had a number of tests:
a brain MRI,
a carotid Doppler study,
and a trans-thoracic echocardiogram with bubble study.
All of these tests were negative.

While I was happy that the tests did not show any
problems, I continued to feel worse.
I averaged a couple of episodes a week, and in addition to
the full complex of symptoms (auras, visual loss in one or
both eyes, headaches, bloating, ambient noise, and reflux),
I felt slightly nauseous, fatigued, and dizzy.

On Friday, February 26, when I was with a group of
colleagues conducting phone interviews for candidates in a
search (we were interviewing for new assistant professor in
the English Department), I lost my entire center field of vision.

We were interviewing the fifth and final candidate, and I
didn't want to mention my situation.
By that time, I'd asked my interview questions so many
times that I didn't need to refer to the interview sheet (which
I could no longer read).
However, in responding to a question the interviewee asked,
I stumbled over two words, and then was completely unable
to pronounce or understand the third word.
In addition, I no longer understood what the words meant
or what I had been trying to say.
At the same time, there was a loud, rushing noise, and I felt
completely confused.
Within a few seconds, when I could conjure up some speech,
I asked the search committee chair if she could "talk for me."
When we completed that interview, I did tell the committee
that I'd been experiencing vision loss, headaches, but had
never had the expressive and receptive aphasia that had
occurred a few minutes earlier.

I didn't have a headache, but I was very dizzy and
disoriented and asked one of the faculty there to walk me
back to my office.
When I called my husband, he insisted on taking me to the
ER immediately.
I was in the ER for several hours while they did histories and
then decided to do a cerebral MRA (they used a contrast
dye).
This test was really the last one left to determine whether these
problems were heart or stroke related,
and the test was negative.

While I was in the ER, I was startled to see that my pulse was
only in the high 50s.
Normally my pulse is high and has been so my entire adult life.
Generally, it has always been in the 80s or higher, no matter
how physically fit I am (and I'm not overweight).
When I fell asleep in the ER, my husband said my pulse
dropped into the 40s.
My blood pressure was equally odd.
Although I take anti-hypertensives, my  normal blood pressure
tends to be borderline high (130-140 over 80-100).
At the hospital it was consistently low -- around 120/60,
which was atypical.
I've since read that Aspartame can mime the symptoms of
hypothyroidism, so I wonder if this could explain my
pulse/blood pressure anomaly.
***Out of curiosity, I just took my pulse.
Although I'm completely relaxed at the moment, my pulse is
83 bpm, which is in my normal range.

Before I was discharged from the ER, they diagnosed
"complex migraines" (and this is a term not really used
anymore), which can mimic strokes, and prescribed
Topomate 25 MG.
I took my first and only dose of that medicine on Saturday
night, February 27.
I had a very strong reaction to the medicine -- a lot of
dizziness, weakness, brain fog, and constant cramping
and diarrhea.
It took over two days to recover from the Topomate, and
the combination of the episode on Friday and my reaction
to the Topomate left me weak, dizzy, and extremely tired
that whole next week.
With the exception of teaching my classes, I missed every
appointment and meeting for the next several days.

Although all serious problems had been ruled out, I
continued to have episodes (negative and positive scotoma,
headaches, nausea, bloating, reflux, etc.) and felt generally
tired, mentally compromised, and weak.
My husband was concerned at my overall poor health, the
continued episodes, and the danger these sudden and
unpredictable vision losses posed, particularly when I was
driving.

On March 8, at my husband's insistence, I saw a neurologist
who specialized in migraines and ophthalmology.
He really had very little to add, other than to suggest that I
try to isolate what my "triggers" might be.
Given that the episodes seemed to occur in varying situations,
I couldn't isolate a specific trigger.
It was, perhaps, a week later, when I remembered I had
started drinking Crystal Light in mid- to late-January.
After reading about Aspartame, I eliminated it from my diet.

Although I did not start to feel better immediately, I have
not had another episode since eliminating Aspartame from
my diet.
I've been diligent about checking food labels for this
substance as well.

It's really been just in the past two weeks that I started to
regain my energy and feel sharper intellectually.

As I started to feel better, I became more angry.
Aspartame effectively compromised my health for months.
I'm a full professor, have published extensively, and, in
addition to teaching, direct a graduate program and a
division of three departments.

This past semester, I've been compromised both
professionally and personally.
My family (my husband and four grown children) have
been very worried, and I've repeatedly had to beg off
any social events because I just wasn't up to it.

Given the clear borders -- my episodes started after taking
Aspartame and ended when it was eliminated -- there is no
doubt in my mind or my husband's that Aspartame caused
the health problems I experienced.

I've been telling friends and relatives to eliminate Aspartame
from their diets.
I have one friend, who drinks several large bottles of diet
Coke a day.
Over the years, she's tried to wean herself from this habit
several times and has failed.
I worry about her addiction as well as the health hazards
Aspartame poses.

I thought it was striking when I read that alcoholics have
described having more severe withdrawal symptoms from
eliminating Aspartame than from giving up alcohol.

I firmly believe that Aspartame poses a serious risk to the
general public and should be removed from the market.
I've studied the techniques of the pharmaceutical companies
at length and know how easy it is to taint what are supposedly
peer-reviewed and credible medical trials.
Substances are often approved by the FDA precipitously and
without sufficient study or with studies that are corrupt.
In the case of Aspartame, the entrenched interests of those
profiting makes this a particularly difficult battle.
Please let me know if there is anything I can do.

Warm regards,

Kristi Siegel, Ph.D., Professor of English
Mount Mary College
_______________________________________________
End of Case

http://www.kristisiegel.com/theory.htm

Dr. Kristi Siegel
Associate Professor, English Dept.
Director, English Graduate Program
Chair -- Languages, Literature, and Communication Division
Mount Mary College
2900 North Menomonee River Pkwy
Milwaukee, WI 53222
(414) 258-4810, ext. 287  siegelkr@...


formaldehyde from 11% methanol part of aspartame causes
severe allergic dermatitis in boy, JE Jacob et al,
Pediatric Dermatology 2009 Nov: Rich Murray 2010.03.30
http://rmforall.blogspot.com/2010_03_01_archive.htm
Tuesday, March 30, 2010
http://groups.yahoo.com/group/aspartameNM/message/1597

Pediatric  Dermatology. 2009 Nov-Dec;26(6):739-43.
Systematized contact dermatitis and montelukast in an atopic
boy.
Castanedo-Tardan MP,
González ME,
Connelly EA,
Giordano K,
Jacob SE.
University of Miami, Miller School of Medicine, Department
of Dermatology and Cutaneous Surgery, Miami, Florida,
USA.

Upon ingestion, the artificial sweetener, aspartame is
metabolized to formaldehyde in the body and has been
reportedly associated with systemic contact dermatitis in
patients exquisitely sensitive to formaldehyde.

We present a case of a 9-year-old Caucasian boy with a
history of mild atopic dermatitis that experienced severe
systematized dermatitis after being started on montelukast
chewable tablets containing aspartame.

Patch testing revealed multiple chemical sensitivities which
included a positive reaction to formaldehyde.

Notably, resolution of his systemic dermatitis only occurred
with discontinuation of the montelukast chewables.
PMID: 20199453

four Murray AspartameNM reviews in SE Jacob & SA
Stechschulte debate with EG Abegaz & RG Bursey of
Ajinomoto re migraines from formaldehyde from aspartame,
Dermatitis 2009 May: TE Hugli -- folic acid with V-C
protects: Rich Murray 2009.08.12
http://rmforall.blogspot.com/2009_08_01_archive.htm
Wednesday, August 12, 2009
http://groups.yahoo.com/group/aspartameNM/message/1582
[ extracts ]

Formaldehyde, aspartame, migraines: a possible connection.
Abegaz EG, Bursey RG.
Dermatitis. 2009 May-Jun;20(3):176-7; author reply 177-9.
No abstract available. PMID: 19470307

Eyassu G. Abegaz *
Robert G. Bursey
Ajinomoto Corporate Services LLC, Scientific & Regulatory
Affairs, 1120 Connecticut Ave., N.W., Suite 1010,
Washington, DC 20036
* Corresponding author. Tel.: +1 202 457 0284;
fax: +1 202 457 0107.
abegazee@... (E.G. Abegaz),
burseyb@... (R.G. Bursey)

"For example, fruit juices, coffee, and alcoholic beverages
produce significantly greater quantities of formaldehyde than
aspartame-containing products. [6]"

"[6] Magnuson BA, Burdock GA, Doull J, et al. Aspartame:
a safety evaluation based on current use levels, regulations,
and toxicological and epidemiological studies.
Crit Rev Toxicol 2007;37:629-727"

[ 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." ]

http://www.medscape.com/viewarticle/579335

Dermatitis. 2008; 19(3): E10-E11.
© 2008  American Contact Dermatitis Society
Formaldehyde, Aspartame, and Migraines:
A Possible Connection
Sharon E. Jacob; Sarah Stechschulte
Published: 09/17/2008
[ Extract ]

Abstract

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.

Case Series

Six patients (ages 16 to 75 years) were referred for evaluation
of recalcitrant dermatitis. By history, five of the patients were
noted  to have developed migraines following aspartame
consumption; the sixth reported dermatitis flares associated
with diet cola consumption of >2 liters/day.

All six patients had current environmental exposures to
formaldehyde or formaldehyde-releasing preservatives in
their personal hygiene products and/or regular consumption
of "sugar-free food" artificially sweetened with aspartame.

Based on their histories and clinical presentations, these
patients were patch-tested with the North American Contact
Dermatitis Group 65-allergen Standard Screening Series and
selected chemicals from the University of Miami vehicle,
fragrance, bakery, and textile trays.

All six patients had positive reactions to formaldehyde, and
four had additional positive reactions to
formaldehyde-releasing preservatives (FRPs).
Expert counseling on allergen avoidance (including avoidance
of formaldehyde, FRPs, and aspartame) and alternative
product recommendations were provided to the patients.

At their follow-up appointments (between 8 and 12 weeks),
all the patients showed clearance of their dermatitis. Four
patients (two inadvertently) resumed their consumption of
aspartame and subsequently returned for an additional
follow-up visit. Three of the first five patients had recurrences
of both their migraines and their dermatitis; the sixth patient
(who had no migraines) had a positive rechallenge dermatitis.
These four patients were again counseled on avoidance
regimen.

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

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@...;
Sarah A. Stechschulte, BA  sstechschulte@...

methanol (11% of aspartame), made by body into
formaldehyde in many vulnerable tissues, causes modern
diseases of civilization, summary of a century of research,
Woodrow C Monte PhD, Medical Hypotheses journal:
Rich Murray 2009.11.15
http://rmforall.blogspot.com/2009_11_01_archive.htm
Sunday, November 15, 2009
http://groups.yahoo.com/group/aspartameNM/message/1589
_______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298  rmforall@...

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 145 members, 1,599 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1218 members, 24,052 posts in a public archive
_______________________________________________

[Non-text portions of this message have been removed]

Vestibulocochlear toxicity in a pair of siblings [doctor & nurse] 15 years
apart secondary to aspartame: two case reports, Paul Pisarik & Dasha Kai,
Cases J 2009.09.15 free full text: Rich Murray 2010.05.04
http://rmforall.blogspot.com/2010_05_01_archive.htm
Tuesday, May 4, 2010
http://groups.yahoo.com/group/aspartameNM/message/1600
_______________________________________________


[ Other formaldehyde sources include alcohol drinks and
tobacco and wood smoke,
while adequate folic acid levels protect most people. ]


"For both, subsequent intentional challenges with aspartame
and unintentional exposures brought back each of their
respective symptoms."

"After the last occurrence of her nausea, headaches, and
vertigo, she has since not consumed aspartame in any product
or form and has been symptom free for 22 years."

"Except for six mild reoccurrences of his symptoms within 24
hours of unintentionally consuming something with aspartame
(hypoesthesia anterior to the tragus and mild tinnitus) lasting
2-4 hours, he has been symptom free for over six years now."


Cases J. 2009 Sep 15; 2: 9237.
Vestibulocochlear toxicity in a pair of siblings 15 years apart
secondary to aspartame: two case reports.
Pisarik P, Kai D.
University of Oklahoma College of Medicine, Tulsa,
1111 S. St. Louis Ave. Tulsa, OK 74120-5440, USA.

Abstract

INTRODUCTION:

Aspartame may have idiosyncratic toxic effects for some
people;
however, there are few case reports published in the medical
literature.
We present two case reports in a pair of siblings, one with a
vestibular and the other with a cochlear toxicity to aspartame.
The cochlear toxicity is the first case to be reported, while
the vestibular toxicity is the second case to be reported.

CASE PRESENTATION:

A 29-year-old white female had a 20-month history of nausea
and headache, progressively getting worse with time and
eventually to also involve vomiting, vertigo, and ataxia.
She was extensively evaluated and diagnosed with a vestibular
neuronitis versus a chronic labyrinthitis and treated
symptomatically with limited success.
In response to a newspaper article, she stopped her aspartame
consumption with total cessation of her symptoms.

Fifteen years later, her then 47-year-old white brother had a
30-month history of an intermittent, initially 5-10 minute long
episode of a mild sensorineural hearing loss in his right ear that
progressed over time to several hour episodes of a moderately
severe high-frequency sensorineural hearing loss to include
tinnitus and a hypoesthetic area in front of his right tragus.
After a negative magnetic resonance scan of the brain, he
remembered his sister's experience with aspartame and
stopped his consumption of aspartame with resolution of
his symptoms, although the very high frequency hearing loss
took at least 15 months to resolve.
For both, subsequent intentional challenges with aspartame
and unintentional exposures brought back each of their
respective symptoms.

CONCLUSION:

Aspartame had a vestibulocochlear toxicity in a pair of siblings,
suggesting a genetic susceptibility to aspartame toxicity.
Even though the yield may be low, asking patients with
dizziness, vertigo, tinnitus, or high-frequency hearing loss
about their aspartame consumption and suggesting cessation
of its use, may prove helpful for some.
PMID: 20126318 [PubMed - in process]
PMCID: PMC2815650
Free PMC Article

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2815650/pdf/1757-1626-0002-000000923\
7.pdf
4 pages 165 KB

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2815650/?tool=pubmed

Cases J. 2009; 2: 9237.
Published online 2009 September 15.
doi: 10.4076/1757-1626-2-9237.
PMCID: PMC2815650
Copyright ©2009 Pisarik and Kai;
licensee Cases Network Ltd. licensee BioMed Central Ltd.

Vestibulocochlear toxicity in a pair of siblings 15 years apart
secondary to aspartame: two case reports
Paul Pisarik 1 and Dasha Kai 2
1 University of Oklahoma College of Medicine, Tulsa,
1111 S. St. Louis Ave. Tulsa, OK 74120-5440, USA
2 University Physician's Hospital,
2800 E. Ajo Way, Tucson, AZ 85713, USA
Corresponding author.
Paul Pisarik: paul-pisarik@...;
Dasha Kai: dasha456@...
Received January 2, 2009; Accepted August 25, 2009.
This is an Open Access article distributed under the terms of
the Creative Commons Attribution License
( http://creativecommons.org/licenses/by/3.0 ), which permits
unrestricted use, distribution, and reproduction in any
medium, provided the original work is properly cited.

Introduction

Aspartame was approved by the United States Food and
Drug Administration (FDA) in 1981 for use in dry products
such as breakfast cereal and as a tabletop sweetener [1].
Later in 1983 it was approved for use in sodas and in 1995
as a general sweetener in all foods and drinks.
Because of its very sweet taste, aspartame has been
extensively used as a food additive.
It is included in over 6000 products and consumed by
200 million people around the world [2].
Because of its ubiquity in our food supply, the FDA has
received many complaints over the years that allege that
aspartame was responsible for a myriad of consumers'
illnesses.

A PubMed search only shows only 14 case reports or case
series regarding potential aspartame toxicity.
The neurotoxic reactions reported include migraines,
carpal tunnel syndrome, a movement disorder of the arms
and legs, an orofacial sensitivity reaction, vertigo and ataxia,
and seizure and mania.
This will be the first paper to show a sensorineural hearing
loss temporally related to aspartame and the second to show
a vestibular toxicity temporally related to aspartame [3].

Case presentation

Case report 1

The first case was a 29-year-old white non-Hispanic female
nurse (one of the authors) who started experiencing nausea
and vomiting 3 weeks after conceiving her first pregnancy that
persisted throughout her pregnancy.
Her pregnancy was complicated with a 114-pound weight
gain and pre-eclampsia.
Her delivery was complicated with shoulder dystocia and
post partum hemorrhage.
After her delivery in January 1985, her symptoms got better
in that she only had nausea in the mornings that cleared by
1 or 2 P.M.
She also had headaches on awakening in the morning up to
3 days a week.

She was on no medications and had no allergies to
medications.
She denied use of alcohol, cigarettes, or any other drugs.
Her past medical history was significant for intermittent
hypertension.
She had multiple right eye surgeries for strabismus in the
early 1960s and a tonsillectomy and adenoidectomy in 1965.
She was 5 foot and 11 inches tall and weighed 165 lbs
prior to her pregnancy, 264 lbs just after her delivery that
decreased over the time to 180 lbs at time of her
self-diagnosis.

She went to see her physician in July 1985 with these
symptoms.
Her physician treated her with oral prochlorperazine and
meclizine;
however, these medications did not have much effect on her.

In January 1986, she again saw her physician with the same
complaints.
The neurological exam was normal except for showing a few
beats of nystagmus on lateral gaze.
She was again treated symptomatically with metoclopramide
and trimethobenzamide.
Over the next several months, the nausea progressed to
encompass the entire day along with some vomiting.
In addition, she was experiencing vertigo with motion and
lying in bed.

She saw her physician in June 1986 and was noted to have
nonfatiguing nystagmus on looking to the right.
She had audiologic testing that was normal but had an
electronystagmograph (ENG) that showed a direction-fixed
right-beating positional nystagmus of about six degrees.
She was referred to an otolaryngologist who noted a
positioning nystagmus consistent with the ENG that was
easily reproduced and persistent.
Radiographs of the internal auditory canals were normal.
Because of the persistence of her symptoms, she was then
referred to a neurologist.
He ordered a brainstem auditory evoked response test and
a magnetic resonance imaging scan of the brain, both of which
were normal.
His final diagnosis was a vestibular neuronitis versus a chronic
labyrinthitis and he gave her diazepam to take as needed.

Over the next two months, her symptoms got worse to where
she was experiencing problems with muscle coordination
manifested by occasionally not being able to negotiate
doorways and occasionally not being able to place a spoon
squarely in her mouth.

In September 1986, she read a doctor-advice column in the
local paper that mentioned aspartame was anecdotally
associated with nausea and headaches.
She had first begun to drink an aspartame-sweetened
drink -- Crystal Light (R) -- right after the birth of her son
and was drinking 16 to 32 ounces per day, sipping on it
throughout the day.
She made sure that she did not consume it during her
pregnancy.
After reading the article, she stopped drinking Crystal
Light (R), her only source of aspartame, and within a week,
she was symptom free.
About a month later, she challenged herself with 8 ounces of
Crystal Light (R) and within 1 to 2 hours started having
nausea, headaches, and vertigo that lasted for 48 hours.
About 3 to 4 weeks later she drank a 12-ounce can of  Diet
Pepsi (R) and within 1 hour started to have the exact same
symptoms, again lasting about 48 hours.
She had a recurrence of the symptoms two times after that,
each time after accidentally drinking a beverage with
aspartame in it.
After the last occurrence of her nausea, headaches, and
vertigo, she has since not consumed aspartame in any product
or form and has been symptom free for 22 years.

Primary diagnosis is a vestibular neuronitis versus chronic
labyrinthitis secondary to aspartame.
Secondary diagnosis is nausea and vomiting of pregnancy.

Case report 2

In January of 2002 at the age of 47, a non-Hispanic white
male physician (one of the authors and brother of case
report 1) had an intermittent right-sided tinnitus associated
with a hearing loss that would last 6-8 hours at a time.
In addition, at the same time, he had a 1.5 cm diameter area
of hypoesthesia in the region just anterior to the tragus of his
right ear.
He had noted a very minor right-sided hearing loss for at
least two years prior to this, but it would never last more
than for a few minutes, perhaps once a month, and he never
thought much about it.
There was no vertigo, nausea, headaches, or other
neurological symptoms associated with this.

He was 6' 3'' tall and weighed 180 pounds.
His past medical history was pertinent for benign prostatic
hypertrophy treated with finasteride since January 1998.
He had no allergies to medications.
He denied use of alcohol, cigarettes, or other drugs.
His past surgical history was pertinent for a tonsillectomy and
adenoidectomy in 1963 and an open reduction and internal
fixation of a comminuted left distal radius fracture in May of
2001 with subsequent removal of hardware in August of 2001.
Family history was pertinent for a sister 15 years earlier having
a vestibular neuronitis versus chronic labyrinthitis secondary to
aspartame.

Between January and August 5, 2002, he had five such prolonged episodes,
along with the episodes that lasted for a few minutes.
On August 5th, he woke up with one such episode that lasted
10 hours before it went away.
On August 8th, he had another episode that started at noon
and unlike his previous episodes, lasted three days with a
severe tinnitus and hearing loss.
He contacted an otolaryngologist and was started on
prednisone.
He had an audiogram on August 9th that showed a
right-sided high frequency sensorineural hearing loss
(see table 1).
By the time he saw the otolaryngologist on August 12th, the
hearing loss resolved clinically and another audiogram was
done and was much improved and similar to a previous
audiogram he had done in 1987, except for a remaining
35-decibel loss at 8000 Hertz (Hz) (see table 1).

At the time of his otolaryngologist appointment, his physical
exam was normal.
A magnetic resonance imaging scan of the brain with and
without gadolinium was normal.

Table 1

Hearing threshold levels in dB (re: ANSI-1969) of case
report 2 for each ear at different points in time

When the otolaryngologist did not have an explanation for his
symptoms, the patient remembered that his sister had the
adverse reaction to aspartame 15 years earlier.
Up until now, he had consumed foods with aspartame,
undeterred by his sister's experience.
At this time, he was consuming aspartame in the form of one
to two cans of Caffeine Free Diet Coke® along with a bowl
of Fiberall (R) cereal a day.
Thereafter he stopped consuming aspartame in any form.
Over the next two months, he had no more severe episodes
of tinnitus and hearing loss but did have two further episodes
of milder right-sided tinnitus and hearing loss (30% of prior
intensity) and only lasting 3-4 hours.

Thinking that it might not be due to aspartame, he drank a can
of Caffeine-free Diet Coke® a day for four days in a row.
On each of these days, he had a mild episode of right-sided
tinnitus and hearing loss for 2-3 hours each day.
He permanently stopped his aspartame consumption after that.
He had one milder episode of tinnitus and hearing loss a couple
of weeks after he finished his challenge.

Follow-up audiograms showed a slowly improving 8000 Hz
hearing loss:
November of 2002 showed only a 20 decibel loss compared
to 1987
and November of 2003 showed a 10 decibel loss compared
to 1987 (see table 1).

Primary diagnosis is tinnitus and sensorineural healing loss
secondary to aspartame.

Except for six mild reoccurrences of his symptoms within 24
hours of unintentionally consuming something with aspartame
(hypoesthesia anterior to the tragus and mild tinnitus) lasting
2-4 hours, he has been symptom free for over six years now.

Conclusion

Aspartame had a vestibulocochlear toxicity in a pair of siblings
suggesting an idiosyncratic genetic predisposition to aspartame
toxicity.
In addition, the cochlear toxicity in case report 2 took at least
15 months to clear after his cessation of aspartame use
suggesting that aspartame's cochlear toxicity can be long
lasting.

Patients with dizziness, vertigo, tinnitus, and hearing loss
present not only to otolaryngologists and neurologists, but
also to primary care clinicians frequently.
Even though the yield may be low, asking them about their
aspartame consumption and suggesting cessation of its use,
may prove helpful for some.

Abbreviations

ENG: electronystagmograph;
FDA: Food and Drug Administration.

Consent

Written informed consent was obtained from the patients for
publication of these case reports.
A copy of the written consent is available for review by the
Editor-in-Chief of this journal.

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

DK obtained copies of her medical records when her health
clinic closed down in the late 1980s and contributed both
subjective and objective findings to case report 1.
PP contributed to case report 2 and did the literature search.
All authors read and approved the final manuscript.

References

US FDA.
Artificial Sweeteners: No Calories ... Sweet!
FDA Consumer Magazine. July-August 2006.

Butchko HH, Stargel WW.
Aspartame: scientific evaluation in the postmarketing period.
Regul Toxicol Pharmacol. 2001;34:221-233.
doi: 10.1006/rtph.2001.1500. [PubMed]

Gulya AJ, Sessions RB, Troost TR.
Aspartame and dizziness: preliminary results of a prospective,
nonblinded, prevalence and attempted cross-over study.
Am J Otol. 1992;13:438-442. [PubMed]

Articles from Cases Journal are provided here courtesy of
BioMed Central
_______________________________________________


recent aspartame (methanol, formaldehyde, formic acid)
symptoms in English professor: Kristi Siegel:
Rich Murray 2010.04.17
http://rmforall.blogspot.com/2010_04_01_archive.htm
Saturday, April 17, 2010
http://groups.yahoo.com/group/aspartameNM/message/1599

"Shortly after seeing the ophthalmologist and about two
weeks or so into my Crystal Light regimen, I had my first
episode of vision loss. [ last week of January ]
This incident was completely different in degree and kind
than the normal visual problems (increased far-sightedness
and visual lability) I had been experiencing.
Rather abruptly, I lost the visual field of the left hemisphere
of my left eye.
The vision loss lasted for about 20 or 30 minutes and after
approximately 15 minutes, I started to develop a crushing
headache which lasted for hours.
I've never had a history of headaches, so the intensity and
duration of this headache was unusual."


formaldehyde from 11% methanol part of aspartame causes
severe allergic dermatitis in boy, JE Jacob et al,
Pediatric Dermatology 2009 Nov: Rich Murray 2010.03.30
http://rmforall.blogspot.com/2010_03_01_archive.htm
Tuesday, March 30, 2010
http://groups.yahoo.com/group/aspartameNM/message/1597

Pediatric  Dermatology. 2009 Nov-Dec;26(6):739-43.
Systematized contact dermatitis and montelukast in an atopic
boy.
Castanedo-Tardan MP,
González ME,
Connelly EA,
Giordano K,
Jacob SE.
University of Miami, Miller School of Medicine, Department
of Dermatology and Cutaneous Surgery, Miami, Florida,
USA.

Upon ingestion, the artificial sweetener, aspartame is
metabolized to formaldehyde in the body and has been
reportedly associated with systemic contact dermatitis in
patients exquisitely sensitive to formaldehyde.

We present a case of a 9-year-old Caucasian boy with a
history of mild atopic dermatitis that experienced severe
systematized dermatitis after being started on montelukast
chewable tablets containing aspartame.

Patch testing revealed multiple chemical sensitivities which
included a positive reaction to formaldehyde.

Notably, resolution of his systemic dermatitis only occurred
with discontinuation of the montelukast chewables.
PMID: 20199453

four Murray AspartameNM reviews in SE Jacob & SA
Stechschulte debate with EG Abegaz & RG Bursey of
Ajinomoto re migraines from formaldehyde from aspartame,
Dermatitis 2009 May: TE Hugli -- folic acid with V-C
protects: Rich Murray 2009.08.12
http://rmforall.blogspot.com/2009_08_01_archive.htm
Wednesday, August 12, 2009
http://groups.yahoo.com/group/aspartameNM/message/1582
[ extracts ]


Formaldehyde, aspartame, migraines: a possible connection.
Abegaz EG, Bursey RG.
Dermatitis. 2009 May-Jun;20(3):176-7; author reply 177-9.
No abstract available. PMID: 19470307

Eyassu G. Abegaz *
Robert G. Bursey
Ajinomoto Corporate Services LLC, Scientific & Regulatory
Affairs, 1120 Connecticut Ave., N.W., Suite 1010,
Washington, DC 20036
* Corresponding author. Tel.: +1 202 457 0284;
fax: +1 202 457 0107.
abegazee@... (E.G. Abegaz),
burseyb@... (R.G. Bursey)

"For example, fruit juices, coffee, and alcoholic beverages
produce significantly greater quantities of formaldehyde than
aspartame-containing products. [6]"

"[6] Magnuson BA, Burdock GA, Doull J, et al. Aspartame:
a safety evaluation based on current use levels, regulations,
and toxicological and epidemiological studies.
Crit Rev Toxicol 2007;37:629-727"

[ 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." ]


http://www.medscape.com/viewarticle/579335

Dermatitis. 2008; 19(3): E10-E11.
© 2008  American Contact Dermatitis Society
Formaldehyde, Aspartame, and Migraines:
A Possible Connection
Sharon E. Jacob; Sarah Stechschulte
Published: 09/17/2008
[ Extract ]

Abstract

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.

Case Series

Six patients (ages 16 to 75 years) were referred for evaluation
of recalcitrant dermatitis. By history, five of the patients were
noted  to have developed migraines following aspartame
consumption; the sixth reported dermatitis flares associated
with diet cola consumption of >2 liters/day.

All six patients had current environmental exposures to
formaldehyde or formaldehyde-releasing preservatives in
their personal hygiene products and/or regular consumption
of "sugar-free food" artificially sweetened with aspartame.

Based on their histories and clinical presentations, these
patients were patch-tested with the North American Contact
Dermatitis Group 65-allergen Standard Screening Series and
selected chemicals from the University of Miami vehicle,
fragrance, bakery, and textile trays.

All six patients had positive reactions to formaldehyde, and
four had additional positive reactions to
formaldehyde-releasing preservatives (FRPs).
Expert counseling on allergen avoidance (including avoidance
of formaldehyde, FRPs, and aspartame) and alternative
product recommendations were provided to the patients.

At their follow-up appointments (between 8 and 12 weeks),
all the patients showed clearance of their dermatitis. Four
patients (two inadvertently) resumed their consumption of
aspartame and subsequently returned for an additional
follow-up visit. Three of the first five patients had recurrences
of both their migraines and their dermatitis; the sixth patient
(who had no migraines) had a positive rechallenge dermatitis.
These four patients were again counseled on avoidance
regimen.

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

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@...;
Sarah A. Stechschulte, BA  sstechschulte@...


methanol (11% of aspartame), made by body into
formaldehyde in many vulnerable tissues, causes modern
diseases of civilization, summary of a century of research,
Woodrow C Monte PhD, Medical Hypotheses journal:
Rich Murray 2009.11.15
http://rmforall.blogspot.com/2009_11_01_archive.htm
Sunday, November 15, 2009
http://groups.yahoo.com/group/aspartameNM/message/1589
_______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298  rmforall@...

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 145 members, 1,600 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1218 members, 24,060 posts in a public archive
_______________________________________________

Woodrow C Monte, PhD, Emiritus Prof. Nutrition gives many PDFs of reseach --
methanol (11% of aspartame) puts formaldehyde into brain and body --
multiple sclerosis, Alzheimer's, cancers, birth defects, headaches: Rich
Murray 2010.05.13
http://rmforall.blogspot.com/2010_05_01_archive.htm
Thursday, May 13, 2010
http://groups.yahoo.com/group/aspartameNM/message/1601
_______________________________________________


[ Other formaldehyde sources include alcohol drinks and
tobacco and wood smoke,
while adequate folic acid levels protect most people. ]


As well as extensive free websites with full texts and videos,
he offers a  $24 145' DVD of a lively talk at the Southland MS
Society of New Zealand, March 29-30, 2009, and soon his
new book, "While Science Sleeps".

http://www.amazon.com/Solving-Mystery-Multiple-Sclerosis-Poisoning/dp/B003L783I0\
/ref=pd_rhf_p_t_1

$24 145' Format NTSC DVD ASIN: B003L783I0

http://whilesciencesleeps.com/about

Curriculum Vitae, publications, photos

http://whilesciencesleeps.com/references

589 references

http://thetruthaboutstuff.com/index.shtml
[ German and Dutch also available ]

http://thetruthaboutstuff.com/news.shtml

http://thetruthaboutstuff.com/videos.shtml

http://thetruthaboutstuff.com/radio.shtml

http://thetruthaboutstuff.com/review1.shtml

http://thetruthaboutstuff.com/listener.shtml

http://thetruthaboutstuff.com/articles.shtml
223 references with abstracts or full and partial texts

http://whilesciencesleeps.com/montediet

Methanol: Where Is It Found? How Can It Be Avoided?

AVOID the following, ranked in order of greatest danger:

1. Cigarettes.
2. Diet foods and drinks with aspartame.
3. Fruit and vegetable products and their juices in bottles,
cans, or pouches.
4. Jellies, jams, and marmalades not made fresh and kept
refrigerated.
5. Black currant and tomato juice products, fresh or
processed.
6. Tomato sauces, unless first simmered at least 3 hours
with an open lid.
7. Smoked food of any kind, particularly fish and meat.
8. Sugar-free chewing gum.
9. Slivovitz: You can consume one alcoholic drink a day
on this diet -- no more! [ no fruit brandies ]
10. Overly ripe or near rotting fruits or vegetables.


Selection from Article 2, Fitness Life, December 2007, and
well discussed in the DVD video:

"Identical Symptoms of MS, Methanol Poisoning
and Aspartame Toxicity

The symptoms of multiple sclerosis (44, 83, 85, 169), chronic
and acute methanol poisoning (13, 144, 189), and Aspartame
toxicity (54, 58, 93, 181), are in all ways identical.

There is nothing that happens to the human body from the toxic
effect of methanol that has not been expressed during the
course of MS... nothing (143, 144).

This generalization extends even to the remarkable
opthomological conditions common to both: transitory optic
neuritis and retrolaminar demyelinating optic neuropathy with
scotoma of the central visual field (which occasionally
manifests as unilateral temporary blindness (85, 138, 163).

In fact, these opthomological symptoms have been thought of
for years in their respective literatures to be "tell tale"
indications for the differential diagnosis for each of these
maladies independently (85, 138, 148, 163, 169).

The common symptoms of
headache (13, 83, 181, 189),
nervousness (13, 83, 181),
depression (58, 83, 189, 181),
memory loss (18, 147, 85, 169, 181),
tingling sensations (13, 85, 168, 138, 169),
pain in the extremities (13, 85, 169),
optic neuritis (85, 138, 148, 163, 169),
bright lights in the visual field (139, 83),
seizures (21, 83, 160),
inability to urinate or to keep from urinating (139, 146, 167)
are all shared by each of these conditions and shared yet again
by complaints from aspartame poisoning (54, 58, 93, 181).

I take these strikingly similar symptom patterns as evidence
that these disorders act on identical components of the central
nervous system and in the same way.

The "Miracle" that MS shares with Methanol poisoning

In the early stages of MS, or when a non-lethal dose of
methanol has been administered, complete recovery is a
possibility.

The only two afflictions for which such dramatic "remissions"
are reported from identical neuromuscular and opthomological
damage, even "blindness" is relapsing-remitting multiple
sclerosis (85) and methyl alcohol poisoning (138, 163).

The pathology of the two maladies is in may ways identical,
particularly when it comes to destruction of the myelin sheath
with no harm to the axon itself (18, 148, 176).

Sex Ratios for MS and Aspartame Reactions

Women bear the brunt of multiple sclerosis (91a-c) and lupus
(SLE)(73) with fully three-fold representations in infliction
numbers over men for both diseases.

This is exactly the proportion represented by adverse reactors
to Aspartame reported by the US Center for Disease Control
in their study of 1984(58).

The Center found three women to every man whose
Aspartame consumption complaints were serious enough to
warrant investigation (93).

Although the female/male ratio for those stricken with MS has
always been high, recent estimates place it at over 3 to 1
(91, 91a, 91c).

What might account for the difference across sexes in
incidence?

A study published in the New England Journal of Medicine
(94) reports biopsies of the gastric lining of men and women.

A result was that the concentration of ADH in the gastric lining
of men was much higher than for woman.

Men have the advantage of removing methanol from the
bloodstream four times faster on an equal-body-size basis
than women.

Thus, for men, methanol is more likely to be removed from the
blood before it reaches the brain.

The brain is spared but the methanol removed would still be
metabolized to formaldehyde in the gut where it would reap its
havoc on a more forgiving organ.

This may help explain why men have more gastrointestinal
complaints from both methanol and Aspartame consumption
(93, 99).

On the other hand, women's complaints from both more
frequently involve serious neurological complications."

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://groups.yahoo.com/group/aspartameNM/message/1498

Monte WC., Is your Diet Sweetener killing you?
Fitness Life. 2007 Nov; 33: 31-33.
Monte WC., A Deadly Experiment.
Fitness Life. 2007 Dec; 34: 38-42.
Monte WC., Bittersweet: Aspartame Breast Cancer Link.
Fitness Life. 2008 Feb; 34: 21-22.

Article 1 http://www.thetruthaboutstuff.com/review1.shtml
Article 2 http://www.thetruthaboutstuff.com/review2.shtml
Article 3 http://www.thetruthaboutstuff.com/review3.shtml

http://www.thetruthaboutstuff.com/articles.shtml
223 references with abstracts or full and partial texts


methanol (11% of aspartame), made by body into
formaldehyde in many vulnerable tissues, causes modern
diseases of civilization, summary of a century of research,
Woodrow C Monte PhD, Medical Hypotheses journal:
Rich Murray 2009.11.15
http://rmforall.blogspot.com/2009_11_01_archive.htm
Sunday, November 15, 2009
http://groups.yahoo.com/group/aspartameNM/message/1589

Methanol: A Chemical Trojan Horse as the Root of the
Inscrutable U, Prepublication Copy; Medical Hypotheses
-- 06 November 2009 (10.1016/j.mehy.2009.09.059)
http://www.medical-hypotheses.com/article/S0306-9877(09)00693-8/abstract
Woodrow C. Monte PhD
Professor of Food Science (retired)
Arizona State University
corresponding author : Woodrow C. Monte PhD
470 South Rainbow Drive
Page, Arizona 86040
Key Words:
food epidemiology; diseases of civilization; methanol;
formaldehyde; aspartame; autism; multiple sclerosis; Alzheimer's;
U-shaped curve.

Abstract:

Until 200 years ago, methanol was an extremely rare
component of the human diet and is still rarely consumed in
contemporary hunter and gatherer cultures.
With the invention of canning in the 1800s, canned and
bottled fruits and vegetables, whose methanol content greatly
exceeds that of' their fresh counterparts, became far more
prevalent.
The recent dietary introduction of aspartame, an artificial
sweetener, 11% methanol by weight, has also greatly
increased methanol consumption.
Moreover, methanol is a major component of cigarette
smoke, known to be a causative agent of many diseases of
civilization (DOC).
Conversion to formaldehyde in organs other than the liver is
the principal means by which methanol may cause disease.
The known sites of class I alcohol dehydrogenase (ADH I),
the only human enzyme capable of metabolizing methanol to
formaldehyde, correspond to the sites of origin for many DOC.
Variability in sensitivity to exogenous methanol consumption
may be accounted for in part by the presence of aldehyde
dehydrogenase sufficient to reduce the toxic effect of
formaldehyde production in tissue through its conversion to
the much less toxic formic acid.
The consumption or endogenous production of small amounts
of ethanol, which acts as a competitive inhibitor of methanol's
conversion to formaldehyde by ADH I, may afford some
individuals protection from DOC.


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


http://groups.yahoo.com/group/aspartameNM/message/870
Aspartame: Methanol and the Public Interest 1984: Monte:
Murray 2002.09.23

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, 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)."
_______________________________________________



"For both, subsequent intentional challenges with aspartame
and unintentional exposures brought back each of their
respective symptoms."

"After the last occurrence of her nausea, headaches, and
vertigo, she has since not consumed aspartame in any product
or form and has been symptom free for 22 years."

"Except for six mild reoccurrences of his symptoms within 24
hours of unintentionally consuming something with aspartame
(hypoesthesia anterior to the tragus and mild tinnitus) lasting
2-4 hours, he has been symptom free for over six years now."

Cases J. 2009 Sep 15; 2: 9237.
Vestibulocochlear toxicity in a pair of siblings 15 years apart
secondary to aspartame: two case reports.
Pisarik P, Kai D.
University of Oklahoma College of Medicine, Tulsa,
1111 S. St. Louis Ave. Tulsa, OK 74120-5440, USA.

Vestibulocochlear toxicity in a pair of siblings [doctor & nurse]
15 years apart secondary to aspartame: two case reports,
Paul Pisarik & Dasha Kai, Cases J 2009.09.15 free full text:
Rich Murray 2010.05.04
http://rmforall.blogspot.com/2010_05_01_archive.htm
Tuesday, May 4, 2010
http://groups.yahoo.com/group/aspartameNM/message/1600



"Shortly after seeing the ophthalmologist and about two
weeks or so into my Crystal Light regimen, I had my first
episode of vision loss. [ last week of January ]
This incident was completely different in degree and kind
than the normal visual problems (increased far-sightedness
and visual lability) I had been experiencing.
Rather abruptly, I lost the visual field of the left hemisphere
of my left eye.
The vision loss lasted for about 20 or 30 minutes and after
approximately 15 minutes, I started to develop a crushing
headache which lasted for hours.
I've never had a history of headaches, so the intensity and
duration of this headache was unusual."

recent aspartame (methanol, formaldehyde, formic acid)
symptoms in English professor: Kristi Siegel:
Rich Murray 2010.04.17
http://rmforall.blogspot.com/2010_04_01_archive.htm
Saturday, April 17, 2010
http://groups.yahoo.com/group/aspartameNM/message/1599


formaldehyde from 11% methanol part of aspartame causes
severe allergic dermatitis in boy, JE Jacob et al,
Pediatric Dermatology 2009 Nov: Rich Murray 2010.03.30
http://rmforall.blogspot.com/2010_03_01_archive.htm
Tuesday, March 30, 2010
http://groups.yahoo.com/group/aspartameNM/message/1597


http://while-science-sleeps.com/references/pdf/247

42 PDF images of media articles since 1974 -- page 2 is
Donnell Alexander, NZ Registered Dietitian,
consultant dietitian to Coca-Cola Oceania,
defends aspartame in Fitness Life,
1 page letter 2009.01.21
http://www.networkpr.co.nz/about-us/our-people/
Donnell (female) is on the national executive of Dietitians NZ,
sits on the Nutrition Society of NZ registration panel, belongs
to the FCG Health and Technical Working Group and is a
member of the New Zealand Institute of Food Science and
Technology, the New Zealand Nutrition Foundation and the
New Zealand Guild of Food Writers.
info@...;  (+ 64 9) 379 3154
(+ 64 4) 460 6610
donnell.alexander@...;  09 306 5806

http://whilesciencesleeps.com/files/stoler_kp_2009_the_research_behind_aspartame\
_fitness_life_vol_42_45.pdf

detailed critique of industry deceit re Donnell letter, 4 pages,
Kenneth P Stoller, MD, medical director,
Hyperbaric Medical Center of New Mexico, Santa Fe
www.hbotnm.com


four Murray AspartameNM reviews in SE Jacob & SA
Stechschulte debate with EG Abegaz & RG Bursey of
Ajinomoto re migraines from formaldehyde from aspartame,
Dermatitis 2009 May: TE Hugli -- folic acid with V-C
protects: Rich Murray 2009.08.12
http://rmforall.blogspot.com/2009_08_01_archive.htm
Wednesday, August 12, 2009
http://groups.yahoo.com/group/aspartameNM/message/1582
[ extracts ]

Formaldehyde, aspartame, migraines: a possible connection.
Abegaz EG, Bursey RG.
Dermatitis. 2009 May-Jun;20(3):176-7; author reply 177-9.
No abstract available. PMID: 19470307

Eyassu G. Abegaz *
Robert G. Bursey
Ajinomoto Corporate Services LLC, Scientific & Regulatory
Affairs, 1120 Connecticut Ave., N.W., Suite 1010,
Washington, DC 20036
* Corresponding author. Tel.: +1 202 457 0284;
fax: +1 202 457 0107.
abegazee@...; (E.G. Abegaz),
burseyb@...; (R.G. Bursey)

"For example, fruit juices, coffee, and alcoholic beverages
produce significantly greater quantities of formaldehyde than
aspartame-containing products. [6]"

"[6] Magnuson BA, Burdock GA, Doull J, et al. Aspartame:
a safety evaluation based on current use levels, regulations,
and toxicological and epidemiological studies.
Crit Rev Toxicol 2007;37:629-727"

[ 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." ]
_______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298  rmforall@...

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 146 members, 1,601 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1219 members, 24,062 posts in a public archive
_______________________________________________

fructose, aspartame, caramel in soft drinks and nonalcoholic fatty liver
disease, W Nseir, F Nassar, N Assy, World J Gastroenterol: Rich Murray
2010.06.07
http://rmforall.blogspot.com/2010_06_01_archive.htm
Monday, June 7, 2010
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1602
[ You may have to Copy and Paste URLs into your browser ]
_______________________________________________


"During regular soft drinks consumption, fat accumulates in the
liver by the primary effect of fructose which increases
lipogenesis, and in the case of diet soft drinks, by the
additional contribution of aspartame sweetener and
caramel colorant which are rich in advanced glycation end
products that potentially increase insulin resistance and
inflammation." 2010.06.07


"From our study, it seems that fructose is not the only risk
factor of liver disease, because 40% of our cohort were
drinking Diet Coke sweetened with aspartame.

Aspartame is absorbed from the intestine and metabolized
by the liver to form phenylalanine, aspartic acid and methanol.
This process causes mitochondrial dysfunction and ATP
depletion, which contribute to accumulation of fat (29).

Also, regarding obesity and aspartame, formaldehyde
converted from the free methyl alcohol accumulates in the
cells and damages mitochondrial DNA, with most toxicity
effects occurring in the liver.

Finally, the effect of caramel colourant has been incriminated
as a cause of elevated liver enzymes and may be a potential
source of advanced glycation end product, which may
promote insulin resistance and can be proinflammatory
(5,6,20)."  2008 October

"29. Trocho C, Pardo R, Rafecas I, et al.
Formaldehyde derived from dietary aspartame binds to tissue
components in vivo.
Life Sci. 1998; 63: 337-49.  [PubMed]"

[ See also:

Woodrow C Monte, PhD, Emiritus Prof. Nutrition gives
many PDFs of reseach -- methanol (11% of aspartame) puts
formaldehyde into brain and body -- multiple sclerosis,
Alzheimer's, cancers, birth defects, headaches:
Rich Murray 2010.05.13
http://rmforall.blogspot.com/2010_05_01_archive.htm
Thursday, May 13, 2010
http://groups.yahoo.com/group/aspartameNM/message/1601

( Other formaldehyde sources include alcohol drinks and
tobacco and wood smoke.
Adequate folic acid levels protect most people from some
harm, but not for the brain and retinas.) ]


World J Gastroenterol. 2010 Jun 7; 16(21): 2579-88.
Soft drinks consumption and nonalcoholic fatty liver disease.
Nseir W, w.nseir@...;
Nassar F,
Assy N. assy.n@...;

Abstract

Nonalcoholic fatty liver disease (NAFLD) is a common
clinical condition which is associated with metabolic syndrome
in 70% of cases.

Inappropriate dietary fat intake, excessive intake of soft
drinks, insulin resistance and increased oxidative stress
combine to increase free fatty acid delivery to the liver, and
increased hepatic triglyceride accumulation contributes to
fatty liver.

Regular soft drinks have high fructose corn syrup which
contains basic sugar building blocks, fructose 55% and
glucose 45%.

Soft drinks are the leading source of added sugar worldwide,
and have been linked to obesity, diabetes, and metabolic
syndrome.

The consumption of soft drinks can increase the prevalence of
NAFLD independently of metabolic syndrome.

During regular soft drinks consumption, fat accumulates in the
liver by the primary effect of fructose which increases
lipogenesis, and in the case of diet soft drinks, by the
additional contribution of aspartame sweetener and caramel
colorant which are rich in advanced glycation end products
that potentially increase insulin resistance and inflammation.

This review emphasizes some hard facts about soft drinks,
reviews fructose metabolism, and explains how fructose
contributes to the development of obesity, diabetes,
metabolic syndrome, and NAFLD.  PMID: 2051807


J Hepatol. 2009 Nov; 51(5): 918-24. Epub 2009 Aug 21.
Soft drink consumption is associated with fatty liver disease
independent of metabolic syndrome.
Abid A,
Taha O,
Nseir W,
Farah R,
Grosovski M,
Assy N.
Liver Unit, Ziv Medical Center, Safed, Israel.
Comment in:
J Hepatol. 2010 Jun;52(6):954; author reply 954.

Abstract

BACKGROUND/AIMS:
The independent role of soft drink consumption in
non-alcoholic fatty liver disease (NAFLD) patients remains
unclear.
We aimed to assess the association between consumption of
soft drinks and fatty liver in patients with or without metabolic
syndrome.
METHODS:
We recruited 31 patients (age: 43+/-12 years) with NAFLD
and risk factors for metabolic syndrome,
29 patients with NAFLD and without risk factors for
metabolic syndrome, and
30 gender- and age-matched individuals without NAFLD.
The degree of fatty infiltration was measured by ultrasound.
Data on physical activity and intake of food and soft drinks
were collected during two 7-day periods over 6 months
using a food questionnaire.
Insulin resistance, inflammation, and oxidant-antioxidant
markers were measured.
RESULTS:
We found that 80% of patients with NAFLD had excessive
intake of soft drink beverages (>500 cm(3)/day) compared to
17% of healthy controls (p<0.001).
The NAFLD group consumed five times more carbohydrates
from soft drinks compared to healthy controls
(40% vs. 8%, p<0.001).
Seven percent of patients consumed one soft drink per day,
55% consumed two or three soft drinks per day, and
38% consumed more than four soft drinks per day for most
days and for the 6-month period.

The most common soft drinks were Coca-Cola
(regular: 32%; diet: 21%)
followed by fruit juices (47%).

Patients with NAFLD with metabolic syndrome had similar
malonyldialdehyde, paraoxonase, and C-reactive protein
(CRP) levels but higher homeostasis model assessment
(HOMA) and higher ferritin than NAFLD patients without
metabolic syndrome
(HOMA: 8.3+/-8 vs. 3.7+/-3.7 mg/dL, p<0.001;
ferritin: 186+/-192 vs. 87+/-84 mg/dL, p<0.01).
Logistic regression analysis showed that soft drink
consumption is a strong predictor of fatty liver
(odds ratio: 2.0; p<0.04) independent of metabolic syndrome
and CRP level.
CONCLUSIONS:
NAFLD patients display higher soft drink consumption
independent of metabolic syndrome diagnosis.
These findings might optimize NAFLD risk stratification.
PMID: 19765850


http://www.ncbi.nlm.nih.gov/pubmed/18925303

Can J Gastroenterol. 2008 Oct; 22(10): 811-6.
Soft drink consumption linked with fatty liver in the absence
of traditiona risk factors.
Assy N, Nasser G, Kamayse I, Nseir W, Beniashvili Z,
Djibre A, Grosovski M.
Liver Unit, Ziv Medical Center, Safed, Israel.
assy.n@...

Abstract

BACKGROUND:
Little is known about dietary habits and their relationships
with liver disease in nonalcoholic fatty liver disease (NAFLD)
patients, particularly in the absence of obesity, diabetes or
hyperlipidemia.
OBJECTIVE:
To assess the association between soft drink consumption and
the presence of fatty liver in NAFLD patients who do not have
classic risk factors.
METHODS:
Three hundred ten patients with NAFLD diagnosed by
ultrasound were assessed for 36 months in a cross-sectional
manner.
Thirty-one patients (10%) who had NAFLD without classic
risk factors were compared with 30 healthy controls.
Physical activity was assessed during the preceding week and
year, and every six months for 36 months.
Data on daily dietary intake of food and soft drink, and the
source of added sugar were collected during two seven-day
periods, at the beginning of the study, and within two weeks
after the metabolic tests by using a validated
food questionnaire given by a trained dietician.
Insulin resistance and lipid peroxidation were assessed by
homeostasis model assessment-insulin resistance index
(HOMA-IRI) and malondialdehyde (MDA) levels,
respectively.
RESULTS:
Eighty per cent of patients (25 of 31) consumed an excessive
amount of soft drink beverages (more than 50 g/day of added
sugar) for 36 months, compared with
20% in healthy controls (P<0.001).
Twenty per cent of patients consumed one drink per day,
40% consumed two to three drinks per day, and
40% consumed more than four drinks per day for most days
during 36 months.

The most common soft drinks consumed were
regular Coca-Cola (40% of patients), Diet Coke (40%)
and flavoured fruit juices (20%).

Ultrasound findings revealed
mild fatty liver in 44% of cases (n=14),
moderate fatty liver in 38% (n=12), and
severe fatty liver in 18% (n=5).
HOMA-IRI and MDA levels were significantly higher in
patients with NAFLD than in healthy controls
(HOMA-IRI, 3.7 versus 1.7, P<0.001; and
MDA, 420+/-300 micromol/mL
versus 200+/-100 micromol/mL; P<0.001).

When controlled for other factors, including dietary
composition and physical activity, soft drink beverage
consumption was the only independent variable that was able
to predict the presence of fatty liver in 82.5% of cases with a
sensitivity of 100%, a specificity of 76%, a positive predictive
value of 57% and a negative predictive value of 100%.

CONCLUSION:
The present study may add important insight into the role of
sugar-sweetened beverage consumption as a cause of fatty
liver in patients without risk factors.
Patients are encouraged to change their long-standing
drinking behaviour.  PMID: 18925303

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661299/?tool=pubmed
free full text

Nimer Assy, MD, 1,2
Gattas Nasser, MD, 3
Iad Kamayse, MD, 4
William Nseir, MD, 5
Zaza Beniashvili, MD, 1
Agness Djibre, MD, 1
and Maria Grosovski, PhD 6
1 Liver Unit, Ziv Medical Center, Safed, Israel
2  Rappaport Faculty of Medicine, Technion -- Israel
Institute of Technology, Haifa, Israel
3 Department of Internal Medicine,
Western Galilee Hospital, Nahariya, Israel
4 Liver Unit, Rambam Medical Center, Haifa, Israel
5 Department of Internal Medicine,
Holy Family Hospital, Nazareth, Israel
6 Department of Biotechnology,
ORT Braude College, Karmiel, Israel
Correspondence: Dr Nimer Assy, Liver Unit,
Ziv Medical Center, PO Box 1008, Safed 13100, Israel.
Telephone 9-724-682-8441, fax 9-724-682-8442, e-mail
assy.n@...; or ; Email: assy.nimer@...;
Received February 13, 2008; Accepted June 4, 2008.

[ selections ]

Normally, less than 5% of the liver is fat by weight, but in
patients with nonalcoholic steatohepatitis (NASH), as much
as 50% to 80% of liver weight may be made up of fat,
mostly in the form of triglycerides (1).
The clinical implications of NASH are derived mostly from its
common occurrence in the general population (10% to 24%)
and its potential to progress to fibrosis (30% to 40%),
cirrhosis (20% to 30%) and hepatocellular carcinoma (2,3).
NASH is the most common cause of cryptogenic cirrhosis
and is an increasingly common indication for liver
transplantation (3).
Nonalcoholic fatty liver disease (NAFLD) is one of the most
important emerging health care issues, and obesity, type 2
diabetes mellitus and hyperlipidemia are conditions frequently
associated with NAFLD (1,2).
However, patients without traditional risk factors have also
been reported to have fatty infiltration of the liver (3).
Identifying new risk factors that permit early diagnosis and
treatment are warranted.

Soft drinks are the leading cause of added sugar in the diet
worldwide.
Recent evidence suggests that sugar-sweetened soft drink
consumption is associated with the risk of obesity and
diabetes because they contain large amounts of high-fructose
corn syrup (HFCS), which raises blood glucose similarly to
sucrose (4).

In addition, soft drinks contain caramel colouring, which is rich
in advanced glycation end products that might increase insulin
resistance and inflammation (4-6).

The intake of nutrients (including sweetened beverages) may
affect insulin resistance, carbohydrate and lipid metabolism,
and hepatic steatosis, yet many other factors may actually play
a role (4).

However, there are few published reports on the intake of
various nutrients in patients with NAFLD.

Recently, it has been reported that patients with fatty liver
consume more simple carbohydrates and less saturated fat
than those in the general population, suggesting that
imbalanced diets play important roles in the development and
progression of NAFLD, and that correction of these diets may
be necessary (7).
High-fructose diets have induced fatty liver in rats and
ducks (8).
Such diets have also caused increases in hepatic lipid
peroxidation and activation of inflammatory pathways in the
liver of rats (9).
Fructose consumption can cause progressive liver disease in
humans, which is demonstrated by the inborn error of
metabolism known as hereditary fructose intolerance.
Aldolase B is a rare disease that results from a deficiency of
the fructose metabolizing enzyme (10).
The extent to which excessive fructose might contribute to the
high prevalence of NAFLD in western societies has not been
systematically investigated.

More recently, soft drink consumption has been linked with
obesity and has been shown to increase the risk of the
metabolic syndrome.

Individuals consuming more than one soft drink per day had
a higher prevalence of the metabolic syndrome than those
consuming less than one drink per day.

Whether soft drink consumption is linked with NAFLD has
not been assessed (11).

The aim of the present study was to assess the association
between soft drink consumption and the presence of fatty
liver by comparing NAFLD patients with no classic risk
factors with age-matched, healthy controls.....

Discussion

The present study compared dietary constituents, physical
activity and liver ultrasound in patients with fatty liver.
We found that NAFLD patients without classic risk factors
consume more soft drinks and juices than healthy controls.
The follow-up data, the correlation between severity of fatty
liver and amount of soft drink consumption, and the fact that
soft drink consumption was the only independent predictor of
fatty liver support the association between soft drink
consumption and fatty liver.
As expected, insulin resistance (HOMA-IRI) and MDA levels
were higher in the group with fatty liver.
However, when controlled for other factors, soft drink
beverage consumption was the only independent variable that
correctly predicted the presence of fatty liver.

The underlying mechanism for this association remains
unknown.
Soft drink consumption is the leading cause of added sugar in
the diet (1 tsp of sugar contains 4.2 g) (17).
Individuals who consume an excessive amount of soft drinks
tend to lead a sedentary lifestyle and eat a higher calorie diet
(an additional 150 kcal/day to 300 kcal/day) that includes
more fructose (18).

Because both regular Coca-Cola and Diet Coke consumption
in our study resulted in an increased risk of fatty liver, factors
other than calories and sugar content likely contribute to the
higher risk.

These factors include the consumption of fructose, aspartame,
caramel (food colourant) and other covariants.

These complexes of sugars and colourants may promote
insulin resistance, lipid peroxidation and hepatic inflammation,
and are a source of glycation end products (5,19,20).

The extent to which excessive fructose, aspartame and
caramel consumption might contribute to the high prevalence
of liver disease in western societies and to the progression of
NAFLD to NASH has not been investigated.

One study of lean women found that four days of overfeeding
with sucrose (glucose plus fructose) drink increased de novo
lipogenesis by 200% to 300% (21).

Another feeding study showed that two days of a
high-fructose diet (30% of the total energy consumed per day,
consumed as a sweetened beverage at every meal) resulted
in decreased postprandial glucose concentration and insulin
response, and prolonged alimentary lipemia in women (22).

Another follow-up study indicated that both surplus calories
and excessive sucrose consumption play a role in the rise of
liver enzyme levels (23).

Additional evidence that fructose can cause steatohepatitis is
that intravenous administration of fructose to healthy volunteers
has resulted in a 75% decrease in hepatic ATP within 10 min
because the liver was overwhelmed and could not metabolize
it (24).

Fructose can also increase triglyceride levels, de novo
synthesis of fatty acids, hyperuricemia and insulin resistance
(25).
The triglyceride response to fructose ingestion appears to
depend on whether a person is carbohydrate-sensitive or
insulin-resistant (26).

Fructose, especially high-fructose corn syrup, is now used
extensively in carbonated beverages and other sweetened
drinks, baked goods, candies, canned fruits, sodas, jams,
jellies and dairy products (27).

After absorption in the small bowel, fructose is transported
via the portal vein to the liver, where it is metabolized by
fructokinase to fructose-1-phosphate.
This molecule is cleaved by aldolase to form glycerone
phosphate and glyceraldehyde-3-phosphate, both of which
can be further metabolized in the glycolytic pathway (28).
An increase in serum triglycerides and, ultimately, increased
low-density lipoprotein cholesterol concentration may result
from enhanced fatty acid synthesis, increased esterification
of fatty acids and increased very low-density lipoprotein
secretion (28).

A soft drink containing 32.6 g of fructose could increase the
fasting serum fructose fourfold.
A 340 g soft drink sweetened with fructose-55 contains
approximately 40 g of the sweetener (ie, 22 g of fructose and
17 g of glucose, representing a fructose excess of 5 g per can)
(20,29).

Fructose affects each of the three major factors that are
believed to contribute to the pathogenesis of diabetic end
organ damage.
These factors are glycosylation of tissue proteins, intracellular
accumulation of sorbitol and oxidative stress (4).
The association between the consumption of beverages
sweetened with sugars such as HFCS and the risk of diabetes
has been established by Schultze et al (20).


From our study, it seems that fructose is not the only risk
factor of liver disease, because 40% of our cohort were
drinking Diet Coke sweetened with aspartame.

Aspartame is absorbed from the intestine and metabolized
by the liver to form phenylalanine, aspartic acid and methanol.
This process causes mitochondrial dysfunction and ATP
depletion, which contribute to accumulation of fat (29).

Also, regarding obesity and aspartame, formaldehyde
converted from the free methyl alcohol accumulates in the
cells and damages mitochondrial DNA, with most toxicity
effects occurring in the liver.

Finally, the effect of caramel colourant has been incriminated
as a cause of elevated liver enzymes and may be a potential
source of advanced glycation end product, which may
promote insulin resistance and can be proinflammatory
(5,6,20).

The extent to which fructose, aspartame and caramel
contributed to severe fatty liver could not be concluded
due to the small size of the cohort.


When controlled for other factors, including dietary
composition and physical activity, soft drink beverage
consumption was the only independent variable that could
correctly classify the presence of fatty infiltration of the liver.

A study by Vartanian et al (30) showed a clear association
among soft drink intake, diabetes and the metabolic
syndrome, confirming our finding.

Although we still do not know the most common soft drink
that induces fatty liver, fructose, caramel and aspartame
constituents may have a role.
These coingestants might also increase the risk for fatty
liver because of their high amount of rapidly absorbable
carbohydrates (20).

They contain a large amount of HFCS, which has a similar
effect on blood glucose as sucrose (31).
The consumption of sugar-sweetened soft drinks therefore
induces a fast and dramatic increase in both glucose and
insulin concentration (32).
In addition, cola-type soft drink caramel colouring is rich
in advanced glycation end products, which may increase
insulin resistance and inflammation (6,33).

The US Food and Drug Administration has established
51 mg of aspartame and 200 mg of caramel colouring
per kg body weight as an acceptable daily intake.

The natural history of NAFLD is not known.
The present study may add important insight into the role of
sugar-sweetened beverage consumption as a cause of fatty
liver in those without risk factors.
The time from NAFLD diagnosis to enrolment in the study
was less than two weeks.
Therefore, the information obtained for dietary food
consumption was a good reflection of the patient's dietary
habits before the diagnosis of NAFLD.....

CONCLUSIONS

Although more studies are needed, the findings of the present
study suggest that soft drink consumption is the most
common risk factor for fatty infiltration of the liver in
patients without classic risk factors.
Patients are encouraged to change their longstanding
drinking behaviour.
Whether consumption of soft drinks contributes to the
progression of simple fatty liver to steatohepatitis in
patients with metabolic syndrome is yet to be determined.

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Nonalcoholic fatty liver disease.
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8. Davail S, Rideau N, Bernadet MD, Andre JM, Guy G,
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9. Kelly GL, Allan G, Azhar S.
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resulting in cholesterol and lipid dysregulation.
Endocrinology. 2004;145:548-55. [PubMed]

10. Santer R, Rischewski J, von Weihe M, et al.
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prevalence of hereditary fructose intolerance in
Central Europe.
Hum Mutat. 2005;25:594. [PubMed]

11. Dhingra R, Sullivan L, Jacques PF, et al.
Soft drink consumption and risk of developing
cardiometabolic risk factors and the metabolic syndrome
in middle-aged adults in the community
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12. Block G, Woods M, Potosky A, Clifford C.
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questionnaire using multiple diet records.
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15. Scatarige JC, Scott WE, Donovan PJ,
Siegelman SS, Sanders RC.
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16. Saverymuttu SH, Joseph AE, Maxwell JD.
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and steatosis.
Br Med J (Clin Res Ed). 1986;292:13-5.

17. Ludwig DS, Peterson KE, Gortmaker SL.
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and childhood obesity: A prospective, observational
analysis.
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18. Popkin BM, Armstrong LE, Bray GM, Caballero B,
Frei B, Willett WC.
A new proposed guidance system for beverage consumption
in the United States.
Am J  Clin Nutr. 2006;83:529-42. [PubMed]

19. Nandhini AT, Balakrishnan SD, Anuradha CV.
Response of liver antioxidant system to taurine in rats fed high
fructose diet.
Indian J Exp Biol. 2002;40:1016-9. [PubMed]

20. 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;292:927-34. [PubMed]

21. McDevitt RM, Bott SJ, Harding M, Coward WA,
Bluck LJ, Prentice AM.
De novo lipogenesis during controlled overfeeding with
sucrose or glucose in lean and obese women.
Am J Clin Nutr. 2001;74:737-46. [PubMed]

22. Teff KL, Elliott SS, Tschop M, et al.
Dietary fructose reduces circulating insulin and leptin,
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ghrelin, and increases triglycerides in women.
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23. Porikos KP, Van Itallie TB.
Diet-induced changes in serum transaminase and
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24. Oberhaensli RD, Galloway GJ, Taylor DJ, Bore PJ,
Radda GK.
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Br J Radiol. 1986;59:695-9. [PubMed]

25. Simko V.
Increase in serum lipids on feeding sucrose:
The role of fructose and glucose.
Am J Clin Nutr. 1980;33:2217. [PubMed]

26. Hallfrisch J, Reiser S, Prather ES.
Blood lipid distribution of hyperinsulinemic men consuming
three levels of fructose.
Am J Clin Nutr. 1983;37:740-8. [PubMed]

27. Vuilleumier S.
Worldwide production of high-fructose syrup and crystalline
fructose.
Am J Clin Nutr. 1993;58(5 Suppl):733S-36S. [PubMed]

28. Michal G, editor.
Biochemical Pathways: An Atlas of Biochemistry and
Molecular Biology. Whily: John Wiley and Sons; 1999. p. 27.

29. Trocho C, Pardo R, Rafecas I, et al.
Formaldehyde derived from dietary aspartame binds to tissue
components in vivo.
Life Sci. 1998;63:337-49. [PubMed]

30. Vartanian LR, Schwartz MB, Brownell KD.
Effects of soft drink consumption on nutrition and health:
A systematic review and meta-analysis.
Am J Public Health. 2007;97:667-75.
[PMC free article] [PubMed]

31. Akgun S, Ertel NH.
The effects of sucrose, fructose, and high-fructose corn syrup
meals on plasma glucose and insulin in non-insulin-dependent
diabetes subjects.
Diabetes Care. 1985;8:279-83. [PubMed]

32. Janssens JP, Shapira N, Debeuf P, et al.
Effects of soft drink and table beer consumption on insulin
response in normal teenagers and carbohydrate drink in
youngsters.
Eur J Cancer Prev. 1999;8:289-95. [PubMed]

33. Yoshida M, McKeown NM, Rogers G, et al.
Surrogate markers of insulin resistance are associated with
consumption of sugar-sweetened drinks and fruit juice in
middle and older-aged adults.
J Nutr. 2007;137:2121-7. [PubMed]

34. Hamaguchi M, Kojima T, Itoh Y, et al.
The severity of ultrasonographic findings in nonalcoholic
fatty liver disease reflects the metabolic syndrome and
visceral fat accumulation.
Am J Gastroenterol. 2007;102:2708-15. [PubMed]

35. Pisani P, Faggiano F, Krogh V, Palli D, Vineis P,
Berrino F.
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Int J Epidemiol. 1997;26(Suppl 1):S152-60.
[PubMed]
_______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298  rmforall@...

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 146 members, 1,602 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1218 members, 24,062 posts in a public archive
_______________________________________________

Betty and Don Martini visit Europe 3 weeks, finding many aware of hazards of
aspartame, 2010.05.16: Rich Murray 2010.06.08
http://rmforall.blogspot.com/2010_06_01_archive.htm
Tuesday, June 8, 2010
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1603
[ You may have to Copy and Paste URLs into your browser ]
_______________________________________________


I really enjoyed, appreciated, and was very grateful for this
informative grassroots account, showing how much impact two
gallant aspartame experts abroad have for the common good.

http://www.mpwhi.com/aspartame_called_poison_around_the_globe.htm

ASPARTAME CALLED POISON
AROUND THE GLOBE
Posted: 17 May 2010

So many of you have asked about my trip and aspartame,
I wrote some notes so you would have an update.
No matter where you go aspartame is known as poison and
people will tell you their horror stories as long as you are
willing to listen.
Even though we were on vacation and to rest we spent
three weeks giving out material and educating people
who wanted to know more.
The stories never stop.
I thought I had brought enough material, but everyday I had
to make more copies.
Sometimes you just had to take a deep breath, because
you felt their suffering as they related the happenings.

I wondered years ago how long it would take to reach
critical mass -- today we are past that point.
You never know when you plant seeds what will grow.
The exponentiation of knowledge has exploded.
If everyone only gave out one flyer a day, imagine how many
hundreds of thousands of lives would be saved.
When Cori Brackett filmed the documentary on aspartame,
she titled it: Sweet Misery: A Poisoned World.
Indeed that is no exaggeration.
I still haven't figured out which is more epidemic with
aspartame, MS or lupus.
It's everywhere.
When Dr. Maria Alemany told me in Barcelona,
"Aspartame will kill 200 million," it was no exaggeration.
If one did a census door by door on aspartame, they would
be shocked by the numbers of the poisoned.

Don and I have been suffering jet lag for a week now, but it
was a wonderful trip.
We feel we accomplished some good in spreading the
word further.
We came back home with only a handful of papers left, and
knowing a lot of people now have more knowledge
to get well.
So read on about some of the countries, and
know you all shared in spreading the word.

All my best, Betty

Dr. Betty Martini, D.Hum.
Mission Possible World Health International
9270 River Club Parkway
Duluth, Georgia 30097
Telephone: 770-242-2599
E-Mail: BettyM19@...

In mutual service, Rich Murray


fructose, aspartame, caramel in soft drinks and nonalcoholic
fatty liver disease, W Nseir, F Nassar, N Assy,
World J Gastroenterol: Rich Murray 2010.06.07
http://rmforall.blogspot.com/2010_06_01_archive.htm
Monday, June 7, 2010
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1602
[ You may have to Copy and Paste URLs into your browser ]


[ See also:

Woodrow C Monte, PhD, Emiritus Prof. Nutrition gives
many PDFs of reseach -- methanol (11% of aspartame) puts
formaldehyde into brain and body -- multiple sclerosis,
Alzheimer's, cancers, birth defects, headaches:
Rich Murray 2010.05.13
http://rmforall.blogspot.com/2010_05_01_archive.htm
Thursday, May 13, 2010
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1601
[ You may have to Copy and Paste URLs into your browser ]

( Other formaldehyde sources include alcohol drinks and
tobacco and wood smoke.
Adequate folic acid levels protect most people from some
harm, but not for the brain and retinas.) ]
_______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298  rmforall@...

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 146 members, 1,603 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1218 members, 24,063 posts in a public archive
_______________________________________________

23andMe.com mass medical data research can check WC Monte (2007) claims,
backed by many PDFs of research on methanol (becomes formaldehyde in body
tissues with high ADH levels) and modern diseases -- multiple sclerosis,
etc: Rich Murray 2010.06.23
http://rmforall.blogspot.com/2010_06_01_archive.htm
Wednesday, June 23, 2010
[at end of each long page, click on Older Posts]
http://groups.yahoo.com/group/aspartameNM/message/1600
[you may have to Copy and Paste URLs into your browser]
_______________________________________________


This review gives references for many probable patterns in the
toxicity of methanol (formaldehyde, formic acid).

According to Thomas Goetz in July, 2010 Wired, which I
read June 21, p 106-113, 138-140, Sergey Brin, 36,
worth $ 15 billion as cofounder of Google,
has the Ashkenazi gene LARRK2,
which increases life risk of Parkingson's Disease to 30-75 %.

His mother Eugenia has mild PD, starting 1996.

He has given $ 50 million for PD research, focussing on new
treatments, and $ 4 million on mining huge data sets of
hundreds of life factors reported by over 4,000 PD patients,
to the Parkinson's Disease Genetic Initiative, part of
23and Me.com, his wife Anne Wojcicki's firm, which now
has genetic data on over 50,000 patients and public reports
on 156 diseases.

Citizens can join and submit a saliva sample for analysis for
$ 499.

"... the genotyping process we use analyzes more than
580,000 locations in a person's genome."

PD patients can join for $ 25 to get a detailed genetic
profile  and submit information about hundreds of facets of
their lives, contributing to reseach on PD.

http://spittoon.23andme.com/  blog 2010.06.22

23andMe and a New Paradigm for Research

40 research surveys in progress
29,000 customers participating in research.so far
9 MILLION research questions answered
650+ genome-wide association studies being run in parallel
100s of genetic associations found -- both replications and
novel discoveries
* The article is in the current issue of Wired,
on newsstands now.
We'll provide a link when the article is available online.

https://www.23andme.com/

https://www.23andme.com/health/all/

research reports on 156 diseases

https://www.23andme.com/for/scientists/

https://www.23andme.com/research/

https://www.23andme.com/health/Multiple-Sclerosis/timeline/

https://www.23andme.com/health/Parkinsons-Disease/

Genes vs. Environment

0-1 % Attributable to Genetics
The heritability of Parkinson's appears to be extremely low
in most populations.
This means that environment generally plays a much bigger
role than genetics in determining a person's risk for the
disease
However, a small fraction of Parkinson's cases are caused
by rare but extremely potent mutations in a small number
of genes, including LRRK2.
That means people with the LRRK2 G2019S mutation
have a much higher than average risk of developing
Parkinson's disease during their lifetimes.
It is not yet understood what genetic and environmental
factors determine whether a person with the
LRRK2 G2019S mutation will develop Parkinson's.

https://www.23andme.com/health/Parkinsons-Disease-Preliminary-Research/

https://www.23andme.com/pd/

Join our research communities.
Parkinson's Disease:
Recent discoveries suggest that genetics plays a greater
role in Parkinson's disease than was previously thought.
You can advance research into the genetic roots of
Parkinson's disease

https://www.23andme.com/howitworks/

Our Scientific Advisors

Joseph Jankovic, MD
Distinguished Chair in Movement Disorders
Director, Parkinson Disease Center and Movement
Disorders Clinic, Baylor College of Medicine
http://www.bcm.edu/neurology/pdcmdc/
josephj@...;

Connie Marras MD, PhD, FRCP(C)
Assistant Professor of Neurology
University of Toronto
Morton and Gloria Shulman Movement Disorders Centre,
Toronto Western Hospital, Toronto, Ontario, Canada.
connie.marras@...;

Bernard Ravina, MD, MSCE
Associate Professor of Neurology
Director of the Movement and Inherited Neurological
Disorders Unit,
Associate Director of the Clinical Trials Coordination
Center, University of Rochester School of Medicine
and Dentistry
bernard.ravina@...;

Caroline M. Tanner, MD, PhD
Director of Clinical Research
The Parkinson's Institute and Clinical Center
[ Mov Disord. 2010; 25 Suppl 1: S58-62.
Advances in environmental epidemiology.
Tanner CM.
Clinical Research, The Parkinson's Institute,
Sunnyvale, California 94085, USA. ctannermd@...;
Abstract
Parkinson's disease (PD) is likely due to the combined
effects of environment and genes in most cases.
Environmental factors inversely associated with PD
(or, putative protective factors) include cigarette smoking,
use of coffee/caffeine, higher uric acid levels, and
anti-inflammatory drug use.
Less well-established inverse associations with PD
include higher cholesterol levels, statin use,
higher dietary vitamin B6, and night shift work.
Putative risk factors are pesticide exposure, head trauma,
certain occupations, and milk consumption.
The pathogenesis of PD may begin decades before motor
symptoms.
PD may have shared determinants with other
neurodegenerative disorders involving abnormal protein
aggregation. PMID: 20187243 ]

https://www.23andme.com/help/  FAQ


(The FASEB Journal. 2008; 22: 715.4.) © 2008 FASEB
715.4
Early environmental exposure to methanol as a sensitization
factor for Parkinson's disease: a closer look into the etiology
of PD
Veronica Renee Mackey and Clivel G. Charlton
Neurobiology and Neurotoxicology,
Meharry Medical College, Nashville, TN

ABSTRACT

Parkinson's disease (PD) is a neurodegenerative disorder
characterized by a progressive loss of substantia nigra (SN)
dopaminergic neurons that project to the striatum.
The etiology of PD is unknown; there is the possibility of
early exposure to toxicants creating a vulnerability stage
for PD to occur later in life.
Here, we investigate whether methanol (MeOH) exposure
in early life causes sensitization of the basal ganglia to
challenges, such as
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)
that precipitates the symptoms of PD.
C57/bl6 mice were exposed to sub-chronic levels of
MeOH in utero.
At 12 wks of age, the offspring were treated with MPTP
for seven days.
Tyrosine hydroxylase (TH) protein was analyzed in the
midbrain and striatum.
MPTP increases the expression of TH in the midbrain
and reduces it in the striatum, suggesting that the increase
of TH in the midbrain may be due to impairment of its
transport from cell bodies in the SN to the terminals in
he striatum.
Lastly, the fetal MeOH sensitized the mice to MPTP
reducing effects, suggesting that fetal exposure to MeOH
may be a pre-disposing factor for PD.
This project was supported, in part by
NIH Grant 1R21 NS 049623-01A1


Clin Pharmacol Ther. 2007 Jan; 81(1): 114-21.
Two cases of rapid onset Parkinson's syndrome following
toxic ingestion of ethylene glycol and methanol.
Reddy NJ, Lewis LD, Gardner TB, Osterling W,
Eskey CJ, Nierenberg DW.
Section of Clinical Pharmacology and Toxicology,
Dartmouth Medical School, Dartmouth Hitchcock
Medical Center, Lebanon, New Hampshire, USA.

Abstract
Ethylene glycol and methanol are toxic alcohols commonly
found in a variety of commercial products.
We report two cases, one associated with ethylene glycol
and one with methanol poisoning, which both led to acute
hemorrhagic necrosis of the basal ganglia and resulted in
acute Parkinson's syndrome.
It is unlikely that oxalate crystal deposition is the only
mechanism for such basal ganglia necrosis, because similar
findings were seen following methanol intoxication.
We discuss other possible mechanisms that may contribute
towards this unusual neurotoxicity.
Both of our patients survived their toxic ingestions, but then
developed acute Parkinson's syndrome within 10 days of
the ingestion.
However, the patient who ingested methanol developed
respiratory muscle stiffness/weakness, which responded
poorly to anti-Parkinsonian drug therapy.
Treatment with carbidopa/levodopa improved cogwheel
rigidity and bradykinesia in both patients.
We conclude that acute Parkinsonism is one of the
lesser-recognized devastating complications of both
ethylene glycol and methanol poisoning. PMID: 17186009


NeuroToxicology
Volume 23, Issues 4-5, October 2002, Pages 521-525
doi:10.1016/S0161-813X(02)00033-5
Copyright © 2002 Elsevier Science Inc. All rights reserved.

Progressive Parkinsonism in a Young Experimental Physicist
Following Long-Term Exposure to Methanol
Yoram Finkelstein,  and Jacob Vardi
Department of Neurology, Shaare Zedek Medical Center
and Faculty of Health Sciences, Ben-Gurion University,
Jerusalem 91031, Israel
Received 3 December 2001;  accepted 20 March 2002.
Available online 25 May 2002.
Abstract
A case is described of an experimental physicist who
developed parkinsonism, apparently as delayed toxic effect
of long exposure to vapors of methanol in the laboratory.
Clinical and magnetic resonance imaging (MRI) supported
the diagnosis, after exclusion of hereditary diseases and
primary degenerative diseases.
Screening for heavy metals in urine and plasma
ceruloplasmin was negative.
This case illustrates the neurotoxic delayed effect of
long-term exposure to methanol with no episodes of acute
intoxication.
The setting of a research laboratory with prolonged exposure
to mixed single crystals and inhalation of methanol vapors
may exist in other academic and hi-tech environments, and
pose the risk of similar delayed toxic influences.
Author Keywords: Parkinsonism; Methanol; Methyl
bromide; Long-term exposure; Delayed toxicity
1. INTRODUCTION
2. CASE HISTORY
3. DISCUSSION
References
Corresponding author. Tel.: +972-2-678-1781;
fax: +972-2-678-1781


Three long, fully referenced reviews by WC Monte (2007),
including PDFs of hundreds of mainstream research studies,
explain the role of new methanol sources since 1800 and the
subsequent rise of many novel diseases, such as multiple
sclerosis, Alzheimer's, and breast cancer.

Alcohol dehydrogenase (ADH) is the enzyme that turns
ethyl alcohol into toxic acetaldehyde, and, when no
ethanol is available, methyl alcohol (methanol) into toxic
formaldehyde, which immediately binds with proteins,
RNA, and DNA in a cumulative durable damage
process, while some of the formaldehyde is further
oxidized into toxic formic acid, and then to water and
carbon dioxide.

Thus, a small amount of ethanol, present in fresh fruits and
vegetables, protects against methanol toxicity.

Methanol is supplied by fruits and vegetables precooked in
sealed glass and metal containers, by the burning of wood
and tobacco, as an impurity in dark wines and liquors, the
additive dimethyl dicarbonate, and an 11% part of
aspartame -- a liter or quart of diet drink gives about half
the amount of methanol as in red wine.

However, for alcohol drinks, ingested methanol is not
converted into formaldehyde until the ethanol, with a blood
half-life of 20 minutes, is gone -- two studies suggest that
this is the main cause of "morning after" hangovers.

The methanol has a blood half-life of about 2.5 hours, so
after 13 hours it would be reduced about 30 fold.

The the Dec, 2005 study by YS Woo et al states:

"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)."

I believe this is ppm = milligrams of methanol per liter of
blood, so the increase in the average was only 1.26
milligrams per liter blood, for strong symptoms in healthy
young Korean males.

There are 4.4 liters blood in a 64 kg (141 lb) adult, the size
of a adult male student volunteer, so 4.4 times an average
ethanol increase of 1.26 milligrams per liter blood gives
5.5 mg increased methanol in the blood, which quickly
produces strong hangover symptoms.

A person who uses 2 L diet drink daily, 5.6 12 oz cans
ingests about 112 mg methanol, about 7 mg methanol/hour
over 16 hours.

The conversion to formaldehyde is fast, varies enormously
from person to person, and is concentrated in tissues with
high blood supply and ADH levels: liver, gut, brain, eye,
skin and sinew.

As one of the smallest molecules, methanol easily penetrates
the blood brain barrier, to be converted by plentiful brain
ADH into formaldehyde in tissues adjacent to blood
capillaries.

The same access occurs for the fetus in pregnant women,
leading to severe birth defects, such as spinal bifida, from use
of alcohol and cigarettes in the fourth week of pregnancy.

Humans and primates are uniquely vulnerable among animals,
so tests on animals led to an incorrect conclusion around
1900 that led to much illness and death for decades, as
methanol was widely used as a food and medicine additive .

New methanol sources in modern civilization include canning
after 1800, expansion of canning, cigarettes, and alcohol
drinks in that century, and aspartame in foods (July, 1981)
and drinks (July, 1983).

Adaquate folic acid levels protect many people,
but not against brain and retinal harm.

Several times more women than men have symptoms
from methanol (formaldehyde).

Methanol and/or formaldehyde also come from vehicle
exhaust, faulty stoves and heaters, many cleaners and body
products, leather, plywood and particleboard, new carpets,
drapes, and furniture, new cars, mobile homes, new
construction (sick buildings), mortuaries, medical and
biology schools, labs, and hospitals, and many other sources.

http://whilesciencesleeps.com/references/pdf/586 free full text

Methanol: A Chemical Trojan Horse as the Root of the
Inscrutable U, Prepublication Copy; Medical Hypotheses
-- 06 November 2009 (10.1016/j.mehy.2009.09.059)
http://www.medical-hypotheses.com/article/S0306-9877(09)00693-8/abstract
Woodrow C. Monte PhD
Professor of Food Science (retired)
Arizona State University
corresponding author : Woodrow C. Monte PhD
470 South Rainbow Drive
Page, Arizona 86040
Key Words:
food epidemiology; diseases of civilization; methanol;
formaldehyde; aspartame; autism; multiple sclerosis;
Alzheimer's; U-shaped curve.

Article 2 http://www.thetruthaboutstuff.com/review2.html
WC Monte, 2007 Dec

"Once methanol runs the gauntlet of first-pass metabolism,
its detoxification is no longer exclusive to the liver.
Formaldehyde, the first metabolite of methanol, can then be
produced within the arteries and veins,[#220] heart,[#503]
brain,[#218] lungs,[#221] breast,[#358] bone,[#503] and
skin.[#221]
These major organs harbor extra hepatic sites of the only
remaining human enzyme capable of metabolizing  methanol,
class I alcohol dehydrogenase (ADH I).[#112]
Methanol transports its potential to become formaldehyde
past normal biological barriers in the brain and elsewhere that
environmental formaldehyde itself cannot usually penetrate.
[#122]"

""Identical Symptoms of MS, Methanol Poisoning
and Aspartame Toxicity

The symptoms of multiple sclerosis (44, 83, 85, 169), chronic
and acute methanol poisoning (13, 144, 189), and Aspartame
toxicity (54, 58, 93, 181), are in all ways identical.

There is nothing that happens to the human body from the toxic
effect of methanol that has not been expressed during the
course of MS... nothing (143, 144).

This generalization extends even to the remarkable
opthomological conditions common to both: transitory optic
neuritis and retrolaminar demyelinating optic neuropathy with
scotoma of the central visual field (which occasionally
manifests as unilateral temporary blindness (85, 138, 163).

In fact, these opthomological symptoms have been thought of
for years in their respective literatures to be "tell tale"
indications for the differential diagnosis for each of these
maladies independently (85, 138, 148, 163, 169).

The common symptoms of
headache (13, 83, 181, 189),
nervousness (13, 83, 181),
depression (58, 83, 189, 181),
memory loss (18, 147, 85, 169, 181),
tingling sensations (13, 85, 168, 138, 169),
pain in the extremities (13, 85, 169),
optic neuritis (85, 138, 148, 163, 169),
bright lights in the visual field (139, 83),
seizures (21, 83, 160),
inability to urinate or to keep from urinating (139, 146, 167)
are all shared by each of these conditions and shared yet again
by complaints from aspartame poisoning (54, 58, 93, 181).

I take these strikingly similar symptom patterns as evidence
that these disorders act on identical components of the central
nervous system and in the same way.

The "Miracle" that MS shares with Methanol poisoning

In the early stages of MS, or when a non-lethal dose of
methanol has been administered, complete recovery is a
possibility.

The only two afflictions for which such dramatic "remissions"
are reported from identical neuromuscular and
opthomological damage, even "blindness" is
relapsing-remitting multiple sclerosis (85) and methyl alcohol
poisoning (138, 163).

The pathology of the two maladies is in may ways identical,
particularly when it comes to destruction of the myelin sheath
with no harm to the axon itself (18, 148, 176).

Sex Ratios for MS and Aspartame Reactions

Women bear the brunt of multiple sclerosis (91a-c) and lupus
(SLE)(73) with fully three-fold representations in infliction
numbers over men for both diseases.

This is exactly the proportion represented by adverse reactors
to Aspartame reported by the US Center for Disease Control
in their study of 1984(58).

The Center found three women to every man whose
Aspartame consumption complaints were serious enough to
warrant investigation (93).

Although the female/male ratio for those stricken with MS has
always been high, recent estimates place it at over 3 to 1
(91, 91a, 91c).

What might account for the difference across sexes in
incidence?

A study published in the New England Journal of Medicine
(94) reports biopsies of the gastric lining of men and women.

A result was that the concentration of ADH in the gastric lining
of men was much higher than for woman.

Men have the advantage of removing methanol from the
bloodstream four times faster on an equal-body-size basis
than women.

Thus, for men, methanol is more likely to be removed from the
blood before it reaches the brain.

The brain is spared but the methanol removed would still be
metabolized to formaldehyde in the gut where it would reap its
havoc on a more forgiving organ.

This may help explain why men have more gastrointestinal
complaints from both methanol and Aspartame consumption
(93, 99).

On the other hand, women's complaints from both more
frequently involve serious neurological complications."

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://groups.yahoo.com/group/aspartameNM/message/1498

Monte WC., Is your Diet Sweetener killing you?
Fitness Life. 2007 Nov; 33: 31-33.

Monte WC., A Deadly Experiment.
Fitness Life. 2007 Dec; 34: 38-42.

Monte WC., Bittersweet: Aspartame Breast Cancer Link.
Fitness Life. 2008 Feb; 34: 21-22.

Article 1 http://www.thetruthaboutstuff.com/review1.html

Article 2 http://www.thetruthaboutstuff.com/review2.html

Article 3 http://www.thetruthaboutstuff.com/review3.html

http://www.thetruthaboutstuff.com/references.html
223 references with abstracts or full and partial texts
[#220 is at http://whilesciencesleeps.com/references/pdf/220 ]

http://thetruthaboutstuff.com/index.shtml
[ German and Dutch also available ]


http://whilesciencesleeps.com/  updated website

http://whilesciencesleeps.com/references 589 references
[ click on titles to get free full text pdfs ]

http://whilesciencesleeps.com/about Woodrow C Monte

http://whilesciencesleeps.com/media videos & audios

http://whilesciencesleeps.com/montediet

Methanol: Where Is It Found? How Can It Be Avoided?

AVOID the following, ranked in order of greatest danger:

1. Cigarettes.
2. Diet foods and drinks with aspartame.
3. Fruit and vegetable products and their juices in bottles,
cans, or pouches.
4. Jellies, jams, and marmalades not made fresh and kept
refrigerated.
5. Black currant and tomato juice products, fresh or
processed.
6. Tomato sauces, unless first simmered at least 3 hours
with an open lid.
7. Smoked food of any kind, particularly fish and meat.
8. Sugar-free chewing gum.
9. Slivovitz: You can consume one alcoholic drink a day
on this diet -- no more! [ no fruit brandies ]
10. Overly ripe or near rotting fruits or vegetables.
[ end of Monte quotes ]


Many scientific studies and case histories report:
headaches;
many body and joint pains (or burning, tingling, tremors,
twitching, spasms, cramps, stiffness, numbness, difficulty
swallowing, acid reflux),
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, scotoma, dry eyes, dry mouth,
mouth sores, burning tongue;
obesity, bloating, edema, anorexia;
poor appetite or excessive hunger or thirst;
breathing problems, shortness of breath, asthma;
nausea, diarrhea or constipation;
coldness;
sweating;
racing heart, low or high blood pressure;
poor blood coagulation;
thrombocytopenia (very low platelets in blood);
diabetes, erratic blood sugar levels;
hypothryroidism or hyperthyroidism (Graves disease);
pseudotumor cerebri;
non-alcoholic steatohepatitis (fatty liver);
interstitial cystitis (bladder pain), urinary problems.
amyotrophic lateral sclerosis;
seizures;
birth defects, problem pregnancies;
addictions;
aggrivates diabetes, autism, allergies, lupus, ADHD,
fibromyalgia, chronic fatigue syndrome, multiple chemical
sensitivity, multiple sclerosis;
drug interactions;

Vestibulocochlear toxicity in a pair of siblings [doctor &
nurse] 15 years apart secondary to aspartame: two case
reports, Paul Pisarik & Dasha Kai, Cases J 2009.09.15
free full text: Rich Murray 2010.05.04
http://rmforall.blogspot.com/2010_05_01_archive.htm
Tuesday, May 4, 2010
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1600
[you may have to Copy and Paste URLs into your browser]

recent aspartame (methanol, formaldehyde, formic acid)
symptoms in English professor: Kristi Siegel:
Rich Murray 2010.04.17
http://rmforall.blogspot.com/2010_04_01_archive.htm
Saturday, April 17, 2010
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1599
[you may have to Copy and Paste URLs into your browser]

formaldehyde from 11% methanol part of aspartame causes
severe allergic dermatitis in boy, JE Jacob et al,
Pediatric Dermatology 2009 Nov: Rich Murray 2010.03.30
http://rmforall.blogspot.com/2010_03_01_archive.htm
Tuesday, March 30, 2010
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1597
[you may have to Copy and Paste URLs into your browser]

kid asthma related to formaldehyde, G McGwin Jr, J Lienert,
JI Kennedy Jr, Environmental Health Perspectives
2009.11.06 abstract: Rich Murray 2009.12.01
http://rmforall.blogspot.com/2009_12_01_archive.htm
Tuesday, December 1, 2009
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1590
[you may have to Copy and Paste URLs into your browser]

re huge reduction in preterm births: folic acid prevents harm
from formaldehyde and formic acid made by body from
methanol in alcohol drinks and aspartame, BM Kapur,
DC Lehotay, PL Carlen at U. Toronto, Alc Clin Exp Res
2007 Dec: Rich Murray 2009.05.12
http://rmforall.blogspot.com/2009_05_01_archive.htm
Tuesday, May 12, 2009
http://groups.yahoo.com/group/aspartameNM/message/1572

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

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

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

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

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

http://groups.yahoo.com/group/aspartameNM/message/1468
Formaldehyde induced urticarial vasculitis in male medical
student, age 40, Michael Pellizzari, Gillian Marshman,
Flinders U., Australasian J. Dermatol. 2007 Aug:
Murray 2007.08.29

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

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/aspartameNMmessage/1452

Subjective symptoms of medical students exposed to
formaldehyde during a gross anatomy dissection course,
Wei CN et al, Center for Policy Studies, Kumamoto
University, Japan, Int J Immunopathol Pharmacol.
2007 Apr. Murray 2008.02.12
http://rmforall.blogspot.com/2008_02_01_archive.htm
Tuesday, February 12, 2008
http://groups.yahoo.com/group/aspartameNM/message/1519

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 2008.02.07
http://rmforall.blogspot.com/2008_02_01_archive.htm
Thursday, February 7, 2008
http://groups.yahoo.com/group/aspartameNM/message/1513

http://groups.yahoo.com/group/aspartameNM/message/1467
4 cases of aspartame-induced thrombocytopenia [very low
platelets in blood ], HJ Roberts MD, Letter in Southern
Medical Journal 2007 May: 100(5); 543:
Murray 2007.08.25

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/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/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/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/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/876
hyperthyroidism (Graves disease) in George and Barbara
Bush, 1991 -- aspartame toxicity? Roberts 1997:
Murray 2002.10.09

http://groups.yahoo.com/group/aspartameNM/message/782
RTM: Smith, Terpening, Schmidt, Gums:
full text: aspartame, MSG, fibromyalgia 2002.01.17


www.who.int/ipcs/publications/training_poisons/basic_analytical_tox/en/index10.h\
tml

"Practical aspects of analytical toxicology  WHO IPCS 1995
Table of contents

Monographs - analytical and toxicological data
(6.46 - 6.78)"

"6.70 Methanol

Methyl alcohol; wood alcohol; CH3OH; relative molecular
mass, 32

Methanol is used as a general and laboratory solvent, and in
antifreeze (often with ethylene glycol), windscreen washer
additives and duplicating fluids.

In an adult, death may follow the ingestion of 20-50 ml of
methanol.

Poisoning with industrial grades of ethanol (methylated
spirit), which often contain methanol as a denaturant, also
occurs, but is generally less serious than with methanol alone.
This is because methanol toxicity results from its metabolism
to formaldehyde and formate by alcohol dehydrogenase, a
reaction inhibited by ethanol....

Acute methanol poisoning is characterized by delayed onset
of coma, cyanosis, respiratory failure, marked metabolic
acidosis, electrolyte imbalance, hyperglycaemia and
blindness, which may be permanent.
Treatment is aimed at correcting metabolic abnormalities,
inhibiting methanol metabolism by giving ethanol and removing
unchanged methanol by peritoneal dialysis or haemodialysis.
Measurement of plasma ethanol concentrations can be useful
in monitoring therapy with this compound
(see section 6.46)."

"6.51 Formaldehyde

Formaldehyde (HCHO; relative molecular mass, 30) is a
colourless, inflammable gas and is normally encountered as
an aqueous solution (formalin, 340-380 ml/l), which also
contains methanol as a stabilizer.
Formalin is used as a disinfectant, an antiseptic and a
tissue-fixing and embalming fluid.
Polymerized formaldehyde (paraformaldehyde) is used as a
fumigant, and other polymeric forms are used as adhesives in
chipboard and plywood, and in the preparation of insulation
materials.

Formaldehyde is rapidly metabolized in vivo to formate and is
itself a metabolite of methanol.

Acute formaldehyde poisoning is uncommon, but 30 ml of
formalin may be fatal in an adult.....

Formaldehyde vapour is very irritating and inhalation may
cause conjunctivitis, coughing and laryngeal and pulmonary
oedema.

Ingestion of formaldehyde solution may give rise to
abdominal pain, vomiting, diarrhoea, hypotension, coma,
metabolic acidosis and acute renal failure.
Treatment is normally symptomatic and supportive."

"6.52 Formic acid and formate

Formic acid (HCOOH; relative molecular mass, 46), a
colourless, aqueous solution, is very corrosive.
Many proprietary descaling agents contain 500-600 ml/l
formic acid.
Formates such as sodium formate (HCOONa) are used as
synthetic intermediates and in the dying, printing and tanning
industries.
Formic acid is itself a metabolite of methanol and
formaldehyde.

The minimum lethal dose of formic acid in an adult is thought
to be about 30 ml.....

Formic acid is very corrosive to tissues, and ingestion may
cause burning and ulceration of the mouth and throat,
corrosion of the glottis, oesophagus and stomach, metabolic
acidosis, intravascular haemolysis, disseminated intravascular
coagulation, circulatory collapse and renal and respiratory
failure.
Treatment is symptomatic and supportive."

"The issue of this document does not constitute formal
publication.
It should not be reviewed, abstracted, or quoted without
the written permission of the Manager,
Programme on Chemical Safety,
WHO, Geneva, Switzerland.

This report contains the collective views of an international
group of experts and does not necessarily represent the
decisions or the stated policy of the United Nations
Environment Programme, the International Labour
Organisation, or the World Health Organization."

"The International Programme on Chemical Safety (IPCS) is a
joint venture of the United Nations Environment Programme,
the International Labour Organisation, and the World Health
Organization.
The main objective of the IPCS is to carry out and
disseminate evaluations of the effects of chemicals on human
health and the quality of the environment.
Supporting activities include the development of
epidemiological, experimental laboratory, and
risk-assessment methods that could produce internationally
comparable results, and the development of manpower in
the field of toxicology.
Other activities carried out by the IPCS include the
development of know-how for coping with chemical
accidents, coordination of laboratory testing and
epidemiological studies, and promotion of research on the
mechanisms of the biological action of chemicals."
_______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298  rmforall@...

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 145 members, 1,604 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1219 members, 24,063 posts in a public archive
_______________________________________________

23andMe publishes in PLoS Genetics, validates revolutionary new paradigm for
fast, flexible mass genetic data research, free full text: more methanol
(formaldehyde) toxicity leads: Rich Murray 2010.06.25
http://rmforall.blogspot.com/2010_06_01_archive.htm
Thursday, June 24, 2010
[at end of each long page, click on Older Posts]
http://groups.yahoo.com/group/aspartameNM/message/1605
[you may have to Copy and Paste URLs into your browser]
_______________________________________________


23andMe.com mass medical data research can check WC
Monte (2007) claims, backed by many PDFs of research on
methanol (becomes formaldehyde in body tissues with high
ADH levels) and modern diseases -- multiple sclerosis, etc:
Rich Murray 2010.06.23
http://rmforall.blogspot.com/2010_06_01_archive.htm
Wednesday, June 23, 2010
[at end of each long page, click on Older Posts]
http://groups.yahoo.com/group/aspartameNM/message/1604
[you may have to Copy and Paste URLs into your browser]


http://spittoon.23andme.com/2010/06/24/plos-genetics-23andme/comment-page-1/#com\
ment-4946

23andMe Publishes in PLoS Genetics,
Validates New Research Paradigm

Published by ErinC at 3:03 pm under 23andMe and you,
inside 23andMe, news, our founders

23andMe is proud to announce the first publication to come
out of 23andWe, our novel participant-driven research
program.

Our results, which encompass replications of previous findings
as well as newly discovered associations, appear online today
in PLoS Genetics.

23andWe is a web-based research framework designed to
facilitate the rapid recruitment of participants to many studies
at once, thus reducing the time and money needed to make
new discoveries.

"This paper announces and validates a revolutionary way of
conducting scientific research," said our President and
Co-Founder, Anne Wojcicki.
"In this paper we confirm that self-reported data from our
customers has the potential to yield data of comparable quality
as data gathered using traditional research methods.
We are excited about moving scientific research forward,
faster," she continued.
[ wife of Sergey Brin, co-founder of Google ]

(Check out "Sergey's Search" in the current issue of Wired to
learn how this approach is allowing us to validate genetic
associations in a fraction of the time traditionally needed.
And check out this recent Spittoon post to read about some
of our other 23andWe successes.)

Over 9,000 people contributed data to our study of 22
separate traits.
Novel SNP associations were revealed for hair curl,
asparagus anosmia (the inability to detect the scent of certain
asparagus metabolites in urine),
the photic sneeze reflex (the tendency to sneeze when entering
bright light),
and freckling.
Previously identified genetic associations between nine genes
and certain pigmentation-related traits (hair color, eye color,
and freckling) were replicated.
23andMe chose to publish its results in PLoS Genetics because
of the journal's open-access policy, which allows
anyone -- including 23andMe customers who contributed to the
research -- to freely access the study.
Customers will also see the results incorporated into the reports
available in their online accounts.

Tags: 23andWe, anosmia, asparagus, hair curl, photic sneeze,
pigmentation, PLOS Genetics, replication, research

Read more in this 23andMe press release:
https://www.23andme.com/about/press/20100624/

23andMe Makes New Discoveries in Genetics Using Novel,
Web-based, Participant-driven Methods

Replication of Known Genetic Associations
Validates New Research Paradigm

MOUNTAIN VIEW, CA -- June 24, 2010 -- 23andMe, Inc.,
a leading personal genetics company, announced today that it
has published the first data to come out of its novel
participant-driven research program.

The results, available online in the journal PLoS Genetics,
replicate several known genetic associations, validating
23andMe's methodology and ushering in an era of more
efficient genetic research.

http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1000993

"This paper announces and validates a revolutionary way of
conducting scientific research," said Anne Wojcicki, 23andMe
President and Co-Founder.
"In this paper we confirm that self-reported data from our
customers has the potential to yield data of comparable quality
as data gathered using traditional research methods.
We are excited about moving scientific research forward,
faster," continued Wojcicki.

In a traditional genome-wide association study (GWAS),
researchers recruit people with (cases) and without (controls)
a particular trait or condition.
The physical characteristics or disease status of both groups
are then correlated with their genetic data to find
single letter differences in the DNA
(single nucleotide polymorphisms, or SNPs)
that are linked to the trait or condition.

Although this method has yielded many exciting insights into
human genetics, it can be a slow and expensive process.
The 23andMe web-based research framework, on the other
hand, facilitates the rapid recruitment of participants to many
studies at once, thus reducing the time and money needed to
make new discoveries.

Principal Scientist Nicholas Eriksson summed up the power
of 23andMe's approach,
"Through 23andMe's web-based platform, the company can
perform hundreds of studies in parallel.
Our ability to contact individuals multiple times and ask
follow-up questions puts us in a position to zero in on
associations that could be the building blocks for future research
aimed at prevention, better treatments, and potentially cures for
a multitude of diseases and conditions."

Over 9,000 people contributed data to this 23andMe study
of 22 separate traits.
In addition to the replications of known genetic associations,
several new discoveries were made.
Novel SNP associations were revealed for hair curl,
asparagus anosmia (the inability to detect the scent of certain
asparagus metabolites in urine),
the photic sneeze reflex (the tendency to sneeze when entering
bright light),
and freckling.
Previously identified genetic associations between nine genes
and certain pigmentation-related traits (hair color, eye color,
and freckling) were replicated.

23andMe chose to publish its results in PLoS Genetics because
of the journal's open-access policy, which allows
anyone -- including 23andMe customers who contributed to the
research -- to freely access the study.
Customers will also see the results incorporated into the reports
available in their online accounts.

About 23andMe

23andMe, Inc. is a leading personal genetics company
dedicated to helping individuals understand their own genetic
information through DNA analysis technologies and web-based
interactive tools.
The company's Personal Genome ServiceT enables individuals
to gain deeper insights into their ancestry and inherited traits.
The vision for 23andMe is to personalize healthcare by making
and supporting meaningful discoveries through genetic research.
23andMe, Inc., was founded in 2006, and the company is
advised by a group of renowned experts in the fields of human
genetics, bioinformatics and computer science.
Its investors include Genentech, Inc.,
Google Inc. (NASDAQ: GOOG)
and New Enterprise Associates.
More information is available at www.23andme.com

Media Contacts:

Rubenstein Communications, 1345 Ave of the Americas,
New York, NY 10105
Contacts:
Jane Rubinstein, 212-843-8287, jrubinstein@...;
Rachel Nagler, 212-843-8017, rnagler@...;
Adam Isserlis, 212-843-8024, aisserlis@...;

Press Releases
June 24, 2010   23andMe Makes New Discoveries in
Genetics Using Novel, Web-based, Participant-driven Methods
June 3, 2010   23andMe Enlists Informed Medical Decisions to
Make Independent Genetic Counseling Services Available to
Customers
October 13, 2009   23andMe Tests NFL Players' DNA for
Athletic Genetic Factors
April 27, 2009   23andMe and Palomar Pomerado Health
Partner to Give PPH Members Access to Their Genetic
Information
March 31, 2009   23andMe Launches Free Online
Community For Moms and Moms-to-Be

March 12, 2009   23andMe Launches Parkinson's Disease
Genetics Initiative

January 28, 2009   23andMe and mondoBIOTECH
Partner to Advance Research of Rare Diseases

December 18, 2008   Silicon Valley Veterans Sarah Imbach
and Larry Tesler Join 23andMe Management Team

December 8, 2008   23andMe Announces Holiday Season
Multi-Pack Discount
October 30, 2008   TIME Magazine Names 23andMe's
Personal Genome Service 2008 Invention of the Year

October 2, 2008   23andMe Announces Breast Cancer
Initiative

September 9, 2008   23andMe Democratizes Personal
Genetics
September 9, 2008   23andMe and Ancestry.com Partner
to Extend Access to Genetic Ancestry Expertise
May 29, 2008   23andMe Launches Consumer-Enabled
Research Program to Actively Engage Individuals in Genetics
Research

May 14, 2008   23andMe and The Parkinson's Institute
Announce Initiative to Advance Parkinson's Disease Research

January 22, 2008   23andMe Launches Web-Based
Personal Genome ServiceT Outside U.S.
November 29, 2007   23andMe Selected as a 2008
Technology Pioneer by the World Economic Forum
November 19, 2007   23andMe Launches Web-Based
Service Empowering Individuals to Access and
Understand Their Own Genetic Information
November 16, 2007   23andMe to Hold Webcast Media
Briefing
May 22, 2007   23andMe, Inc. Completes Series A
Financing


http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1000993

Web-Based, Participant-Driven Studies Yield Novel Genetic
Associations for Common Traits

Abstract
Author Summary
Introduction
Results
Discussion
Methods
Supporting Information
Acknowledgments
Author Contributions
References

Nicholas Eriksson1*,
J. Michael Macpherson 1,
Joyce Y. Tung 1,
Lawrence S. Hon 1,
Brian Naughton 1,
Serge Saxonov 1,
Linda Avey 1,
Anne Wojcicki 1,
Itsik Pe'er 2,
Joanna Mountain 1,3*
1 23andMe, Mountain View,
California, United States of America,
2 Department of Computer Science, Columbia University,
New York, New York, United States of America,
3 Department of Anthropology, Stanford University,
Stanford, California, United States of America

Abstract

Despite the recent rapid growth in genome-wide data, much
of human variation remains entirely unexplained.
A significant challenge in the pursuit of the genetic basis for
variation in common human traits is the efficient, coordinated
collection of genotype and phenotype data.
We have developed a novel research framework that facilitates
the parallel study of a wide assortment of traits within a single
cohort.
The approach takes advantage of the interactivity of the Web
both to gather data and to present genetic information to
research participants, while taking care to correct for the
population structure inherent to this study design.
Here we report initial results from a participant-driven study
of 22 traits.
Replications of associations (in the genes OCA2, HERC2,
SLC45A2, SLC24A4, IRF4, TYR, TYRP1, ASIP,
and MC1R) for hair color, eye color, and freckling validate
the Web-based, self-reporting paradigm.
The identification of novel associations for hair morphology
(rs17646946, near TCHH; rs7349332, near WNT10A;
  and rs1556547, near OFCC1),
freckling (rs2153271, in BNC2),
the ability to smell the methanethiol produced after eating
asparagus (rs4481887, near OR2M7),
and photic sneeze reflex (rs10427255, near ZEB2,
and rs11856995, near NR2F2)
illustrates the power of the approach.

Author Summary

Twin studies have shown that many human physical
characteristics, such as hair curl, earlobe shape,
and pigmentation are at least partly heritable.
In order to identify the genes involved in such traits, we
administered Web-based surveys to the customer base of
23andMe, a personal genetics company.

Upon completion of surveys, participants were able to see how
their answers compared to those of other customers.

Our examination of 22 different common traits in nearly
10,000 participants revealed associations among several
single-nucleotide polymorphisms
(SNPs, a type of common DNA sequence variation)
[ 580,000 single nucleotide polymorphisms (SNPs)
found for each of ~50,000 participants in 23andMe];
and freckling,
hair curl,
asparagus anosmia (the inability to detect certain urinary
metabolites produced after eating asparagus),
and photic sneeze reflex (the tendency to sneeze when
entering bright light).

Additionally our analysis verified the association of a large
number of previously identified genes with variation
in  hair color, eye color, and freckling.

Our analysis not only identified new genetic associations, but
also showed that our novel way of doing research -- collecting
self-reported data over the Web from involved participants
who also receive interpretations of their genetic data -- is a
viable alternative to traditional methods.

Citation:
Eriksson N, Macpherson JM, Tung JY, Hon LS, Naughton B,
et al. (2010)
Web-Based, Participant-Driven Studies Yield
Novel Genetic Associations for Common Traits.
PLoS Genet 6(6): e1000993. doi:10.1371/journal.pgen.
1000993

Editor: Greg Gibson, Georgia Institute of Technology,
United States of America
Received: June 22, 2009; Accepted: April 12, 2010;
Published: June 24, 2010

Copyright: © 2010 Eriksson 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.

Funding: This study was funded by the participants and by
23andMe.
Company co-president and co-author AW has provided
financial support to 23andMe for its general operational needs.

Competing interests:
NE, JMM, JYT, LSH, BN, SS, LA, AW, and JM are or have
been employed by 23andMe and own stock options in the
company.
23andMe co-president AW has provided general guidance,
including guidance related to the company's research
undertakings and direction.
PLoS Genetics' Editor-in-Chief Gregory S. Barsh is a
potential consultant to 23andMe and therefore recused
himself from the editorial and peer-review process.
PLoS co-founder Michael B. Eisen is a member of the
23andMe Scientific Advisory Board.

* E-mail: nick@...; (NE);
joanna@...; (JM)
_______________________________________________


This review continues to give references for many probable
patterns in the toxicity of methanol (formaldehyde, formic acid).

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, along with tobacco and alcohol use, maybe folic acid
status.

It is available to any qualified research team.


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

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
http://groups.yahoo.com/group/aspartameNM/message/1475

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 cohert ------------- 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.

"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."

http://cebp.aacrjournals.org/cgi/content/full/15/9/1654
free full text
http://cebp.aacrjournals.org/cgi/reprint/15/9/1654
free full text pdf

Cancer Epidemiology Biomarkers & Prevention
Vol. 15, 1654-1659, September 2006
© 2006 American Association for Cancer Research

Consumption of Aspartame-Containing Beverages and
Incidence of Hematopoietic and Brain Malignancies

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@...;

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 >/=600 mg/d, 0.98; 95% CI, 0.76-1.27),
glioma (RR for >/=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 (1,200 or 2,000 mg/d, which is equivalent to
~7 to 11 cans of soft drinks daily) compared with the
lowest categories."


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

aspartame, caffeine, MSG, alcohol may cause migraine
headaches, C Sun-Edelstein, A Mauskop, The New York
Headache Center, Clin J Pain 2009 June:
Rich Murray 2009.05.25
http://rmforall.blogspot.com/2009_05_01_archive.htm
Monday, May 25, 2009
http://groups.yahoo.com/group/aspartameNM/message/1573

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

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

Seizures and hyponatremia after excessive intake of diet coke,
LJ Mortelmans, M Van Loo, HG De Cauwer, K Merlevede,
Klina General Hospital, Brasschaat, Belgium, EJEM
2008 Feb: Mark D. Gold critique: Murray 2008.01.10
http://rmforall.blogspot.com/2008_01_01_archive.htm
Thursday, January 10, 2008
http://groups.yahoo.com/group/aspartameNM/message/1502

possible neurologic effects of aspartame, TJ Maher,
RJ Wurtman, Environ. Health Persp. 1987 Nov, full text:
other seizure reports re aspartame, methanol, formaldehyde,
formic acid: Murray 2008.01.10
http://rmforall.blogspot.com/2008_01_01_archive.htm
Thursday, January 10, 2008
http://groups.yahoo.com/group/aspartameNM/message/1501

interstitial cystitis symptoms worse for coffee, tea, soda,
alcoholic beverages, citrus fruits and juices, hot pepper,
artificial sweeteners (not sucralose), B Shorter et al, Long
Island U., J. Uriology 2007 July: Murray 2007.11.13
http://groups.yahoo.com/group/aspartameNM/message/1489

"The most frequently reported and most bothersome
comestibles were coffee, tea, soda, alcoholic beverages,
citrus fruits and juices, artificial sweeteners and hot pepper."


aspartame decreases evoked extracellular dopamine levels in
the rat brain, Brian P Bergstrom, Muskingum College,
Neuropharmacology 2007.09.29: Murray 2007.11.06
http://groups.yahoo.com/group/aspartameNM/message/1485

13,620 seniors using more than 1 can/week artificially
sweetened [aspartame] soft drinks had 8% higher death risk,
1981-2004, Paganini-Hill A, Kawas CH, Corrada MM,
U. Southern Cal., Prev. Med. 2007 April 44(4) 305-10:
Murray 2007.10.12
http://RMForAll.blogspot.com October 12, 2007
http://groups.yahoo.com/group/aspartameNM/message/1479

Formaldehyde induced urticarial vasculitis in male medical
student, age 40, Michael Pellizzari, Gillian Marshman,
Flinders U., Australasian J. Dermatol. 2007 Aug:
Murray 2007.08.29
http://groups.yahoo.com/group/aspartameNM/message/1468

"A complete recovery occurred only after strict elimination of
all exposure to formaldehyde, both occupationally and in the
home environment, was achieved."


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/1459

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/aspartameNMmessage/1452

Is aspartame really safer in reducing the risk of hypoglycemia
during exercise in patients with type 2 diabetes? Ferland A,
Brassard P, Poirier P, Universite Laval, Quebec,
Diabetes Care 2007 July: Murray 2007.07.06
http://groups.yahoo.com/group/aspartameNMmessage/1450

"Although it has been reported that various forms of
carbohydrate intake before exercise is safer for patients with
diabetes in the prevention of exercise-induced hypoglycemia,
we have reported severe symptoms of hypoglycemia on four
occasions following sucrose - and/or aspartame sweetened
meals (6).

Considering the lack of evidence on the aspartame utilization
in patients with type 2 diabetes (7-9), we consider that these
clinical observations, in a exercise setting, raise important
concerns regarding the safety of aspartame as suggested
by international guidelines."

aspartame and sucrose each raise blood glucose in diabetes 2,
Annie Ferland, Paul Poirier, et al, talk 2005.05.13
Laval Hospital Research Center, Laval University,
Sainte-Foy, Canada: Murray 2007.01.11
http://groups.yahoo.com/group/aspartameNM/message/1401

Wellington, NZ lady, 25, free by 24 hours of severe muscle
cramps (5 months) after quitting 4-8 packs daily aspartame
chewing gum (past few years): Murray 2007.06.20
http://groups.yahoo.com/group/aspartameNM/message/1442

[ 6-8 mg aspartame per stick chewing gum, so 8 packs,
5 sticks each, gives 240-320 mg, while a 12 oz can aspartame
diet soda has 200 mg -- however, aspartame from gum is
absorbed directly into the mucosal membranes in the mouth,
close to the brain. ]


man 51 still blind with brain lesions 2 years later from formic
acid toxicity after 4 days of methanol exposure in cheap
whiskey, Sudipta Chattopadhyay, Puvana Chandra, NEJM:
Murray 2007.05.31
http://groups.yahoo.com/group/aspartameNM/message/1439

effect of aspartame on oncogene and suppressor gene
expressions in mice, Katalin Gambos, Istvan Ember, et al,
University of Pecs, Hungary, In Vivo 2007 Jan; scores of
their relevant past studies since 1977: Murray 2007.04.14
http://groups.yahoo.com/group/aspartameNM/message/1414

Quaternium-15, a formaldehyde source, also causes some
allergic contact dermatitis, role of methanol from aspartame:
Murray 2006.11.20
http://groups.yahoo.com/group/aspartameNM/message/1381

eyelid contact dermatitis by formaldehyde from aspartame,
AM Hill & DV Belsito, Nov 2003: Murray 2004.03.30
[150 KB]
http://groups.yahoo.com/group/aspartameNM/message/1067

fibromyalgia, MSG, aspartame, full text, Smith, Terpening,
Schmidt, Gums: Murray 2002.01.07 2006.09.09
http://groups.yahoo.com/group/aspartameNM/message/1368

Possible role of aspartame in risperidone-associated pituitary tumors,
H.J. Roberts MD: Murray 2006.06.26
http://groups.yahoo.com/group/aspartameNM/message/1355

aspartame groups and books: updated research review of
2004.07.16: Murray 2006.05.11
http://groups.yahoo.com/group/aspartameNM/message/1340

Comet assay finds DNA damage from sucralose, cyclamate,
saccharin, aspartame in mice: Sasaki YF & Tsuda S
Aug 2002: Murray 2006.05.08
http://groups.yahoo.com/group/aspartameNM/message/1337

[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.]


aspartame or MSG affects circadian rhythms in rats,
two studies, P. Subramanian, T. Manivasagam et al 2004:
Murray 2006.04.27
http://groups.yahoo.com/group/aspartameNM/message/1329

California Office of Environmental Health Hazard Assessment
in 2004 rejected poor 2003 NTP studies of aspartame
(methanol, formaldehyde) carcinogenicity (highly praised by
industry PR): Murray 2006.03.03
http://groups.yahoo.com/group/aspartameNM/message/1311


Aspartame and smoking give the same toxic metabolite as
does benzene, Lin YS et al, U N Carolina, Chapel Hill,
2006 Jan., Center for Environmental Health and
Susceptibility: Murray 2006.03.01
http://groups.yahoo.com/group/aspartameNM/message/1310

"Multiple linear regression models identified several significant
contributors to 1,4-BQ-Alb levels,
including gender,
body mass index (BMI),
the gender-BMI interaction,
automobile refueling,
smoking status,
and consumption of fruit
and the artificial sweetener, aspartame.

The authors predicted that these background levels of
1,4-BQ-Alb were equivalent to occupational exposures
between 1 and 3 parts per million of benzene.

Mixed effects linear models indicated that the random
variation in adduct levels was about equally divided between
and within subjects.

The observations indicate that levels of 1,4-BQ-Alb
cover a wide range in the general population,
and they support the hypotheses that demographic,
diet and lifestyle factors are contributing sources."

1: Biomarkers. 2006 Jan-Feb; 11(1): 14-27.
Variability of albumin adducts of 1,4-benzoquinone,
a toxic metabolite of benzene, in human volunteers.
Lin YS, McKelvey W, Waidyanatha S, Rappaport SM.
Department of Environmental Sciences and Engineering,
University of North Carolina, Chapel Hill, NC, 27599, USA.
smr@...;

History and origin of benzene in soft drinks,
Ross E. Getman, Esq, Wash DC and NY State Bars,
http://argentina.indymedia.org: Murray 2006.03.01
http://groups.yahoo.com/group/aspartameNM/message/1309

http://groups.yahoo.com/group/aspartameNM/message/1279
all three aspartame metabolites harm human erythrocyte
[red blood cell] membrane enzyme activity, KH Schulpis et al,
two studies in 2005, Athens, Greece, 2005.12.14:
2004 research review, RL Blaylock: Murray 2006.01.14

"High or abuse concentrations of ASP hydrolysis products
significantly decreased the membrane enzyme activity,
which was completely or partially prevented by L-cysteine
or reduced GSH."


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/1271

neurotoxic synergy of aspartame with Quinoline Yellow,
and L-glutamic acid with Brilliant Blue, in mouse cells,
Lau K, McLean WG, Williams DP, Howard CV, U. of
Liverpool, Toxicol Sci 2005.12.13: Murray
http://groups.yahoo.com/group/aspartameNM/message/1270

[Rich Murray:
  This study by an expert mainstream research team shows
that both aspartame and MSG harm developing mouse
neuroblastoma cells: "Inhibition of neurite outgrowth was
found at concentrations of additives theoretically achievable
in plasma by ingestion of a typical snack and drink."]



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/1263

Gubisne-Haberle D, Yu PH, et al, September, 2004 full text:

"Methylamine,
a major metabolite of creatine (Mitchell and Zhang, 2001),
can also be derived from adrenaline,
lecithin,
dietary sources,
and cigarette smoke (Yu, 1998).

SSAO converts methylamine into formaldehyde,
hydrogen peroxide,
and ammonium,
all of which are cytotoxic.

Aminoacetone is derived from threonine and glycine,
and its deamination
leads to the production of cytotoxic methylglyoxal.

Formaldehyde and methylglyoxal are extremely reactive
chemicals, which can interact with free amino or amide groups
to form Schiff's base, subsequently methylene bridges, and
produce irreversible covalently cross-linked complexes
between proteins, as well as between proteins
and single-stranded DNA (Bolt, 1987).

Increased protein aggregation and deposition is associated
with the aging process and with numerous pathological
conditions, such as the formation of plaques in the pancreas,
brain, kidney, and other organs."
_______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298  rmforall@...

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 146 members, 1,605 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1219 members, 24,065 posts in a public archive
_______________________________________________

23andMe.com, wired.com, Sergey Brin's Search for a Parkinson's Cure, Thomas
Goetz 2010 July free full text: some more methanol (formaldehyde, formic acid)
toxicity leads: Rich Murray 2010.06.26
http://rmforall.blogspot.com/2010_06_01_archive.htm
Saturday, June 26, 2010
[at end of each long page, click on Older Posts]
http://groups.yahoo.com/group/aspartameNM/message/1606
[you may have to Copy and Paste URLs into your browser]
_______________________________________________


http://whilesciencesleeps.com/references 589 references
[ click on titles to get free full text pdfs ]

Article 2 http://www.thetruthaboutstuff.com/review2.html
WC Monte, 2007 Dec

"Once methanol runs the gauntlet of first-pass metabolism,
its detoxification is no longer exclusive to the liver.

Formaldehyde, the first metabolite of methanol, can then be
produced within the arteries and veins,[#220] heart,[#503]
brain,[#218] lungs,[#221] breast,[#358] bone,[#503] and
skin.[#221]

These major organs harbor extra hepatic sites of the only
remaining human enzyme capable of metabolizing methanol,
class I alcohol dehydrogenase (ADH I).[#112]

Methanol transports its potential to become formaldehyde
past normal biological barriers in the brain and elsewhere that
environmental formaldehyde itself cannot usually penetrate.
[#122]"


23andMe has initiated a chain-reacting, exponentially evolving
global revolution for good in medicine -- a capitalist public
service profit firm that enables medical research and practice to
be democratic, populist, citizen funded, self-organizing, open,
creative, adaptable, efficient, cost-effective, fast, and beneficial
for prevention as well as treatment.

One bottom line result in a decade will be trillions of dollars of
benefits in the health and productivity of citizens.

With 50,000 participants now, yearly doubling for 10 years
would reach 50 million -- at a fee of $ 500 each, that is $ 25
billion.


Any way to get into this data gold mine?
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, along with tobacco and alcohol use,
maybe folic acid status.

It is available to any qualified research team.


23andMe publishes in PLoS Genetics, validates revolutionary
new paradigm for fast, flexible mass genetic data research,
free full text: more methanol (formaldehyde) toxicity leads:
Rich Murray 2010.06.25
http://rmforall.blogspot.com/2010_06_01_archive.htm
Thursday, June 24, 2010
[at end of each long page, click on Older Posts]
http://groups.yahoo.com/group/aspartameNM/message/1605
[you may have to Copy and Paste URLs into your browser]


23andMe.com mass medical data research can check WC
Monte (2007) claims, backed by many PDFs of research on
methanol (becomes formaldehyde in body tissues with high
ADH levels) and modern diseases -- multiple sclerosis, etc:
Rich Murray 2010.06.23
http://rmforall.blogspot.com/2010_06_01_archive.htm
Wednesday, June 23, 2010
[at end of each long page, click on Older Posts]
http://groups.yahoo.com/group/aspartameNM/message/1604
[you may have to Copy and Paste URLs into your browser]


Sergey Brin's Search for a Parkinson's Cure
By Thomas Goetz  June 22, 2010,12:00 pm, Wired July 2010

Buried deep within each cell in Sergey Brin's body -- in a
gene called LRRK2, which sits on the 12th chromosome -- is
a genetic mutation that has been associated with higher rates
of Parkinson's.
Illustration: Rafa Jenn

Several evenings a week, after a day's work at Google
headquarters in Mountain View, California, Sergey Brin drives
up the road to a local pool.
There, he changes into swim trunks, steps out on a 3-meter
springboard, looks at the water below, and dives.

Brin is competent at all four types of springboard
diving -- forward, back, reverse, and inward.
Recently, he's been working on his twists, which have been
something of a struggle.
But overall, he's not bad; in 2006 he competed in the
master's division world championships.
(He's quick to point out he placed sixth out of six in his
event.)

The diving is the sort of challenge that Brin, who has also
dabbled in yoga, gymnastics, and acrobatics, is drawn to:
equal parts physical and mental exertion.
"The dive itself is brief but intense," he says.
"You push off really hard and then have to twist right away.
  It does get your heart rate going."

There's another benefit as well:
With every dive, Brin gains a little bit of leverage -- leverage
against a risk, looming somewhere out there, that someday he
may develop the neurodegenerative disorder Parkinson's
disease.
Buried deep within each cell in Brin's body -- in a gene called
LRRK2, which sits on the 12th chromosome -- is a genetic
mutation that has been associated with higher rates of
Parkinson's.

Not everyone with Parkinson's has an LRRK2 mutation; nor
will everyone with the mutation get the disease.
But it does increase the chance that Parkinson's will emerge
sometime in the carrier's life to between 30 and 75 percent.
(By comparison, the risk for an average American is about 1
percent.)
Brin himself splits the difference and figures his DNA gives him
about 50-50 odds.

That's where exercise comes in.
Parkinson's is a poorly understood disease, but research has
associated a handful of behaviors with lower rates of disease,
starting with exercise.
One study found that young men who work out have a 60
percent lower risk.
Coffee, likewise, has been linked to a reduced risk.
For a time, Brin drank a cup or two a day, but he can't stand
the taste of the stuff, so he switched to green tea.
("Most researchers think it's the caffeine, though they don't
know for sure," he says.)
Cigarette smokers also seem to have a lower chance of
developing Parkinson's, but Brin has not opted to take up the
habit.
With every pool workout and every cup of tea, he hopes to
diminish his odds, to adjust his algorithm by counteracting his
DNA with environmental factors.

"This is all off the cuff," he says, "but let's say that based on
diet, exercise, and so forth, I can get my risk down by half, to
about 25 percent."
The steady progress of neuroscience, Brin figures, will cut his
risk by around another half -- bringing his overall chance of
getting Parkinson's to about 13 percent.
It's all guesswork, mind you, but the way he delivers the
numbers and explains his rationale, he is utterly convincing.

Brin, of course, is no ordinary 36-year-old.
As half of the duo that founded Google, he's worth about $15
billion.
That bounty provides additional leverage:
Since learning that he carries a LRRK2 mutation, Brin has
contributed some $50 million to Parkinson's research, enough,
he figures, to "really move the needle."
In light of the uptick in research into drug treatments and
possible cures, Brin adjusts his overall risk again, down to
"somewhere under 10 percent."
That's still 10 times the average, but it goes a long way to
counterbalancing his genetic predisposition.

It sounds so pragmatic, so obvious, that you can almost miss a
striking fact:
Many philanthropists have funded research into diseases they
themselves have been diagnosed with.
But Brin is likely the first who, based on a genetic test, began
funding scientific research in the hope of escaping a disease in
the first place.

His approach is notable for another reason.
This isn't just another variation on venture philanthropy -- the
voguish application of business school practices to scientific
research.
Brin is after a different kind of science altogether.
Most Parkinson's research, like much of medical research,
relies on the classic scientific method: hypothesis, analysis,
peer review, publication.
Brin proposes a different approach, one driven by
computational muscle and staggeringly large data sets.
It's a method that draws on his algorithmic sensibility -- and
Google's storied faith in computing power -- with the aim of
accelerating the pace and increasing the potential of scientific
research.
"Generally the pace of medical research is glacial compared to
what I'm used to in the Internet," Brin says.
"We could be looking lots of places and collecting lots of
information.
And if we see a pattern, that could lead somewhere."

In other words, Brin is proposing to bypass centuries of
scientific epistemology in favor of a more Googley kind of
science.
He wants to collect data first, then hypothesize, and then
find the patterns that lead to answers.
And he has the money and the algorithms to do it.

Given what seems like very bad news, most of us would
actually do what Brin did:
Go over our options, get some advice, and move on with life.
Illustration: Nathan Fox

Brin's faith in the power of numbers -- and the power of
knowledge, more generally -- is likely something he inherited
from his parents, both scientists.
His father, Michael, is a second-generation mathematician;
his mother Eugenia is trained in applied mathematics and spent
years doing meteorology research at NASA.
The family emigrated from Russia when Brin was 6. [1980]
At 17, [1991] he took up mathematics himself at the University
of Maryland, later adding a second major in computer science.
When he reached Stanford for his PhD -- a degree he still
hasn't earned, much to his parents' chagrin -- he focused on
data mining.
That's when he began thinking about the power of large data
sets and what might come of analyzing them for unexpected
patterns and insights.

Around the same time, in 1996, Brin's mother started to feel
some numbness in her hands.
The initial diagnosis was repetitive stress injury, brought on by
years of working at a computer.
When tests couldn't confirm that diagnosis, her doctors were
stumped.
Soon, though, Eugenia's left leg started to drag.
"It was just the same as my aunt, who had Parkinson's years
ago," she recalls.
"The symptoms started in the same way, at the same age.
To me, at least, it was obvious there was a connection."

At the time, scientific opinion held that Parkinson's was not
hereditary, so Brin didn't understand his mother's concern.
"I thought it was crazy and completely irrational," he says.
After further tests at Johns Hopkins and the Mayo Clinic,
though, she was diagnosed with Parkinson's in 1999.

Even after the LRRK2 connection was made in 2004, Brin still
didn't connect his mother's Parkinson's to his own health.
Then, in 2006, his wife-to-be, Anne Wojcicki, started the
personal genetics company 23andMe (Google is an investor).
As an alpha tester, Brin had the chance to get an early look at
his genome.
He didn't find much of concern.
But then Wojcicki suggested he look up a spot known as
G2019S -- the notch on the LRRK2 gene where an adenine
nucleotide, the A in the ACTG code of DNA, sometimes
substitutes for a guanine nucleotide, the G.
And there it was:
He had the mutation.
His mother's 23andMe readout showed that she had it, too.

Brin didn't panic;
for one thing, his mother's experience with the disease has
been reassuring.
"She still goes skiing," he says.
"She's not in a wheelchair."
Instead, he spent several months mulling over the results.
He began to consult experts, starting with scientists at the
Michael J. Fox Foundation and at the Parkinson's Institute,
which is not far from Google's headquarters.
He quickly realized it was going to be impractical to keep his
risk from the public.
"I can't talk to 1,000 people in secret," he says.
"So I might as well put it out there to the world.
It seemed like information that was worthy of sharing and
might even be interesting."

So one day in September 2008, Brin started a blog.
His first post was called simply "LRRK2."

"I know early in my life something I am substantially
predisposed to," Brin wrote.
"I now have the opportunity to adjust my life to reduce
those odds (e.g., there is evidence that exercise may be
protective against Parkinson's).
I also have the opportunity to perform and support research
into this disease long before it may affect me.
And, regardless of my own health, it can help my family
members as well as others."

Brin continued: "I feel fortunate to be in this position.
Until the fountain of youth is discovered, all of us will have
some conditions in our old age, only we don't know what
they will be.
I have a better guess than almost anyone else for what ills may
be mine -- and I have decades to prepare for it."

In a sense, we've been using genetics to foretell disease risk
forever.
When we talk about "family history," we're largely talking
about DNA, about how our parents' health might hint at our
own.
A genetic scan is just a more modern way to link our familial
past with our potential future.
But there's something about the precision of a DNA test that
can make people believe that chemistry is destiny -- that it
holds dark, implacable secrets.
This is why genetic information is sometimes described as
"toxic knowledge":
Giving people direct access to their genetic information, in the
words of Stanford bioethicist Hank Greely, is out and out
"reckless."

It's true that in the early days of the science, genetic testing
meant learning about a dreaded degenerative disease like
Huntington's or cystic fibrosis.
But these diseases, although easy to identify, are extremely
rare.
Newer research has shown that when it comes to getting sick,
a genetic predisposition is usually just one factor.
The vast majority of conditions are also influenced by
environment and day-to-day habits, areas where we can
actually take some action.

But, surprisingly, the concept of genetic information as toxic
has persisted, possibly because it presumes that people
aren't equipped to learn about themselves.
But research shows this presumption to be unfounded.
In 2009, The New England Journal of Medicine published
results of the Risk Evaluation and Education for Alzheimer's
Disease study, an 11-year project that sought to examine
how people react to finding out that they have a genetic risk
for Alzheimer's.
Like Parkinson's, Alzheimer's is a neurodegenerative
condition centering on the brain.
But unlike Parkinson's, Alzheimer's has no known treatment.
So learning you have a genetic predisposition should be
especially toxic.

In the study, a team of researchers led by Robert Green, a
neurologist and geneticist at Boston University, contacted
adults who had a parent with Alzheimer's and asked them to
be tested for a variation in a gene known as ApoE.
Depending on the variation, an ApoE mutation can increase a
person's risk for Alzheimer's from three to 15 times the
average.
One hundred sixty-two adults agreed; 53 were told they had
the mutation.

The results were delivered to the participants with great care:
A genetic counselor walked each individual through the data,
and all the subjects had follow-up appointments with the
counselor.
Therapists were also on call.
"People were predicting catastrophic reactions," Green recalls.
"Depression, suicide, quitting their jobs, abandoning their
families.
They were anticipating the worst."

But that isn't what happened.
People told that they were at dramatically higher risk for
developing Alzheimer's later in life seemed to process the
information and integrate it into their lives, often choosing to
lead more healthy lifestyles.
"People are handling it," Green says.
"It doesn't seem to be producing any clinically apparent
distress."

In other experiments, Green has further challenged the
conventional wisdom about the toxicity of genetic
information:
He has begun questioning the need for counselors and
therapists.
"We're looking at what happens if you don't do this
elaborate thing.
What if you do it like a lab test in your doctor's office?
We're treating it more like cholesterol and less like
Huntington's disease."

In other words, given what seems like very bad news, most of
us would do what Sergey Brin did:
Go over our options, get some advice, and move on with life.
"Everyone's got their challenges; everyone's got something to
deal with," Brin says.
"This is mine.
To me, it's just one of any number of things that I could get in
old age.
And the most important factor is that I can do something about
it."


High-Speed Science

Can a model fueled by data sets and computational power
compete with the gold standard of research?
Maybe: Here are two timelines -- one from an esteemed
traditional research project run by the NIH,
the other from the 23andMe Parkinson's Genetics Initiative.
They reached almost the same conclusion about a possible
association between Gaucher's disease and Parkinson's
disease, but the 23andMe project took a fraction of the time.
-- Rachel Swaby

Traditional Model

1. Hypothesis: An early study suggests that patients with
Gaucher's disease (caused by a mutation to the GBA gene)
might be at increased risk of Parkinson's.
2. Studies: Researchers conduct further studies, with varying
statistical significance.
3. Data aggregation: Sixteen centers pool information on more
than 5,500 Parkinson's patients.
4. Analysis: A statistician crunches the numbers.
5. Writing: A paper is drafted and approved by 64 authors.
6. Submission: The paper is submitted to The New England
Journal of Medicine. Peer review ensues.
7. Acceptance: NEJM accepts the paper.
8. Publication: The paper notes that people with Parkinson's
are 5.4 times more likely to carry the GBA mutation.

Total time elapsed: 6 years

Parkinson's Genetics initiative

1. Tool Construction: Survey designers build the questionnaire
that patients will use to report symptoms.
2. Recruitment: The community is announced, with a goal of
recruiting 10,000 subjects with Parkinson's.
3. Data aggregation: Community members get their DNA
analyzed. They also fill out surveys.
4. Analysis: Reacting to the NEJM paper, 23andMe
researchers run a database query based on 3,200 subjects.
The results are returned in 20 minutes.
5. Presentation: The results are reported at a Royal Society of
Medicine meeting in London: People with GBA are 5 times
more likely to have Parkinson's, which is squarely in line with
the NEJM paper. The finding will possibly be published at a
later date.

Total time elapsed: 8 months


If Brin's blog post betrayed little fear about his risk for
Parkinson's, it did show a hint of disappointment with the state
of knowledge on the disease.
(His critique was characteristically precise:
"Studies tend to have small samples with various selection
biases.")

His frustration is well founded.
For decades, Parkinson's research has been a poor cousin to
the study of Alzheimer's, which affects 10 times as many
Americans and is therefore much more in the public eye.
What is known about Parkinson's has tended to emerge from
observing patients in clinical practice, rather than from any
sustained research.
Nearly all cases are classified as idiopathic, meaning there's no
known cause.
Technically, the disease is a result of the loss of brain cells that
produce the neurotransmitter dopamine, but what causes those
cells to die is unclear.
The classic symptoms of the condition -- tremors, rigidity,
balance problems -- come on gradually and typically don't
develop until dopamine production has declined by around 80
percent, meaning that a person can have the disease for years
before experiencing the first symptom.

As far as treatments go, the drug levodopa, which converts to
dopamine in the brain, remains the most effective.
But the drug, developed in 1967, has significant side effects,
including involuntary movements and confusion.
Other interventions, like deep-brain stimulation, are invasive
and expensive.
Stem cell treatments, which generated great attention and
promise a decade ago, "didn't really work," says William
Langston, director of the Parkinson's Institute.
"Transferring nerve cells into the brain and repairing the brain
has been harder than anybody thought."

There are, however, some areas of promise -- including the
2004 discovery of the LRRK2 connection.
It's especially common among people of Ashkenazi descent,
like Brin, and appears in just about 1 percent of Parkinson's
patients.
Rare as the mutation is, however, LRRK2 cases of
Parkinson's appear indistinguishable from other cases, making
LRRK2 a potential window onto the disease in general.

LRRK2 stands for leucine-rich repeat kinase.
Kinases are enzymes that activate proteins in cells, making them
critical to cell growth and death.
In cancer, aberrant kinases are known to contribute to tumor
growth.
That makes them a promising target for research.
Drug companies have already developed kinase inhibitors for
cancer; it's a huge opportunity for Parkinson's treatment, as
well:
If overactive kinases interfere with dopamine-producing cells
in all Parkinson's cases, then a kinase inhibitor may be able to
help not just the LRRK2 carriers but all people with the
disease.

Another promising area for research is that delay between the
loss of dopamine-producing cells and the onset of symptoms.
As it stands, this lag makes treatment a much more difficult
problem.
"By the time somebody has full-blown Parkinson's, it's way
too late," Langston says.
"Any number of promising drugs have failed, perhaps because
we're getting in there so late."
But doctors can't tell who should get drugs earlier, because
patients are asymptomatic.
If researchers could find biomarkers -- telltale proteins or
enzymes detected by, say, a blood or urine test -- that were
produced before symptoms emerged, a drug regimen could
be started early enough to work.

And indeed, Brin has given money to both these areas of
research, predominantly through gifts to the Parkinson's
Institute and to the Michael J. Fox Foundation, which is
committed to what's called translational research -- getting
therapies from researchers to the clinic as quickly as possible.
Last February the Fox Foundation launched an international
consortium of scientists working on LRRK2, with a mandate
for collaboration, openness, and speed.
"The goal is to get people to change their behavior and share
information much more quickly and openly," says Todd
Sherer, head of the Fox Foundation's research team.
"We need to change the thinking."

As Brin's understanding of Parkinson's grew, though, and as
he talked with Wojcicki about research models, he realized
that there was an even bolder experiment in the offing.

In 1899, scientists at Bayer unveiled Aspirin, a drug it offered
as an effective remedy for colds, lumbago, and toothaches,
among other ills.
How aspirin -- or acetylsalicylic acid -- actually worked was
a mystery.
All people knew was that it did (though a discouraging side
effect, gastric bleeding, emerged in some people).

It wasn't until the 1960s and '70s that scientists started to
understand the mechanism:
Aspirin inhibits the production of chemicals in the body called
prostaglandins, fatty acids that can cause inflammation and
pain.
That insight proved essential to understanding the later
discovery, in 1988, that people who took aspirin every other
day had remarkably reduced rates of heart attack -- cases
in men dropped by 44 percent.
When the drug inhibits prostaglandins, it seems, it inhibits the
formation of blood clots, as well -- reducing the risk of heart
attack or stroke.

The second coming of aspirin is considered one of the triumphs
of contemporary medical research.
But to Brin, who spoke of the drug in a talk at the Parkinson's
Institute last August, the story offers a different sort of lesson --
one drawn from that period after the drug was introduced but
before the link to heart disease was established.
During those decades, Brin notes, surely "many millions or
hundreds of millions of people who took aspirin had a variety
of subsequent health benefits."
But the association with aspirin was overlooked, because
nobody was watching the patients.
"All that data was lost," Brin said.

In Brin's way of thinking, each of our lives is a potential
contribution to scientific insight.
We all go about our days, making choices, eating things,
taking medications, doing things -- generating what is
inelegantly called data exhaust.

A century ago, of course, it would have been impossible to
actually capture this information, particularly without a specific
hypothesis to guide a researcher in what to look for.
Not so today.
With contemporary computing power, that data can be
tracked and analyzed.
"Any experience that we have or drug that we may take, all
those things are individual pieces of information," Brin says.
"Individually, they're worthless, they're anecdotal.
But taken together they can be very powerful."

In computer science, the process of mining such large data
sets for useful associations is known as a market-basket
analysis.
Conventionally, it has been used to divine patterns in retail
purchases.
It's how Amazon.com can tell you that "customers who
bought X also bought Y."

But a problem emerges as the data in a basket become less
uniform.
This was the focus of much of Brin's work at Stanford, where
he published several papers on the subject.
One, from 1997, argued that given the right algorithms,
meaningful associations can be drawn from all sorts of
unconventional baskets -- "student enrollment in classes, word
occurrence in text documents, users' visits of Web pages, and
many more."
It's not a stretch to say that our experiences as patients might
conceivably be the next item on the list.

This is especially true given the advances in computational
power since 1997, when Brin and his fellow Stanford
comp-sci student Larry Page were starting Google.

"When Larry and I started the company," Brin says, "we had
to get some hard drives to, you know, store the entire Web.
We ended up in a back alley in San Jose, dealing with some
shady guy.
We spent $10,000 or $20,000, all our life savings.
We got these giant stacks of hard drives that we had to fit in
our cars and get home.
Just last week I happened to go to Fry's and I picked up a
hard drive that was 1 terabyte and cost like $100.
And it was bigger than all those hard drives put together."

This computing power can be put to work to answer questions
about health.
As an example, Brin cites a project developed at his
company's nonprofit research arm, Google.org.
Called Google Flu Trends, the idea is elegantly simple:
Monitor the search terms people enter on Google, and pull
out those words and phrases that might be related to
symptoms or signs of influenza, particularly swine flu.
In epidemiology, this is known as syndromic surveillance,
and it usually involves checking drugstores for purchases of
cold medicines, doctor's offices for diagnoses, and so forth.

But because acquiring timely data can be difficult, syndromic
surveillance has always worked better in theory than in
practice.
By looking at search queries, though, Google researchers were
able to analyze data in near real time.
Indeed, Flu Trends can point to a potential flu outbreak two
weeks faster than the CDC's conventional methods, with
comparable accuracy.
"It's amazing that you can get that kind of signal out of very
noisy data," Brin says.
"It just goes to show that when you apply our newfound
computational power to large amounts of data -- and
sometimes it's not perfect data -- it can be very powerful."
The same, Brin argues, would hold with patient histories.
"Even if any given individual's information is not of that great
quality, the quantity can make a big difference.
Patterns can emerge."

Brin's tolerance for "noisy data" is especially telling, since
medical science tends to consider it poisonous.
Biomedical researchers often limit their experiments to narrow
questions that can be rigorously measured.
But the emphasis on purity can mean fewer patients to study,
which results in small data sets.
That limits the research's "power" -- a statistical term that
generally means the probability that a finding is actually true.
And by design it means the data almost never turn up insights
beyond what the study set out to examine.

Increasingly, though, scientists -- especially those with a
background in computing and information theory -- are
starting to wonder if that model could be inverted.
Why not start with tons of data, a deluge of information, and
then wade in, searching for patterns and correlations?

This is what Jim Gray, the late Microsoft researcher and
computer scientist, called the fourth paradigm of science, the
inevitable evolution away from hypothesis and toward
patterns.

Gray predicted that an "exaflood" of data would overwhelm
scientists in all disciplines, unless they reconceived their notion
of the scientific process and applied massive computing tools
to engage with the data.
"The world of science has changed," Gray said in a 2007
speech -- from now on, the data would come first
.
Gray's longtime employer, Bill Gates, recently made a small
wager on the fourth paradigm when he invested $10 million in
Schrödinger, a Portland, Oregon-based firm that's using
massive computation to rapidly simulate the trial and error of
traditional pharmaceutical research.

And Andy Grove, former chair and CEO of Intel, has likewise
called for a "cultural revolution" in science, one modeled on the
tech industry's penchant for speedy research and development.

Grove, who was diagnosed with Parkinson's in 2000 and has
since made the disease his casus belli, shakes his fist at the
pace of traditional science:
"After 10 years in the Parkinson's field, we may finally have
three drugs in Phase I and Phase II trials next year -- that's
more than ever before.
But let's get real.
We'll get the results in 2012, then they'll argue about it for a
year, then Phase III results in 2015, then argue about that for
a year -- if I'm around when they're done ."
He doesn't finish his thought.
"The whole field is not pragmatic enough.
They're too nice to themselves."

Grove disagrees somewhat with Brin's emphasis on patterns
over hypothesis.
"You have to be looking for something," he says.
But the two compare notes on the disease from time to time;
both are enthusiastic and active investors in the Michael J. Fox
Foundation.
(Grove is even known to show up on the online discussion
forums.)

In the world of traditional drug research, however, there's
more than a little skepticism about swapping out established
biomedical approaches for technological models.
Derek Lowe, a longtime medicinal chemist and author of a
widely read drug industry blog, grants that big hardware and
big data can be helpful.
But for a disease as opaque as Parkinson's, he argues, the
challenge of drug development will always come down to
basic chemistry and biology.
"I don't have a problem with data," Lowe says.
"The problem is that the data is tremendously noisy stuff.
We just don't know enough biology.
If Brin's efforts will help us understand that, I'm all for it. But
I doubt they will."

To be sure, biomedicine, and pharmaceutical research in
particular, is not the same as software or computer chips.
It's a much more complicated process, and Brin acknowledges
as much:
"I'm not an expert in biological research.
I write a bunch of computer code and it crashes, no big deal.
But if you create a drug and it kills people, that's a different
story."
Brin knows that his method will require follow-up research to
get through the traditional hoops of drug discovery and
approvals.
But, he adds, "in my profession you really make progress
based on how quick your development cycle is."

So, with the cooperation of the Parkinson's Institute, the
Fox Foundation, and 23andMe, he has proposed a new
development cycle.
Brin has contributed $4 million to fund an online Parkinson's
Disease Genetics Initiative at 23andMe:
10,000 people who've been diagnosed with the disease and
are willing to pour all sorts of personal information into a
database.
(They've tapped about 4,000 so far.)

Volunteers spit into a 23andMe test tube to have their DNA
extracted and analyzed.
That information is then matched up with surveys that extract
hundreds of data points about the volunteers' environmental
exposures, their family history, disease progression, and
treatment response.
The questions range from the mundane
("Are you nearsighted?") -- to the perplexing
("Have you had trouble staying awake?").
It is, in short, an attempt to create the always-on
data-gathering project that Brin believes could aid all medical
research -- and, potentially, himself.
"We have no grand unified theory," says Nicholas Eriksson,
a 23andMe scientist.
"We have a lot of data."

Tags: chromosome, DNA, genetic mutation, google,LRRK2,
parkinson's, research, Sergey Brin
_______________________________________________



formaldehyde and other toxins in new cars restricted in
Sweden and Japan, Severin Carrell, The Independent, UK:
Murray 2005.10.16
http://groups.yahoo.com/group/aspartameNM/message/1235

James S. Turner, Esq. letter on improper approval of
aspartame by FDA in 1981, to New Mexico Environmental
Improvement Board 2005.09.20, plain text:
Murray 2005.09.23
http://groups.yahoo.com/group/aspartameNM/message/1218

diabetic Richard Larson free of headaches by giving up
aspartame, Fae Woodward, The Willits News, California:
Murray 2005.09.15
http://groups.yahoo.com/group/aspartameNM/message/1214

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/1213

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 2004.07.27
http://groups.yahoo.com/group/aspartameNM/message/1189

diet soda (aspartame) goes with more obesity, Sharon P
Fowler, University of Texas Health Science Center, San
Antonio, Charlotte E. Grayson, MD, WebMD.com,
foxnews.com 2005.06.15: related articles:
Murray 2005.06.27
http://groups.yahoo.com/group/aspartameNM/message/1177

five recent abstracts on formaldehyde damage to cells --
vitamin E and selenium protect, Yoshiro Saito and Yasukazu
Yoshida et al, O'Brien PJ et al, Costa M et al:
Murray 2005.06.07
http://groups.yahoo.com/group/aspartameNM/message/1173

three independent double-blind experiments on aspartame
and headache in 1988, 1993, 1994: Murray 2005.06.04
http://groups.yahoo.com/group/aspartameNM/message/1171

EPA Preliminary Remedial Goals (PRG) 2003 Oct, air and
tap water -- methanol, formaldehyde, formic acid -- sources
omitted are methanol from aspartame, dark wines and
liquors, fruit pectins: Murray 2005.01.18 rmforall
http://groups.yahoo.com/group/aspartameNM/message/1145

Toxicological Profile for Formaldehyde 3/4 plain text,
229 to 342 of 468 pages
USA DHHS PHS ATSDR 1999 July: Murray 2004.09.03
http://groups.yahoo.com/group/aspartameNM/message/1111

This is really buried in the 1999 468-page ATSDR report:

" b. Water:

EPA 1-d Health Advisory (child)-draft 10 mg/L EPA 1995;

IRIS 1999 10-d Health Advisory (child)-draft 5 mg/L

Lifetime Health Advisory (adult)-draft 1 mg/L "


Four state water limits are 10 to 100 times more stringent:

" b. Water

Water Quality Criteria: Human Health

CA Drinking water (guideline) 30 µg/L FSTRAC 1995

MD Drinking water (guideline) 10 µg/L

ME Drinking water (guideline) 30 µg/L

NJ Drinking water (guideline) 100 µg/L "


antiseptic? antifungal? antiviral? 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/1143

re: Lenore S. Greenstein reply: three highly proclaimed, but
flawed, pro-aspartame studies: Leon 1989, Schiffman 1987,
Spiers 1998: Murray 2004.11.11
http://groups.yahoo.com/group/aspartameNM/message/1137

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/1131



continuing aspartame debate in British Medical Journal,
John Biffra, Bob Dowling, Nick Finer, Ian J Gordon:
Murray 2005.02.09
http://groups.yahoo.com/group/aspartameNM/message/1155

Mark Gold, most recent of 14 Rapid Responses to
Aspartame and its effects on health, BMJ:
Murray 2004.11.06
http://groups.yahoo.com/group/aspartameNM/message/1133

8 more Rapid Responses to Aspartame and its effects on
health, BMJ: Murray 2004.10.18
http://groups.yahoo.com/group/aspartameNM/message/1124

5 critical Rapid Responses to Aspartame and its effects on
health, Michael E J Lean and Catherine R Hankey,
BMJ 2004; 329: 755-756: Murray 2004.10.05
http://groups.yahoo.com/group/aspartameNM/message/1120

Aspartame and its effects on health, Michael E.J. Lean,
Catherine R. Hankey, Glasgow UK, British Medical Journal:
11% methanol component of aspartame, and same level of
methanol in dark wines and liquors, turns to formaldehyde
and formic acid, the main cause of chronic hangover
symptoms: Murray 2004.10.04
http://groups.yahoo.com/group/aspartameNM/message/1117

http://bmj.bmjjournals.com/cgi/eletters/329/7469/755#76712

http://www.bmj.com/cgi/content/full/329/7469/755


genotoxins, Comet assay in mice: Ace-K, stevia fine;
aspartame poor; sucralose, cyclamate, saccharin bad:
Sasaki YF, Aug, Dec 2002: Rencuzogullari E et al,
Aug 2004: Murray 2003.01.27, 2004.10.17
http://groups.yahoo.com/group/aspartameNM/message/1123


Alcohol Hangover (formaldehyde from methanol impurity),
Robert M Swift, Dena Davidson 1998: Murray 2004.11.17
http://groups.yahoo.com/group/aspartameNM/message/1138

hangover symptoms from methanol from dark wines and
liquors or 11% methanol part of aspartame, review of
research: Jones AW 1988: Murray 2004.10.23
http://groups.yahoo.com/group/aspartameNM/message/1128


[ For a 60 kg person,
this would be 90 mg bourbon, 0.09 liter,
giving 2.34 mg methanol, which led to twice as many
symptoms as the 0.35 mg methanol from vodka.
The bourbon gave as about as much methanol
as an ounce of diet soda. ]

http://bmj.bmjjournals.com/search.dtl
[ search to get free full text ]
British Medical Journal 1997 (4 January); 314(7073): 2.
Ian Calder, F.R.C.A.
Tel/Fax: 0171 720 9279
Consultant Anaesthetist at
the National Hospital for Neurology and Neurosurgery,
London WCIN 3BG, UK

Editorials
Hangovers: Not the ethanol -- perhaps the methanol

"Wine is only sweet to happy men," wrote an unhappy John
Keats to his sweetheart.(1)  His observation seems to have
been vindicated.

Harburg et al found that psychosocial factors such as guilt
about drinking, a neurotic personality, becoming angry or
depressed while drinking, and having suffered "negative life
events" in the past 12 months are better predictors of
symptoms of hangover than the amount of ethanol drunk.(2)

In fact, ethanol itself may play only a minor part in producing
the thirst, headache, fatigue, nausea, sweating, tremor,
remorse, and anxiety that hangover sufferers report.

Hangover symptoms are worst at a time when almost all
ethanol and its metabolite acetaldehyde have been cleared
from the blood, and peak blood ethanol or acetaldehyde
levels are not related to the severity of hangover.(3 )

Between a quarter and a half of drinkers claim not to
experience hangover symptoms despite having been
intoxicated.(2, 3, 4)

Congeners -- complex organic molecules such as polyphenols,
higher alcohols including methanol, and histamine, which occur
in varying amounts in ethanolic drinks -- are probably more to
blame than ethanol.

Chapman found that hangover symptoms were almost twice as
common in volunteers who drank 1.5 ml/kg [ body weight ] of
bourbon whiskey -- which has methanol concentrations of
26 mg/l -- as in those drinking the same dose of vodka
( 3.9 mg of methanol per litre ). (5)

[ For a 60 kg person,
this would be 90 mg bourbon,  0.09 liter,
giving 2.34 mg methanol, which led to twice as many
symptoms as the 0.35 mg methanol from vodka.
The bourbon gave as about as much methanol
as an ounce of diet soda. ]

Pawan compared the hangover produced by different types of
drink (but only one brand of each) in his study of 20
volunteers. The severity of hangover symptoms declined in the
order of brandy, red wine, rum, whisky, white wine, gin,
vodka, and pure ethanol.(6)  Vodka and pure ethanol caused
only mild headaches in two volunteers.

Jones has suggested that it is the metabolism of methanol to
formaldehyde and formic acid that causes symptoms of
hangover, with quicker methanol metabolisers suffering
more.(7)  The justification for this suggestion is threefold:
the types of drink associated with more severe hangovers
contain higher levels of methanol;
the time course of methanol metabolism corresponds to the
onset of symptoms;
and a small dose of ethanol, which blocks the formation of
formaldehyde and formic acid, provides an effective treatment
for hangovers ("the hair of the dog").

The economic and social consequences of hangovers are
probably considerable but difficult to quantify. Performance
accuracy is impaired synergistically by sleep deprivation and
hangover.(8)
Drivers perform less well in simulators when tested the
morning after drinking ethanol.(9)
Making driving with a hangover a criminal offence might be
logical, but is probably impractical in the absence of a simple
diagnostic test like breath alcohol.

Many pathophysiological disturbances occur during hangover,
including dehydration; metabolic acidosis; hypoglycaemia;
disturbed prostaglandin synthesis; abnormal secretion of
vasopressin, cortisol, aldosterone, renin, and testosterone;
increased cardiac output; tachycardia; and vasodilatation.

Hypoglycaemia and acidosis can be treated with fructose or
glucose,(9) and the cardiovascular abnormalities with
B blockade,(10) but symptoms are not alleviated.
However, rehydration and anti-inflammatory analgesics are
helpful, particularly if treatment is started before bedtime.(11)

A completely effective treatment is probably unattainable
(since so many factors -- such as lack of sleep, active or
passive smoking, dietary indiscretions, unaccustomed
physical activity, intermittent upper airway obstruction, and
emotional disturbances -- must play a part) and is arguably
undesirable since the fear of hangover prompts most people
to moderate their ethanol intake.(4 )

Even moderate amounts of ethanol can be damaging,(12) so
a penalty for consumption is in our interests. Perhaps those
who aspire to be one of Dr Johnson's "heroes" by drinking
brandy (13) are sensible as well as brave.

Ian Calder, Consultant anaesthetist, Department of
Neuroanaesthesia,
National Hospital for Neurology and Neurosurgery,
Queen Square, London WC1N 3BG UK

1. Keats J. Letter to Fanny Brawne. In: Tripp RT, ed.
The international thesaurus of quotations.
England: Penguin, 1976: 266.

2. Harburg E, Gunn R, Gleiberman L, DiFranceisco W,
Schork A.
Psychosocial factors, alcohol use and hangover signs among
social drinkers: a reappraisal.
J Clin Epidemiol 1993; 46: 413-22. [Medline]

3. Ylikahri RH, Huttunen M, Eriksson CJ, Nikkila EA.
Metabolic studies on the pathogenesis of hangover.
Eur J Clin Invest 1974; 4: 93-100.

4. Smith CM, Barnes GM.
Signs and symptoms of hangover; prevalence and relationship
to alcohol use in a generally adult population.
Drug Alcohol Depend 1983; 11: 249-69. [Medline]

5. Chapman LF.
Experimental induction of hangover.
Q J Stud Alcohol 1970; 5: 67-85. [Medline]

6. Pawan GLS.
Alcoholic drinks and hangover effects.
Proc Nutr Soc 1973; 32: 15A.

7. Jones AW.
Elimination half-life of methanol during hangover.
Pharmacol Toxicol 1987; 60; 217-20.

8. Peeke SC, Callaway E, Jones RT, Stone GC, Doyle J.
Combined effect of alcohol and sleep deprivation in normal
young adults.
Psychopharmacol 1980; 67: 279-87. [Medline]

9. Seppala T, Leino T, Linnoila M, Huttunen MO,
Ylikahri RH.
Effects of hangover on psychomotor skills related to driving:
modification by fructose and glucose.
Acta Pharmacol Toxicol 1976; 38: 209-18.

10. Bogin RM, Nostrant TT, Young MJ.
Propranolol for the treatment of the alcoholic hangover.
Am J Drug Alcohol Abuse 1986; 12: 279-84.

11. Khan MA, Jensen K, Krogh HJ.
Alcohol induced hangover. A double blind comparison of
pyritinol and placebo in preventing hangover symptoms.
Q J Stud Alcohol 1973; 34: 1195-201. [Medline]

12. Karhunen PJ, Erkinjuntti T, Laippala P.
Moderate alcohol consumption and loss of cerebellar
Purkinje cells.
BMJ 1994; 308: 1663-7.

13. Boswell J.
Life of Johnson. April 7th 1779.
Oxford University Press: Oxford, 1970.
_______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298  rmforall@...

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 146 members, 1,606 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1219 members, 24,066 posts in a public archive
_______________________________________________


[Non-text portions of this message have been removed]

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, Lyme disease: Murray 2004.08.08 2010.06.27
http://groups.yahoo.com/group/aspartameNM/message/1607
64 KB truncated version 2010.06.27

http://rmforall.blogspot.com/2010_06_01_archive.htm
Sunday, June 27, 2010 full text
http://health.groups.yahoo.com/group/aspartameNM/files/
205 KB full text


Herein I offer abstracts and three full texts of dozens of studies by a
world-class biochemist and her associates, mostly experiments with rats, on
ethanol toxicity since 1984 and methanol toxicity since 1993. Enough
details are provided to show the competency and credibility of E.
Skrzydlewska and her colleagues over two decades, and to make access to
their literature more convenient for professionals.

For instance, anyone can click on this post at the above URL, and in Outlook
Express, use Control F to search the text for any word. Yahoo Groups also
includes a fine search function.

A conscientious, responsible review of any reseach that affects the
interests of vast commercial vested interests has to provide justified
criticism of dubious studies, reviews, and conclusions, that are
characteristically the main sources for private and professional
information. My experience since I first started investigating toxicity
issues in 1999 is, count on it, wolves guard the sheep.

To be effective, this criticism has to be calm, civil, detailed, specific,
reasonable, founded on evidence, focused on issues and not on persons, and
based on easily accessed public sources, so that anyone interested in basing
their conclusions on facts can start the laborous process of deciding for
themselves.

http://groups.yahoo.com/group/aspartameNM/message/667
25 rules of disinformation , Sweeney 1997: Murray 2001.07.04 rmforall

As a medical layman, age 68, after two decades as a home health care
giver, my volunteer public service for toxicity issues on the Net since
January 1999 depends entirely on earning credibility by deserving it.

http://groups.yahoo.com/group/aspartameNM/messages
146 members, 1,607 posts in a public searchable archive

I regret that I almost never receive negative feedback based on any
specifics of this work, for this would enable me, in the finest tradition
of science, to either reverse, amend, or clarify my positions, to the
benefit of humanity, as well as deepening my own satisfaction and confidence
in a long-term effort.

However, it is indubitable that the best disinformation strategy is to
simply ignor any inconvenient researchers and their work, or, if that
becomes problematic due to the quality of the worker and his work, to firmly
repeat the exact opposite of truth, for example, "Aspartame is the most
tested food additive in history," while using ad hominen statements to
dismiss, ridicule, and marginalize the opposition. Fanning a "flame war" of
escalating incivility is a virtually infallible strategy for muddying the
waters, preventing any real examination of actual facts.

I should also here assert that, so far, I have not ever received a
penny of support for my toxicity service, save for about $ 300 of free
books, from both sides of the debate. Furthermore, when the happy day
ensues when I receive payment of any sort, I will immediately and forever
make this clearly and completely known on the Net, along with full details
for contacting the sources, who must agree to repond responsibly,
immediately, and publicly to all inquiries. All my financial information
about this work will be immediately, clearly, and forever public. I cannot
be bought, bent, or borrowed. I don't deal in secret.

A persistent, consistent campaign that provides facts about an actual toxin
can only succeed.

Fact is, the 11% methanol component of aspartame, readily released into the
G.I. tract, is within hours converted into potent amounts of formaldehyde
and formic acid, in amounts scores of times higher than that allowed by the
EPA for daily drinking water.

I have recently summarized mainstream evidence that the similar amounts of
methanol impurity, about one part in ten thousand, in dark wines and
liquors, are largely responsible for the famed "morning after" hangover:

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 2004.08.06 rmforall

Similar potent levels of methanol, and its inevitable products in the human
body, formaldehyde and formic acid, can also ensue from fermentation of
fruits by certain yeast and bacteria in the colon:

Alcohol Clin Exp Res. 1997 Aug; 21(5): 939-43.
Endogenous production of methanol after the consumption of fruit.
Lindinger W, Taucher J, Jordan A, Hansel A, Vogel W.
Institut fur Ionenphysik, Leopold Franzens Universitat Innsbruck, Austria.

After the consumption of fruit, the concentration of methanol
in the human body increases by as much as an order of magnitude.
This is due to the degradation of natural pectin
(which is esterified with methyl alcohol) in the human colon.
In vivo tests performed by means of proton-transfer-reaction
mass spectrometry show that consumed pectin
in either a pure form (10 to 15 g)
or a natural form (in 1 kg of apples) induces a
significant increase of methanol in the breath
(and by inference in the blood) of humans.
The amount generated from pectin (0.4 to 1.4 g)
[ 400 -1400 mg ] is approximately
equivalent to the total daily endogenous production
(measured to be 0.3 to 0.6 g/day) [ 300 to 600 mg ]
or that obtained from 0.3 liters of 80-proof brandy
(calculated to be 0.5 g). [ 500 mg ]
This dietary pectin may contribute to the development
of nonalcoholic cirrhosis of the liver. PMID: 9267548

[ Methanol has a blood half-life of about 2.5 hours,
so after 13 hours, its blood level is reduced to about
3 %, which would be 12 to 42 mg for the whole body,
if the degradation of pectin by bacteria in the GI tract
is fast, while slower production of methanol from pectin
would produce lower peak methanol levels.

The ADH enzyme does not start to convert methanol
into formaldehyde until blood levels of ethanol have
become very low -- then the resulting conversion of the
residual methanol into formaldehyde in specific tissues
is the main cause of "morning after" hangover symptoms.

High levels of folic acid protect many people
from this toxic production of formaldehyde,
but not for the brain or retina. ]

Alcohol Clin Exp Res. 1995 Oct; 19(5): 1147-50.
Methanol in human breath.
Taucher J, Lagg A, Hansel A, Vogel W, Lindinger W.
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 = 64 mg ethanol and 0.19 ml = 0.33 mg methanol ] PMID: 8561283


These three potent dietary sources of methanol, formaldehyde, and formic
acid, which impact many people, and cause the same symptoms in vulnerable
and sensitized people, are ignored in the following prestigious, official
source:


[ Extracts ] [ My comments are in square brackets. ]

http://www.atsdr.cdc.gov/toxprofiles/tp111.pdf

[ I saved this document as 4 plain text files of 250 to 289 KB each:

http://health.groups.yahoo.com/group/aspartameNM/files/ ]

TOXICOLOGICAL PROFILE FOR FORMALDEHYDE
U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES
Public Health Service Agency for Toxic Substances and Disease Registry
July 1999

[ http://www.atsdr.cdc.gov atsdric@... 888-42-ATSDR
404-498-0110 fax 404-498-0093

Agency for Toxic Substances and Disease Registry Division of Toxicology
1600 Clifton Road NE, Mailstop E-29 Atlanta, GA 30333
* Information line and technical assistance Phone: (800) 447-1544 Fax:
(404) 639-6359

* To order toxicological profiles, contact
National Technical Information Service 5285 Port Royal Road Springfield,
VA 22161 Phone: (800) 553-6847 or (703) 487-4650

The National Center for Environmental Health (NCEH) focuses on preventing or
controlling disease, injury, and disability related to the interactions
between people and their environment outside the workplace.
http://www.cdc.gov/nceh/ 888-232-6789
http://www2.cdc.gov/nceh/contactnceh/frmSubmit.asp email contact
Contact: NCEH, Mailstop F-29, 4770 Buford Highway, NE, Atlanta, GA
30341-3724 . Phone: 770-488-7000 . FAX: 770-488-7015.

The National Institute for Occupational Safety and Health (NIOSH) conducts
research on occupational diseases and injuries, responds to requests for
assistance by investigating problems of health and safety in the workplace,
recommends standards to the Occupational Safety and Health Administration
(OSHA) and the Mine Safety and Health Administration (MSHA), and trains
professionals in occupational safety and health.
http://www.cdc.gov/niosh/homepage.html eidtechinfo@...
Contact: NIOSH, 200 Independence Avenue, SW, Washington, DC 20201 . Phone:
513-533-8328 800-356-4674 or NIOSH Technical Information Branch, Robert A.
Taft Laboratory, Mailstop C-19, 4676 Columbia Parkway, Cincinnati, OH
45226-1998 Phone: 800-35-NIOSH fax 513-533-8573

The National Institute of Environmental Health Sciences (NIEHS) is the
principal federal agency for biomedical research on the effects of chemical,
physical, and biologic environmental agents on human health and well-being.
http://www.niehs.nih.gov/
Contact: NIEHS, PO Box 12233, 104 T.W. Alexander Drive,
Research Triangle Park, NC 27709 . Phone: 919-541-3212.
Office of Communications 919-541-3345 TTY 919-541-0731


Referrals
The Association of Occupational and Environmental Clinics (AOEC) has
developed a network of clinics in the United States to provide expertise in
occupational and environmental issues. Contact:
AOEC, 1010 Vermont Avenue, NW, #513, Washington, DC 20005
Phone: 202-347-4976 FAX: 202-347-4950
Web Page: http://www.aoec.org/ e-mail: AOEC@...

AOEC Clinic Director: http://occ-envmed.mc.duke.edu/oem/aoec.htm.

The American College of Occupational and Environmental Medicine (ACOEM) is
an association of physicians and other health care providers specializing in
the field of occupational and environmental medicine.
http://www.acoem.org/ http://www.acoem.org/feedback/ email contact
Contact: ACOEM, 55 West Seegers Road, Arlington Heights, IL 60005
Phone: 847-818-1800 FAX: 847-818-9266. ]

FORMALDEHYDE page iii

UPDATE STATEMENT
Toxicological profiles are revised and republished as necessary, but no less
than once every three years. [ I could not locate any more recent updates
than July 1999 via Google. ]

FORMALDEHYDE ix

CONTRIBUTORS
CHEMICAL MANAGER(S)/AUTHORS(S):
Sharon Wilbur, M.A. [ Not a PhD level degree ]
[ Environmental Health Scientist ]
ATSDR, Division of Toxicology, Atlanta, GA

M. Olivia Harris, M.A. [ Not a PhD level degree ]
ATSDR, Division of Toxicology, Atlanta, GA
[ Environmental Health Scientist
1600 Clifton Road NE, E29 Atlanta, GA 30333
P: 404-639-5091 F: 404-639-6315 oxh0@... ]

Peter R. McClure, Ph.D., DABT [ Veterinarian ]
Syracuse Research Corporation, North Syracuse, NY
[ Syracuse Research Corporation Environmental Science Center
301 Plainfield Road Suite 350 Syracuse, New York 13212 (315) 452 8420
mcclure@... ]

Wayne Spoo, DVM, DABT, DABVT [ Veterinarian ]
Research Triangle Institute, Research Triangle Park, NC
[ Jerry Wayne Spoo Operations Director, Life Sciences and Toxicology
919-541-6000 jwspoo@... http://www.rti.org http://www.abvt.org/

CPT Spoo, HHC, USACAPOC, AOCP-MS, 910-432-2209.
jerry.w.spoo@... ]

FORMALDEHYDE xi

PEER REVIEW
A peer review panel was assembled for formaldehyde. The panel consisted of
the following members:
1. Carson Conaway, Research Scientist, American Health Foundation, Valhalla,
New York 10595;
[ http://www.ahf.org/contact/ 914-789-7210 914-789-7243
1 Dana Road Valhalla, NY 10595
300 E. 42nd. Street New York, NY 10017

http://www.ifcp.us/Scientists-Scientists-Carson_Conaway.cfm
Carson Clifford Conaway, Ph. D., DABT [ Veterinarian ]
Research Scientist phone: (914) 789-7210 email: cconaway@...
Institute for Cancer Prevention
In addition to his research work, Dr. Conaway is an Adjunct Associate
Professor in the Department of Pharmacology, New York Medical College. In
that capacity, he is called upon to present lectures in toxicology to
graduate students in the College of Basic Medical Sciences and in the School
of Public Health.

2. John Egle, Jr., Professor, Department of Pharmacology and Toxicology,
Medical College of Virginia, Smith Bldg., Room 656, Richmond, VA 23219; and
[ http://www.medschool.vcu.edu/ John L. Egle, Jr no longer listed. Last
PubMed study in 1995 . Studies on formaldehyde, 2 in 1974, 1 in 1972, no
PubMed abstracts for these. ]

3. Vincent Garry, Director, Environmental Medicine, University of Minnesota,
421 29th Ave., SE Minneapolis, MN 55414.

[
http://www.iatp.org/foodandhealth/library/admin/uploadedfiles/Vincent_Garry_Bio.\
pdf
Vincent F Garry Title: Professor
Department: Lab Medicine/Pathology (office: Lab Med/Pathology Department)
Dept Campus: UMN Twin Cities
E-mail Address: garry001@...
Office Address: Lab Med/Pathology Department
225 Mayo 8609 420 Delaware St SE Minneapolis, MN 55455
Campus Mail: Lab Medicine and Pathology
MMC 609 Mayo 8609 420 Delaware St SE Minneapolis, MN 55455
Office Phone:+1 612-626-3354 Fax:+1 612-626-3380
Address: 4829 Girard Ave So Minneapolis, MN 55409
Phone:+1 612-827-7316

Toxicol Appl Pharmacol. 2004 Jul 15; 198(2): 152-63.
Pesticides and children.
Garry VF.
Department of Laboratory Medicine and Pathology and Program in Toxicology,
University of Minnesota School of Medicine, Minneapolis, MN 55455, USA.

Prevention and control of damage to health, crops, and property by insects,
fungi, and noxious weeds are the major goals of pesticide applications.
As with use of any biologically active agent, pesticides have unwanted
side-effects. In this review, we will examine the thesis that adverse
pesticide effects are more likely to occur in children who are at special
developmental and behavioral risk. Children's exposures to pesticides in the
rural and urban settings and differences in their exposure patterns are
discussed.
The relative frequency of pesticide poisoning in children is examined.
In this connection, most reported acute pesticide poisonings occur in
children younger than age 5.
The possible epidemiological relationships between parental pesticide use or
exposure and the risk of adverse reproductive outcomes and childhood cancer
are discussed.
The level of consensus among these studies is examined.
Current concerns regarding neurobehavioral toxicity and endocrine disruption
in juxtaposition to the relative paucity of toxicant mechanism-based studies
of children are explored. PMID: 15236951 ]

These experts collectively have knowledge of formaldehyde's physical and
chemical properties, toxicokinetics, key health end points, mechanisms of
action, human and animal exposure, and quantification of risk to humans.

All reviewers were selected in conformity with the conditions for peer
review specified in Section 104(I)(13) of the Comprehensive Environmental
Response, Compensation, and Liability Act, as amended.

Scientists from the Agency for Toxic Substances and Disease Registry (ATSDR)
have reviewed the peer reviewers' comments and determined which comments
will be included in the profile.

A listing of the peer reviewers' comments not incorporated in the profile,
with a brief explanation of the rationale for their exclusion, exists as
part of the administrative record for this compound. [ Not easily accessible
by public ]

A list of databases reviewed and a list of unpublished documents cited are
also included in the administrative record. [ Not easily accessible by
public ]

The citation of the peer review panel should not be understood to imply its
approval of the profile's final content. The responsibility for the content
of this profile lies with the ATSDR.... [ Apparently, the peer review
panel's opinions carry little weight. ]

1. PUBLIC HEALTH STATEMENT
This public health statement tells you about formaldehyde and the effects of
exposure....

1.2 WHAT HAPPENS TO FORMALDEHYDE WHEN IT ENTERS THE
ENVIRONMENT?

Most of the formaldehyde you are exposed to in the environment is in the
air.... [ A very misleading statement, as already pointed out above ]

There is usually more formaldehyde present indoors than outdoors.
[ Ignors the issue of dietary sources ]

Formaldehyde is released to the air from many home products and you may
breath in formaldehyde while using these products.

Latex paint, fingernail hardener, and fingernail polish release a large
amount of formaldehyde to the air. [ Bound to be much less than the potent
amounts in dietary sources, which have immediate strong effects on sensitive
and sensitivized persons and other vulnerable groups ]

Plywood and particle board, as well as furniture and cabinets made from
them, fiberglass products, new carpets, decorative laminates, and some
permanent press fabrics give off a moderate amount of formaldehyde.
[ This shows why new buildings, and especially mobile homes and RVs are
toxic for many people. ]

Some paper products, such as grocery bags and paper towels, give off small
amounts of formaldehyde.

Because these products contain formaldehyde, you may also be exposed on the
skin by touching or coming in direct contact with them.

You may also be exposed to small amounts of formaldehyde in the food you
eat. [ The amounts in dietary sources are the most potent sources for most
people. ]

You are not likely to be exposed to formaldehyde in the water you drink
because it does not last a long time in water. [ This ignores the fact that
methanol, always turned into formaldehyde and formic acid in humans, does
indeed last a very long time in water and dietary sources. ]

Many other home products contain and give off formaldehyde although the
amount has not been carefully measured. [ Potent dietary sources have been
systematically ignored for decades. ]

These products include household cleaners, carpet cleaners, disinfectants,
cosmetics, medicines, fabric softeners, glues, lacquers, and antiseptics.
[ Notice "cosmetics", "medicines", "disinfectants", "antiseptics" -- to this
list of direct skin contact items, we can add hair care products, shoe
leather, and some permanent press clothes. ]

You may also breath formaldehyde if you use unvented gas or kerosene heaters
indoors or if you or someone else smokes a cigar, cigarette, or pipe
indoors.

The amount of formaldehyde in mobile homes is usually higher than it is in
conventional homes because of their lower air turnover. [ Evades the issue
that particleboard and other materials common in mobile homes are strong
formaldehyde sources, which this study showed caused symptoms and immune
system signs:

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 toxicology@... ]

People who work at or near chemical plants that make or use formaldehyde can
be exposed to higher than normal amounts of formaldehyde.

Doctors, nurses, dentists, veterinarians, pathologists, embalmers, workers
in the clothing industry or in furniture factories, and teachers and
students who handle preserved specimens in laboratories also might be
exposed to higher amounts of formaldehyde. The National

FORMALDEHYDE 4 1. PUBLIC HEALTH STATEMENT

Institute for Occupational Safety and Health (NIOSH) estimates that
1,329,332 individuals in the United States have had the potential for
occupational exposure to formaldehyde. [ Common sense suggests that health
professionals who have been exposed to formaldehyde and have become
sensitized and symptomatic naturally will have a prejudice against
discovering the real extent of the danger. ]

1.4 HOW CAN FORMALDEHYDE ENTER AND LEAVE MY BODY?

Formaldehyde can enter your body after you breath it in, drink or eat it, or
when it comes in contact with your skin....

Once absorbed, formaldehyde is very quickly broken down. [ Notice the phrase
"very quickly broken down", which skirts the issue that potent levels of
formaldehyde and formic acid are inevitably produced in humans, and retained
in complex, unresearch amounts. ]

Almost every tissue in the body has the ability to break down formaldehyde.
[ Again the dangers are waved away by definition. The correct way to say
this is that formaldehyde and formic acid toxicity affects every tissue in
the body. ]

It is usually converted to a non-toxic chemical called formate, which is
excreted in the urine. [ This is an astonishing, brazen deceit, defining
formic acid as "non-toxic". Notice the qualification "usually". ]

Formaldehyde can also be converted to carbon dioxide and breathed out of the
body. [ Notice the qualification "can" . ]

It can also be broken down so the body can use it to make larger molecules
needed in your tissues, or it can attach to deoxyribonucleic acid (DNA) or
to protein in your body.... [ In one sentence, formaldehyde is portrayed as
a useful food, while the very serious and complex issue of formaldehyde
adducts to DNA and proteins in all tissues and cells is minimalized:

C. Trocho (1998 July 26): [ Not cited in this lengthy tome. ]
"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.
[ 60 to 120 mg aspartame for a 60-kg person, of which 11% is methanol,
6.6 to 13.2 mg ]
Many headache studies in humans used doses of about 30 mg/kg daily.
[ 1800 mg aspartame for a 60-kg person, of which 11% is methanol, 198 mg ]

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 rmforall

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." ]

Some people are more sensitive to the effects of formaldehyde than
others....
[ Again a very significant, complex, and problematic issue is mentioned and
minimalized in one sentence-- notice the phrase "some people". ]

The Department of Health and Human Services (DHHS) has determined that
formaldehyde may reasonably be anticipated to be a human carcinogen (NTP).

The International Agency for Research on Cancer (IARC) has determined that
formaldehyde is probably carcinogenic to humans.

This determination was based on specific judgements that there is limited
evidence in humans and sufficient evidence in laboratory animals that
formaldehyde can cause cancer.

The Environmental Protection Agency (EPA) has determined that formaldehyde
is a probable human carcinogen based on limited evidence in humans and
sufficient evidence in laboratory animals.... [ These extremely alarming
admissions ought to be emphasized and used to support calls for urgent
research, action, and public warning. ]

The most common way for children to be exposed to formaldehyde is by
breathing it. [ Again, kids are kept at risk with this policy of denial of
the potent role of dietary sources. ]

Children may also be exposed by wearing some types of new clothes or
cosmetics.

A small number of studies have looked at the health effects of formaldehyde
in children. [ Notice the term "small number", which serves to both mention
and minimalize the problem of a dire shortage of adaquate research. ]

It is very likely that breathing formaldehyde will result in nose and eye
irritation (burning feeling, itchy, tearing, and sore throat). [ The focus
is placed on the most unimportant symptoms. ]

We do not know if the irritation would occur at lower concentrations in
children than in adults. [ Research that could threaten vested interests
somehow just doesn't get funded. ]

Studies in animals suggest that formaldehyde will not cause birth defects in
humans. [ Notice the qualification "suggest". ]

Inhaled formaldehyde or formaldehyde applied to the skin is not likely to be
transferred from mother to child in breast milk or to reach the developing
fetus.... [ Notice the qualification "not likely".

ttp://groups.yahoo.com/group/aspartameNM/message/915
formaldehyde toxicity: Thrasher & Kilburn: Shaham: EPA: Gold:
Wilson: CIIN: Murray 2002.12.12 rmforall

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 ]

Formaldehyde is usually found in the air.

Formaldehyde levels are also higher indoors than outdoors.

Opening windows or using a fan to bring in fresh air is the easiest way to
lower formaldehyde levels in the home and reduce the risk of exposure to
your family. [ This reassuring, simple advice is dangerous, since the potent
dietary sources are ignored. ]

Removing formaldehyde sources from the house will also reduce the risk of
exposure.

Since formaldehyde is found in tobacco smoke, not smoking or smoking outside
will reduce exposure to formaldehyde.

Unvented heaters, such as portable kerosene heaters, also produce
formaldehyde. If you do not use these heaters in your home or shop, you help
to prevent
the build up of formaldehyde indoors.

Formaldehyde is found in small amounts in many consumer products including
antiseptics, medicines, dish-washing liquids, fabric softeners, shoe-care
agents, carpet cleaners, glues, adhesives, and lacquers.

If you or a member of your family uses these products, providing fresh
outdoor air when you use them, this will reduce your exposure to
formaldehyde.

Some cosmetics, such as nail hardeners, have very high levels of
formaldehyde.

If you do not use these products in a small room, or if you have plenty of
ventilation when you use them, you will reduce your exposure to
formaldehyde.

If your children are not in the room when you use these products, you will
also reduce their exposure to formaldehyde.

Formaldehyde is emitted from some wood products such as plywood and particle
board, especially when they are new.

The amount of formaldehyde released from them decreases slowly over a few
months. [ Notice "slowly over a few months". ]

If you put these materials in your house, or buy furniture or cabinets made
from them, opening a window will lower formaldehyde in the house. [ What
happens in winter? ]

The amount of formaldehyde emitted to the house will be less if the wood
product is covered with plastic laminate or coated on all sides.

If it is not, sealing the unfinished sides will help to lower the amount of
formaldehyde that is given off.

Some permanent press fabrics emit formaldehyde. [ Why aren't there warning
labels? ]

Washing these new clothes before use will usually lower the amount of
formaldehyde and reduce your family's risk of exposure.

FORMALDEHYDE 7 1. PUBLIC HEALTH STATEMENT

1.8 IS THERE A MEDICAL TEST TO DETERMINE WHETHER I HAVE BEEN EXPOSED TO
FORMALDEHYDE?

We have no reliable test to determine how much formaldehyde you have been
exposed to or whether you will experience any harmful health effects....
[ Another casual mention of an alarming reality ]

1.9 WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO PROTECT HUMAN
HEALTH?

The federal government develops regulations and recommendations to protect
public health.

Regulations can be enforced by law.

Federal agencies that develop regulations for toxic substances include the
EPA, the Occupational Safety and Health Administration (OSHA), and the Food
and Drug Administration (FDA).

Recommendations provide valuable guidelines to protect public health but
cannot be enforced by law. [ Not reassuring... ]

Federal organizations that develop recommendations for toxic substances
include the Agency for Toxic Substances and Disease Registry (ATSDR) and the
NIOSH. [ ATSDR and NIOSH cannot enforce their recommendations. ]

Regulations and recommendations can be expressed in not-to-exceed levels in
air, water, soil, or food that are usually based on levels that affect
animals,
then they are adjusted to help protect people. [ This bypasses the
issue that the reseach on humans is very inadequate to determine the actual,
complex toxicity of methanol, formaldehyde, and formic acid. ]

Sometimes these not-to-exceed levels differ among federal organizations
because of different exposure times (an 8-hour workday or a 24-hour day),
the use of different animal studies, or other factors....
[ An outstanding example of disharmony in the EPA is the fact that the
1998.05.05 EPA IRIS level for oral methanol in humans (Oral Rfd) is 0.5
mg/kg/day, or 30 mg oral methanol daily for a 60 kg human. The animal
study used was:

U.S. EPA. 1986. Rat oral subchronic toxicity study with methanol. Office of
Solid Waste, Washington, DC.

I have not found on the Net any information as to the authors, institution,
abstract, or full text of this study.

But the EPA ATSDR 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 rmforall

http://www.atsdr.cdc.gov/tfacts111.html
[excerpts]

Agency for Toxic Substances and Disease Registry Division of Toxicology
1600 Clifton Road NE, Mailstop E-29Atlanta, GA 30333 888-422-8737 FAX:
(404)498-0057 ATSDRIC@... http://www.atsdr.cdc.gov/contacts.html

"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."

This stringent limit means that if over 13% of the oral methanol limit
results in production of formaldehyde in the human body by the liver, then
the formaldehyde limit would be exceeded. This is cutting things pretty
close.

http://www.epa.gov/iris/subst/0305.htm
also http://www.china-pops.net/enwww/IRIS-Mirror/subst/0305.htm 1998.05.05

USA Environmental Protection Agency EPA
Integrated Risk Information System IRIS

This site explains that the harmful rat dose of 500 mg/kg body weight per
day was
divided by 10 for "interspecies extrapolation" (the higher vulnerability of
humans than rats),
by 10 for "range of sensitivity" (the variation of individual human
vulnerability), and
by 10 for "subchronic to chronic exposure" (the increased danger from
lifetime as compared to the 3 month exposure in the rat test),
giving a total reduction of 10x10x10 = 1000 for the UF = Uncertainty Factor.

The human Oral RfD is the rat Oral RfD divided by 1000, so
500 mg/kg/day is reduced to 0.5 mg/kg/day , so that the allowed dose for a
60 kg human is 30 mg oral methanol daily.


Moreover, a recent study found that after 4 months of moderate oral
aspartame, rats took four times longer to finish a simple, one-turn maze--
an alarming level of neurotoxicity:

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 rmforall

"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) 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."

The 11% methanol component of aspartame is immediately released in the GI
tract, so these rats were being exposed to only 27.5 mg/kg/day methanol.

The EPA IRIS on 1998.05.05 used a 1986 90 day rat study to find a
No-Observed-Effect Level (NOEL) value of 500 mg/kg/day, which, divided by
1000, became their human long-term safe methanol level of 0.5 mg per kg body
weight per day, which for a 60 kg average person is 30 mg methanol daily,
for oral exposure.

However, the rat level is 18 times greater than that for the level of
dramatic memory loss and clear-cut brain changes found by McConnaughey M,
May 2004.

This suggests reducing the human long-term safe level twenty times to
.025 mg/kg/day = 25 micrograms per kg body weight per day,
which for a 60 kg average person is 1.5 mg oral methanol per day.


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), about 22 mg
methanol per can.

If only 10% of the methanol accumulates 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.

If about 30% of oral methanol is retained as formaldehyde and formic acid,
then this EPA ATSDR formaldehyde limit of 2 mg daily for 2 L drinking water
suggests a corresponding methanol limit of 6.7 mg daily, about 4.5 times the
safe limit based on the McConnaughey data. This is much closer than the
1998 EPA IRIS limit of 30 mg daily oral methanol, which is 20 times the
McConnaughey data limit. ]
_______________________________________________________



Returning to the voluminous work of Elzbieta Skrzydlewska, it is important
that many of her studies suggest that many safe substances may prevent or
treat toxicity from methanol and its inevitable toxic human body products,
formaldehyde and formic acid:

N-acetylcysteine (2000); U-83836E containing a trolox ring (1997);
green tea (2004); vitamins E, C, A, and beta-carotene (2004);
glutathione (2001); N-Acetylcysteine (NAC) (2001); melatonin (2001);
low and medium levels of cysteine (1990).



"Methanol, when introduced into all mammals, is oxidized into formaldehyde
and then into formate, mainly in the liver.

Such metabolism is accompanied by the formation of free radicals....

The consequences of methanol metabolism and toxicity distinguish the human
and monkey from lower animals.

Formic acid is likely to be the cause of the metabolic acidosis and ocular
toxicity in humans and monkeys,
which is not observed in most lower animals.

Nevertheless, chemically reactive formaldehyde and free radicals may damage
most of the components of the cells of all animal species, mainly proteins
and lipids...."

http://taylorandfrancis.metapress.com/openurl.asp?genre=article&eissn=1537-6524&\
volume=13&issue=4&spage=277

Toxicology Mechanisms and Methods
Publisher: Taylor & Francis Health Sciences, part of the Taylor & Francis
Group Issue: Volume 13, Number 4 / Oct-Dec 2003 Pages: 277 - 293

Toxicological and Metabolic Consequences of Methanol Poisoning
Elzbieta Skrzydlewska, Assoc. Professor, MSc, PhD, Deputy Dean of Faculty of
Pharmacy, Head of Department of Analytical Chemistry, Medical University of
Bialystok, Mickiewicza 2A 15-230 Bialystok 8, P.O. Box 14, Poland
skrzydle@...
http://www.amb.edu.pl/en/sites/university.html dzss@...
Kilinskiego 1 15-089 Bialystok, Poland fax (48 85)7485408

Abstract:
Methanol, when introduced into all mammals, is oxidized into formaldehyde
and then into formate, mainly in the liver.

Such metabolism is accompanied by the formation of free radicals.

In all animals, methanol oxidation, which is relatively slow, proceeds via
the same intermediary stages, usually in the liver,
and various metabolic systems are involved in the process, depending on the
animal species.

In nonprimates, methanol is oxidized by the catalase-peroxidase system,
whereas in primates, the alcohol dehydrogenase system takes the main role in
methanol oxidation.

The first metabolite (formaldehyde is rapidly oxidized by formaldehyde
dehydrogenase) is the reduced glutathione (GSH)-dependent enzyme.

Generated formic acid is metabolized into carbon dioxide with the
participation of H4folate and two enzymes, 10-formyl H4folate synthetase and
dehydrogenase,
whereas nonprimates oxidize formate efficiently.

Humans and monkeys possess low hepatic H4folate and 10-formyl H4folate
dehydrogenase levels
and are characterized by the accumulation of formate after methanol
intoxication.

The consequences of methanol metabolism and toxicity distinguish the human
and monkey from lower animals.

Formic acid is likely to be the cause of the metabolic acidosis and ocular
toxicity in humans and monkeys,
which is not observed in most lower animals.

Nevertheless, chemically reactive formaldehyde and free radicals may damage
most of the components of the cells of all animal species, mainly proteins
and lipids.

The modification of cell components results in changes in their functions.

Methanol intoxication provokes a decrease in the activity and concentration
of antioxidant enzymatic as well as nonenzymatic parameters,
causing enhanced membrane peroxidation of phospholipids.

The modification of protein structure by formaldehyde as well as by free
radicals results changes in their functions,
especially in the activity of proteolytic enzymes and their inhibitors,
which causes disturbances in the proteolytic-antiproteolytic balance toward
the proteolytics and enhances the generation of free radicals.

Such a situation can lead to destructive processes because components of the
proteolytic-antiproteolytic system during enhanced membrane lipid
peroxidation may penetrate from blood into extracellular space, and an
uncontrolled proteolysis can occur.

This applies particularly to extracellular matrix proteins.

Keywords:
Free Radicals, Methanol Metabolism, Methanol Poisoning, Proteases, Protease
Inhibitors

If you are not subscribed, this publisher offers secure article or
subscription sales from this site. The price for this article is $25.00.
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Taylor & Francis Group
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_______________________________________________________



J Pharm Pharmacol. 2000 May; 52(5): 547-52.
Protective effect of N-acetylcysteine on rat liver cell membrane during
methanol intoxication. kasacka@...
Dobrzynska I, Skrzydlewska E, Kasacka I, Figaszewski Z.
Institute of Chemistry, University in Bialystok, Poland.

Methanol is oxidized in vivo to formaldehyde and then to formate, and these
processes are accompanied by the generation of free radicals.
We have studied the effect of N-acetylcysteine on liver cell membrane from
rats intoxicated with methanol (3.0 g kg(-1)).
Evaluation of the effect was achieved by several methods.
Lipid peroxidation and surface charge density were measured.
An ultrastructural study of the liver cells was undertaken.
The concentration of marker enzymes of liver damage (alanine
aminotransferase and aspartate aminotransferase) in blood serum was
measured.
Methanol administration caused an increase in lipid peroxidation products
(approximately 30%) as well as in surface charge density (approximately
60%).
This might have resulted in the membrane liver cell damage visible under
electron microscopy and a leak of alanine aminotransferase and aspartate
aminotransferase into the blood (increase of approximately 70 and 50%,
respectively).
Ingestion of N-acetylcysteine with methanol partially prevented these
methanol-induced changes.
Compared with the control group, lipid peroxidation was increased by
approximately 3% and surface charge density by approximately 30%.
Alanine aminotransferase and aspartate aminotransferase activity increased
by 9 and 8%, respectively, compared with the control group.
The results suggested that N-acetylcysteine was an effective antioxidant in
methanol intoxication.
It may have efficacy in protecting free radical damage to liver cells
following methanol intoxication. PMID: 10864143



"Changes in protein structure resulted both from free radical action and
formaldehyde generation during methanol intoxication."

J Appl Toxicol. 2000 May-Jun; 20(3): 239-43.
Effect of methanol intoxication on free-radical induced protein oxidation.
Skrzydlewska E, Elas M, Farbiszewski R, Roszkowska A.
Department of Analytical Chemistry, Medical University, 15-230 Bialystok 8,
Poland.

Oxygen free radicals are generated during methanol-induced liver injury, as
was shown for ethanol.
The effect of methanol intoxication (6 g kg(-1) body wt.) on protein
modification in the liver of rats was investigated.
Electron spin resonance determination indicated an increase in the free
radical signal 6 and 12 h after intoxication.
After 7 days of treatment, the contents of malondialdehyde and carbonyl
groups in proteins were significantly increased.
The level of amino groups and sulphydryl groups and the amount of tryptophan
in proteins were decreased,
whereas the amount of bi-tyrosine was increased significantly.
Changes in protein structure resulted both from free radical action and
formaldehyde generation during methanol intoxication.
Copyright 2000 John Wiley & Sons, Ltd. PMID: 10797478



Toxicology. 2000 Dec 7; 156(1): 47-55.
N-acetylcysteine or trolox derivative mitigate the toxic effects of methanol
on the antioxidant system of rat brain.
Farbiszewski R, Witek A, Skrzydlewska E.
Department of Analytical Chemistry, Bialystok Medical Academy, Mickiewicza
Str 2, P.O. Box 14, 15-230 Bialystok 8, Poland.

The effect of two compounds: N-acetylcysteine (NAC) and trolox derivative
(U-83836E) on the methanol induced impairment of the antioxidant system of
the rat brain was studied in male Wistar rats (approx. 250 g body weight).
The animals were divided into six main groups:
control group (0.5 ml of physiological saline intragastrically),
NAC group (150 mg/kg intraperitoneally-i.p),
U-83836E group (10 mg/kg i.p.),
methanol group (3 g/kg intragastrically),
NAC+methanol and U-83836E+methanol groups.
In these particular groups the changes in antioxidant parameters were
observed for 6,12,24,48 h and 5 and 7 days.
The results proved that the use of methanol and N-acetylcysteine increased
the activities of Cu,Zn-superoxide dismutase, glutathione peroxidase and
glutathione reductase by about 15,15 and 41%, respectively, in comparison to
the group of rats receiving methanol alone.
Similarly, the level of GSH increased by about 17%, the concentration of
ascorbate by 20%, while the thiobarbituric acid-reactive substances (TBA-rs)
diminished to the values as in control group.
The use of new antioxidant U8383E and methanol showed less beneficial effect
in the measured parameters however,
it serves as a better protector for the methanol induced decrease in
GSH-content. These data suggest that NAC and U-83836E mitigate the toxic
effects of methanol on the antioxidant system of the rat brain.
PMID: 11162875



Rocz Akad Med Bialymst. 1999; 44: 89-101.
Morphological changes in the liver of rats intoxicated with methanol.
Kasacka I, Skrzydlewska E.
Department of Histology and Embryology, Medical Academy of Bialystok.

On the basis of morphological examinations in light and electron microscope,
the evaluation of methanol influence on the liver of rats was conducted.
The examination was carried out in the group of 36 rats that were given a
single dose of methanol (1.5 g/kg b.w.) into the stomach through a gastric
tube.
The liver was taken from rats under the ether anaesthesia after 6, 12, and
24 hours as well as after 2, 5, and 7 days of methanol administration.
Results showed that methanol intoxication caused visible changes in the
examined organ.
Only 6 h after intoxication, lobular peripheral hepatocytes presented
characteristic features of vacuolar degradation persisting up to 48 h.
Since the second day of intoxication, many cells with double nuclei were
found more frequently than in controls.
Single hepatocytes or small hepatocytic clusters with the features of
deliquescent necrosis could be seen after 5 and 7 days of examination.
All animals intoxicated with methanol showed distinct weakness of glycogen
reaction.
The loss of glycogen resources was highest at 24 h after methanol
administration.
The results indicate, that methanol causes morphological changes in the rat
liver and that intensification of these changes depends on the time after
intoxication. PMID: 10697423



Rocz Akad Med Bialymst. 1999; 44: 76-88.
Activity of lysosomal proteases in the liver and in the plasma from rats
intoxicated with methanol.
Skrzydlewska E.
Department of Analytical Chemistry, Medical Academy of Bialystok.

The activity of lysosomal proteolytic enzymes (cathepsin A, B, C, D and E)
in cytosol and in the whole homogenate of the liver and in the blood plasma
from rats intoxicated with 1.5, 3.0 and 6.0 g methanol/kg b.w. was measured
6, 12 and 24 h and 2, 5 and 7 days after the intoxication.
The activity of all proteases was increased in the cytosol from 12 h to 5
days of intoxication, whereas the activity of these enzymes was decreased in
the whole liver homogenate during the same time.
The magnitude of the decrease in proteolytic activity in the whole
homogenate of the liver depended on the amino acid active center of the
enzyme.
The greatest decrease was observed for sulfhydryl and hydroxyl proteases and
smaller one for carboxyl proteases.
The proteases activity in the plasma was increased from 12 h to 5 days after
methanol intoxication.
These results suggest that during methanol intoxication the cellular and
lysosomal membranes are impaired and proteases are translocated into the
blood. However, changes in proteases activities and proteases distribution
within the hepatocytes may lead to disturbances in the catabolism of
cell proteins and to destruction of liver cells. PMID: 10697422



"The primary metabolic appropriation of methanol is oxidation to
formaldehyde and then to formate.
These processes are accompanied by formation of superoxide anion and
hydrogen peroxide....
Methanol administration,[ by ] increasing concentration of the lipid
peroxidation products, decreased the liver glutathione-peroxidase and
glutathione reductase (GSSG-R) activities, GSH concentration and total
antioxidant status (TAS)."

Drug Alcohol Depend. 1999 Nov 1; 57(1): 61-7.
Protective effect of N-acetylcysteine on reduced glutathione, reduced
glutathione-related enzymes and lipid peroxidation in methanol intoxication.
Skrzydlewska E, Farbiszewski R. skrzydle@...
Department of Analytical Chemistry, Bialystok Medical University, Poland.

The primary metabolic appropriation of methanol is oxidation to formaldehyde
and then to formate.
These processes are accompanied by formation of superoxide anion and
hydrogen peroxide.
This paper reports data on the effect of N-acetylcysteine (NAC) on reduced
glutathione (GSH) and on activity of some GSH-metabolising enzymes in the
liver, erythrocytes and serum of rats intoxicated with methanol (3 g/kg
b.w.) during 7 days after intoxication.
Methanol administration,[ by ] increasing concentration of the lipid
peroxidation products, decreased the liver glutathione-peroxidase and
glutathione reductase (GSSG-R) activities, GSH concentration and total
antioxidant status (TAS).
The use of NAC after methanol ingestion apparently diminished lipid
peroxidation, elevated the GSH level in the liver and erythrocytes, and
increased activity of GSH-related enzymes in the serum, erythrocytes and in
the liver.
These results suggest that NAC exerts its protective effect by acting as a
precursor for glutathione, the main low molecular antioxidant and as a free
radical scavenger. PMID: 10617314



"Methanol ingestion in humans caused changes in activities of proteases and
their inhibitors with similar direction as in rats.
These changes in activity of proteases and their inhibitors produce signific
ant disturbances in proteolytic-antiproteolytic balance after methanol
administration."

J Toxicol Environ Health A. 1999 Jul 23; 57(6): 431-42.
Activity of cathepsin G, elastase, and their inhibitors in plasma during
methanol intoxication.
Skrzydlewska E, Szmitkowski M, Farbiszewski R.
Department of Analytical Chemistry, Medical University, Bialystok, Poland.
skrzydle@...

Methanol oxidation in the liver is accompanied by formation of formaldehyde
and free radicals.
These compounds can react with biologically active proteins, including
proteolytic enzymes and their inhibitors.
The activity of cathepsin G and elastase and their inhibitors such as
alpha-1-antitrypsin and alpha-2-macroglobulin in plasma of rats given
methanol orally in doses of 1.5, 3, and 6 g/kg was investigated for 7 days.
The activity of cathepsin G and elastase was increased from 12 h to 5 d,
proportionally to methanol dose.
At the same time, activity of their inhibitors was reduced.
Methanol ingestion in humans caused changes in activities of proteases and
their inhibitors with similar direction as in rats.
These changes in activity of proteases and their inhibitors produce signific
ant disturbances in proteolytic-antiproteolytic balance after methanol
administration. PMID: 10478824



Folia Histochem Cytobiol. 1999; 37(2): 111-2.
Parenchymal cell mitochondria in the liver of rats after methanol
intoxication.
Kasacka I, Skrzydlewska E.
Department of Histology, Medical University, Bialystok, Poland.
PMID: 10352983



"Our findings indicate decreased antioxidative potential both in the brain
and in the liver of rats after methanol ingestion."

Comp Biochem Physiol C Pharmacol Toxicol Endocrinol. 1998 Aug; 120(2):
289-94.
The comparison of the antioxidant defense potential of brain to liver of
rats after methanol ingestion.
Skrzydlewska E, Witek A, Farbiszewski R.
Department of Instrumental Analysis, Bialystok Medical University, Poland.

The antioxidant enzymatic and nonenzymatic potential in the brain of rats
given methanol orally was investigated for 7 days consecutively and compared
to that one in the liver.
Glutathione (GSH) and the activities of superoxide dismutase (Cu, Zn-SOD),
glutathione peroxidase (GSH-Px) and glutathione reductase (GSSG-R) were
reduced in the brain after the first 24 h, whereas
in the liver these parameters were diminished after 6 h.
The brain catalase (CAT) activity was very low and constant in contrast to
high and changeable CAT in the liver.
At the beginning of intoxication, the activities of Cu, Zn-SOD and CAT in
the liver were increased;
after 5 days they were restored to normal values
while Cu, Zn-SOD diminished gradually in the brain.
An early change that occurred 6 h after intoxication was a decrease of
ascorbate in the brain and in the liver.
The increase in thiobarbituric acid-reactive substances (TBA-rs) in the
liver was preceded by their increase in the brain.
Our findings indicate decreased antioxidative potential both in the brain
and in the liver of rats after methanol ingestion.
The regulatory mechanisms of the antioxidant enzymes in the brain of
intoxicated rats differ from those ones in the liver. PMID: 9827043



Acta Biol Hung. 1998; 49(2-4): 345-52.
Formaldehyde-induced modification of hemoglobin in vitro.
Farbiszewski R, Skrzydlewska E, Roszkowska A.
Department of Analytical Chemistry, Medical University, Bialystok, Poland.

Formaldehyde is known to react with proteins.
The purpose of our experiments was to analyse in vitro the effect of
formaldehyde on the physicochemical and biological properties of hemoglobin
molecules.
The effect of formaldehyde concentration, reaction time, pH and temperature
on hemoglobin free amino groups was estimated.
The modified hemoglobin was analysed using electrophoretic, potentiometric
and spectrophotometric techniques.
Reaction between formaldehyde and hemoglobin was accelerated by increasing
concentration of formaldehyde and higher temperature.
This reaction was most intensive during the first few hours at pH 7.4 so the
amount of free amino groups of hemoglobin was significantly diminished by
directly mixing formaldehyde with hemoglobin.
The modified protein was characterized by the increase in electrophoretic
mobility and the decrease in maximum absorption derived from porphyrin
rings. Formaldehyde modified hemoglobin was less susceptible to the action
of cathepsin D. PMID: 10526979



"These results indicate that methanol intoxication in rats leads to an
increase in the lipid peroxidation and impairment in the antioxidant
mechanisms in liver, erythrocytes, and blood serum."

J Toxicol Environ Health A. 1998 Apr 24; 53(8): 637-49.
Lipid peroxidation and antioxidant status in the liver, erythrocytes, and
serum of rats after methanol intoxication.
Skrzydlewska E, Farbiszewski R.
Department of Instrumental Analysis, Medical Academy, Bialystok, Poland.

Lipid peroxidation products measured as a malondialdehyde and activities of
superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione
reductase (GSSG-R), and concentrations of ascorbic acid, alpha-tocopherol,
and glutathione (GSH) were measured in the liver, erythrocytes, and serum of
rats 6, 14, and 24 h and 2, 5, and 7 d after treatment with 3 g methanol/kg.
GSH-Px and GSSG-R activities, GSH level, and ascorbate concentration in the
liver, erythrocytes, and blood serum were significantly decreased.
In addition, SOD and alpha-tocopherol in erythrocytes were diminished, while
malondialdehyde (MDA) in liver, erythrocytes, and serum were elevated.
Further, erythrocyte counts, hemoglobin levels, hematocrit, and mean
corpuscular volume (MCV) were reduced.
These results indicate that methanol intoxication in rats leads to an
increase in the lipid peroxidation and impairment in the antioxidant
mechanisms in liver, erythrocytes, and blood serum. PMID: 9572161



Rocz Akad Med Bialymst. 1997; 42 Suppl 2: 47-55.
Ultrastructural evaluation of lysosomes and biochemical changes in cathepsin
D distribution in hepatocytes in methanol intoxication.
Skrzydlewska E, Szynaka B.
Department of Instrumental Analysis, Medical Academy of Bialystok.

Methanol oxidation is accompanied by free radicals and formaldehyde
formation.
It is likely to cause damage of lysosomal membranes.
Lysosomal ultrastructure under transmission electron microscope and
biochemical localization of cathepsin D were estimated after rats
intoxication with methanol.
The examination was carried out 6, 12 and 24 h and 2.5 and 7 days after
intoxication.
Ultrastructural examination showed that methanol causes
extension of Golgi apparatus cisterns and an increase in a number of
lysosomes.
>From 12 h to 2 days lysosomes were characterized by damage of structure of
membrane enclosing lysosomes.
During the first days of intoxication activity of cathepsin D decreased in
lysosomes and increased in cytosol.
These changes may lead to uncontrolled extralysosomal proteolysis in the
liver cells and to the onset of liver tissue destruction. PMID: 9646682



Rocz Akad Med Bialymst. 1997; 42 Suppl 2: 39-46.
Ultrastructural evaluation of hepatocytes membranes and changes in cytosolic
enzymes distribution in methanol intoxication.
Skrzydlewska E, Szynaka B.
Department of Instrumental Analysis, Medical Academy of Bialystok.

Acute methanol intoxication causes metabolic and structural disturbances of
liver cells.
The aim of this paper, therefore, was to evaluate the
ultrastructure of liver cells membrane and the amount of lipid peroxidation
products, as well as the concentration of marker enzymes of liver damage
(ALT and AST) in blood serum.
The experiment was done on Wistar rats which once received intragastrically
6.0 g methanol/kg b.w. as a 50% solution.
The animals were decapitated 6, 12 and 24 h and 2, 5 and 7 days after the
methanol administration.
The liver was evaluated under transmission electron microscope and lipid
peroxidation products were determined in the liver homogenate.
The serum ALT and AST activity were also assayed.
The biochemical results indicate the increase in lipid peroxidation
products.
The consequence of this is probably the membrane liver cell damage visible
in the electron microscope. PMID: 9646681



"The primary metabolic fate of methanol is oxidation to formaldehyde and
then to formate by enzymes of the liver....

Changes due to methanol ingestion may indicate impaired antioxidant defense
mechanisms in the liver tissue. "

Free Radic Res. 1997 Oct; 27(4): 369-75.
Decreased antioxidant defense mechanisms in rat liver after methanol
intoxication.
Skrzydlewska E, Farbiszewski R.
Department of Instrumental Analysis, Medical Academy, Poland.

The primary metabolic fate of methanol is oxidation to formaldehyde and then
to formate by enzymes of the liver.
Cytochrome P-450 and a role for the hydroxyl radical have been implicated in
this process.
The aim of the paper was to study the liver antioxidant defense system in
methanol intoxication, in doses of 1.5, 3.0 and 6.0 g/kg b.w., after
methanol administration to rats.
In liver homogenates, the activities of Cu,Zn-superoxide dismutase and
catalase were significantly increased after 6 h following methanol ingestion
in doses of 3.0 and 6.0 g/kg b.w. and persisted up to 2-5 days,
accompanied by significant decrease of glutathione reductase and glutathione
peroxidase activities.
The content of GSH was significantly decreased during 6 hours to 5 days.
The liver ascorbate level was significantly diminished, too, while MDA
levels were considerably increased after 1.5, 3.0 and 6.0 g/kg b.w. methanol
intoxication.
Changes due to methanol ingestion may indicate impaired antioxidant defense
mechanisms in the liver tissue. PMID: 9416465



Arch Toxicol. 1997; 71(12): 741-5.
Glutathione consumption and inactivation of glutathione-related enzymes in
liver, erythrocytes and serum of rats after methanol intoxication.
Skrzydlewska E, Farbiszewski R.
Department of Instrumental Analysis, Medical Academy, Bialystok, Poland.

The primary metabolic fate of methanol is oxidation to formaldehyde and then
to formate.
These processes are accompanied by formation of superoxide anion
and further hydrogen peroxide.
Glutathione plays a unique role in the cellular defense system against
xenobiotics.
The glutathione (GSH) content and glutathione peroxidase (GSH-Px) and
glutathione reductase (GSSG-R) activities were measured in liver,
erythrocytes and serum of rats.
Rats were intoxicated with 3.0 and 6.0 g methanol/kg body wt. and
measurements taken after 6, 12 and 24 h and 2, 5 and 7 days of intoxication.
The decrease in GSH content and in GSH-related enzyme activity was observed
during the whole time-course of the intoxication.
The most significant changes were observed in the erythrocytes.
The results obtained show that the protection against oxidative damage due
to methanol intoxication in rats seems to be less efficient than in control
rats. PMID: 9388006



Acta Biochim Pol. 1997; 44(2): 339-42.
Activity of liver proteases in experimental methanol intoxication.
Skrzydlewska E, Skrzydlewski Z, Worowski K.
Department of Instrumental Analysis, Medical Academy, Bialystok, Poland.

Intoxication of rats with methanol (1.5 and 3.0 g/kg body weight) led to a
significant, time- and dose-dependent decrease in the activities of
cathepsins A, B and C, while the activity of cathepsin D was unaffected.
The decrease was associated with a different partial release of individual
cathepsins to the post-lysosomal fraction. PMID: 9360724



Fundam Clin Pharmacol. 1997; 11(5): 460-5.
Trolox-derivative antioxidant protects against methanol-induced damage.
Skrzydlewska E, Farbiszewski R.
Department of Instrumental Analysis, Medical Academy, Bialystok, Poland.

This paper reports data on the effect of a new antioxidant, U-83836E, on the
lipid peroxidation and antioxidant status of liver, red blood cells (RBCs)
and blood serum of rats intoxicated with methanol (3.0 g/kg body weight).
Methanol administration slightly increased the levels of peroxidation
products in the liver, and markedly increased them in RBCs and serum.
In contrast, glutathione-peroxidase, glutathione-reductase activity, reduced
glutathione concentration and total antioxidant status were decreased.
The use of U-83836E, containing a trolox ring, appeared to be beneficial in
reducing lipid peroxidation products and in partially in preventing the
decrease in glutathione and antioxidant enzymes induced by methanol in liver
and serum.
These results show that antioxidant U-83836E may partially prevent methanol
toxicity. PMID: 9342600



"These results indicate that methanol in rats leads to the impairment of
antioxidant mechanisms in the liver, erythrocytes, and blood serum. "

Alcohol. 1997 Sep-Oct; 14(5): 431-7.
Antioxidant status of liver, erythrocytes, and blood serum of rats in acute
methanol intoxication.
Skrzydlewska E, Farbiszewski R.
Department of Analytical Chemistry, Medical Academy, Poland.

SOD, CAT, GSH-Px, GSSG-R, ascorbic acid, alpha-tocopherol, nonprotein- and
protein-bound sulfhydryl compounds, and TBA-rs content
in the liver, erythrocytes, and blood serum of rats treated with methanol
after 6, 12, and 24 h and 2, 5, and 7 days were investigated.
Furthermore, hematological parameters of erythrocytes were analysed.
GSH-Px, GSSG-R, sulfhydryl compounds, and ascorbic acid in the liver,
erythrocytes, and in blood serum were significantly decreased.
In addition, Cu,Zn-SOD and tocopherol in erythrocytes were diminished,
whereas TBA-rs in the three biological materials was enhanced.
Simultaneously, erythrocytes amount, hemoglobin level, hematocrit, and MCV
were reduced.
These results indicate that methanol in rats leads to the impairment of
antioxidant mechanisms in the liver, erythrocytes, and blood serum. PMID:
9305457



Alcohol. 1997 May-Jun; 14(3): 295-9.
Influence of methanol and its metabolites on the activity of
alpha1-antitrypsin.
Skrzydlewska E, Mielczarska J.
Department of Instrumental Analysis, Medical Academy, Bialystok, Poland.

Among methanol and its metabolites, formaldehyde was found to have the
strongest inactivating effect on the activity of alpha1-antitrypsin
preparation and inhibitor existing in blood serum.
The influence of formaldehyde on the activity of serum alpha1-antitrypsin is
lower in comparison with purified inhibitor.
alpha1-Antitrypsin modified by formaldehyde inactivates the trypsin in its
action on the BAPA to a smaller degree than on the hemoglobin.
The effective formaldehyde concentration in the case of the BAPA is about 64
mM and in the case of the hemoglobin is about 256 mM.
The significant inhibitory effect of methanol on alpha1-antitrypsin appears
only at a high concentration of this compound.
Formate does not decrease alpha1-antitrypsin activity.
In people intoxicated with methanol, alpha1-antitrypsin activity decreases,
whereas the content of this inhibitor does not change. PMID: 9160807



Acta Biochim Pol. 1997; 44(1): 139-45.
Liver and serum antioxidant status after methanol intoxication in rats.
Skrzydlewska E, Farbiszewski R.
Department of Instrumental Analysis, Medical Academy, Bialystok, Poland.

Activities of superoxide dismutase (SOD), catalase, glutathione peroxidase
(GSH-Px) and glutathione reductase (GSSG-R) and concentration of ascorbate,
alpha-tocopherol, non-protein and protein-bound sulfhydryl compounds and
thiobarbituric acid-reactive substances (TBA-rs) were measured in liver and
serum of rats 6, 12 and 24 h and 2, 5 and 7 days after intoxication with
1.5 g or 3.0 g methanol/kg b.w.
Liver GSH-Px and GSSG-R activities and SH-groups and ascorbate content were
significantly diminished at 6 and 24 h,
while TBA-rs were increased.
Serum SOD, GSH-Px and GSSG-R activities and SH-groups concentration were
reduced, while TBA-rs were elevated.
The changes were more intensive after application of the higher dose of
methanol.
It is concluded that methanol impairs the liver and blood serum antioxidant
mechanisms in rats. PMID: 9241366



Vet Hum Toxicol. 1996 Dec; 38(6): 429-33.
Diminished antioxidant defense potential of liver, erythrocytes and serum
from rats with subacute methanol intoxication.
Skrzydlewska E, Farbiszewski R.
Department of Analytical Chemistry, Medical Academy, Bialystok, Poland.

The activities of superoxide dismutase (SOD), catalase glutathione
peroxidase (GSH-Px) and glutathione reductase (GSSG-R) and the concentration
of ascorbate, alpha-tocopherol, non-protein and protein-bound sulfhydryl
compounds, and thiobarbituric acid-reactive substances (TBA-rs)
in liver, erythrocytes and serum of rats dosed with 1.5 g methanol/kg bw
were measured after 6, 12 and 24 h and 2, 5 and 7 d.
Hematological erythrocyte parameters were also determined.
Liver GSH-Px and GSSG-R activities, SH-groups and ascorbate were
significantly diminished at 12 and 24 h, while TBA-rs increased.
Blood SOD, GSH-Px and GSSG-R activities and sulfhydryl-group concentrations
were reduced while TBA-rs were elevated.
Methanol given to rats impaired liver, erythrocyte and blood serum
antioxidant mechanisms. PMID: 8948074



Rocz Akad Med Bialymst. 1996; 41(2): 397-404.
Decreased antioxidant status and increased lipid peroxidation in rats after
methanol intoxication.
Skrzydlewska E.
Department of Instrumental Analysis, Medical Academy of Bialystok.

The liver is the main metabolic place where the methanol is oxidized to
formaldehyde and to formate.
The aim of this paper was to study the liver antioxidant system in acute
methanol intoxication, after 6, 12, 24 hours and 2, 5 and 7 days of alcohol
administration into rats.
In liver homogenates the superoxide dismutase, catalase, peroxidase and
reductase glutathione activity and content of malondialydehyde (MDA),
SH-compounds in protein and non-protein fraction and ascorbate were
estimated.
Activity of superoxide dismutase and catalase was significantly increased
after 6 hours following methanol ingestion and persisted up to 2-5 days of
intoxication.
It was accompanied by significant decreased of reductase and peroxidase
glutathione activities.
The protein and non-protein SH-groups were significantly decreased during 6
hours to 5 days following methanol ingestion.
The liver MDA content was considerably increased.
After 2 days since methanol intoxication the liver vitamin C content was
significantly decreased in comparison with the control group.
The obtain results demonstrated that during methanol induced liver injury
there are increase of lipid peroxidation and impairment of proantioxidant
equilibrium in favour to prooxidant. PMID: 9020552



Pol Tyg Lek. 1993 May 3-10; 48(18-19): 433-6.
[Metabolism and toxic effects of methanol]
[Article in Polish]
Skrzydlewska E.
Zakladu Analizy Instrumentalnej AM, Bialymstoku.
Publication Types: Review Review, Tutorial PMID: 8309827



Cell Mol Biol Lett. 2003; 8(2): 391-413.
DNA damage caused by lipid peroxidation products.
Luczaj W, Skrzydlewska E.
Department of Analytical Chemistry, Medical Academy of Bialystok,
Mickiewicza 2A, P.O. Box 14, 15-230 Bialystok 8, Poland.

Lipid peroxidation is a process involving the oxidation of polyunsaturated
fatty acids (PUFAs), which are basic components of biological membranes.
Reactive electrophilic compounds are formed during lipid peroxidation,
mainly alpha, beta-unsaturated aldehydes.
These compounds yield a number of adducts with DNA.
Among them, propeno and substituted propano adducts of deoxyguanosine with
malondialdehyde (MDA), acrolein, crotonaldehyde and etheno adducts,
resulting from the reactions of DNA bases with epoxy aldehydes, are a very
important group of adducts.
The epoxy aldehydes are more reactive towards DNA than the parent
unsaturated aldehydes.
The compounds resulting from lipid peroxidation mostly react with DNA
showing both genotoxic and mutagenic action;
among them, 4-hydroxynonenal is the most genotoxic, while MDA is the most
mutagenic.
DNA damage caused by the adducts of lipid peroxidation products
with DNA can be removed by the repairing action of glycosylases.
The formed adducts have been hitherto analyzed using the IPPA
(Imunopurification-(32)P-postlabelling assay) method and via gas
chromatography/electron capture negtive chemical ionization/mass
spectrometry (GC/EC NCI/MS).
A combination of liquid chromatography with electrospray tandem mass
spectrometry (LC/ES-MSMS) with labelled inner standard has mainly been used
in recent years. PMID: 12813574



Hepatogastroenterology. 2003 Jan-Feb; 50(49): 126-31.
Antioxidant potential in esophageal, stomach and colorectal cancers.
Skrzydlewska E, Kozuszko B, Sulkowska M, Bogdan Z, Kozlowski M,
Snarska J, Puchalski Z, Sulkowski S, Skrzydlewski Z.
skrzydle@...
Department of Analytical Chemistry Medical Academy, 15-230 Bialystok 8, P.O.
Box 14, Poland.

BACKGROUND/AIMS: The gastrointestinal tract is particularly susceptible to
reactive oxygen species attack which lead to carcinogenesis.
An important role in defense strategy against reactive oxygen species is
played by antioxidants.
The present study aims at examining antioxidant parameters and
malondialdehyde-- the product of lipid peroxidation as well as the marker of
cancer progression-- and cancer procoagulant in esophageal, gastric and
colorectal cancer patients.
METHODOLOGY: The activity of superoxide dismutase, catalase, glutathione
peroxidase and reductase and the level of glutathione, vitamin C,
malondialdehyde and cancer procoagulant were determined in tumors and normal
mucous from 18 patients with esophageal cancer, 18 patients with stomach
tumor and 62 patients with colorectal cancer.
RESULTS: In esophageal tumor the activity of all enzymes has been increased
compared with normal mucous.
Stomach tumor has been also characterized by an increase in antioxidant
enzymes activity except glutathione peroxidase and reductase whose
activities have been decreased.
However in colorectal tumor the activity of enzymes has been increased apart
from catalase.
In all cases the glutathione level has been increased while the vitamin C
content has been significantly decreased.
Tumor malondialdehyde level was significantly increased, too.
The level of cancer procoagulant also increased in cancer tissues as well as
in the serum.
CONCLUSIONS: Antioxidant potential in all cases of
gastrointestinal tract cancer has been unbalanced which has lead to increase
in reactive oxygen species action and enhancement of lipid peroxidation and
cancer procoagulant generation. PMID: 12630007



J Toxicol Environ Health A. 2004 Apr 9; 67(7): 595-606.
Green tea protection against age-dependent ethanol-induced oxidative stress.
Luczaj W, Waszkiewicz E, Skrzydlewska E, Roszkowska-Jakimiec W.
Department of Analytical Chemistry, Medical University of Bialystok,
Bialystok, Poland.

Ethanol intoxication leads to oxidative stress, which may be additionally
enhanced by aging.
The aim of this study was to investigate the influence of green tea as a
source of water-soluble antioxidants on the ability to prevent oxidative
stress in aged rats sub-chronically intoxicated with ethanol.
Two-, 12-, and 24-mo-old male Wistar rats were divided into 4 experimental
groups: (1) control, (2) green tea, (3) ethanol, and (4) ethanol and green
tea. Ethanol intoxication produced age-dependent decrease in the activity of
serum superoxide dismutase, glutathione peroxidase, and reductase and in
levels of glutathione (GSH), vitamins C, E, and A, and beta-carotene.
Changes in the serum antioxidative ability were accompanied by enhanced
oxidative modification of lipid (increase in lipid hydroperoxides,
malondiadehyde, and 4-hydroxynonenal levels) and protein (rise in carbonyl
group levels).
Green tea partially protected against changes in antioxidant enzymatic as
well as nonenzymatic parameters produced by ethanol and enhanced by aging.
Administration of green tea significantly protects cellular components such
as lipids and proteins against oxidative modification.
Results indicate that green tea effectively protects blood serum against
oxidative stress produced by ethanol as well as aging. PMID: 15129554



Postepy Hig Med Dosw (Online). 2004 Mar 30; 58: 194-201.
[Antioxidative abilities during aging] [Article in Polish]
Augustyniak A, Skrzydlewska E.
Zaklad Chemii Nieorganicznej i Analitycznej Akademii Medycznej w
Bialymstoku.

Biological aging is associated with increased cellular levels of reactive
oxygen species (ROS) as well as the formation and accumulation of oxidized
biomolecules.
During evolution, organisms developed a highly-efficient and adaptive
antioxidant defense system.
Antioxidants can generally be divided into two categories: enzymatic and
non-enzymatic. During the aging process the activity of antioxidant enzymes,
e.g. SOD, CAT, GSH-Px, and GSSG-R, depends on factors such as race, gender,
tissue and subcellular localization of enzymes.
The age-dependent decrease in antioxidant enzyme activity may be attributed
to oxidative modifications of enzymes.
During the aging process, ROS may also lead to the induction of some enzyme
activity which is explained as an adaptive phenomenon.
The decrease in GSH concentration with age can be explained by decreased GSH
synthesis and/or increased GSH consumption in the removal of peroxides and
xenobiotics.
In plasma albumin, ferritin, transferrin, and caeruloplasmin exert
protective action.
Plasma proteins can inhibit ROS generation and lipid peroxidation by
chelating free transition metals.
Plasma protein concentrations changes with age.
The major exogenous antioxidants, mostly derived from the diet, are vitamin
E, C, A, and beta-carotene.
During the aging process the level of vitamins may decrease or increase,
depending on such factors as diet, and diseases. PMID: 15077054



Folia Morphol (Warsz). 2004 Feb; 63(1): 123-6.
Green tea as an antioxidant which protects against alcohol induced injury in
rats -- a histopathological examination.
Baltaziak M, Skrzydlewska E, Sulik A, Famulski W, Koda M.
Department of General Pathology, Medical University, Bialystok, Poland.
drbal@...

Our study with animal models was designed to test the hypothesis that green
tea protects against chronic (over 4 weeks) alcohol induced liver injury in
rats.
The research was conducted on Wistar male rats divided into 4 research
groups:
I - received the Libera-De Carli control diet (L-DC),
II - received (L-DC) and green tea,
III - received (L-DC) and ethanol and
IV - received (L-DC), green tea and ethanol.
When comparing groups I and II we saw less intensive steatosis in group II
than in group I, which can suggest that green tea may affect the
accumulation of fat in the hepatocytes and protect them against steatosis
and disruption.
In III, the ethanol group, the steatosis of the liver increased considerably
and the green tea which was given with ethanol in group IV did not halt
this,
as in group IV we also observed intensive steatosis in the liver.
>From this data we conclude that green tea has an important, although not
fully understood role in preventing liver injury. PMID: 15039917



Alcohol. 2004 Jan; 32(1): 25-32.
Green tea protects against ethanol-induced lipid peroxidation in rat organs.
Ostrowska J, Luczaj W, Kasacka I, Rozanski A, Skrzydlewska E.
Department of Analytical Chemistry, Medical Academy of Bialystok,
PO Box 14, 15-230 Bialystok, Poland.

Ethanol metabolism is accompanied by generation of free radicals, which
stimulates lipid peroxidation.
Natural antioxidants are particularly useful in such a situation.
The current study was designed to investigate the efficacy of green tea, as
a source of water-soluble antioxidants (catechins), on lipid peroxidation in
liver, brain, and blood induced by chronic (4 weeks) ethanol intoxication in
rats. Feeding of ethanol led to a significant increase in lipid
peroxidation, as measured by increased concentrations
of lipid hydroperoxides, 4-hydroxynonenal, and malondialdehyde.
Feeding of ethanol also changed the glutathione-dependent lipid
hydroperoxide decomposition system, resulting in a decrease in both reduced
glutathione concentration and activity of glutathione peroxidase.
Observed changes were statistically significant in all examined tissues.
Enhancement in lipid peroxidation was associated with disruption of
hepatocyte cell membranes, as observed through electron microscopic
evaluation.
Green tea protects phospholipids from enhanced peroxidation and prevents
changes in biochemical parameters and morphologic changes observed after
ethanol consumption.
These results support the suggestion that green tea protects membranes from
peroxidation of lipids associated with ethanol consumption. PMID: 15066700



Journal of Toxicology and Environmental Health Part A
Publisher: Taylor & Francis Health Sciences, part of the Taylor & Francis
Group Issue: Volume 67, Number 7 / April 9, 2003 Pages: 595 - 606

Green Tea Protection Against Age-Dependent Ethanol-Induced Oxidative Stress
Wojciech Luczaj A1, Ewa Waszkiewicz A1, Elzbieta Skrzydlewska A1,
Wiesawa Roszkowska-Jakimiec A2

A1 Department of Analytical Chemistry, Medical University of Bialystok,
Bialystok, Poland
A2 Department of Instrumental Analysis, Medical University of Bialystok,
Bialystok, Poland

Abstract:
Ethanol intoxication leads to oxidative stress, which may be additionally
enhanced by aging.
The aim of this study was to investigate the influence of green tea as a
source of water-soluble antioxidants on the ability to prevent oxidative
stress in aged rats sub-chronically intoxicated with ethanol.
Two-, 12-, and 24-mo-old male Wistar rats were divided into 4 experimental
groups: (1) control, (2) green tea, (3) ethanol, and (4) ethanol and green
tea. Ethanol intoxication produced age-dependent decrease in the activity of
serum superoxide dismutase, glutathione peroxidase, and reductase and in
levels of glutathione (GSH), vitamins C, E, and A, and g-carotene.
Changes in the serum antioxidative ability were accompanied by enhanced
oxidative modification of lipid (increase in lipid hydroperoxides,
malondiadehyde, and 4-hydroxynonenal levels) and protein (rise in carbonyl
group levels).
Green tea partially protected against changes in antioxidant enzymatic as
well as nonenzymatic parameters produced by ethanol and enhanced by aging.
Administration of green tea significantly protects cellular components such
as lipids and proteins against oxidative modification.
Results indicate that green tea effectively protects blood serum against
oxidative stress produced by ethanol as well as aging.



Addict Biol. 2002 Jul; 7(3): 307-14.
Green tea as a potent antioxidant in alcohol intoxication.
Skrzydlewska E, Ostrowska J, Stankiewicz A, Farbiszewski R.
Department of Analytical Chemistry, Medical Academy of Bialystok, Bialystok,
Poland. skrzydle@...

Ethanol oxidation to acetaldehyde and next to acetate is accompanied by free
radical generation.
Free radicals can affect cell integrity when antioxidant mechanisms are no
longer able to cope with the free radical generation observed in ethanol
intoxication.
Natural antioxidants are particularly useful in such a situation.
The present study was designed to investigate the efficacy of green tea as a
source of water-soluble antioxidants (catechins) on the liver and blood
serum antioxidative potential of rats chronically (28 days) intoxicated with
ethanol.
Alcohol caused a decrease in liver superoxide dismutase, glutathione
peroxidase and catalase activities and an increase in activity of
glutathione reductase.
Moreover, a decrease in the level of reduced glutathione, ascorbic acid,
vitamins A and E and beta-carotene were observed.
The activity of serum glutathione peroxidase decreased while glutathione
reductase activity increased.
The level of serum non-enzymatic antioxidants was also decreased in the
liver.
Alcohol administration caused an increase in the liver and serum lipid
peroxidation products, measured as thiobarbituric acid-reactive substances.
However, green tea prevents the changes observed after ethanol intoxication.
Green tea also protects membrane phospholipids from enhanced peroxidation.
These results indicate a beneficial effect of green tea in alcohol
intoxication. PMID: 12126490



Phytomedicine. 2002 Apr; 9(3): 232-8.
Protective effect of green tea against lipid peroxidation in the rat liver,
blood serum and the brain.
Skrzydlewska E, Ostrowska J, Farbiszewski R, Michalak K.
Department of Analytical Chemistry, Medical Academy of Bialystok, Poland.
skrzydle@... michalak@...

This paper reports data on the effect of green tea on the lipid peroxidation
products formation and parameters of antioxidative system of the liver,
blood serum and central nervous tissue of healthy young rats drinking green
tea for five weeks.
The rats were permitted free access to solubilized extract of green tea.
Bioactive ingredients of green tea extract caused in the liver an increase
in the activity of glutathione peroxidase and glutathione reductase and in
the content of reduced glutathione as well as marked decrease in lipid
hydroperoxides (LOOH), 4-hydroksynonenal (4-HNE) and malondialdehyde (MDA).
The concentration of vitamin A increased by about 40%.
Minor changes in the measured parameters were observed in the blood serum.
GSH content increased slightly, whereas the index of the total antioxidant
status increased significantly.
In contrast, the lipid peroxidation products, particularly MDA was
significantly diminished.
In the central nervous tissue the activity of superoxide dismutase and
glutathione peroxidase decreased while the
activity of glutathione reductase and catalase increased after drinking
green tea.
Moreover the level of LOOH, 4-HNE and MDA significantly decreased.
The use of green tea extract appeared to be beneficial to rats in reducing
lipid peroxidation products.
These results support and substantiate traditional consumption of green tea
as protection against lipid peroxidation in the liver, blood serum, and
central nervous tissue. PMID: 12046864



Rocz Akad Med Bialymst. 2001; 46: 240-50.
The influence of green tea on the activity of proteases and their inhibitors
in plasma of rats after ethanol treatment.
Skrzydlewska E, Roszkowska A, Makiela M, Skrzydlewski Z.
Department of Analytical Chemistry, Medical Academy of Bialystok, Bialystok,
Poland.

Ethanol oxidation in the liver is accompanied by formation of acetaldehyde
and free radicals.
These compounds can react with biologically active proteins, including
proteolytic enzymes and their inhibitors.
The aim of this paper was to determine the influence of green tea on the
activity of cathepsin G and elastase and their inhibitors such as
alpha-1-antitrypsin and alpha-2-macroglobulin, total antioxidant status and
lipid peroxidation in plasma of young rats chronically intoxication with
ethanol.
The activity of cathepsin G and elastase was increased, while the activity
of their inhibitors was reduced after ethanol treatment.
At the same time, the total antioxidant status was significantly decreased
while lipid peroxidation measured as malondialdehyde and 4-hydroxynonenal
was significantly increased.
Giving green tea to rats did not change the proteases and their inhibitors
activity, but significantly increased total antioxidant status and decreased
lipid peroxidation.
Drinking green tea with ethanol partially prevents the changes observed
after ethanol intoxication. PMID: 11780568



J Toxicol Environ Health A. 2001 Oct 12; 64(3): 213-22.
Antioxidant status and lipid peroxidation in colorectal cancer.
Skrzydlewska E, Stankiewicz A, Sulkowska M, Sulkowski S, Kasacka I.
Department of Analytical Chemistry, Medical Academy of Bialystok, Poland.
skrzydle@...

Colon carcinogenesis is a multistep process where oxygen radicals were found
to enhance carcinogenesis at all stages: initiation, promotion, and
progression.
Since insufficient capacity of protective antioxidant system can result in
cancer, the aim of this study was to examine the activity of antioxidant
enzymes (superoxide dismutase, catalase, glutathione peroxidase, and
glutathione reductase) and the levels of reduced glutathione, vitamin C, and
vitamin E.
The lipid peroxidation products were also determined by measuring
malondialdehyde and 4-hydroxynonenal levels in colorectal cancer tissue
collected from 55 patients.
In these cases the activity of superoxide dismutase, glutathione peroxidase,
and glutathione reductase was significantly increased
while the activity of catalase was significantly decreased in cancer tissue.
However, the level of nonenzymatic antioxidant parameters (glutathione,
vitamin C, and vitamin E) was significantly decreased in cancer tissue.
Further lipid peroxidation was enhanced during cancer development,
manifested by a significant increase in malondialdehyde and 4-hydroxynonenal
levels.
The obtained results indicate significant changes in antioxidant capacity of
colorectal cancer tissues, which lead to enhanced action of oxygen radicals,
resulting in lipid peroxidation. PMID: 11594700



Postepy Hig Med Dosw. 2001; 55(6): 871-89.
[Melatonin as an antioxidant] [Article in Polish]
Skrzydlewska E.
Zaklad Chemii Nieorganicznej i Analitycznej Akademii Medycznej w
Bialymstoku.

This review describes the structure and properties of melatonin.
The interaction of melatonin with reactive oxygen species and its protective
action in relation to DNA, lipids and proteins are presented.
The effect of melatonin on antioxidant and prooxidant enzymes is discussed,
too. Publication Types: Review Review, Tutorial PMID: 11875783



Rocz Akad Med Bialymst. 2001; 46: 133-44.
Ethanol and N-acetylcysteine influence on the development of liver changes
in experimental methanol intoxication.
Kasacka I, Skrzydlewska E.
Departments of Histology & Embriology, Medical Academy of Bialystok,
Bialystok, Poland.

The evaluation of ethanol and N-Acetylcysteine (NAC) influence on
histopathological changes in rat liver intoxicated with 3 g of methanol/kg
b.w. was conducted, based on morphological examinations in light and
electron microscope.
The rats received intragastrically 3.0 g of methanol/kg b.w. as a 50%
solution, 10% ethanol for 24 hours before methanol and next 48 hours after
methanol ingestion and NAC (150 mg/kg b.w.) after 15 min. methanol
administrated.
The results indicate that methanol intoxication causes pronounced
morphological changes in the examined organ.
Ethanol administered to methanol-intoxicated rats caused intensification of
certain parameters of hepatocytes morphological damage.
A simultaneous administration of methanol and NAC resulted in a lower degree
of parenchymal damage. PMID: 11780556




Psychiatr Pol. 1992 Sep-Oct; 26(5): 421-9.
[The influence of disulfiram on the metabolism of ethanol] [Article in
Polish]
Skrzydlewska E.
Zakladu Analizy Instrumentalnej AM, Bialymstoku.

The author discusses the metabolism of disulfiram and the enzymes which
metabolize ethanol.
The restraining of the activity of ALDH in the liver by disulfiram causes an
accumulation of acetaldehyde which in their turn cause a series of
psychophysical symptoms which are unpleasant and in some instances dangerous
for the patient.
Thus, it is important to monitor changes in the activity of ALDH after
administration of disulfiram.
Publication Types: Review Review, Tutorial PMID: 1302340


Postepy Hig Med Dosw. 1992; 46(1): 117-30.
[Metabolism of liver proteins in ethanol poisoning] [Article in Polish]
Skrzydlewska E, Worowski K, Roszkowska-Jakimiec W.
Zaklad Analizy Instrumentalnej AM, Bialymstoku.

The present paper reviews the literature on influence of ethanol and
acetaldehyde on synthesis, export and degradation of liver proteins.
Direction and intensification changes caused by ethanol and acetaldehyde
depend on concentration, time of activity and the way of administration of
these compounds, and the way of feeding.
Publication Types: Review Review Literature PMID: 1641374


Postepy Hig Med Dosw. 1992; 46(2): 159-72.
[Proteolytic enzymes of the digestive tract in ethanol poisoning] [Article
in Polish]
Skrzydlewska E, Worowski K, Roszkowska-Jakimiec W.
Zaklad Analizy Instrumentalnej Akademii Medycznej, Bialymstoku.

The present paper reviews the literature on changes of proteolytic enzymes
activity, disorders of protein digestion and absorption of protein
degradation products from digestive tract in ethanol intoxication.
Magnitude of the change depends on concentration, dose and time of ethanol
consumption.
Acute ethanol intoxication causes increase in gastric and pancreatic
proteolytic enzymes secretion and reduces amino acids and peptides
absorption.
Chronic ethanol consumption results in reduced synthesis and secretion of
gastric and pancreatic proteinases.
Publication Types: Review Review Literature PMID: 1470579



Postepy Hig Med Dosw. 1992; 46(4): 417-30.
[Interaction of acetaldehyde and proteins] [Article in Polish]
Skrzydlewska E, Roszkowska-Jakimiec W.
Zaklad Analizy Instrumentalnej Akademii Medycznej, Bialymstoku.

A review of literature dealing with acetaldehyde-proteins reactions in vitro
and in vivo was done.
The changes in proteins structure and functions resulting from acetaldehyde
binding were discussed.
Publication Types: Review Review, Academic PMID: 1293589


Rocz Akad Med Bialymst. 1990-91; 35-36: 119-27.
[Histopathological evaluation of protective effect of L-cysteine in
ethanol-induced liver damage in rats] [Article in Polish]
Worowski K, Chyczewski L, Skrzydlewska E.
Zakladu Analizy Instrumentalnej, Akademii Medycznej Bialymstoku.

Rats fed standard diet were intoxicated during 4 weeks with ethanol at the
dose of 0.6 g/100 g of the body weight.
This poisoning causes vacuolar degeneration, disappearance of glycogen
granules, steatosis of hepatocytes and focal necrosis changes in the liver.
The intake of food with cysteine at the dose of 0.012 and 0.024 g/100 g/24
hrs markedly prevents histopathological changes in the liver of rats
intoxicated with ethanol.
Larger amounts of cysteine (0.044 g/100 g/24 hrs) intensify
histopathological changes caused by ethanol in the liver of rats. PMID:
2136542



Rocz Akad Med Bialymst. 1990-91; 35-36: 129-41.
[Effect of cysteine on protein metabolism in the liver of rats with
ethanol-induced liver damage] [Article in Polish]
Skrzydlewska E, Worowski K, Chyczewski L.
Zakladu Analizy Instrumentalnej, Akademii Medycznej, Bialymstoku.

Rats intoxicated with ethanol at the dose of 0.6 g/100 g of the body weight
during 4 weeks were fed on standard diet and the one containing 0.125, 0.25
and 0.5% L-cysteine.
Intoxication of rats fed standard food causes an increase in the activity
of cathepsin D and gamma-glutamyl-transpeptidase in the liver and an
increase in the activity of alanine aminotransferase and
gamma-glutamyl-transpeptidase in the blood serum.
Consuming by rats food containing small and medium quantity of cysteine
causes normalization of the activity of all enzymes,
whereas consuming food containing large quantity of cysteine does not give
such effect. PMID: 1983788



Rocz Akad Med Bialymst. 1990-91; 35-36: 163-75.
[Effect of immunomodulating drugs on the release and activities of lysosomal
proteinases of the liver of rats with ethanol poisoning] [Article in
Polish]
Skrzydlewska E, Chyczewski L, Worowski K.
Zakladu Analizy Instrumentalnej, Akademii Medycznej, Bialymstoku.

Increased activity of cathepsin A and D in the cytosol fraction and
homogenate of the liver of rats intoxicated for 4 weeks with ethanol (0.6
g/100 g of the body weight) was found.
The cytosol cathepsin A and D activities were unaffected under the influence
of Levamisole and isoprinosine++.
Encorton reduced the activity of both cathepsins in the cytosol fraction
while it did not diminish their activities in the liver homogenates.
Encorton, and to a markedly lesser degree, Levamisole and isoprinosine++
caused a regression of vacuolar degeneration and of necrotic lesions and
an increase in the number of glycogen granules in the livers of
ethanol-intoxicated rats. PMID: 1726679



Mater Med Pol. 1989 Jul-Sep; 21(3): 225-7.
Inhibitory effect of ethanol and acetaldehyde on the amidolytic activity of
trypsin and chymotrypsin.
Skrzydlewska E, Worowski K, Zakrzewska I, Prokopowicz J, Puchalski Z,
Piotrowski Z.
Department of Instrumental Analysis, Bialystok, Poland.

Ethanol and in higher degree acetaldehyde displayed inhibitory effect
directed against amidolytic activity of trypsin and chymotrypsin.
The decrease of the activity of both enzymes is related to the concentration
of these compounds.
The rate of inhibition of amidolytic activity of chymotrypsin with both
reagents is more evident in comparison to trypsin. PMID: 2491274



Acta Med Pol. 1988; 29(1-2): 41-5.
Effect of ethanol and acetaldehyde on the enzymatic activity of human
pancreatic juice in vitro. I. Inhibition of alpha-amylase and lipase
activity. Zakrzewska I, Worowski K, Skrzydlewska E, Prokopowicz J,
Puchalski Z, Piotrowski Z. PMID: 3267162



Acta Med Pol. 1988; 29(1-2): 47-52.
Effect of ethanol and acetaldehyde on the enzymatic activity of human
pancreatic juice in vitro. II. Inhibition of the activity of proteolytic
enzymes. Skrzydlewska E, Worowski K, Zakrzewska I, Prokopowicz J,
Puchalski Z, Piotrowski Z. PMID: 3076740



Folia Med Cracov. 1987; 28(1-2): 205-14.
[Effect of ethanol and acetaldehyde on the release and activity of proteases
and protein degradation in the rat liver (in vitro and in vivo studies)]
[Article in Polish] Skrzydlewska E. PMID: 3623321



Rocz Akad Med Im Juliana Marchlewskiego Bialymst. 1986-87; 31-32: 3-18.
[Effects of ethanol and acetaldehyde on proteolytic enzyme activity of the
stomach] [Article in Polish] Skrzydlewska E. PMID: 3152147



Rocz Akad Med Im Juliana Marchlewskiego Bialymst. 1986-87; 31-32: 19-28.
[Effects of ethanol and acetaldehyde on proteolytic enzyme activity of the
small intestine and pancreas] [Article in Polish]
Skrzydlewska E. PMID: 3152145



Acta Biochim Pol. 1985; 32(3): 271-7.
Release of acid proteolytic activity from lysosomes and degradation of
protein in organs of rats intoxicated with ethanol and acetaldehyde.
Skrzydlewski Z, Worowski K, Skrzydlewska E.

Intoxication with ethanol and acetaldehyde resulted in a marked increase of
the acid proteolytic activity in the post-lysosomal supernatant of rat
kidney, lung, and liver, while the content of protein and acid-soluble
tyrosine remained practically unchanged.
Proteins of the post-lysosomal supernatant were degraded in vitro by the
endogenous proteinase(s) of lysosomal origin at pH 3.5 and 5.5 but not at pH
7.0. PMID: 3911694



Rocz Akad Med Im Juliana Marchlewskiego Bialymst. 1984-85; 29-30: 59-76.
[Effect of ethanol and acetaldehyde on the activity and release of
cathepsins from lysosomes of the canine liver (studies in vitro)]
[Article in Polish] Skrzydlewska E, Worowski K. PMID: 6443826



Rocz Akad Med Im Juliana Marchlewskiego Bialymst. 1984-85; 29-30: 153-62.
Influence of ethanol and acetaldehyde on blood coagulation (examinations in
vitro). Skrzydlewska E, Worowski K. PMID: 6443814



Rocz Akad Med Im Juliana Marchlewskiego Bialymst. 1984-85; 29-30: 163-73.
Influence of ethanol and acetaldehyde on fibrinolytic system (examinations
in vitro). Skrzydlewska E, Worowski K. PMID: 6242841
_______________________________________________________


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Postepy Higieny I Medycyny Doswiadczalnej http://www.phmd.pl

Postepy Hig Med Dosw (Online). 2004 Mar 30; 58: 194-201.
[Antioxidative abilities during aging]
[Article in Polish] [ Abstract and 80 References, in English, are given
here. ]
Augustyniak A, Skrzydlewska E.
Zaklad Chemii Nieorganicznej i Analitycznej Akademii Medycznej w
Bialymstoku.

Biological aging is associated with increased cellular levels of reactive
oxygen species (ROS) as well as the formation and accumulation of oxidized
biomolecules.
During evolution, organisms developed a highly-efficient and adaptive
antioxidant defense system.
Antioxidants can generally be divided into two categories: enzymatic and
non-enzymatic. During the aging process the activity of antioxidant enzymes,
e.g. SOD, CAT, GSH-Px, and GSSG-R, depends on factors such as race, gender,
tissue and subcellular localization of enzymes.
The age-dependent decrease in antioxidant enzyme activity may be attributed
to oxidative modifications of enzymes.
During the aging process, ROS may also lead to the induction of some enzyme
activity which is explained as an adaptive phenomenon.
The decrease in GSH concentration with age can be explained by decreased GSH
synthesis and/or increased GSH consumption in the removal of peroxides and
xenobiotics.
In plasma albumin, ferritin, transferrin, and caeruloplasmin exert
protective action. Plasma proteins can inhibit ROS generation and
lipid peroxidation by chelating free transition metals.
Plasma protein concentrations changes with age.
The major exogenous antioxidants, mostly derived from the diet, are vitamin
E, C, A, and beta-carotene.
During the aging process the level of vitamins may decrease or increase,
depending on such factors as diet, and diseases. PMID: 15077054

www.phmd.pl
Review
Postepy Hig Med Dosw (online), 2004; 58: 194-201

page 194

Zdolnosci antyoksydacyjne w starzejacym
sie organizmie
Antioxidative abilities during aging
Agnieszka Augustyniak, Elzbieta Skrzydlewska
Zaklad Chemii Nieorganicznej i Analitycznej Akademii Medycznej
w Bialymstoku Streszczenie
Received: 2003.04.22
Accepted: 2003.08.08
Published: 2004.03.30
Key words: aging . antioxidant enzymes . non-enzymatic antioxidants
Full-text PDF: http://www.phmd.pl/pub/phmd/vol_58/5343.pdf
Word count: 3953
Tables: -
Figures: 1
References: 80
Source of support: Praca finansowana z grantu KBN 6PO5F01720.
Adres autorki: dr hab. Elzbieta Skrzydlewsdka, Zaklad Chemii Nieorganicznej
i Analitycznej AM, ul. Mickiewicza 2a,
15-230 Bialystok, e-mail: skrzydle@...

page 196

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page 200

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page 201

Augustyniak A. i Skrzydlewska E. - Zdolnosci antyoksydacyjne.

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_______________________________________________________




"CONCLUSION
There is much strong evidence that the background of etheno-DNA and
propano-DNA detected in tissues from unexposed humans and rodents arises
from endogenous lipid peroxidation products, such as MDA.

With the advent of ultrasensitive, specific detection methods for this kind
of DNA damage in human tissues and cells, new insights can be gained into
the mechanisms involved in human cancers.

Moreover, etheno-DNA adducts can now be used as biomarkers to investigate
the potential role of lipid peroxidation in human cancers."

Cell Mol Biol Lett. 2003; 8(2): 391-413.
DNA damage caused by lipid peroxidation products.
Luczaj W, Skrzydlewska E.
Department of Analytical Chemistry, Medical Academy of Bialystok,
Mickiewicza 2A, P.O. Box 14, 15-230 Bialystok 8, Poland.

Lipid peroxidation is a process involving the oxidation of polyunsaturated
fatty acids (PUFAs), which are basic components of biological membranes.
Reactive electrophilic compounds are formed during lipid peroxidation,
mainly alpha, beta-unsaturated aldehydes.
These compounds yield a number of adducts with DNA.
Among them, propeno and substituted propano adducts of deoxyguanosine with
malondialdehyde (MDA), acrolein, crotonaldehyde and etheno adducts,
resulting from the reactions of DNA bases with epoxy aldehydes,
are a very important group of adducts.
The epoxy aldehydes are more reactive towards DNA than the parent
unsaturated aldehydes.
The compounds resulting from lipid peroxidation mostly react with DNA
showing both genotoxic and mutagenic action;
among them, 4-hydroxynonenal is the most genotoxic,
while MDA is the most mutagenic.
DNA damage caused by the adducts of lipid peroxidation products
with DNA can be removed by the repairing action of glycosylases.
The formed adducts have been hitherto analyzed using the IPPA
(Imunopurification-(32)P-postlabelling assay) method and via gas
chromatography/electron capture negtive chemical ionization/mass
spectrometry (GC/EC NCI/MS).
A combination of liquid chromatography with electrospray tandem mass
spectrometry (LC/ES-MSMS) with labelled inner standard has mainly been used
in recent years. PMID: 12813574

http://www.cmbl.org.pl/vol8/V8Page391.pdf

CELLULAR & MOLECULAR BIOLOGY LETTERS
Volume 8, (2003) pp 391 - 413
http://www.cmbl.org.pl
Received 6 January 2003
Accepted 16 April 2003

Abbreviations used: eA - 1,N6-ethenoadenine;
eC - 3,N4-ethenocytosine; edA - 1,N6-
ethenodeoxyadenosine; edC - 3,N4-ethenodeoxycytidine;
AdG - acrolein-derived 1,N2-propanodeoxyguanosine;
CdG - crotonaldehyde-derived 1,N2-propanodeoxyguanosine;
EH - 2,3-epoxy-4-hydroxynonanal;
GC/EC NCI/MS - gas chromatography with mass spectrometry with electron
capture negative chemical ionization detection;
GSH - gluthatione; HNE - trans-4-hydroxy-2-nonenal;
IPPA - Imunopurification-32Ppostlabelling assay;
LC/ES-MSMS - liquid chromatography with electrospray tandem mass
spectrometry;
M1 C - N4-(3-oxo-propenyl)deoxycytidine;
M1 G - pirymido[1,2a]purin-10(3H)-one); M1A -
N6-(3-oxo-propenyl)deoxyadenosine; MDA - malondialdehyde; PUFAs -
polyunsaturated fatty acids.



DNA damage caused by lipid peroxidation products.
Wojciech Luczaj and Elzibieta Skrzydlewska.
Department of Analytical Chemistry, Medical Academy of Biaystok,
Mickiewicza 2A, P.O. Box 14, 15-230 Biaystok 8, Poland

Abstract:
Lipid peroxidation is a process involving the oxidation of
polyunsaturated fatty acids (PUFAs), which are basic components of
biological membranes. Reactive electrophilic compounds are formed during
lipid
peroxidation, mainly a,b-unsaturated aldehydes. These compounds yield a
number of adducts with DNA. Among them, propeno and substituted propano
adducts of deoxyguanosine with malondialdehyde (MDA), acrolein,
crotonaldehyde and etheno adducts, resulting from the reactions of DNA bases
with epoxy aldehydes, are a very important group of adducts. The epoxy
aldehydes are more reactive towards DNA than the parent unsaturated
aldehydes. The compounds resulting from lipid peroxidation mostly react with
DNA showing both genotoxic and mutagenic action; among them, 4-
hydroxynonenal is the most genotoxic, while MDA is the most mutagenic. DNA
damage caused by the adducts of lipid peroxidation products with DNA can be
removed by the repairing action of glycosylases. The formed adducts have
been hitherto analyzed using the IPPA (Imunopurification-32P-postlabelling
assay) method and via gas chromatography/electron capture negtive chemical
ionization/mass spectrometry (GC/EC NCI/MS). A combination of liquid
chromatography with electrospray tandem mass spectrometry (LC/ES-MSMS)
with labelled inner standard has mainly been used in recent years.

Key Words: Lipid Peroxidation, Etheno Adducts, Propano Adducts, á,â-
Unsaturated Aldehydes



CELL. MOL. BIOL. LETT. Vol. 8. No. 2. 2003

page 392

INTRODUCTION
Carcinogenesis was induced by chronic infections caused by viruses, bacteria
or parasites and the inflammation accompanying them. A hypothesis explaining
carcinogenesis mechanisms suggested that endogenic compounds causing DNA
damage are formed by the organism in the inflammation state [1]. The main
species/compounds involved in them are oxygen and nitrogen (species). The
production of these species markedly increases in such conditions, and they
can induce enhanced lipid peroxidation in direct reactions and/or cause DNA
damage [1].

Various reactive electrophilic compounds can be formed by lipid
peroxidation and some of them, showing mutagenic and genotoxic properties,
reaily react with proteins and DNA. This is particularly true for trans-4-
hydroxynonenal, malondialdehyde, and crotonaldehyde, which form adducts
with DNA [7]. The formation of these compounds was described as early as in
the eighties, but their identification and quantitative determination in
animal organisms under physiological conditions has only been possible in
recent studies, in which ultrasensitive analytical methods such as IPPA
(Imunopurification-32P-postlabelling assay) and gas chromatography/electron
capture negtive chemical ionization/mass spectrometry (GC/EC NCI/MS) were
used [86-89]. This also created chances to obtain evidence of the toxic and
genetic consequences of such DNA damage [1].

LIPID PEROXIDATION
Lipid peroxidation occurs in physiological conditions. It involves the
oxidation of polyunsaturated fatty acids (PUFAs), which are basic biological
membrane components. Many unsaturated components, mainly aldehydes, are then
formed [2]. Fundamental reactions occurring during peroxidation are showing
in Fig. 1 [2].

Polyunsaturated fatty acids contain active methylene groups situated between
cis double bonds. Such groups readily react with oxidizing agents and their
hydrogen atoms are removed to form carbon-centered radicals (compound 1,
Fig. 1) [2]. These radicals react with molecular oxygen-yielding peroxyl
radicals, which are the initial products of polyunsaturated fatty acid
oxidation [3].

Further transformations of peroxyl radicals depend on their position in
the carbon chain of the fatty acids [3]. If the peroxyl radical exists at
the
end of a double bond system (compound 2, Fig. 1) then it can be reduced to a
hydroperoxide. Conjugated diene hydroperoxides formed in this way (compound
4, Fig. 1) are relatively stable lipid peroxidation products in the absence
of transition metal ions [2]. Peroxyl radicals can be also reduced to
hydroperoxides by other fatty acid molecules or by vitamin E [4].

The reduction of a peroxyl radical by another fatty acid molecule results in
the formation of a new carbon centered radical which propagates the fatty
acid oxidation. In this way, an oxidized molecule can induce the oxidation
of many other fatty acid molecules. Approximately 60 linoleic acid molecules
and 200 molecules of arachidonic acid

CELLULAR & MOLECULAR BIOLOGY LETTERS 393

are oxidized as the result of transformations initiated by one free-radical
reaction [4]. The length of the free-radical reaction chain depends on many
factors.

The main factor determining the free-radical reaction chain length in vivo
is vitamin E concentration in the lipid bilayer [5]. This vitamin reduces
peroxyl radicals to hydroperoxides, thereby breaking the reaction chain and
slowing
the rate of lipid peroxidation [6].
However, vitamin E can initiate other free-radical chain reactions if
present in very small concentrations [6].

Fig. 1. The pathways of lipid peroxidation [3].

If the peroxyl radical is located within a fatty acid chain
(compound 3, Figure 1) then it can undergo cyclization owing to a
neighbouring double bond [7], yielding a cyclic peroxide
located in vicinity of a carbon-centered radical
(compound 5, Fig. 1). This radical can undergo further transformations. It
can bind an oxygen molecule, yielding a peroxyl radical which can be reduced
to hydroperoxide (compound 6, Fig. 1), as described earlier, or it can
undergo
a new cyclization, yielding a bicyclic peroxide. This can bind another
oxygen molecule and be reduced to a compound (compound 7, Fig. 1)
structurally
analogous to prostaglandin endoperoxide but lacking a stereochemical control
[7]. The chemical conversion of the bicyclic peroxide group of this compound
gives malondialdehyde (MDA) and isoprostanes [8] and 17-carbon fatty acids
are simultaneously formed as side products (compound 8, Fig. 1) [9].

There is a growing belief that the most valuable biomarkers of lipid
peroxidation in the human body are the isoprostanes [10-14]. Highly
sensitive and accurate spectrophotometric methods have
hitherto been used to determine isoprostane

CELL. MOL. BIOL. LETT. Vol. 8. No. 2. 2003 394

concentration in blood serum [13, 15, 16]. Isoprostates undergo relatively
rapid metabolic transformations. Therefore, lipid peroxydation in various
organs can be readily monitored by determining the level of their
decomposition
products in urine [13, 17].

It is known that transition metal ions initiate free-radical reactions
including lipid peroxidation because they participate in generating reactive
oxygen species (O2-*, *OH). At the same time, they contribute to the
propagation
of the process by reducing lipid hydroperoxides [18, 19]. Compounds of such
ions as
Cd(II), Co(II), Cu(II), Hg(II), Ni(II), Pb(II), Sn(II), V(V), Fe(II), and
Fe(III) provoke enhanced lipid peroxidation under both in vitro and in vivo
conditions [20-25].

All the hydroperoxides presented in Fig. 1, as well as their regio- and
stereoisomers, can be reduced to their akoxyl radicals by transition metal
cations and then they can undergo b-cleavage yielding many products
[26,27].

This results in a number of epoxy compounds (e.g. 2,3-epoxybutanal or
2,3-epoxy-4-hydroxynonanal), hydroperoxides (e.g. compounds 4, 6, 7, Fig. 1)
and saturated and á,â-unsaturated aldehydes (e.g. acrolein, crotonaldehyde,
4-hydroxynonenal, 2,4-nonadienal, 2,4-decadienal) [28]. These compounds are
formed from fatty acids in various amounts depending on their stucture and
oxidation conditions.

Recently, a new product of lipid peroxidation, 4-oxo-2-nonenal, was reported
to be generated by the decomposition of linoleic acid hydroperoxide [13(S)-
hydroperoxy-(Z,E)-9, 11-octadecadienoic acid] [29].

All lipid peroxidation pathways leading to product formation are not known
in sufficient detail. Nevertheless, it has been found that crotonaldehyde is
mainly generated from a-linoliec acid and linoleate.

Crotonaldehyde is also formed in small amounts by the peroxidation
of arachidonate and such acids as cis-5,8,11,14,17-eicosapentaenoic
and cis-4,7,10,13,16,19-docosahexaenoic [30].
It is interesting that arachidonate and w-3-polyunsaturated fatty acids were
earlier stated to be primary compounds of acrolein generation [31].

It was also found that hexanal and 4-hydroxynonenal (HNE) were formed from
lipids containing w-6-polyunsaturated fatty acids (18:2, 20:4),
whereas 4-hydroxyhexenal and propanal are formed from
w-3-polyunsaturated fatty acids (22:6) [32]. It was
shown that hexanal is formed as a result of the â-cleavage of
15-hydroperoxyarachidonic acid or 13-hydroperoxy-linoleic acid [32, 33].

However, it was suggested that HNE could be formed by the transformation of
w-6-polyunsaturated fatty acids like 11-hydroperoxy-arachidonic acid (or 9-
hydroperoxy-linoleic acid) or from isomers of 15-hydroperoxy-arachidonic
acid and 13-hydroperoxy-linoleic acid [34]. On the other hand, lipids
containing polyunsaturated fatty acids with three or more double bonds
separated
by methylene groups, mainly arachidonic acid (20:4) and docosahexaenoic acid
(22:6), yield malondialdehyde (MDA) [32, 33]. It is believed that oleic and
linoleic acid to a small degree take part in MDA formation [32, 35].
Bicyclic peroxides with an oxygen bridge located inside the molecule are
involved as intermediates in the pathway of MDA formation; at higher
temperatures or in an acid medium, they undergo decomposition to free MDA
[7]. Two other

CELLULAR & MOLECULAR BIOLOGY LETTERS 395

pathways to MDA formation from polyunsaturated fatty acids were proposed
[36]. The main stages of MDA formation by the oxidation of arachidonic acid
are presented in Fig. 2: â-cleavage of the fatty acid giving
hydroperoxyaldehyde, which further yields MDA or the acrolein radical; the
latter undergoes transformation to the enol form of MDA in reaction with a
hydroxyl radical [2].

ADDUCTS OF LIPID PEROXIDATION PRODUCTS WITH DNA

There are many known adducts formed by low molecular weight compounds
resulting from lipid peroxidation with DNA bases, but the compounds formed
by a,b-unsaturated aldehydes have been studied the most thoroughly [37, 38].
Among them, there are etheno and substituted ethano adducts of
deoxyadenosine, deoxyguanosine, and deoxycytidine, propeno and substituted
propano adducts of deoxyguanosine, and bicyclic adducts with deoxyguanosine.

A particularly important group of these compounds are propeno and
substituted propano adducts of deoxyguanosine with malondialdehyde,
acrolein,
or crotonaldehyde. Their content in human liver DNA is from 1500 to 5000
adducts per cell [86, 39].

Fig. 2. Possible mechanisms of the formation of MDA through the autoxidation
of intermediate polyunsturated aldehydes derived from â-cleavage of
5-hydrperoxy or 15-hydrperoxy arachidonic acid [7].

It has been proved in numerous studies carried out in various laboratories
that propano adducts are mainly formed in reactions of small-molecule a,b-
unsaturated aldehydes with deoxyguanosine [1, 40-42, 48]. The mechanism of

CELL. MOL. BIOL. LETT. Vol. 8. No. 2. 2003 396

the nucleophilic Michael addition of the nitrogen atom of deoxyguanosine
amino group to the aldehyde double bond followed
by cyclization in position N-1 of
deoxyguanosine is presented in Fig. 3a.
Reactivity of enals with deoxyguanosine
during the formation of propano adducts varies with increasing alkyl chain
length: acrolein > crotonaldehyde > HNE [41, 59]. Accordingly, adduct
formation rate in the case of HNE is considerably lower than in the case of
shorter chain unsaturated aldehydes [48]. In addition, the modification
degree of nucleic acid is lower in the case of double-stranded DNA than in
the case of single-stranded DNA, because two nitrogen atoms of the
bases must then be bonded to form a cyclic adduct, which are normally
bonded by a hydrogen bond in the DNA a-helix [59].

Fig. 3. The mechanism of the reaction of 4-hydroxyalkenals with
deoxyguanosine.
(a) The reaction of the parent unsaturated aldehyde;
(b) the reaction of epoxyaldehyde [48].

Acrolein is the most electrophilic of the á,â-unsaturated aldehydes. This is
reflected by its great ability to react with thiol and amino groups [43,
44].
It was found, for example, that acrolein reacts with GSH 110-150 times
more rapidly than HNE or crotonaldehyde [45]. Acrolein yields cyclic adducts
with deoxyguanosine, deoxyadenosine and deoxycytidine, but it is its
compounds
with deoxyguanosine that have been studied the most extensively [46]. Three
stereoisomeric adducts are formed in the reaction with deoxyguanosine:
AdG 1, AdG 2, and AdG 3 (Fig. 4).
AdG 1 and AdG 2 are a pair of diastereoisomers and
AdG 3 is a regio-isomer formed by ring closure in the opposite direction; it
is supposedly composed of AdG 1 and AdG 2 stereoisomers. With these
compounds, the formation mechanism is based on the Michael addition of
nitrogen N-1 of the deoxyguanosine amino group to the third acrolein carbon
atom, followed by ring closure between deoxyguanosine nitrogen N-2 and the
carbon C-1 of acrolein [41].

Crotonaldehyde, a homolog of acrolein, reacts with deoxyguanosine like
acrolein, mainly yielding 1,N2-propano adducts: CdG 1 and CdG 2 (Fig. 4)
[36].

CELLULAR & MOLECULAR BIOLOGY LETTERS 397

However, the number of guanosine modifications caused by crotonaldehyde is
considerably smaller than in the case of acrolein [46]. The Michael addition
between the nitrogen N-1 and the double-bond carbon atom is not possible in
this case because of steric hindrance generated by the methyl group and the
oxygen atom at the C-6 carbon atom. As a result, only one diastereoisomer
pair is formed. The trans configuration was assigned to the CdG isomers on
the ground of NMR magnetic coupling constants [47].

Fig. 4. The reaction of acrolein (1) and crotonaldehyde (2) with
deoxyguanosine [47].
4-Hydroxyalkenals, including HNE, have three exceptionally reactive groups:
the aldehyde group, the double carbon-carbon bond, and the hydroxyl group.

All of them can react with other molecules, either independently from each
other of or in cooperation. In a neutral medium, 4-hydroxyalkenals readily
react
with the sulfhydryl groups (SH) of thiols such as glutathione, or they react
with
protein or nucleic acid base amino groups, mainly of guanine, adenine, and
cytosine [36].

As in the case of acrolein and crotonaldehyde, Michael addition of the
nitrogen deoxcyguanosine amino group to the HNE double bond followed by
cyclization in the N-1 position of deoxyguanosine are involved in the
mechanism of the HNE reaction with deoxyguanosine [48]. It results in the
formation of two pairs of
1,N2-propano-dG (HNE-dG 1,2 and 3,4) diastereomeric adducts [48,49].
The formation of four different adducts is a consequence of the
trans configuration of the hydroxy group and
the side alkyl chain with a chiral carbon atom [50].
An HNE adduct with deoxyguanosine is presented in Fig. 5.

MDA also reacts with DNA bases yielding various compounds (Fig. 6). The
problem of MDA interaction with DNA is somewhat complicated by the ability
of MDA to oligomerize to dimers and trimers which are also able to react
with DNA.
However, MDA oligomerization is relatively slow in a neutral medium,
and compounds of the monomers presented in Fig. 6 are considered to be the
main products formed in physiological conditions [51, 52]. The in vitro
experiments suggest that the adducts M1G (pirymido[1,2a]purin-10(3H)-one)
and M1A (N6-(3-oxo-propenyl)deoxyadenosine)
are the main products of MDA reaction with DNA [57, 1].
The amount of M1G was found to be approximately
five times greater than that of M1A [57]. Trace amounts of N4-(3-oxo-

CELL. MOL. BIOL. LETT. Vol. 8. No. 2. 2003 398

propenyl)deoxycytidine (M1C) were also formed [53]. It should be stressed
that the main adduct of malondialdehyde
with dG is not a malondialdehyde-specific lesion.
Dedon et al. demonstrated that base propenals as structural analogs
of MDA derived from oxidative DNA damage are capable of forming the M1G.
Adenine propenal was predicted to be more reactive than malondialdehyde in
the formation of M1G [58].

Fig. 5. The formation of 1,N2-propano-dG adduct in a reaction of HNE with
deoxyguanosine [50].

Fig. 6. The formation of MDA-DNA adducts [3].

It was demonstrated that unsaturated aldehydes could be converted to
epoxyaldehydes (aldehydes with an oxygen bridge in the molecule) in the
presence of H2O2 or fatty acid hydroperoxides or in conditions in which
these oxidants are formed [54-56]. Epoxyaldehydes are more reactive towards
DNA than parent unsaturated aldehydes, particularly those formed from
long-chained enals [54-56]. Reactions of epoxy aldehydes with DNA bases
yield etheno or ethano adducts [1], mainly 1,N2-ethenoguanosine (or
1,N2-ethanoguanosine), 1,N6-ethenoadenosine, and 3,N4-ethenocytidine (Fig.
7). Acrolein epoxide (glycidaldehyde) reacts with guanine yielding
substituted 1,N2-ethano and 1,N2-

CELLULAR & MOLECULAR BIOLOGY LETTERS 399

Fig. 7. The formation of various etheno adducts from reactions of
deoxyrybonucleosides with epoxyaldehydes. The substituted etheno adducts are
formed by a loss of H 2O from the intermediate ethano adducts and the
unsubstituted etheno adducts are formed by base-catalyzed losses of R'CHO
and H2O [47].

etheno adducts and an unsubstituted 1,N2-etheno adduct [57] while 2,3-
epoxybutanal obtained from crotonaldehyde yields 1,N2-ethenoguanosine, 1,N6-
ethenoadenosine, and 3,N4-ethenocytidine [54]. The relative generation
yields of substituted and unsubstituted etheno adducts depend on
epoxyaldehyde and on the pH of the reaction. 2,3-epoxy-4-hydroxynonanal (EH)
is a mixture of two diastereomers, I and II;
it is formed in vitro in the reaction of HNE with
t-butyl hydroperoxide. It reacts with deoxyguanosine yielding a unique
tetracyclic 1,N2 ethano adduct as two pairs of diastereomers [55, 56].
Adducts formed at pH 10 and 37ºC readily undergo conversion to
1,N2-ethenodeoxyguanosine (1,N2-edG)

CELL. MOL. BIOL. LETT. Vol. 8. No. 2. 2003 400

- compound 9 in Fig. 3b [55]. 2,3-Epoxy-4-hydroxynonanal reacting with
deoxyadenosine yields edA adduct (1,N6-ethenoadenosine) and the pair of its
substituted isomers. It was also demonstrated that both 2,3-epoxy-4-
hydroxynonanal isomers (I and II) react stereoselectively with
deoxyadenosine and deoxyguanosine, yielding etheno adducts; isomer I
preferentially
modifies adenine over guanine, while isomer II exhibits similar rectivity to
both purine bases [59].
Isomer II of 2,3-epoxy-4-hydroxynonanal is more mutagenic than
isomer I because of its higher reactivity towards nucleic acids. These
results suggest that epoxidation is possibly an important transition stage
activating relatively unreactive long-chain enals. Unfortunately, there is
no evidence
that epoxidation of 4-hydroxy-2-nonenal can occur in vivo, as the compound
is a convenient substrate of glutathione S-transferases and aldo-keto
reductases
[60].

Recent studies have also furnished us with information on DNA damage caused
by 2,4-decadienal (DDE), a highly toxic lipid peroxidation product [61, 62].
Initially, the formation of 1,N6-etheno-2'-deoxyadenosine
and of two etheno adducts:
1-[3-(2-deoxy-beta-D-erythro-pentafuranosyl)-3H-imidazo[2,1-i]purin-
7-yl]-1,2,3-octanetriol (adduct 1) and
1-[3-(2-deoxy-beta-D-erythropentafuranosyl)-
3H-imidazo[2,1-i]purin-7-yl]-1,2-heptanediol (adduct 2) are
generated in the reaction of the aldehyde with deoxyadenosine [61, 62]. On
the other hand, Loureiro et al. proved that the interaction of DDE with
deoxyguanosine yielded the adduct which is a tautomer of 1,N2-ethene-2'-
deoxyguanosine (the commonly known reaction product of epoxy aldehydes
with dG) and, in addition, two new diastereomeric products [63]. The
formation mechanism that was proposed for these compounds involved double
DDE
epoxidation, nucleophilic addition of the dG amino group nitrogen atom to
the C1 carbon atom of the aldehyde, followed by cyclization as the result of
nucleophilic attack of the N1 nitrogen atom on the C2 carbon atom of the
epoxy group, and dehydratation [63].

Similarly, 4-oxo-2-nonenal, a recently discovered lipid peroxidation
product, forms adducts with the DNA of the structure corresponding to that
of substituted etheno adducts [64].
The three initially formed ethano adducts arose from
the highly regioseletive nucleophilic addition of the nitrogen N-2 of dG to
the C-1 aldehyde of 4-oxo-2-nonenal, followed by the reaction of N-1 at the
C-2
of the resulting á,â-unsaturated ketone. All three ethano adducts then
dehydrated to a single heptanone etheno-dG adduct
(3-(2-deoxy-beta-D-erythropentafuranosyl)
imidazo-7-(heptane-2-one)-9-hydroxy[1,2-alpha]purine) [64]. Nucleophilic
addition of the N-6 of dA to the C-1 aldehyde of 4-oxo-2-nonenal followed by
the reaction of N-1 at the C-2 of the resulting á,â-unsaturated ketone
results in the generation of a mixture of two ethano adducts that could
inter-convert
to each other. The ethano adducts are subsequently dehydrated, yielding a
single heptanone etheno-dA adduct
(1''-[3-(2'-deoxy-beta-D-erythropentafuranosyl)-3H-imidazo[2,1-i]purin-7-yl]
heptane-2''-one) [65, 66].

CELLULAR & MOLECULAR BIOLOGY LETTERS 401

THE GENOTOXICITY AND MUTAGENEITY OF LIPID
PEROXIDATION PRODUCTS AND OF THEIR ADDUCTS WITH DNA

Most compounds formed by lipid peroxidation react with DNA and proteins.
These processes have genotoxic and mutagenic effects. The most genotoxic
lipid peroxidation product is 4-hydroxynonenal [70]. HNE and other 4-
hydroxyalkenals provoke genotoxic phenomena in various animal tissues as
well as in the Salomonella typhimurium bacteria cell [71]. A similar action
was observed in the case of 2-nonenal, whereas nonanal shows no genotoxic
action
even at high non-physiological concentration (100 mM) [70]. On the other
hand, HNE was found to provoke chromosomal aberrations and sister chromatid
exchange even at 0.1 mM [70]. It should be taken into account that HNE
concentration in the liver is in the range of about 0.1-0.5 mM and, for this
reason, the aldehydes generated by lipid peroxidation
are a constant source of DNA mutagenic DNA damage [36].

Mutagenic properties, both towards eukaryotic and bacterial cells, are
characteristic for acrolein, crotonaldehyde, and MDA [67-69]. MDA appears to
be the most mutagenic product of lipid peroxidation [70]. MDA shows
mutagenic activity towards Salomonella typhimurium bacteria culture [72] and
towards eukaryotic cells and is carcinogenic in rodents. The mutagenic
abilities of MDA-DNA adducts were based on MDA reaction (in a neutral
medium) with the single-stranded M13 vector
containing the lacZá gene giving rise to
mutation during the formation of the lacZá- phenotype [76]. The mutation was
found to be related to the increase in the
amount of M1G-major MDA-doexyguanosine
adduct. Most sequence changes induced by MDA were base pair substitutions.
43% of these substitutions were transversions (most of which were G.T) and
57% were C.T and A.G transitions [76]. The ability of MDA to induce base
pair substitution mutation at dG, dA, and dC is due to the possibility of
forming adducts with these deoxynucleosides. No mutation was detected in the
case of dT, which is concurrent with the fact
that MDA does not form adducts with this deoxynucleoside.
An experiment in which M1G was positioned at a defined site
in a duplex M13 genome was used to determine the mutagenic potential of the
lesion. M1G-modified and unmodified genomes were transoformed into E. coli
strains [77]. A 500-fold increase in mutations was observed compared to the
unadducted genome. The recent work of Lloyd and Harris shows that cyclic
adducts can be reactive species that participate in intra- and interchain
crosslinking reactions in the genome. They demonstrated that the primary
acrolein adduct of deoxyguanosine,
3-(2-deoxy-beta-D-erythro-pentofuranosyl)-
5,6,7,8-tetrahydro-8-hydroxypyrimido[1,2-a]purin-10(3H)-one (2), can
spontaneously but reversibly be forme as an interchain cross-link with the
exocyclic amino group of deoxyguanosine in the opposing chain [78].

The carcinogenic action of MDA was known of as early as 1972 [73]. This
compound, administered locally to mice, provokes a rapidly propagating skin

CELL. MOL. BIOL. LETT. Vol. 8. No. 2. 2003 402

tumour without showing characteristics which are typical for a mouse skin
assay [74]. In addition, MDA was found to induce thyroid tumours in rats
[75].
DNA damage caused by the formation of adducts with lipid peroxidation
products can be repaired.
This is mainly mediated by the action of
glycosylase, which results in apurinic/apyrimidinic sites [79].
Human cells contain a protein signalling the ranges of damaged DNA
owing to its high binding affinity to the etheno adducts of DNA,
and glycosylase acts there as the repairing enzyme [80].

This protein is able to detect nucleic acid damage in the position of åA
(1,N6-ethenoadenine) coupled either
with thymine or with cytosine [80], while the
range where eA is bonded to adenine is poorly detectable and the adduct of
eA with guanine is undetectable. It is worth noting that the molecular
weight of the discussed protein is similar to those of many animal DNA
glycosylases [81].
Since it was found that 3-methyladenine-DNA glycosylase was able to remove
eA and 3-methyladenine cooperating with a protein having affinity to eA, the
repairing action to eA in the human organism was assigned to
3-methyladenine-DNA glycosylase [79]. In further studies, it was found that
all four etheno adducts:
eA, 3,N4-ethenocytosine (eC), N2,3-ethenoguanine (N2,3-eG) and
1,N2-ethenoguanine (1N2-eG) can be removed both
by human glycosylase and by Escherichia coli expressing
cloned human 3-methyladenine-DNA glycosylase [82].
It is also supposed that etheno adducts of adenine and cytosine are
removed much more effectively than the guanine adducts [83]. It was recently
reported that human alkylpurine-DNA N-glycosylase (APNG) is able to remove
both 1,N6-ethenoadenine(eA) and 1,N6-ethanoadenine (EA);
unlike eA, EA has a single bond in its five-membered ring instead of double
bond [84].
It was also found experimentally that the ability of this enzyme to remove
EA is 65
times lower than its ability to remove eA [84].
It should be stressed that the possibility to remove etheno adducts of DNA
by ubiquitous and non-specific DNA glycosylase suggests an
endogenous origin of these adducts.

METHODS OF IDENTIFICATION AND QUANTITATIVE
DETERMINATION OF THE ADDUCTS OF LIPID PEROXIDATION
PRODUCTS WITH DNA

Etheno and propano DNA adducts are formed in small amounts in vivo. For this
reason, sensitive separation and detection methods are needed in their
analysis to monitor their formation and to determine their role in
pathological states
including carcinogenesis.

The first method applied in the quantitative analysis of the etheno adducts
of dA and of dC occurring in the lung and liver DNA of rats after a short
exposure
to vinyl chloride involved the resolution of DNA hydrolysis products by HPLC
and the determination of the level of the resulting adducts via the
radioimmunoassay (RIA) technique using monoclonal antibodies [85].
Parallelly, a sensitive method was developed to determine the level of
etheno dG adducts based on electrophore labelling followed by negative ion
chemical ionization [86].
The

CELLULAR & MOLECULAR BIOLOGY LETTERS 403

detection limit, depending on the sensitivity of the methods, was three
adducts (edA or edC) per 108 parent bases and six edG adducts per 107 parent
bases, respectively.
Unfortunately, several mg of DNA were needed to carry out the
determination using these methods.

A method combining gas chromatography with mass spectrometry with electron
capture negative chemical ionization detection (GC/EC NCI/MS) used in
quantitative determination of etheno adducts, mainly MDA with dG, proved to
be more sensitive [86, 88]. The detection limit of this method is about 1
M1G adduct per 108 parent bases, and the required DNA amount is 1 mg [87,
88].
In this method, deoxyribonucleosides are separated using monoclonal
antibodies against M1G-deoxyribose-albumine and M1G-deoxyribose conjugates.
The M1G base is converted in its derivative using pentafluorobenzyl bromide
(PFB) and the derivative is analysed using the GC/EC NCI/MS method.

The ultrasensitive IPPA method (Imunopurification-32P-postlabelling assay)
involves the isolation of modified DNA bases using immunoaffinity followed
by labelling e-deoxyribonucleoside 3'-monophosphates
with 32P phosphorus [89-91].
This was the basic method in determining the level of etheno adducts of
deoxyadenosine and deoxycytidine (edA and edC, respectively) isolated from
normal nucleotides using monoclonal antibodies against those adducts. The
attainable detection limit of this method is about 1 adduct per 107-109
parent DNA bases, and the required DNA amount is only 10-50 mg. Thus, it is
applicable to determinations in human tissues, where the expected
concentration of etheno adducts of DNA is close to one per 108 parent bases
[77, 79].
The use of large amounts of an energetic radioisotope and a great amount of
work were needed in the sensitive 32P-postlabelling method and, in addition,
this method was very time-consuming.
For this reason, another method has recently been applied -- liquid
chromatography and electrospray tandem mass
spectrometry (LC/ES-MSMS) with the use of a labelled inner standard.
It was applied in quantitative determination of the etheno adducts of dA
with guanine formed in the placenta [92, 93] and of etheno adducts of
guanine in
the human liver [94]. The resulting detection limit was about 1 adduct per
106-107 parent DNA bases. The LC/ES-MSMS method proved to be more sensitive
than the 32P-postlabelling method, but 1 mg DNA was needed to carry out the
analysis.
For this reason Roberts et al. have recently taken advantage of the unique
properties of graphitized carbon to attain maximal efficiency of
chromatographic separation [95]. Such a modification of the method made it
possible to
determine the level of the etheno adducts of dC of the order of 5 adducts
per 108 parent bases using an amount of DNA less than 100 mg.

Examples of the occurrence of etheno adducts in various tissues and the
techniques used for their identification and quantitative determination are
presented in Tab. 1.

CELL. MOL. BIOL. LETT. Vol. 8. No. 2. 2003 404

Tab. 1. Etheno adducts in various tissues and the methods of their
determination.
Adducts Tissue Technique Reference
M1G liver 32P [96, 97]
M1G kidney 32P [98]
M1G white cells 32P [99, 100]
M1G breats 32P [99, 101]
M1G liver GC/MS [87]
M1G leukocyte DNA GC/EC NCI/MS [88]
M1G pancreas GC/EC NCI/MS [102]
M1G liver GC/EC NCI/MS [103]
edA liver 32P [90, 104, 105, 108]
edC liver 32P [90, 104, 105, 108]
edA spleen 32P [106]
edC spleen 32P [106]
edA white cells 32P [107]
edC white cells 32P [107]
1,N2-propano-dG liver 32P [50]
1,N2-propano-dG colon 32P [50]
edA placenta GC/ECNCI/MS [92]
edA placenta LC/MS/MS [93]
edA liver LC/MS/MS [93]
edC liver LC/ES-MS/MS [93, 94]
1,N2-propano-dG brain 32P [109]

CONCLUSION

There is much strong evidence that the background of etheno-DNA and
propano-DNA detected in tissues from unexposed humans and rodents arises
from endogenous lipid peroxidation products, such as MDA.
With the advent of ultrasensitive, specific detection methods for this kind
of DNA damage in human tissues and cells, new insights can be gained into
the mechanisms involved in human cancers.
Moreover, etheno-DNA adducts can now be used as biomarkers to investigate
the potential role of lipid peroxidation in human cancers.

Acknowledgements. This study was supported by the Polish State Committee
for Resesarch, grant No. 3P05B07922.

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Med Sci Monit. 2001 Nov-Dec; 7(6): 1230-5.
Role of reactive oxygen species (ROS) in patients with erythema migrans, an
early manifestation of Lyme borreliosis.
Pancewicz SA, Skrzydlewska E, Hermanowska-Szpakowicz T, Zajkowska JM,
Kondrusik M.
Department of Infection Diseases and Neuroinfections, Medical University,
Bialystok, Poland.

BACKGROUND: Lyme borreliosis is a tick-transmitted, chronic, zoogenous
disease caused by Borrelia burgdorferi spirochete.
The clinical picture of Lyme disease is characterized by the variety of
tissue and organ involvement and differing severity of symptoms.
One of the pathogenic symptoms of early Lyme disease is a skin lesion called
erythema migrans.
MATERIAL AND METHODS: The purpose of our research was to estimate the
parameters of the antioxidant system and the concentration of lipid
peroxidation products in the plasma of patients with erythema migrans (EM).
The parameters measured included the activity levels of superoxide dismutase
(SOD) according to Sykes,
gluthatione reductase (GSSG-R) according to Mize and Langdon,
glutathione peroxidase (GSH-Px) according to Paglia and Valentine;
the concentrations of malondialdehyde (MDA)
were examined by means of a Bioxytech LPO-586 kit.
The total sulphydryl groups (-SH) according to Ellman and
reduced glutathione (GSH)
were measured using a Bioxytech GSH-400 test
in plasma samples collected from 20 patients with EM aged from 19 to 50,
taken before (examination 1) and after (examination 2) therapy with
amoxycycline.
The control group consisted of 8 healthy people.
RESULTS: The results of our examinations prove that beta-lactamase
antibiotic therapy brings non-enzymatic antioxidant parameters to control
values, though the treatment causes no change in enzymatic antioxidant
parameters,
resulting in the further activation of free radicals.
CONCLUSIONS: In patients with Erythema migrans, the decreased capability to
reduce lipid superoxidants leads to maintaining a high concentration of
membrane lipid peroxidation products. PMID: 11687735


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Clinical Research

page 1230

Med Sci Monit, 2001; 7(6): 1230-1235
Role of reactive oxygen species (ROS) in patients with erythema
migrans, an early manifestation of Lyme borreliosis
Slawomir A. Pancewicz1, Elzbieta Skrzydlewska2, Teresa
Hermanowska-Szpakowicz1,
Joanna Zajkowska1, Maciej Kondrusik1
1 Department of Infection Diseases and Neuroinfections, Medical University,
Bialystok, Poland
2 Department of Analytical Chemistry, Medical University, Bialystok, Poland
key words: Lyme borreliosis, erythema migrans, reactive oxygen species,
antioxidants

SUMMARY
Background: Lyme borreliosis is a tick-transmitted, chronic, zoogenous
disease caused by Borrelia burgdorferi
spirochete. The clinical picture of Lyme disease is characterized by the
variety of tissue and organ involvement
and differing severity of symptoms. One of the pathogenic symptoms of early
Lyme disease is a skin lesion called erythema migrans.
Material and methods: The purpose of our research was to estimate the
parameters of the antioxidant system
and the concentration of lipid peroxidation products in the plasma of
patients with erythema migrans (EM).
The parameters measured included the activity levels of superoxide dismutase
(SOD) according to Sykes, gluthatione
reductase (GSSG-R) according to Mize and Langdon, glutathione peroxidase
(GSH-Px) according to
Paglia and Valentine; the concentrations of malondialdehyde (MDA) were
examined by means of a Bioxytech
LPO-586 kit. The total sulphydryl groups (-SH) according to Ellman and
reduced glutathione (GSH) were measured
using a Bioxytech GSH-400 test in plasma samples collected from 20 patients
with EM aged from 19 to
50, taken before (examination 1) and after (examination 2) therapy with
amoxycycline. The control group consisted
of 8 healthy people.
Results: The results of our examinations prove that beta-lactamase
antibiotic therapy brings non-enzymatic antioxidant
parameters to control values, though the treatment causes no change in
enzymatic antioxidant parameters,
resulting in the further activation of free radicals.
Conclusions: In patients with Erythema migrans, the decreased capability to
reduce lipid superoxidants leads to
maintaining a high concentration of membrane lipid peroxidation products.
Received: 2000.08.28
Accepted: 2001.09.28
Correspondence address: S.awomir A. Pancewicz, Department of Infection
Diseases and Neuroinfections, Medical University,
ul. °urawia 14, 15-540 Biaystok, Poland

BACKGROUND
Lyme borreliosis (tick spirochaetosis, Lyme disease)
is a tick-transmitted, chronic, multisystem, zoogenous
disease of worldwide distribution, caused by
Borrelia burgdorferi spirochete, and in Europe also
by Borrelia garini and Borrelia afzeli. Ticks of the
Ixodes type are main carriers of B. burgdorferi. In
Europe, I. ricinus and I. persulcatus are main carriers
of B. burgdorferi, whereas in the Unites States
I. dammini is present in the North-eastern states
and I. pacificus in the Western states. I. neotomae,
I. spinipalpis, I. hexagonus, and I. granulatus ticks
are of less importance in the transmission of B.
burgdorferi [1-4].

Research done in Poland by Sifski et al. revealed
B. burgdorferi infection in 3.5% to 58.33% of ticks,
depending on the region of Poland [3]. Wegner et
al. documented infection in 11.5% of the I. ricinus
ticks in the region of Olsztyn, and in 4.0% to
15.6% in the region of Bia.ystok [5].

1231

Pancewicz SA et al - Role of reactive oxygen species (ROS) in patients.
The tests performed by many authors, both in Poland
and elsewhere, show that B. burgdorferi is
commonly present in high risk groups, especially
among forestry employees and farmers. Pancewicz
et al. in 1993-1997 examined 1466 forestry employees
from the northeastern region of Poland,
and found B. burgdorferi antibodies in 23.81% of
their subjects [6]. Hulsse C. von Stenglin found B.
burgdoferi infection in 7.8% of the ticks in the
Mecklenbug-Vorpmmern region of Germany, and
detected B. burgdorferi antibodies in 31.4% of forestry
employees [7]. According to Rath et al, 53%
of forestry workers reported tick bites, but erythema
migrans appeared after the bite only in 8% of
these persons. IgG antibodies to B. burgdorferi (immunoblot
assay) were found in 18% of the persons
examined [8]. Burek et al. discovered IgG antibodies
to B. burgdorferi in 9.7% of their total research
population, but in the group coming from
a high risk region the figure rose to 44%, as against
8% in the group from a low risk region; moreover,
antibodies were found in 42.9% of forestry workers [9].

The pathomechanisms controlling the course of
Lyme borreliosis have not yet been fully explained.
It is known, however, that the accompanying
inflammatory states are characterized by the
increased stimulation of phagocytes, which leads
to the increased generation of reactive oxygen
species (ROS) [10,11]. The presence of ROS causes
modifications to occur in low- and macromolecular,
endo- and exogenous compounds [10]. It
has been proved that B. burgdorferi induces O2 generation,
and that ROS derived from macrophages,
mainly nitrous oxide (NO), take part in the inactivation
of B. burgdorferi spirochete [12-15].
The balance between free radicals and antioxidants
is the main factor in the defense against
harmful processes at the cellular and tissue levels.
According to current findings, excessive ROS production
in the organism and imbalance between
the concentrations of ROS and defense antioxidants
may be related to such pathologic processes
as intestinal inflammation, joint inflammation, local
ischemic processes, cardiovascular diseases,
multiple sclerosis, or central and peripheral nervous
system diseases [16-26].

The prevalence of Lyme borreliosis among the population
in the northeastern region of Poland and
difficulties in the treatment and prognosis of the
course of the disease have prompted us to evaluate
selected parameters of the antioxidant system and
lipid peroxidation products in patients with erythema
migrans, an early manifestation of Lyme borreliosis.

MATERIAL AND METHODS
Twenty patients aged from 21 to 66 years (x=41.9)
treated for Lyme borreliosis in the form of erythema
migrans (EM) were enrolled in the study. The
diagnosis of the disease was based on the patients'
epidemiological history and the characteristic clinical
picture. The examinations were carried out
from July to September of 1998. All the patients reported
for treatment within 2 to 4 weeks after
a tick bite. Skin changes of 5 to 30 cm in diameter
and characteristic of EM were found on the patients'
skin, primarily on the extremities. Four weeks
of therapy with Amoxycycline at a dosage of
2.0 g daily resulted in complete remission of pathological
skin changes.

IgM class antibodies to B. burgdorferi were measured
in serum by means of the ELISA method, using
Borrelia recombinant IgG and IgM High Sensitivity
kits from Biomedica (Austria) within 4 to 6 weeks
after treatment.

The control group consisted of 8 healthy individuals
(2 women and 6 men) aged 21 to 45 years (x= 31 years).

Enzyme activity and the concentration of micromolecular
substances were assessed twice: before
Amoxycycline treatment (examination 1) and after
4 weeks of therapy (examination 2).

The activity of Cu, Zn-SOD (EC. 1.15.1.1) was determined
by the method of Misra and Fridovich
[27] as modified by Sykes et al. [24]. A standard
curve for SOD activity was made by using SOD
from bovine erythrocytes (Sigma Biochemicals, St.
Louis, Missouri, USA). One unit of SOD was defined
as the amount of the enzyme needed to inhibit
epinephrine oxidation to adrenochrome by
50%. Enzyme activity was expressed in units per
mg of protein for liver and serum, or per mg of hemoglobin
for erythrocytes.

Glutathione peroxidase (EC. 1.11.1.6) activity was
measured in the liver, erythrocytes and serum specrophotometrically
using a technique based on Paglia
and Valentine [28], whereas GSH formation was
assayed by measuring the conversion of NADPH to
NADP. Enzyme activity was expressed as micromoles
of NADP/min per mg of protein for the liver and
per mg of hemoglobin for erythrocytes.
The activity of glutathione reductase (EC. 1.6.4.2)
was measured by the method of Mize and Langdon,
which involves monitoring the oxidation of nicotinamide
adenine dinucleotide phosphate
(NADPH) at 340 nm [29].

Sulfhydryl compounds were estimated according to
Ellman using 5,5'-dithiobis (nitrobenzoic acid,
DTNB) [30].

The glutathione (GSH) concentration was measured
using a Bioxytech GSH-400 test. This method
proceeds in two steps. The first step leads to the
formation of substitution products between a patented
reagent and all the mercaptans (GSH) present
in the sample. The second step transforms
specifically the substitution product obtained with
GSH into a chromophoric thione whose maximum
absorbency wavelength is 400 nm.
Lipid peroxidation in liver, erythrocytes and serum
was assayed using a Bioxytech LPO-586 kit that
measures MDA together with 4-hydroxyalkanals or
MDA alone. The colorimetric assay uses a chromogenic
reagent which reacts with the products mentioned
above, generating a stable chromophore
which is measured spectrophotometrically at 586
nm. This technique requires sample incubation at
45°C, thus avoiding undesirable artifacts.

Statistical analysis
The results of our examinations were analyzed statistically
by calculating the arithmetic mean and
standard deviation for each variable. The evaluation
of statistical significance was performed by
means of the Wilcoxon test for two related and
unrelated trials, since the variables were not subjected
to normal distribution. The value p<0.05
was taken as the limit of statistical significance.

RESULTS
SOD activity in healthy controls was 3.02 u/ml,
whereas in patients with erythema migrans, it was
lower before treatment than in the controls, and
decreased insignificantly after treatment, to 2.77
u/ml (Tables 1 and 2).

GSSG-R activity was insignificantly higher than in
the controls, amounting to 26.46 u/ml in examination
1, before treatment. After 4 weeks' treatment
with Amoxycycline this figure increased to 29.57
u/ml (Tables 1 and 2).

GSH-Px activity was insignificantly lower in both
examination 1 and 2 in comparison with controls:
93.15% in examination 1, decreasing after treatment
to 91.74% of the values found in controls
(Tables 1 and 2).

The total concentration of SH-groups was significantly
lower (76.71%) in examination 1 when
compared to the concentration in the controls.
After treatment, an insignificant increase to 183.3
nmol/l was observed in the total concentration of
SH-groups, which again was significantly lower in
comparison to the controls (92.19%) (Tables 1
and 2).

1232

Clinical Research
Enzymes examined p= p<
SOD
GSSG-R
GSH-Px
-SH
GSH
MDA
* statistical significance p< 0.05
Test 1 - Test 2
Test 1 - controls
Test 2 - controls
Test 1 - Test 2
Test 1 - controls
Test 2 - controls
Test 1 - Test 2
Test 1 - controls
Test 2 - controls
Test 1 - Test 2
Test 1 - controls
Test 2 - controls
Test 1 - Test 2
Test 1 - controls
Test 2 - controls
Test 1 - Test 2
Test 1 - controls
Test 2 - controls
0.72
0.0932
0.627
0.66
0.6437
0.381
0.75
0.0776
0.0336
0.02
0.0119
0.3393
0.05
0.0076
0.1675
0.21
0.00001
0.00001
0.8
0.100
0.700
0.7
0.700
0.400
0.8
0.080
0.05*
0.05*
0.02*
0.400
0.06
0.008*
0.200
0.3
0.0001*
0.0001*

Table 2. Comparison of enzyme and micromolecular substance
activity in patients with Erythema migrans before and after
treatment in comparison with controls.
Enzymes examined Examination 1 Examination 2 Controls
SOD (u/ml)
GSSG-R (u/ml)
GSH-Px (u/ml)
-SH (nmol/l)
GSH (nmol/l)
MDA (nmol/l)
2.93±1.14
26.46±11.88
132.0±7.21
152.52±19.58
15.66±3.66
15.66±4.21
2.77±1.14
29.57±5.28
130.00±9.11
183.30±53.22
18.14±2.39
14.21±3.99
3.02±2.50
24.87±10.73
141.71±12.52
198.83±65.02
21.23±5.89
4.76±3.13

Table 1. Activity of antioxidation parameters and peroxidation products
(MDA) in patients with Erythema migrans before and after
treatment and in healthy controls.

1233

Pancewicz SA et al - Role of reactive oxygen species (ROS) in patients.
The GSH concentration was 26.24% lower in comparison
to controls in examination 1. After treatment,
it increased insignificantly to 18.14 nmol/ml,
and did not differ significantly when compared to
healthy controls (Tables 1 and 2).

The mean MDA concentration was significantly higher
in both examinations 1 and 2 than in the controls.
In examination 1, before treatment, it was
328.99% of control value; after treatment it decreased
insignificantly, but was still significantly higher
than in the controls (298.53%).

DISCUSSION
The skin lesion called erythema migrans is an early
pathogenic symptom of Lyme disease, appearing
from 10 days to several weeks after infection. Erythema
migrans is present as a ring-like or homogeneous
erythema at the site of B. burgdorferi spirochete
penetration. Afterwards, it spreads concentrically
in the intercellular matrix, which explains why
erythema migrans is later so dispersed [4,31]

Patients with erythema migrans present with nonspecific
symptoms, such as malaise, fatigue, fever,
cephalalgia, atralgia and myalgia.
Neutrophils and macrophages belong to the most
important elements of the host's defense system
against the bacterial infection. The activation of
neutrophils and macrophages greatly intensifies
their metabolism, causing an increase in oxygen
absorption, and in glucose, lipid, and protein metabolism,
the production of proinflammatory cytokin,
and the release of proteolytic enzymes from
these cells, such as collagenase and elastase. Neutrophils
are capable of producing active oxygen
metabolites, which act as bactericidal agents, but
when produced excessively they may cause harmful
reactions [32].

Suhonen et al. examined oxidative burst, calcium
mobilization and phagocytosis induced by B. burgdoferi
proper, B. afzeli and B. garini. They proved
that each genotype of B. burgdorferi induces all
neutrophil functions, depending on the complement.
The CR3 (CD11b) integrin was shown to have
a role in the oxidative burst and calcium mobilization
induced by B. burgdorferi [15].

Modolell et al. examined B. burgdorferi's interaction
with murine macrophages derived from bone
marrow. They found that this interaction caused
microorganized phagocytosis, the induction of nitric
oxide (NO) and oxygen free radicals, and the
elimination of spirochete. The phagocytosis of B.
burgdorferi by macrophages and the generation of
NO and free oxygen radicals was intensified through
spirochete opsonization with monoclonal antibodies.

The addition of NO-synthesis specific inhibitors
to macrophage and spirochete cultures,
together or separately, caused only a partial reduction
in the effector cell-killing potential. The
data they obtained suggest that NO and oxygen
free radicals are essential but insufficient for the
complete elimination of B. burgdorferi by macrophages.
The authors concluded that the defense
against B. burgdorferi infection is associated with
the humoral response, and that specific antibodies
play an important role in the spirochete control
mediated by macrophages [14].

Harter L. et al. stated that mRNA regulation of nitric
oxide (NO) synthetasis, one of the free radicals,
was part of the host's immune response to B. burgdorferi
infection. They suggested that NO may play
a role in arthritis in dogs [33].

Georgili et al. have proved that all B. burgdorferi
strains have a different susceptibility to elimination
through phagocytosis; however, all of them provoked
oxidative burst [13].

Active oxygen metabolites, especially the hydroxylic
radical, exhibit a high level of chemical activity,
and in they organism they interact with proteins, lipids,
carbohydrates and nucleinic acids, which
causes changes in cell function and structure. However,
the excessive release of these compounds
by the cell may cause tissue damage. An excess of
reactive oxygen species activates the mechanisms
which immobilize them by means of enzymatic superoxide
dismutase, catalase and glutathione peroxidation.
The activity of oxygen reactive species is
harmful when the antioxidant system is disturbed
or when it is unable to eliminate the results of ROS
activity [10,11,18].

The excess of ROS together with the inefficiency
of the antioxidant mechanisms intensifies lipid peroxidation,
causing a decrease in cell membrane
flow, damage to the nucleinic acid structure, and
enzyme inactivation. Lipid peroxidation is an avalanche
process, continually supplying free radicals
that initiate further peroxidation reactions. The
products of lipid peroxidation and their reactions
with other cell components cause changes in cell
membrane properties, resulting in cell homeostasis
disorder, which leads to cell death [10,11,18,32].

1234

Clinical Research
The results obtained in our studies indicate that there
are changes in the serum antioxidant system of
patients with Lyme borreliosis presenting in the
form of erythema migrans. The activity of antioxidant
enzymes (SOD and GSH-Px) in patients before
treatment was significantly lower than in the controls.
After treatment, despite complete remission of
pathological changes, a further decrease was observed
in the activity of these enzymes. The concentration
of SH- and GSH- group micromolecular substances,
which was significantly lower before treatment
when compared to controls, increased after
treatment, and did not differ significantly from the
values of healthy individuals. The MDA concentration
was significantly higher both before and after
treatment than the values found in the controls.
These results indicate that beta-lactamase antibiotic
therapy brings non-enzymatic antioxidant parameters
to control values, though no change is observed
in the enzymatic antioxidant parameters,
resulting in the further activation of free radicals.
This may suggest an ongoing asymptomatic pathological
process, leading to the appearance of late
borreliosis symptoms.

A constant decrease in the activation of glutathion
peroxidase indicates a decreased capability to reduce
lipid superoxidants, thus maintaining a high concentration
of membrane lipid peroxidation products.

CONCLUSIONS
1. In Lyme borreliosis presenting as erythema migrans,
changes in the antioxidant system are observed in the plasma of patients,
i.e. a decrease in the activity of SOD and GSH-Px antioxidant enzymes,
a decrease in the concentration of antioxidant -SH and GSH non-enzymatic
parameters, and an increase in MDA concentration.

2. Beta-lactamase antibiotic therapy brings non-enzymatic antioxidant
parameters to control values,
though it has no influence on enzymatic antioxidant parameters.

3. In erythema migrans, the decreased ability to reduce lipid superoxidants
leads to maintaining a high concentration of membrane lipid peroxidation
products.

REFERENCES:
1. Burgdorfer W: Lyme disease - a tick-borne spirochetosis. Science,
1982; 216: 1317-1318

2. Gustafson R: Epidemiological studies on Lyme borreliosis and tick-
-borne encephalitis. Scand J Inf Dis, 1994; Sup. 92: 8-21

3. Sifski E, Karbowiak G, Siuda K et al: Zaka½enie kleszczy Borrelia
burgdorferi w wybranych rejonach Polski. Przeg Epidemiol, 1994; 4: 385

4. Stanek G, O'Connell S, Cimmino M et al: European Union concerted
action on risk assessment in Lyme borreliosis: clinical case definition
for Lyme borreliosis. Wien Klin Wochenschr, 1996; 108/23: 741-747

5. Wegner Z, Stafczak J, Racewicz N et al: Wyst´powanie kr´tków Borrelia
burgdorferi w kleszczach Ixodes ricinus na terenie województwa bia-
.ostockiego. Mat Mi´dz Symp Borelioza z Lyme. Bia.owie½a 1995, 12

6. Pancewicz SA, Zajkowska JM, Kondrusik M et al: WykrywalnoÊç
przeciwcia. przeciwko B. burgdorferi wÊród pracowników leÊnictwa
w pó.nocno-wschodnim regionie Polski. Med Prac, 1998; 49(3): 253

7. Hulsse C, von Stenglin M: Incidence of Lyme borreliosis in Mecklenburg-
Vorpommern. Gesundheitswesen, 1995; 57(1): 21-4

8. Rath PM, Obershoff B, Mohnhaupt A et al: Seroprevalence of Lyme
borreliosis in forestry workers from Brandenburg, Germany. Eur
J Clin, Microbiol Infect Dis, 1996; 15(5): 372 -7

9. Burek V, Misic-Mayerus L, Maretic T: Antibodies to Borrelia burgdorferi
in various population groups in Croatia. Scan. J Infect Dis, 1992; 24(5):
683-4

10. Conner EM, Grisham MB: Inflammation, free radicals and antioxidants.
Nutrition, 1996; 12: 274-277

11. Kehrer JP: Free radicals as mediators of tissue injury and disease, Crit
Rev Toxicol, 1993; 23: 21-48

12. Garcia-Monco JC, Benach JL: Mechanism of injury in Lyme
neuroborreliosis, Semin Neurol, 1997; 171: 67

13. Georgilis K, Steere AC, Klempner MS: Infectivity of Borrelia burgdorferi
correlates with resistance to elimination by phagocytic cells. J Infect
Dis, 1991; 163: 150-155

14. Modolell M, Schaible UE, Ritting M, Simon MM: Killing of Borrelia
burgdorferi by macrophages is dependent on oxygen radicals and nitric
oxide and can be enhanced by antibodies to outer surface proteins of
the spirochete. Immunol Lett, 1994; 40(2): 139-146

15. Suhonen J, Hartiala K, Tuominen-Gustafsson H, Viljanen MT: Borrelia
burgdorferi-induced oxidative burst, calcium mobilization and phagocytosis
of human neutrophils are complement dependent. J Infectious
Dis, 2000; 181: 195-202

16. Bruckdorfer KR, Hillary JB, Bunce T et al: Increased susceptibility to
oxidation of low-density lipoproteins isolated from patients with systemic
sclerosis. Arthritis Rheum, 1995; 38(8): 1060-1067

17. De Deyn PP, Hiramatsu M, Borggreve F et al: Superoxide dismutase
activity in cerebrospinal fluid of patients with dementia and some other
neurological disorders. Alzheimer Dis Assoc Disord, 1998; 12(1): 26-32

18. Eapen CE, Madesh M, Balasubramanian KA et al: Mucosal mitochondrial
function and antioxidant defences in patients with gastric
carcinoma. Scand J Gastroenterol, 1998; 33(9): 975-981

19. Hall ND, Maslen CL, Blake DR: The oxidation of serum sulphhydryl
groups by hydrogen peroxide secreted by stimulated phagocytic cells in
rheumatoid arthritis, Rheumatol Int, 1984; 4: 35-38

20. Honkkanen VEA: The factors affecting plasma glutathione peroxidase
and selenium in rheumatoid arthritis: a multiple linear regression analysis.
Scan J Rheumatol, 1991; 20: 385-391

21. Kiziltunc A, Cogalgil S, Cerrahoglu L: Carinitine and antioxidants
levels in patients with Rheumatoid Arthritis, Scand J Rheumatol, 1998;
27: 441-445

1235

Pancewicz SA et al - Role of reactive oxygen species (ROS) in patients.
22. Maeda H, Akaike T: Nitric oxide and oxygen radicals in infection,
inflammation and cancer. Biochemistry (Mosc) 1998; 63(7): 854-865

23. Stoessl AJ: Etiology of Parkinson's disease. Can J Neurol Sci, 1999;
26(suppl 2): 5-12

24. Sykes JA, McCormac FX, O'Brien TJ: Preliminary study of the superoxide
dismutase content of some human tumours. Cancer Res, 1978,
38, 2759-2762

25. Tarp U, Hansen JC, Overvad K et al: Glutathione peroxidase activity in
patients with rheumatoid arthritis and in normal subjects: effects of long-
-term selenium supplementation. Arthritis Rheum, 1987; 30: 1162-1165

26. Tarp U, Stengaard Pedersen K, Hansen JC, Thorling EB: Glutathione
redox cycle enzymes and selenium in severe rheumatoid arthritis: lack
of antioxidative response to selenium supplementation in polymorphonuclear
leucocytes. Ann. Rheum. Dis, 1992; 51: 1044-1049

27. Blum J, Fridovich I: Inactivation of glutathione peroxidase by
superoxide radical. Arch Biochem Biophys, 1985; 240: 500-508.

28. Paglia DE, Valentine WN: Glutathione peroxidase and selenoprotein
activity in various tissue. Biol Chem, 1967; 145: 233

29. Mize CE, Langdon. RG: Hepatic glutathione reductase. Purification
and general kinetic properties. J Biol Chem, 1962; 237: 1589

30. Ellman GL: SH groups determination in biological fluids. Anal Biochem,
1970; 46: 237

31. Sigal LH: Lyme disease: a review of aspects of its immunology and
immunopathogenesis. Annu Rev Immunol, 1997; 15: 63-92

32. Zeman K: Rola neutrofilów w procesach zapalnych. W: Zapalenie.
Patofizjologia i klinika, red. H. Tchórzewski. Medpress Warszawa,
1998; 76.

33. Harter L, Straubinger RK, Summers BA et al: Up-regulation of inducible
nitric oxide synthase mRNA in dogs experimentally with Borrelia burgdorferi.
Vet Immunol Immunopathol, 1999; 22, 67(3): 271-284
_______________________________________________________



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 rmforall

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).
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 same
amount that produces hangover from red wine.

The expert review by Monte WC (1984) states: "An alcoholic consuming 1500
calories a day from alcoholic sources alone may consume between 0 and 600 mg
of methanol each day depending on his choice of beverages (Table 1)...."
Table 1 lists red wine as having 128 mg/l methanol, about one part in ten
thousand.

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, 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)."

"Fruit and vegetables contain pectin with variable methyl ester content.
However, the human has no digestive enzymes for pectin (6, 25) particularly
the pectin esterase required for its hydrolysis to methanol (26).

Fermentation in the gut may cause disappearance of pectin (6) but the
production of free methanol is not guaranteed by fermentation (3).
In fact, bacteria in the colon probably reduce methanol directly to formic
acid or carbon dioxide (6) (aspartame is completely absorbed before
reaching the colon).
Heating of pectins has been shown to cause virtually no demethoxylation;
even temperatures of 120 deg C produced only traces of methanol (3).
Methanol evolved during cooking of high pectin foods (7) has been accounted
for in the volatile fraction during boiling and is quickly lost to the
atmosphere (49).
Entrapment of these volatiles probably accounts for the elevation in
methanol levels of certain fruits and vegetable products during canning (31,
33)."
______________________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298 rmforall@...

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 146 members, 1,607 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1219 members, 24,066 posts in a public archive
_______________________________________________

WC Monte gives 1917 rabbit study that shows blood vessel thickening by
formic acid, made by ADH in many tissues from methanol -- sources are canned
fruits, wood & tobacco smoke, alcohol drinks, aspartame: Rich Murray
2010.07.04
http://rmforall.blogspot.com/2010_07_01_archive.htm
Sunday, July 4, 2010
[at end of each long page, click on Older Posts]
http://groups.yahoo.com/group/aspartameNM/message/1608
[you may have to Copy and Paste URLs into your browser]
_______________________________________________


Rich,

Yes there is a lot of thickening of connective tissue lining the vessels of
individuals poisoned with methanol who live long enough for the changes to
occur.  This is to be expected since the layers of the veins and arteries
that contain ADH are indeed the  the ones that are involved in thickening.
I have attached an article from 1917 -- take a look at page 770.

Woody 2010.07.03 12:36 PM MST


"My impression is that the apparent increase of the connective tissue is due
not only to the fact that the parenchyma cells have disappeared, but to the
actual proliferation of the fixed tissue cells, as seen by the very marked
thickening of the adventitia and the media of the blood-vessels."

'In cases of long standing, in addition to the above general appearance
there is also a marked increase of the connective tissue, especially around
the blood-vessels."

http://whilesciencesleeps.com/references

589 references -- click on each title for free full pdf

15 Eisenberg AA.;  1917.  "Visceral Changes in Wood Alcohol Poisoning by
Inhalation",  American Journal of Public Health  7:765

http://whilesciencesleeps.com/references/pdf/15 7 pages

[ This is the time before Roe when it was unknown that humans were many
times more sensitive to methanol than any other animal.

Keen eyes, a century ago, noted a progression of horrors in a variety of
tissues -- worth quoting at length. ]

Arthur Alexander Eisenberg, BA, MD
Director, Pathological Laboratories, St. Vincent's Charity Hospital,
Cleveland.

"But Pohl (8) observed experimentally that while no bad effects followed
immediately after the administration to an animal of a small dose of methyl
alcohol, very serious results were noticeable a few days later, the
experiment in many instances terminating fatally.  If a small non-lethal
dose be repeated a few times, fatal issue occurs invariably, while ethyl
alcohol, similarly administered, produces no such effects.

How are we to explain such paradoxical phenomenon?  Why does a substance,
non-lethal in a single dose, become lethal after a few repeated doses, and
vice versa?  The explanation as given by Pohl is as follows:  Ethyl alcohol
is very rapidly oxidized in the animal body, in fact so rapidly that over 90
per cent. of it is converted to carbon dioxide and water, whereas methyl
alcohol is oxidized very slowly, with the formation of formaldehyde and then
formic acid.

It is formic acid and its cumulative action that is responsible for the
untoward effects of methyl alcohol, the variability of individual results
depending on the individual power of oxidation, the action of wood alcohol
thus becoming especially dangerous in those who are ill nourished...

The histo-chemical investigations of Placet (9) show that the power of
fixing methyl alcohol varies with the different tissues, the following
organs being given in the order of their affinity: brain, liver, kidney and
muscles.  This statement of Placet finds abundant confirmation in the
results of my experiments...

The most striking observation was the uniformity of lesions (practically in
every case the same organs, and those only, were involved), the extent of
lesions varying with the duration of time exposure, thus the fatty
degeneration of the cardiac muscle or destruction of the perenchyma cells of
the cerebrum being more extensive in the rabbit which had been exposed for
6 months than in the one which had inhaled wood alcohol or Columbian
spirits [ more refined] for but 2 months...

...the central nervous system -- notably the cerebrum -- appears to bear the
brunt of the attack, it being together with the optic nerve the most
frequently as well as the most extensively involved organ.  Next in
frequency, but not necessarily in extent, of involvement are the kidneys,
the liver, and the muscle -- the latter again showing a very marked
inequality of involvement, the cardiac muscle being affected in every case
while the striated and the smooth muscle were involved but in 10 per cent.
of the cases...no difference between the effects of wood alcohol when
imbided and when inhaled.

The lesions found in the various parts of the cerebrum, the cerebellum, the
medulla and the pons consisted of different degrees of inflammatory and
degenerative processes.  Macroscopically the tissues appear yellowish,
glistening; the line of demarcation between the grey and the white matter is
not as sharp as in the control animals, in the more prolonged cases the gray
matter appearing quite thinned -- the entire picture being one of a
nonspecific atrophy.

Microscopically, the neurocytes are diminished, assuming a spindle-like
shape, Nissl's granules also are diminished, with brownish pigment scattered
here and there.

In the more severe cases the parenchyma cells are greatly reduced in numbers
as well as in size.  Thus, for example, the brain of the rabbit which had
been exposed to the inhalation of Columbian Spirits showed practically
nothing but neuroglia cells, and no trace of parenchyma cells, the latter
being represented by masses of granular debris and fat droplets, partly
taken up by the so-called contractile cells, i.e. leucocytes, lymphocytes,
and according to Birch-Hirschfield, endothelial cells.

The different states of parenchymatous degeneration depend, of course, on
the length of the exposure to which the animal has been subjected, the
nuclear changes varying from the wandering of the nucleus to the periphery
of the cell to the total karyolysis.

My impression is that the apparent increase of the connective tissue is due
not only to the fact that the parenchyma cells have disappeared, but to the
actual proliferation of the fixed tissue cells, as seen by the very marked
thickening of the adventitia and the media of the blood-vessels.

The entire microscopical picture corresponds very closely to Adami's
"exhaustion" condition, which is "anatomically recognized by the
disappearance of cells and fibres and the secondary overgrowth of glial
tissue filling in the space."

The lesions of the liver and the kidney present, both macroscopically and
microscopically, the typical characteristic of albuminous degeneration
(cloudy swelling) and fatty degeneration -- the increased size of the organ,
softened consistence, the tissue being almost friable (etat crible),
glistening yellowish color, the protoplasm being uniformly dull-grey, the
outline of the cells in most cases being altered or lost.  The nuclei are
much smaller than they normally are, lost in many cases, and appearing as
vague, shadowy structures in others.  The cell bodies are filled with
granular, dust-like masses.

In cases of long standing, in addition to the above general appearance there
is also a marked increase of the connective tissue, especially around the
blood-vessels.

The muscle cells, especially the heart, present an appearance very similar
to that of the liver and the kidney, as well as both fragmentation and
segmentation, in some of the cases.

The lung shows in many cases patches of broncho-pneumonia, which, however,
are not uniform, either in distribution or in extent."


Woodrow C Monte, PhD, Emiritus Prof. Nutrition gives many PDFs of reseach --
methanol (11% of aspartame) puts formaldehyde into brain and body --
multiple sclerosis, Alzheimer's, cancers, birth defects, headaches: Rich
Murray 2010.05.13
http://rmforall.blogspot.com/2010_05_01_archive.htm
Thursday, May 13, 2010
http://groups.yahoo.com/group/aspartameNM/message/1601


[ Other formaldehyde sources include alcohol drinks and
tobacco and wood smoke,
while adequate folic acid levels protect most people,
but not for brain and retina harm.

http://whilesciencesleeps.com/montediet

Methanol: Where Is It Found? How Can It Be Avoided?

AVOID the following, ranked in order of greatest danger:

1. Cigarettes.
2. Diet foods and drinks with aspartame.
3. Fruit and vegetable products and their juices in bottles,
cans, or pouches.
4. Jellies, jams, and marmalades not made fresh and kept
refrigerated.
5. Black currant and tomato juice products, fresh or
processed.
6. Tomato sauces, unless first simmered at least 3 hours
with an open lid.
7. Smoked food of any kind, particularly fish and meat.
8. Sugar-free chewing gum.
9. Slivovitz: You can consume one alcoholic drink a day
on this diet -- no more! [ no fruit brandies ]
10. Overly ripe or near rotting fruits or vegetables.


http://whilesciencesleeps.com/references

589 references -- click on each title for free full pdf

Article 2 http://www.thetruthaboutstuff.com/review2.html

Selection from Article 2, Fitness Life, December 2007, and
well discussed in the DVD video:

"Identical Symptoms of MS, Methanol Poisoning
and Aspartame Toxicity

The symptoms of multiple sclerosis (44, 83, 85, 169), chronic
and acute methanol poisoning (13, 144, 189), and Aspartame
toxicity (54, 58, 93, 181), are in all ways identical.

There is nothing that happens to the human body from the toxic
effect of methanol that has not been expressed during the
course of MS... nothing (143, 144).

This generalization extends even to the remarkable
opthomological conditions common to both: transitory optic
neuritis and retrolaminar demyelinating optic neuropathy with
scotoma of the central visual field (which occasionally
manifests as unilateral temporary blindness (85, 138, 163).

In fact, these opthomological symptoms have been thought of
for years in their respective literatures to be "tell tale"
indications for the differential diagnosis for each of these
maladies independently (85, 138, 148, 163, 169).

The common symptoms of
headache (13, 83, 181, 189),
nervousness (13, 83, 181),
depression (58, 83, 189, 181),
memory loss (18, 147, 85, 169, 181),
tingling sensations (13, 85, 168, 138, 169),
pain in the extremities (13, 85, 169),
optic neuritis (85, 138, 148, 163, 169),
bright lights in the visual field (139, 83),
seizures (21, 83, 160),
inability to urinate or to keep from urinating (139, 146, 167)
are all shared by each of these conditions and shared yet again
by complaints from aspartame poisoning (54, 58, 93, 181).

I take these strikingly similar symptom patterns as evidence
that these disorders act on identical components of the central
nervous system and in the same way.

The "Miracle" that MS shares with Methanol poisoning

In the early stages of MS, or when a non-lethal dose of
methanol has been administered, complete recovery is a
possibility.

The only two afflictions for which such dramatic "remissions"
are reported from identical neuromuscular and opthomological
damage, even "blindness" is relapsing-remitting multiple
sclerosis (85) and methyl alcohol poisoning (138, 163).

The pathology of the two maladies is in may ways identical,
particularly when it comes to destruction of the myelin sheath
with no harm to the axon itself (18, 148, 176).

Sex Ratios for MS and Aspartame Reactions

Women bear the brunt of multiple sclerosis (91a-c) and lupus
(SLE)(73) with fully three-fold representations in infliction
numbers over men for both diseases.

This is exactly the proportion represented by adverse reactors
to Aspartame reported by the US Center for Disease Control
in their study of 1984(58).

The Center found three women to every man whose
Aspartame consumption complaints were serious enough to
warrant investigation (93).

Although the female/male ratio for those stricken with MS has
always been high, recent estimates place it at over 3 to 1
(91, 91a, 91c).

What might account for the difference across sexes in
incidence?

A study published in the New England Journal of Medicine
(94) reports biopsies of the gastric lining of men and women.

A result was that the concentration of ADH in the gastric lining
of men was much higher than for woman.

Men have the advantage of removing methanol from the
bloodstream four times faster on an equal-body-size basis
than women.

Thus, for men, methanol is more likely to be removed from the
blood before it reaches the brain.

The brain is spared but the methanol removed would still be
metabolized to formaldehyde in the gut where it would reap its
havoc on a more forgiving organ.

This may help explain why men have more gastrointestinal
complaints from both methanol and Aspartame consumption
(93, 99).

On the other hand, women's complaints from both more
frequently involve serious neurological complications."

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://groups.yahoo.com/group/aspartameNM/message/1498

Monte WC., Is your Diet Sweetener killing you?
Fitness Life. 2007 Nov; 33: 31-33.
Monte WC., A Deadly Experiment.
Fitness Life. 2007 Dec; 34: 38-42.
Monte WC., Bittersweet: Aspartame Breast Cancer Link.
Fitness Life. 2008 Feb; 34: 21-22.

Article 1 http://www.thetruthaboutstuff.com/review1.html
Article 2 http://www.thetruthaboutstuff.com/review2.html
Article 3 http://www.thetruthaboutstuff.com/review3.html

http://www.thetruthaboutstuff.com/articles.html
223 references with abstracts or full and partial texts


methanol (11% of aspartame), made by body into
formaldehyde in many vulnerable tissues, causes modern
diseases of civilization, summary of a century of research,
Woodrow C Monte PhD, Medical Hypotheses journal:
Rich Murray 2009.11.15
http://rmforall.blogspot.com/2009_11_01_archive.htm
Sunday, November 15, 2009
http://groups.yahoo.com/group/aspartameNM/message/1589

Methanol: A Chemical Trojan Horse as the Root of the
Inscrutable U, Prepublication Copy; Medical Hypotheses
-- 06 November 2009 (10.1016/j.mehy.2009.09.059)
http://www.medical-hypotheses.com/article/S0306-9877(09)00693-8/abstract
Woodrow C. Monte PhD
Professor of Food Science (retired)
Arizona State University
corresponding author : Woodrow C. Monte PhD
470 South Rainbow Drive
Page, Arizona 86040
Key Words:
food epidemiology; diseases of civilization; methanol;
formaldehyde; aspartame; autism; multiple sclerosis; Alzheimer's;
U-shaped curve.

Abstract:

Until 200 years ago, methanol was an extremely rare
component of the human diet and is still rarely consumed in
contemporary hunter and gatherer cultures.
With the invention of canning in the 1800s, canned and
bottled fruits and vegetables, whose methanol content greatly
exceeds that of' their fresh counterparts, became far more
prevalent.
The recent dietary introduction of aspartame, an artificial
sweetener, 11% methanol by weight, has also greatly
increased methanol consumption.
Moreover, methanol is a major component of cigarette
smoke, known to be a causative agent of many diseases of
civilization (DOC).
Conversion to formaldehyde in organs other than the liver is
the principal means by which methanol may cause disease.
The known sites of class I alcohol dehydrogenase (ADH I),
the only human enzyme capable of metabolizing methanol to
formaldehyde, correspond to the sites of origin for many DOC.
Variability in sensitivity to exogenous methanol consumption
may be accounted for in part by the presence of aldehyde
dehydrogenase sufficient to reduce the toxic effect of
formaldehyde production in tissue through its conversion to
the much less toxic formic acid.
The consumption or endogenous production of small amounts
of ethanol, which acts as a competitive inhibitor of methanol's
conversion to formaldehyde by ADH I, may afford some
individuals protection from DOC.


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


http://groups.yahoo.com/group/aspartameNM/message/870
Aspartame: Methanol and the Public Interest 1984: Monte:
Murray 2002.09.23

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, 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)."
_______________________________________________


"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."

7 Trocho C. Pardo R. Fafecas I. Virgili J. Remesar X. Fernandez-Lopez. J;
"A.1988. Formaldehyde derived from dietary aspartame binds to tissue
components in vivo",  Life Sci  63: 337

http://whilesciencesleeps.com/references/pdf/7  13 pages

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


-----Original Message-----
From: Rich Murray [mailto:rmforall@...]
Sent: Friday, July 02, 2010 8:06 PM
To: Woodrow Monte
Cc: Rich Murray; RichMurray.rmforall@...
Subject: neck vein narrowing & MS -- any methanol connection? Monte: Murray
2010.07.02

neck vein narrowing & MS -- any methanol connection? Monte: Murray
2010.07.02

http://www.nytimes.com/2010/06/29/health/29vein.html

http://www.nytimes.com/2010/06/29/health/29vein.html?pagewanted=print

June 28, 2010
From M.S. Patients, Outcry for Unproved Treatment
By DENISE GRADY

For her first appointment with Dr. Daniel Simon, Neelima Raval showed up
with a rolling file cabinet full of documents. She had downloaded every word
written by or about Dr. Paolo Zamboni, a vascular surgeon from Italy with a
most unorthodox theory about multiple sclerosis.

Dr. Zamboni believes that the disease, which damages the nervous system, may
be caused by narrowed veins in the neck and chest that block the drainage of
blood from the brain. He has reported in medical journals that opening those
veins with the kind of balloons used to treat blocked heart arteries-an
experimental treatment he calls the "liberation procedure" -- can relieve
symptoms....

She has a degree in toxicology and works for a drug company...

Dr. Zamboni, 53, (no relation to the inventor of the ice-rink machine) began
studying the medical literature on multiple sclerosis in 1995 when his wife
learned she had the disease.

"What I found was like a detective story," he said.

He discovered reports of vein abnormalities and of brain lesions forming
around veins. But the research had been abandoned. Vein disorders are his
specialty; he has been studying them for 25 years. He began using ultrasound
and other imaging techniques to examine veins, and found narrowings in the
neck and chest veins in people with the disease, but not in healthy ones. He
suspected that abnormal blood flow and pressure in the veins -- not just
narrowing alone -- might cause minute amounts of bleeding in the brain,
leading to an immune reaction and inflammation that damaged myelin and
nerves. Iron deposits could also form, and add to the damage. He wondered if
opening the narrowed areas might help.
In 2006 he began using balloons to treat patients, including his wife, whose
symptoms went away and, he says, have not come back....


Int Angiol. 2010 Apr;29(2):140-8.
CSF dynamics and brain volume in multiple sclerosis are associated with
extracranial venous flow anomalies: a pilot study.
Zamboni P, Menegatti E, Weinstock-Guttman B, Schirda C, Cox JL, Malagoni AM,
Hojnacki D, Kennedy C, Carl E, Dwyer MG, Bergsland N, Galeotti R, Hussein S,
Bartolomei I, Salvi F, Ramanathan M, Zivadinov R.
Vascular Diseases Center, University of Ferrara-Bellaria Neurosciences,
Ferrara and Bologna, Italy.
Paolo Zamboni <zmp@...>;
_______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298  rmforall@...

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 146 members, 1,608 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1216 members, 24,072 posts in a public archive
_______________________________________________

sweeteners (aspartame), methanol (becomes formaldehyde), and premature babies in
Denmark, TI Halldorsson et al 2010.06.30 AmJClinNutr: Erik Millstone: Betty
Martini: Rich Murray 2010.07.08
http://rmforall.blogspot.com/2010_07_01_archive.htm
Thursday, July 8, 2010
[at end of each long page, click on Older Posts]
http://groups.yahoo.com/group/aspartameNM/message/1609
[you may have to Copy and Paste URLs into your browser]
_______________________________________________


Am J Clin Nutr. 2010 Jun 30. [Epub ahead of print] 8 pages
Intake of artificially sweetened soft drinks and risk of preterm
delivery: a prospective cohort study of 59,334 Danish
pregnant women.
Halldorsson TI,  lur@...;
Strøm M, mrm@...;
Petersen SB, marp@...;
Olsen SF. sfolsen@...;
Centre for Fetal Programming, Division of Epidemiology,
Statens Serum Institut, Copenhagen, Denmark, Reykjavik,
Iceland.
Thorhallur I Halldorsson,
Marin Strøm,
Sesilje B Petersen,
and Sjurdur F Olsen

Abstract

BACKGROUND:
Sugar-sweetened soft drinks have been linked to a number
of adverse health outcomes such as high weight gain.
Therefore, artificially sweetened soft drinks are often
promoted as an alternative.
However, the safety of artificial sweeteners has been
disputed, and consequences of high intakes of artificial
sweeteners for pregnant women have been minimally
addressed.
OBJECTIVE:
We examined the association between intakes of
sugar-sweetened and artificially sweetened soft drinks
and preterm delivery.
DESIGN:
We conducted prospective cohort analyses of 59,334
women from the Danish National Birth Cohort (1996-2002).
Soft drink intake was assessed in midpregnancy by using a
food-frequency questionnaire.
Preterm delivery (<37 wk) was the primary outcome
measure.
Covariate information was assessed by telephone interviews.
RESULTS:
There was an association between intake of artificially
sweetened carbonated and noncarbonated soft drinks
and an increased risk of preterm delivery
(P for trend: </=0.001, both variables).
In comparison with women with no intake of artificially
sweetened carbonated soft drinks, the adjusted odds ratio
for women who consumed >/=1 serving of artificially
sweetened carbonated soft drinks/d was
1.38 (95% CI: 1.15, 1.65).
The corresponding odds ratio for women
who consumed >/=4 servings of artificially sweetened
carbonated soft drinks/d was
1.78 (95% CI: 1.19, 2.66).
The association was observed for normal-weight and
overweight women.
A stronger increase in risk was observed for early preterm
and moderately preterm delivery than with late-preterm
delivery.
No association was observed for sugar-sweetened
carbonated soft drinks (P for trend: 0.29)
or for sugar-sweetened noncarbonated soft drinks
(P for trend: 0.93).
CONCLUSIONS:
Daily intake of artificially sweetened soft drinks may increase
the risk of preterm delivery.
Further studies are needed to reject or confirm these findings.
PMID: 20592133

1. From the Centre for Fetal Programming,
Division of Epidemiology,
Statens Serum Institut, Copenhagen, Denmark
(TIH, MS, SBP, and SFO);
the Unit for Nutrition Research,
Faculty of Food Science and Nutrition,
School of Health Sciences, University of Iceland (TIH),
Reykjavik, Iceland;
and the Department of Nutrition,
Harvard School of Public Health. Boston, MA (SFO).

2 Supported by the European Union (EU)
Integrated Research Project
EARNEST (FOOD-CT-2005-007036).
The EU project EARNEST
http://www.metabolic-programming.org receives financial
support from the Commission
of the European Communities under the FP 6 priority 5:
food quality and safety.
The Danish National Birth Cohort has been financed by the
March of Dimes Birth Defects Foundation,
the Danish Heart Association,
the Danish Medical Research Council,
and the Sygekassernes Helsefond,
Danish National Research Foundation,
Danish Pharmaceutical Association,
Ministry of Health, National Board of Health,
Statens Serum Institut.

3 Address correspondence to TI Halldorsson,
Centre for Fetal Programming,
Division of Epidemiology, Statens Serum Institut,
Artillerivej 5, Building 206, DK-2300
Copenhagen S, Denmark. E-mail: lur@...;
Received November 19, 2009.
Accepted for publication June 3, 2010.
doi: 10.3945/ajcn.2009.28968.

Of the 59,334 pregnant women,

over 4 artificially sweetened
carbonated soft drinks daily __ 340  0.6 %

noncarbonated soft drinks __ 1,753 3.0 %

2-3 cans daily artificially
carbonated _______________ 834 1.4 %

noncarbonated ___________ 3,643 6.1 %


So, over 3% of pregnant women in 1996-2002
used 4 or more artificially sweetened soft drinks daily,
while over 6 % had 2-3 drinks daily.

This does not include aspartame from other foods.

"A monitoring survey from 2005 quantified artificial
sweeteners in 76 soft drinks from the Danish market (30).
For carbonated soft drinks, aspartame and
acesulfame-K were primarily used in products from the
major international brands, and the average concentration of
these 2 sweeteners was around 2--3-fold higher
in carbonated than in noncarbonated soft drinks (30)."

"After ingestion, aspartame is broken down into aspartic acid,
phenylalanine, and methanol.
Methanol is oxidized into formaldehyde and then to
formic acid, which is considered responsible
for the toxic effects of methanol.
Despite arguments that aspartame intake should not affect
blood methanol concentrations (34), animal studies have
reported the accumulation of formaldehyde adducts derived
from aspartame in tissue components (22).
This might be one explaining factor for reports on headaches
linked to the intake of aspartame (10).
More relevant to our findings, a study in low dose methanol
exposure through inhalation in nonhuman primates observed
a significant decrease in the length of gestation in exposed
animals compared with control animals (21).
A shortening of gestation was even observed at methanol
vapor concentrations that barely affected blood methanol
concentrations in these animals (200 ppm; 2.5 h/d).
Furthermore, 5 out of 28 exposed animals needed medical
intervention and were delivered by cesarean delivery either
because of vaginal bleeding (n = 4) or unproductive labor
(n = 1).
None of the 9 control animals required cesarean delivery.
The authors suggested that the observed shortening of
gestation could either be related to the effects of methanol
on the fetal neuroendocrine system
(hypothalamic-pituitary-adrenal axis) or an indirect
action of methanol on the maternal uterine environment.
The latter explanation would be more compatible with our
findings of an increased risk of medically induced preterm
deliveries."

http://whilesciencesleeps.com/references

589 references -- click on each title for free full pdf

http://whilesciencesleeps.com/references/pdf/7
22. Trocho C. Pardo R. Fafecas I. Virgili J. Remesar X.
Fernandez-Lopez. J;
"A.1998. Formaldehyde derived from dietary aspartame
binds to tissue components in vivo",  Life Sci  63: 337

http://whilesciencesleeps.com/references/pdf/538
21. Burbacher T, Grant K, Shen D, Sheppard L,
Damian D, Ellis S, et al.;  2004. tmb@...;
"Chronic maternal methanol inhalation in nonhuman primates
(Macaca fascicularis): reproductive performance and
birth outcome.",  Neurotoxicol Teratol  26(5):639-50

http://whilesciencesleeps.com/references/pdf/328
10. Jacob SE. Stechschulte S.;  2008
"Formaldehyde, aspartame, and migraines:
a possible connection", Dermatitis  19(3):E10-1

http://whilesciencesleeps.com/references/pdf/544
Abegaz E, Bursey R.;  2009.
"Formaldehyde, aspartame, migraines: a possible connection.
(comment on).",  Dermatitis  20(3):176-7.

http://whilesciencesleeps.com/references/pdf/543
Stechschulte S, Jacob S.;  2009.
"Formaldehyde, aspartame, migraines: a possible connection.
(author reply).",  Dermatitis  20(3):177-9.


----- Original Message -----
From: "Dr. Betty Martini,D.Hum."
<bettym19@...>
To: <bettym19@...>
Sent: Thursday, July 08, 2010 11:19 AM
Subject: Fwd: Sweeteners, methanol and
premature deliveries - new study

Dear Erik,

Thank you so much.

Of course, fetal tissue does not tolerate  methanol and
aspartame triggers birth defects and mental  retardation.
http://www.rense.com/general/asp.htm

Interestingly, in  restaurants so many times you see these
signs, "If you're pregnant,  don't use alcohol -- can cause birth
defects".
If just alcohol is  known to cause birth defects, anyone of
intelligence knows that  methanol or wood alcohol, a severe
metabolic poison, would be worse.

Then you have the phenylalanine
www.mpwhi.com/louis_elsas_testifying_to_congress.htm

Yet,  government agencies refuse to put a warning for
pregnant  women.
There is only a PKU warning.
Big Pharma still runs  government agencies.
I remember about 15 years ago I spoke with somebody
who worked for Monsanto and was told one of their people
said, "When we say something the FDA jumps.  They do
what we  say!"
So innocent babies are born autistic, with Tourettes, mentally
retarded and more, because the FDA are cowards,
and the manufacturers are criminals.

Glad to see this.

All my best, Betty

www.mpwhi.com
www.dorway.com
www.wnho.net
Aspartame Toxicity Center www.holisticmed.com/aspartame

Subject: Sweeteners, menthanol and premature deliveries
Originator-Info: login-id=mhfa1; server=mail.sussex.ac.uk;
token_authority=http://www.sussex.ac.uk/its/help/support.php

Dear Jim and colleagues

Please find attached a copy of a paper that has just come out
in the American Journal of Clinical Nutrition.
It is a huge study of Danish women, indicating that women
who consumed artificially sweetened beverages were
significantly more likely than women who consumed
sugar-sweetened to have premature deliveries of their
babies.
You will be interested in particular because they suggest
that methanol may be implicated in an underlying mechanism
This may therefore be grist to your mill,

with best wishes from Erik

Prof Erik Millstone
SPRU - Science and Technology Policy Research
Freeman Centre
University of Sussex
Brighton BN1 9QE, ENGLAND
Phone +44 (0)1273 877380

See 'Can Science and Politics help keep each other honest?'
Professorial Lecture 11 May 2010,
available at
See recent Professorial Lecture at the University of Sussex on
'Can Science and Politics help keep each other honest?',
11 May 2010  available at
www.sussex.ac.uk/newsandevents/sussexlectures/2010.php


[ Adequate folic acid protects most mothers from having
children with  birth defects from methanol and
its products in their bodies, formaldehyde and formic acid. ]

Food Nutr Bull. 2008 Jun;29(2 Suppl):S205-9.
Folic acid for the prevention of neural tube defects:
the Danish experience.
Olsen SF, Knudsen VK.
Maternal Nutrition Group, Division of Epidemiology,
Statens Serum Institut, Copenhagen, Denmark.
sfolsen@...;

Abstract

Evidence from controlled trials suggests that ingestion of
0.4 mg of folic acid per day in the periconceptional period
is effective in preventing neural tube defects (NTD).
For this reason, most countries recommend that women
planning pregnancy take folic acid supplements in the
periconceptional period, and some countries even fortify
stable foods with folic acid.
Denmark exemplifies a country with a relatively conservative
attitude with respect to taking action in these matters.
In 1999, a national information campaign was launched that
recommended women planning pregnancy take 0.4 mg of
folic acid periconceptionally, but with the moderation that
women who eat a healthy diet do not need to take folic acid
supplement.
The campaign was repeated during 2001.
The results of the latter campaign were evaluated by using
data from a national survey among pregnant women
conducted simultaneously with the campaign by the
Danish National Birth Cohort.
An increase in the proportion of folic acid users took place
concomitantly with the launching of the information events,
but the increase was limited.
Among women who did not plan their pregnancy, a small
proportion had taken folic acid supplements
periconceptionally, and this proportion did not change
concomitantly with the campaign.
Young age and low education were factors associated
with low likelihood of taking folic acid.
It seems that different and more efficient actions are
needed if a more substantial proportion of Danish women
and their fetuses are going to benefit from the knowledge
that folic acid supplementation in the periconceptional
period can prevent NTD.
PMID: 18709894
_______________________________________________


Woodrow C Monte, PhD, Emiritus Prof. Nutrition gives many
PDFs of reseach -- methanol (11% of aspartame) puts
formaldehyde into brain and body -- multiple sclerosis,
Alzheimer's, cancers, birth defects, headaches:
Rich Murray 2010.05.13
http://rmforall.blogspot.com/2010_05_01_archive.htm
Thursday, May 13, 2010
[at end of each long page, click on Older Posts]
http://groups.yahoo.com/group/aspartameNM/message/1601
[you may have to Copy and Paste URLs into your browser]


[ Other formaldehyde sources include alcohol drinks and
tobacco and wood smoke,
while adequate folic acid levels protect most people,
but not for brain and retina harm.

http://whilesciencesleeps.com/references

589 references -- click on each title for free full pdf

Article 2 http://www.thetruthaboutstuff.com/review2.html
_______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298  rmforall@...

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 146 members, 1,609 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1216 members, 24,073 posts in a public archive
_______________________________________________

The Rise of the Power Vegan, 6 page revolutionary, lucid, thorough article
in Men's Journal, Kevin Gray: Rich Murray 2010.09.13
http://rmforall.blogspot.com/2010_09_01_archive.htm
Monday, September 13, 2010
[ at the end of each long post, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1610
[ you may have to Copy and Paste URLs into your browser ]
_______________________________________________


page 12 Contributors
Kevin Gray
This month's story about eating animal-free was a change of pace for Gray,
whose regular beats have him traveling the world:
He's interviewed the president of Congo and right-wing paramilitaries
accused of murdering banana workers in Columbia, and motorcycled across
Mongolia.
But few stories have affected his life as much as this piece on
high-performing vegans.
"It's changed my whole diet, says the Brooklyn-based writer. "I now eat 80
percent vegan."

[ Three vegans give their daily diet:
Tony Gonzalez (football) -- build muscle
Scott Jurek (ultramarathoner) -- gain stamina
Biz Stone (Co-founder of Twitter) -- increase mental sharpness ]

http://www.mensjournal.com/in-the-october-2010-issue-michael-douglas

Most Popular Articles
#1. The Men's Journal Guide to Going Vegan

6 pages, 96-101, October, 2010

From Kevin Gray's "The Rise of the Power Vegan":

For years the gospel of the vegan convert centered on Teva wearers fighting
for animal rights or on righteous punks sticking it to their parents at the
dinner table.

It did not include $7-million-a-year freight trains like Atlanta Falcons
tight end Tony Gonzalez, hockey brawlers like former Montreal Canadiens
winger Georges Laraque, or seven-time Western States Endurance Run champ
Scott Jurek. But vegan athletes -- who eschew all animal products for a
plant-based diet -- and their vegetarian cousins, who may or may not eat
eggs and dairy, are challenging meat eaters on every field.

Even former heavyweight champ Mike Tyson ditched the burgers and went vegan
several months ago and, as a result, is looking a lot like the old
lean-and-mean Mike (except for that face tattoo, which is still just
bizarre).

No one is saying that eating vegan will make you stronger, but the rap that
you cannot build muscle or get enough protein for competitive strength
training, or have the stamina for endurance training, turns out to be a
myth.

Even more compelling, though, is new evidence that eating vegan can reduce
your risk of heart disease, diabetes, and cancer. "People can bulk up and
knock other people around with animal-based proteins -- that we know," says
T. Colin Campbell, a retired Cornell University professor and author of "The
China Study", which outlines the link between animal-based proteins and
disease. "But it comes at a cost. Your life span is much shorter. Cancer and
diabetes risk goes up. You pay a big price." In his 2005 bestseller,
Campbell says he first discovered a relationship between protein and cancer
while working in the Philippines, where children were getting liver cancer
because of high levels of animal protein in their diets. A study on rats
showed that those given a diet of 20 percent protein got the cancer. Those
given only 5 percent protein did not.

And it's not just athletes looking to shave time off their marathon bests or
add inches to their guns. Hard-charging Fortune 500 types, watching their
blood pressure spike every time stock prices dip, are equipping their corner
offices with raw-food Kind bars and enough locavore produce to choke a
rabbit.

Among them are social-networking wunderkind Biz Stone, the 36-year-old
co-founder of Twitter; real estate magnate Mort Zuckerman, who is worth some
$2 billion; and, perhaps less surprisingly, the co-CEO of Whole Foods, John
Mackey, who oversees a $6.3 billion empire with 55,000 employees < whom he
urges to eat green.

Mackey, who has been a vegetarian for 27 years and a vegan for seven,
recently set up a program to teach his employees and customers the benefits
of eating a plant-strong, nutrient-dense diet. "I feel satiated and
empowered, and have a sense of vitality that I haven't felt in years," he
says.

Interest in whole grains and health foods has, of course, skyrocketed in the
past decade, with a Whole Foods in every city. Even Burger King has a veggie
burger on its menu. Three percent of the U.S. adult population now calls
itself vegetarian, according to a 2009 Vegetarian Resource Group poll. (The
fact that there's a resource group counting leaf eaters says a lot in
itself.) That's some 9 million people, nearly quadruple what it was in 1994
when the VRG asked the same question. Of that population, around a third are
vegans and eat no dairy or eggs, and sometimes no honey.

Still, kicking the meat habit doesn't automatically make you healthy --
there are risks, especially if you're an athlete. Tony Gonzalez found that
out three weeks into his new diet. It was the spring of 2007, and he had
quit "eating flesh," as he likes to put it, after meeting a fellow passenger
on a flight who refused nearly all the food offered to him. The guy told him
about The China Study. Gonzalez had already suffered a bout of Bell's Palsy,
which temporarily paralyzed his face that year. He was convinced that the
NFL diet, which fattens players with burgers and ice cream, was slowly
killing him. Forty pages into the book, he was hooked.

But when he showed up for training, he found he had shed 10 pounds and
struggled to lift the 100-pound dumbbells that he used to throw around. "The
diet killed me," says Gonzalez, still visibly shaken. "There was no way I
could do this and play football, at least not the way I was doing it."

Read the full article in MJ's October issue.


http://www.mensjournal.com/category/food-drink

[ also 24 comments... ]

The Men's Journal Guide to Going Vegan
Posted By MJ On September 7, 2010 @ 1:39 pm In Food & Drink

All it takes is three weeks of eating vegan before you start to feel
positive effects. But it isn't easy changing lifelong eating habits. Here's
all you need to know at the grocery store and in the kitchen.

I. First, the Ground Rules

* Obviously red meat, poultry, and fish are all off the menu. But also no
eggs or dairy, which includes ice cream, cheese, butter, and even cream in
your morning coffee. Eggs and milk are also common ingredients in pastas and
bread. In fact, nearly all commercial baked goods have an ingredient that's
not vegan, so it's usually best to steer clear.

* You'll also need to start scouring labels for egg and milk derivatives
like casein or whey, two popular health-food protein sources. They're found
in a lot of snack bars, fitness foods, and, of course, protein powder
supplements.

* Don't forget multivitamins: Gelatin isn't vegan, so find pills with a
vegan coating, as listed on the label.


II. What to Expect

Week One:

Your entire body will feel lighter, as the meat built up in your gut is
literally forced out by the deluge of fiber from all the vegetables. You
will also feel less sluggish. "You start to come out of this fog that many
people have from eating heavy, fatty foods," says Susan Levin, the director
of nutrition education at the non-profit Physicians Committee for
Responsible Medicine. "When you give up dairy, you immediately breathe
easier." You'll also have to deal with cravings for things like cheese. Find
an appropriate substitute, like soy cheese. Your taste buds will adjust
within a week.

Week Two:

You will have noticeably increased energy, and you're likely to see some
slight weight loss, because your overall calorie intake has likely gone
down. "Not much weight loss," says Levin. "We don't want people dropping
weight like crazy." With increased energy, she says, you will find your
workouts getting better and, as pro athletes have noted, your recovery time
will become shorter. By the end of your second week, says vegan
ultramarathoner Scott Jurek, you won't feel as achy after your workouts.

With more energy, says Levin, comes a brighter mood and outlook. According
to a 2009 Arizona State University study, people who cut all meat from the
diets, including fish, showed less tension and stress.

Week Three:

"Enjoy everything you had in week two, but even more energy and probably a
final layer of weight loss," says Levin. But really, this week is where it
gets molecular. "If you were someone who was meticulous and into blood labs,
you'd actually see your blood sugars and cholesterol levels go down," says
Levin. "Your blood pressure will also fall as you're breathing better and
your arteries are clearing out."

III. Your New Shopping List

"Eating organic, whole foods does not have to be expensive," says Jurek.
"Put your dollars in fresh produce and bulk foods. The less packaged food
you eat, the more you will save, and the quality of your diet will increase.
And get out and explore your local farmers market."

**Protein:

These will ensure you get plenty of it.

* Firm tofu: It's easier to treat firm tofu like meat when cooking. It doesn't
break down as easily as soft tofu, which is mainly used in dips and
desserts.

* Tempeh: a great ground-meat substitute for tacos and bolognese sauce

* Beans: black or pinto -- no refried beans because of the lard

* Hemp or rice milk: better than soymilk, which is heavily processed

* Nuts: Nuts are a rich source of protein but often high in fat. However, it's
unsaturated fat, which may help lower cholesterol. Cashews are great for
snacks between meals and when cooking Asian dishes. Pine nuts are ideal for
salads.

* Almond butter: This is your peanut butter substitute. Use it for
sandwiches or on toast to add protein to your breakfast. We like Once Again,
found in most health-food stores; Nature's Promise, from Stop & Shop's
organic food line; and the Trader Joe's brand.

* Hemp or brown-rice protein: for your smoothies and to sprinkle on salads

**Vegetables and Fruits:

This is your new meat, not in terms of protein, but in terms of the real
centerpiece of your daily meals and snacks. So go to town. Below is a list
of particularly versatile options, some that pack more nutrients and
proteins per gram than any others.

* Broccoli: At thirty-three percent protein, broccoli fills you up and keeps
you full.

* Spinach: This is where you get your calcium now that you've given up milk.
It's also packed with antioxidants.

* Avocadoes: bursting with vitamins, 18 amino acids and omega-3 and -6 fatty
acids, which help lubricate joints and reduce inflammation

* Kale: This "superplant" is rich in phytochemicals sulforaphane and
indoles, which research suggests protects against cancer.

* Yams and sweet potatoes: staples of the vegan diet for their density and
carbs

* Leafy greens: any of the lettuces: romaine, arugula, and watercress, plus
bok choy, collard greens, and artichokes

* Tomatoes, cucumbers, and carrots: for salads, sandwiches, and snacking

* Blueberries, strawberries, and raspberries: for smoothies, snacks, and
breakfast cereals

**Grains, Seeds, and Cereals:

* Quinoa

* Brown rice

* Whole-wheat bread: preferably from a bakery

* Steel-cut oats: The inner parts of the oat kernel, much less processed
than rolled oats or old-fashioned oatmeal. Great for a hearty fall or winter
breakfast.

* Chia seeds: This new vegan fad food is the offspring of those claymate
Chia Pet sproutings. It was the main source of fuel for Aztec warriors and
has recently caught on with the health crowd, thanks to its superfood
qualities. Chia seeds are packed with protein, omega-3 and -6 fatty acids,
and soluble fiber, which helps stabilize blood-glucose levels. Bake them
into cookies or eat them by the handful.

* Granola: Some granola may contain eggs, honey, or other non-vegan
ingredients, so be careful.

* Whole grain-based cereals: like Kashi brand

**Vegan Energy Bars: Your best friends at the airport, long car rides, and
between office meetings. Here are some of the best.

* Vega bars: Triathlete Brendan Brazier concocted these himself. His entire
Vega food line is worth checking out.

* ProBar

* Kind Bar

* Raw Revolution

* 18 Rabbits

**Supplements: If you're superathletic and working on strength training, you
can build your daily protein intake by adding these to your shakes, cereals,
or salads.

* Hemp protein

* Brown-rice protein

**Ready-made meals: This is all cook-and-eat food. Have a few of these in
your fridge or freezer for those late work nights when you can't prepare
anything yourself.

* Field Roast: Its Celebration Roast is great for a large party or days of
leftovers.

* Gardein: Everything from meatless buffalo wings and ribs to "Chick'n
Scaloppini."

* Turtle Island Foods: Creator of the much-mocked holiday Tofurky, it also
makes Tofurky pizza.

IV. Your Meal Plan: Six Go-To Vegan Recipes

BREAKFAST

**Scott Jurek's Blueberry Ultra Power Smoothie

Ingredients:

1 banana, fresh or frozen
1/2 cup pre-soaked almonds (soak 1/4 cup almonds in water 3 to 4 hours or
overnight)
1 cup frozen or fresh blueberries
2 1/2 cups of water
3 tbsp Green Foods Vegan Protein Powder
6 dates or 2 to 3 tbsp natural sweetener
3 tbsp Udo's Oil DHA 3-6-9 Blend
2 tbsp raw maca powder
1/2 tsp sea salt
1/2 tsp vanilla extract or raw vanilla powder

Directions:

Blend all until smooth. (For an extra-hardy breakfast, eat with 6 to 8 oz
soy or coconut-milk yogurt, mixed with 2 tbsp hemp protein powder and one
banana.)

**Apple-Spice Oatmeal

Ingredients:

1/2 cup steel-cut oats
2 cups water
1/2 tsp salt
1/2 tsp cinnamon
1 large organic apple, coarsely chopped
1/4 tsp nutmeg, freshly grated
1/8 tsp ground cloves
1/4 cup of walnuts

Directions:

Put all ingredients in a medium-sized pot. Bring to a boil, and reduce heat
to very low. Cover and simmer for about 30 to 45 minutes, or until oats are
tender and water is mostly absorbed. Serve with sweetener of your choice
with a little freshly grated nutmeg on top.

LUNCH

**The Big Salad (with side of quinoa and/or lentils)

Ingredients/Directions:

*Salad:

3 cups dark leafy greens or raw lacinato/black kale
1 roma tomato
1/4 cucumber
1/2 carrot
1/4 cup pumpkin seeds

*Dressing:

1 tbsp olive oil
1 tbsp balsamic vinegar, dash sea salt and black pepper

*Quinoa:

3 cups cooked quinoa
Top with 1 tbsp olive oil, 1 to 2 tbsp nutritional yeast, 1/4 tsp sea salt,
1/4 tsp paprika.

*Lentils:

2 cups cooked green lentils
Top with 1 tsp each of olive oil, minced garlic, ginger, and curry spice,
plus 1/4 tsp sea salt.

*Spicy BLT Wrap

Ingredients:

1/2 (6-oz) package smoky bacon-style tempeh
1 tsp cooking oil
1/2 tsp Bragg's or soy sauce (divided)
1/2 tsp liquid smoke (divided)
1/2 to 3/4 tsp Tabasco or other hot sauce, to taste
1-1/2 tsp veggie bacon bits
About 1 cup of salad greens (a mix of red lettuce/green lettuce/spinach)
2 tbsp vegan mayonnaise (Nayonaise)
6 to 8 grape or cherry tomatoes
2 large flatbreads, or burrito-sized tortillas of choice

Directions:

1. Chop tempeh into1/2-inch to 1-inch pieces. Mix oil with 1/4 tsp each of
Bragg's, liquid smoke, and hot sauce. Heat oil mixture, and sauté tempeh for
5-8 minutes over medium heat, stirring occasionally.

2. While the tempeh cooks, mix vegan mayo with remaining 1/4 tsp each of
Bragg's and liquid smoke. Add 1/4 to 1/2 tsp hot sauce, to taste. Halve the
cherry tomatoes.

3. When tempeh is ready, combine it with 1-1/2 tsp of veggie "bacon" bits,
and remove from heat.

4. Heat flatbread/tortillas slightly, in microwave/oven/large skillet
(whichever you prefer). Spread half of the mayo mixture down the middle of
each flatbread/tortilla; add half the tempeh mixture to each, and top with
greens & tomatoes. Wrap up and enjoy!

Courtesy of Vegweb.com

DINNER

**Tempeh Tacos

Ingredients:
1/2 medium-size onion, chopped
3 cloves garlic, minced
1 jalapeño pepper, minced
2 tbsp olive oil
2 8-ounce packages tempeh, diced into 1/8- to 1/16-inch cubes
4 tbsp Mexican seasoning
1 tsp salt
1 cup water
1/4 cup chopped cilantro
12 whole-grain or corn tortillas
2 Roma tomatoes, chopped
1 avocado, thinly sliced
1/4 head romaine lettuce, chopped
1/4 cup cilantro, chopped
1/2 cup diced red bell peppers
1 jalapeño, finely minced (if more spice desired)

Directions:

1. Sauté onion, garlic, and jalapeño in olive oil until soft. Add diced
tempeh and continue to sauté for 2 minutes. Add seasoning, salt, and water.
Cook the mixture 10 to 25 minutes, until enough liquid evaporates that you're
left with a thickened sauce.

2. Just before serving add cilantro and stir. Heat tortillas over a griddle
or wrapped in foil in the oven.

3. Fill each tortilla with 2 or 3 tbsp of tempeh.

Makes 4 to 6 servings

**Roasted Vegetables with Pasta

Ingredients:

1 red onion
1 large red bell pepper
1 lb fresh asparagus
2 cups button mushrooms
1 tsp garlic powder or granules
1 tsp mixed Italian herbs
1 tsp chili powder
1/4 tsp salt
1/4 tsp black pepper
8 to 12 oz dry pasta
2 tomatoes, chopped (optional)

Preheat oven to 500°.

Directions:

1. Cut onion and bell pepper into generous bite-sized pieces. Remove tough
ends from asparagus, then break into 1- to 2-inch pieces. Clean mushrooms
and cut off any tough stems.

2. Place all the vegetables into a large bowl and sprinkle with garlic
powder or granules, Italian herbs, chili powder, salt, and black pepper.
Toss to mix.

3. Spread in a single layer in 1 or 2 large baking dishes. Bake 10 to 12
minutes or until the vegetables are just tender.

4. While the vegetables are cooking, cook the pasta according to directions,
then drain and arrange on a large platter.

5. Top with the roasted vegetables and chopped tomatoes.

**Easy Bean Dip

Ingredients:

1 15-oz can black beans, drained and rinsed
1 cup salsa
1/2 tsp ground cumin (optional)

Directions:

Combine all ingredients in a food processor or blender; process until
smooth.

Makes 6 servings; courtesy of Nutritionmd.org

Article printed from Men's Journal: http://www.mensjournal.com

URL to article: http://www.mensjournal.com/vegan

EDITORIAL QUESTIONS or COMMENTS should be e-mailed to
letters@..., or sent to Letters, Men's Journal, 1290 Avenue of
the Americas, New York, NY 10104-0298. Fax number: 212-484-3433. Please
include your address and daytime telephone number. Letters may be edited for
space and clarity.

Copyright © 2009 Men's Journal. All rights reserved.

http://www.bykevingray.com/biography.php

Kevin Gray is a senior writer at Conde Nast Portfolio magazine, which he
joined in July 2006 to help prepare for the magazine's launch in May 2007.
Prior to joining Portfolio, Gray served as articles editor and senior
features writer at Details, where he covered business, politics and
international affairs. Since joining Details in 2000 to assist in its
re-launch, Gray has traveled the globe covering stories on several different
continents.

In the past six years, this has meant, among other things, tracking down
Joseph Kabila, the 32-year-old president of the Congo, for an exclusive
interview; infiltrating a sex slave trafficking ring in Romania; and getting
caught in a shoot-out as he interviewed the new police chief of a
drug-plagued Mexican border town. Gray has driven a motorcycle across
Mongolia, and written about Mongolia's homeless orphans; gone to Vietnam
with the U.S. Army to dig up the remains of dead servicemen; chronicled the
rise of the Falun Gong in China; profiled a group of violent white
supremacists in South Africa; and traveled to Libya to interview Saif
Gaddafi, Moamar Gaddafi's son and likely successor.

Prior to joining Details, Gray worked at CNN as a business producer on the
show Business Unusual with Lou Dobbs. His work has also appeared in The New
York Times Magazine, USA Today, The Washington Post, People and Newsweek.
Gray is a graduate of the University of Michigan. He also holds a master's
degree in English from the Center for Writers at the University of Southern
Mississippi
_______________________________________________


See also:

www.drmcdougall.com

www.vegsource.com


sweeteners (aspartame), methanol (becomes formaldehyde),
and premature babies in Denmark, TI Halldorsson et al
2010.06.30 AmJClinNutr: Erik Millstone: Betty Martini:
Rich Murray 2010.07.08
http://rmforall.blogspot.com/2010_07_01_archive.htm
Thursday, July 8, 2010
http://groups.yahoo.com/group/aspartameNM/message/1609

Woodrow C Monte, PhD, Emiritus Prof. Nutrition gives many
PDFs of reseach -- methanol (11% of aspartame) puts
formaldehyde into brain and body -- multiple sclerosis,
Alzheimer's, cancers, birth defects, headaches:
Rich Murray 2010.05.13
http://rmforall.blogspot.com/2010_05_01_archive.htm
Thursday, May 13, 2010
http://groups.yahoo.com/group/aspartameNM/message/1608
_______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298  rmforall@...

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 148 members, 1,610 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1215 members, 24,083 posts in a public archive

http://groups.yahoo.com/group/rmforall/messages

http://groups.yahoo.com/group/AstroDeep/messages

participant, Santa Fe Complex www.sfcomplex.org
_______________________________________________

JH Mercola gives WC Monte paradigm for methanol (from wines and liquors,
cigarettes, canned fruits, aspartame) conversion into toxic formaldehyde in
tissues, somewhat mitigated by ethyl alcohol [and folic acid] 2010.09.14:
Rich Murray 2010.09.17
http://rmforall.blogspot.com/2010_09_01_archive.htm
Friday, September 17, 2010
[ at the end of each long post, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1611
[ you may have to Copy and Paste URLs into your browser ]
_______________________________________________


[ Joseph H. Mercola, DO  Certified Physician and Surgeon
State of Illinois ]

[ http://aspartame.mercola.com/  many articles ]

172,000 views by Sept. 16, and 183 comments,
1,148 people like this

http://articles.mercola.com/sites/articles/archive/2010/09/14/why-do-heavy-drink\
ers-outlive-nondrinkers.aspx

Call Toll Free: 877-985-2695

The World's #1 Free Natural Health Newsletter

Why Do Researchers Recommend this Common Drink that Can Poison Your Brain?
Posted By Dr. Mercola,  September 14 2010, 172,000 views, Share1148

Research has consistently found that people who don't drink actually tend to
die sooner than those who do.
A new paper suggests that abstainers' mortality rates are actually higher
than those of heavy drinkers.

Even after controlling for many possible variables, such as socioeconomic
status, level of physical activity, and number of close friends, the
researchers found that over a 20-year period, mortality rates were highest
for those who had never been drinkers.

One reason for this may be that low levels of ethanol in your bloodstream
will prevent the formation of formaldehyde from dietary methanol.
In fact, ethanol is used as the preferred antidote for accidental methanol
poisoning in an emergency for this reason.

Time Magazine reports:
"The authors of the new paper are careful to note that even if drinking is
associated with longer life, it can be dangerous: it can impair your memory
severely and it can lead to nonlethal falls and other mishaps".

Sources:

Time Magazine August 30, 2010
http://www.time.com/time/health/article/0,8599,2014332,00.html?xid=rss-topstorie\
s&utm_source=feedburner&utm_medium=feed&utm_campaign=Feed:+time/topstories+%28TI\
ME:+Top+Stories%29

Clinical and Experimental Research November 2010; 34(11): 1-11
http://onlinelibrary.wiley.com/doi/10.1111/j.1530-0277.2010.01286.x/pdf

Medical Hypothesis March 2010; 74(3):493-6  Woodrow C Monte, Prof. Nutrition
(retired)
"Methanol: A chemical Trojan horse as the root of the inscrutable U"
http://www.ncbi.nlm.nih.gov/pubmed/19896282

  SweetPoison.com -- Medical Hypothesis November 6, 2009
Prepublication copy (Full PDF)
http://www.sweetpoison.com/articles/Monte%20%20WC.%20Methanol%3B%20A%20chemical%\
20Trojan%20horse%20as%20the%20root%20of%20the%20inscrutable%20U.%20Medical%20Hyp\
otheses%2006%20November%202009.pdf

Dr. Mercola's Comments:

This is not the first time we've been told that drinking alcohol is actually
good for you.
What's surprising however, not to mention potentially troublesome, are the
scientific claims that moderate and even heavy drinking is beneficial -- in
this case, more beneficial for your longevity than abstaining from alcohol
entirely!
It's difficult to reconcile this claim with everything we already know about
the devastating health effects of excessive alcohol consumption and the fact
that ethyl alcohol is neurotoxic..
However, I will offer one potential explanation for this oxymoron a bit
later in this article.

Moderate Drinkers Live Longer than Non-Drinkers, Study Finds

According to the recent study published in the journal Clinical and
Experimental Research, epidemiological research suggests that moderate to
high alcohol consumption is associated with a reduced overall mortality risk
compared to non- and light drinkers.
Their study included over 1,800 people, aged 55 to 65 when the study began.
Sixty-nine percent of the participants were men.
The subjects were followed for 20 years.
Surprisingly, the group with the lowest mortality rate was moderate
drinkers, who had one to three alcoholic drinks per day, followed by heavy
drinkers, and then light drinkers, while non-drinkers had the highest
mortality rate of them all.

The study states:
"Controlling only for age and gender, compared to moderate drinkers,
abstainers had a more than 2 times increased mortality risk,
heavy drinkers had 70% increased risk,
and light drinkers had 23% increased risk.

A model controlling for former problem drinking status, existing health
problems, and key sociodemographic and social-behavioral factors, as well as
for age and gender, substantially reduced the mortality effect for
abstainers compared to moderate drinkers.

However, even after adjusting for all covariates, abstainers and heavy
drinkers continued to show increased mortality risks of 51 and 45%,
respectively, compared to moderate drinkers."

Time Magazine writes that "moderate alcohol use (especially when the
beverage of choice is red wine) is thought to improve heart health,
circulation and sociability."

But is that enough to explain these findings?
I believe it's unwise to ignore the big picture when it comes to health, and
when it comes to alcohol, I'm just not convinced that the potential benefits
outweigh all the risks, particularly when it comes to having multiple drinks
per day.
So I hope these latest findings will not be used as justification to further
promote a dangerous and health-damaging habit that can easily lead to
alcoholism.

The Health Hazards of Alcohol

Before we get into the potential benefits, it's important to realize that
alcohol is a neurotoxin that can poison your brain.
It can also disrupt your hormonal balance, which could potentially explain
why women do not appear to reap the same health benefits from alcohol
consumption as men do.

According to the Harvard School of Public Health, "moderate" consumption for
women is just one drink per day, whereas "moderate" consumption for men is
two drinks.
Hence, women who consume two to three drinks a day will actually fall into
the category of "heavy" drinkers.

Another important consideration is that wine or other alcoholic beverages
will increase your insulin levels, which will eventually have a negative
impact on your health.
As I've stated on many previous occasions, insulin resistance is a hallmark
of nearly every chronic disease there is.

Heavy drinkers also face increased risk of cancer, heart disease, high blood
pressure, and cirrhosis of the liver.

According to the Harvard School of Public Health, women who drink two or
more drinks a day increase their risk of breast cancer by more than 40
percent!
http://www.ncbi.nlm.nih.gov/pubmed/9480365?dopt=Citation

Other types of cancer linked to excessive alcohol consumption include cancer
of the:
Mouth, larynx and esophagus
Liver
Colon
Pancreas
Lungs

Alcohol consumption also inhibits your body's natural stress response by
reducing a key stress hormone, known as corticotropin-releasing factor
(CRF).
CRF is produced by your hypothalamus and helps trigger your body's reaction
to stress.

If your stress response is impaired, your immune system will also be
inhibited, which can have any number of health implications, from reducing
your ability to fight infections to increasing your cancer risk
http://articles.mercola.com/sites/articles/archive/2007/07/11/how-to-supercharge\
-your-immune-system.aspx
http://articles.mercola.com/sites/articles/archive/2007/12/13/your-immune-system\
-can-keep-cancer-dormant.aspx

Alcohol also clearly needs to be avoided during pregnancy.

Beyond Resveratrol -- Explaining the Health Benefits of Alcohol

One of the most widely accepted health benefits of alcohol comes from
resveratrol, an antioxidant found in red wine, which acts as a:
Cancer-preventing agent
Blood thinner
Vaso-expanding agent
Blood pressure lowering compound
Anti-aging chemical

But resveratrol cannot explain the health benefits ascribed to the moderate
consumption of other types of alcohol (ethanol).

Interestingly, research into ethanol's impact on dietary methanol may offer
clues that could potentially rival the late breaking science into fructose
and its devastating impact on health.
http://articles.mercola.com/sites/articles/archive/2010/01/02/HighFructose-Corn-\
Syrup-Alters-Human-Metabolism.aspx

One possible explanation for why mortality rates are higher for non-drinkers
may be that low levels of ethanol (alcohol) in your bloodstream helps
prevent the formation of formaldehyde from dietary methanol.
(In fact, ethanol is used as the preferred antidote for accidental methanol
poisoning in an emergency for this reason.)

What is dietary methanol and how could this possibly have ANY significance?

New Concern in Your Food: Wood Alcohol (Methanol)

Fresh fruits and vegetables contain small amounts of naturally-occurring
methanol, and the artificial sweetener aspartame converts into methanol in
your body.
Normally this is not a problem as the methanol is typically bound to pectin,
and since your body has no enzyme to metabolize that bond it is simply
excreted in your stool and none of the methanol is absorbed into your body.

However, the problem occurs when you can or bottle fruit- or vegetable
juice, as the methanol tends to then dissociate from the pectin into free
methanol, which you do absorb.

The methanol you absorb readily passes the blood brain barrier where it can
be  converted to form formaldehyde, which is a potent toxin that actually
causes most of the damage.

Why Ethanol May Protect You From Methanol

An exciting paper that delves into this topic is food scientist Woody Monte's
"Methanol: A chemical Trojan horse as the root of the inscrutable U,"
published in the March, 2010 issue of Medical Hypotheses.

In it, he explains that:
"Very low levels of ethanol in your bloodstream would substantively prevent
all formaldehyde production from dietary methanol anywhere in the body.
Protection from formaldehyde production may account for the yet unexplained
dose region of apparent improvement in the U-shaped curve of alcohol
consumption.
Epidemiologic studies show moderate consumption of alcohol is associated
with a reduced risk of myocardial infarction, dementia, lupus, and other
diseases of civilization.
Low doses of ethanol appear to provide a preventative measure against the
causes of diseases of civilization.
Recent studies of individuals who consumed at least one alcoholic drink per
day show subjects had an additional 86 percent reduction in risk of
myocardial infarction if they were genetically endowed with a genotype of
ADH I that was 2.5 times slower to metabolize ethanol than the control.
These findings were ''consistent with the hypothesis that a slower rate of
clearance of alcohol enhances the beneficial effect of moderate alcohol
consumption on the risk of cardiovascular disease.""
It is important to understand that the primary treatment for methanol
poisoning in the emergency room is to give them ethanol, for the reasons
described above.
The ethanol will preferentially be broken down before the methanol.
The methanol then remains unmetabolized, and in its base form it is
relatively nontoxic.
It becomes a problem when your body breaks it down to formaldehyde.
So while your body is breaking down the ethanol it has enough time to
breathe out the methanol unchanged in your lungs and excrete it unchanged in
your urine.

A Little Alcohol Might Be Good, But More is Definitely Dangerous

As I mentioned earlier, if this theory is correct, it could rival the
scientific findings on fructose in terms of importance, and could explain
not only the health benefits of low-to moderate alcohol consumption, but
also how aspartame affects some people more negatively than others.

It may still be too early to draw definitive conclusions, but the arguments
are compelling and I'll be following this line of research with great
interest in the years to come.

In his paper, Dr. Monte continues to connect the dots and shows how greater
alcohol consumption ceases to be beneficial at a certain point, and instead
starts to take its toll on your health:
"A compelling explanation of the dose region of adverse effects of the
U-shaped curve with high ethanol consumption, which shows increased risk of
these same diseases, could be the mechanism by which humans habituate to
high consumption of ethanol.
The induction of the P450 hepatic microsomal ethanol-oxidizing system
results in a considerably higher clearance rate of ethanol from the
bloodstream for an extended period of time, thus accounting for more
consumption leading to statistically less time of protection.
Small amounts of supplemental alcohol not sufficient to induce P450 might be
expected to prolong the residence time and avoid gaps in the protection
afforded by ethanol in preventing methanol-placed formaldehyde. "
P450 is a class, or family, of liver enzymes whose main functions include
catalyzing the metabolism of drugs and the oxidation of organic substances.

In simplistic terms, higher alcohol consumption sends this system into high
gear, and starts clearing ethanol from your system.
Again, a simplified explanation for how you become a habitual drinker (which
also tends to lead to drinking increasing amounts of alcohol) is that the
more you drink, the more efficient this ethanol-clearing system becomes, and
you begin to be able to drink more before you notice the effects of the
alcohol.

What this all means is that in order for the alcohol to provide you with the
health benefit of preventing formaldehyde formation, it must below enough to
not activate the P450 system.

Hence you get a U-shaped curve, where low- to moderate alcohol consumption
gives you increasing amounts of health benefits, until you reach the
"threshold," at which point the more you drink, the more harm it causes.

It's important to realize that formaldehyde is a class 1 carcinogen and a
mutagen, and in the form of methanol, it can easily be transported
throughout your entire body and brain.

Wherever you have a lot of ADH1 (the enzyme metabolizes methanol to
formaldehyde), such as in your brain, methanol can be particularly
troublesome.

But as long as there's just enough ethanol in your system to keep the
methanol moving along, without ever being metabolized to formaldehyde, no
damage is caused.

It's worth noting here also that the average person typically has some
naturally-occurring ethanol in their system, as it is also created through
the fermentation process in your gut.

However, the addition of small amounts of ethanol in the form of alcohol may
be able to more fully prevent formaldehyde from forming, which could explain
why low- to moderate alcohol consumption appears to be even more healthful
than total abstinence.

How Can You Get the Same Benefits Without Drinking Alcohol?

It is not my recommendation to start drinking alcohol or to use this
information as a justification to continue drinking alcohol.
I am not convinced it is physiologically beneficial for you in the long run.
The purpose of running this article was to merely inform you of a recent
appreciation of methanol toxicity, and how ethanol can interact with it.
If this theory is true then the primary benefit of using ethanol would be to
prevent methanol from converting to formaldehyde.

So what is the main source of methanol in your diet?
Remember that fresh fruits and vegetables have it but it's harmless if you
eat them fresh, as the methanol is then bound to pectin and cannot
dissociate and cause you harm.

They key is to avoid ALL canned (or bottled) fruit or vegetable juices as
they will have free methanol.

Another large source of free methanol would be aspartame which is 11 percent
methanol by weight.

So if this theory is correct, you would likely receive very little benefit
from consuming ethanol if you just avoid canned fruits and vegetables and
asparatame.

Do You Drink Too Much?

It's dangerous to place too much weight on recommendations that include
imbibing alcohol on a regular basis.
And even if you do take that recommendations to heart, it's important to
remember that health benefits have ONLY been found in people who drink small
amounts of alcohol on a daily basis, NOT a week's worth of alcohol over the
weekend...

This fact also further strengthens the theory that the benefit is derived
from having low amounts of ethanol circulating almost continuously, or at
least regularly, through your system, keeping formaldehyde from forming and
doing any damage.

Unfortunately, alcohol abuse is a major problem in most countries, so I
certainly hope you will not use this information as an excuse to hit the
bottle every day.

Most alcohol misuse and abuse stems from deep emotional challenges.
Addressing these issues at a deep level is imperative to avoid the negative
health consequences -- both physical and mental -- that inevitably result
from excessive drinking.

The Emotional Freedom Technique (EFT) can be helpful if this is an issue for
you.
This psychological acupressure technique is routinely used in my clinic and
it works better than any other traditional or alternative method I am
currently aware of.
http://www.mercola.com/Forms/eftcourse.aspx

However, if you try the technique yourself and find that you are not
improving, consider consulting a trained EFT therapist to facilitate the
process.
You can find a list of qualified EFT practitioners near you at this link.
For more information, feel free to review Pat Carrington's site
TappingCentral.
http://www.masteringeft.com/

Related Links:

How Alcohol Changes Your Brain
http://articles.mercola.com/sites/articles/archive/2009/06/30/How-Alcohol-Change\
s-Your-Brain.aspx

How Heart-Healthy is Alcohol?
http://articles.mercola.com/sites/articles/archive/2005/12/24/how-heart-healthy-\
is-alcohol.aspx

Alcohol Use Linked to More Cancers
http://articles.mercola.com/sites/articles/archive/2006/02/18/alcohol-use-linked\
-to-more-cancers.aspx

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© Copyright 2010 Dr. Joseph Mercola. All Rights Reserved.
_______________________________________________


Woodrow C Monte, PhD, Emiritus Prof. Nutrition gives many
PDFs of reseach -- methanol (11% of aspartame) puts
formaldehyde into brain and body -- multiple sclerosis,
Alzheimer's, cancers, birth defects, headaches:
Rich Murray 2010.05.13
http://rmforall.blogspot.com/2010_05_01_archive.htm
Thursday, May 13, 2010
http://groups.yahoo.com/group/aspartameNM/message/1601
_______________________________________________


[ Other formaldehyde sources include alcohol drinks and
tobacco and wood smoke,
while adequate folic acid levels protect most people,
but not for brain and retina harm.

See also:

sweeteners (aspartame), methanol (becomes formaldehyde),
and premature babies in Denmark, TI Halldorsson et al
2010.06.30 AmJClinNutr: Erik Millstone: Betty Martini:
Rich Murray 2010.07.08
http://rmforall.blogspot.com/2010_07_01_archive.htm
Thursday, July 8, 2010
http://groups.yahoo.com/group/aspartameNM/message/1609 ]

http://whilesciencesleeps.com/references

589 references -- click on each title for free pdf of abstract
or whole paper

Article 2 http://www.thetruthaboutstuff.com/review2.html

Selection from Article 2, Fitness Life, December 2007

http://whilesciencesleeps.com/montediet

Methanol: Where Is It Found? How Can It Be Avoided?

AVOID the following, ranked in order of greatest danger:

1. Cigarettes.
2. Diet foods and drinks with aspartame.
3. Fruit and vegetable products and their juices in bottles,
cans, or pouches.
4. Jellies, jams, and marmalades not made fresh and kept
refrigerated.
5. Black currant and tomato juice products, fresh or
processed.
6. Tomato sauces, unless first simmered at least 3 hours
with an open lid.
7. Smoked food of any kind, particularly fish and meat.
8. Sugar-free chewing gum.
9. Slivovitz: You can consume one alcoholic drink a day
on this diet -- no more! [ no fruit brandies ]
10. Overly ripe or near rotting fruits or vegetables.
_______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298  rmforall@...

http://groups.yahoo.com/group/AstroDeep/messages

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 148 members, 1,611 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1215 members, 24,084 posts in a public archive

http://groups.yahoo.com/group/rmforall/messages

participant, Santa Fe Complex www.sfcomplex.org
_______________________________________________

Bill Clinton went vegan since May to reverse heart disease, 2 minute video: Rich
Murray 2010.09.19
http://rmforall.blogspot.com/2010_09_01_archive.htm
Sunday, September 19, 2010
[ at the end of each long post, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1612
[ you may have to Copy and Paste URLs into your browser ]
_______________________________________________


http://www.vegsource.com/news/2010/09/bill-clinton-goes-vegan-to-reverse-heart-d\
isease-video.html

Sunday, September 19, 2010

Bill Clinton Goes Vegan To Reverse Heart Disease (VIDEO)
YAHOO.COM 09/17/10
Read More: bill clinton, health, heart disease

Comments (3)

Bill Clinton talks about going veg to reverse heart disease, so he can be
healthy in the years ahead to see his potential grandchildren.

Scroll down for video.

We also have this from ecorazzi.com:

"I'm trying to be one of those experimenters," said Clinton.
"Since 1986, several hundred people who have tried essentially a plant-based
diet, not ingesting any cholesterol from any source, has seen their bodies
start to heal themselves -- break up the arterial blockage, break up the
calcium deposits around the heart.
82 percent of the people who have done this have had this result, so I want
to see if I can be one of them."

Just hours ago, Ecorazzi received exclusive information from a friend of
Clinton (who wishes to remain anonymous) regarding first-hand conversations
with the former president about his vegan diet.

According to our source, Clinton decided to adopt the diet in the early part
of May.
While he does occasionally eat fish, the former president otherwise follows
a strict vegan diet.

What made him go vegan?
According to our source, Clinton has read many books on the topic, including
books by T. Colin Campbell, Caldwell Esselstyn and Dr. Dean Ornish. Although
losing weight was a benefit of the dietary change, the choice to go vegan
was about more than just losing weight.
"I've never known him not to say what's on his mind," says our source.
"And he knows quite a bit and likely has a lot to say about the benefits of
a vegan diet.
He has read The China Study, and he knows the issues.
With time, I think it's likely he could become the most outspoken proponent
of a complete vegan diet."

Bill Clinton Goes Vegan To Reverse Heart Disease (VIDEO)
YAHOO.COM | 09/17/10
Read More: bill clinton, health, heart disease

http://bit.ly/dvowMY

http://news.yahoo.com/video#video=21941869
working to stay healthy... 2:03 minutes

Fri Sep 17, 12:48 am ET
Clinton: Working to stay healthy for his grandchildren
By Willow Bay

On a mission to keep off the weight he lost this summer for daughter
Chelsea's wedding, President Bill Clinton is experimenting with a
low-cholesterol, vegetarian diet.
Clinton, apparently eager to fit some exercise into his busy schedule,
walked across Time Square on Thursday evening for an interview with Yahoo!
News and The Huffington Post.
Clinton is in New York gearing up for the Clinton Global Initiative's (CGI)
Annual Meeting.
In this part of the interview, President Clinton explains the way potential
grandchildren motivate him to stick to the diet, and shares one of his
favorite moments from Chelsea's recent wedding to Marc Mezvinksky.
_______________________________________________


The Rise of the Power Vegan, 6 page revolutionary, lucid,
thorough article in Men's Journal, Kevin Gray:
Rich Murray 2010.09.13
http://rmforall.blogspot.com/2010_09_01_archive.htm
Monday, September 13, 2010
[ at the end of each long post, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1610
[ you may have to Copy and Paste URLs into your browser ]


Woodrow C Monte, PhD, Emiritus Prof. Nutrition gives many
PDFs of reseach -- methanol (11% of aspartame) puts
formaldehyde into brain and body -- multiple sclerosis,
Alzheimer's, cancers, birth defects, headaches:
Rich Murray 2010.05.13
http://rmforall.blogspot.com/2010_05_01_archive.htm
Thursday, May 13, 2010
http://groups.yahoo.com/group/aspartameNM/message/1608
_______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298  rmforall@...

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 148 members, 1,612 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1215 members, 24,104 posts in a public archive

http://groups.yahoo.com/group/rmforall/messages

http://groups.yahoo.com/group/AstroDeep/messages

participant, Santa Fe Complex www.sfcomplex.org
_______________________________________________

formaldehyde from 0.2 mg daily methanol from aspartame in Singulair
(montelukast) chewable asthma medicine causes severe allergic dermatitis in
boy, SE Jacob et al, Pediatric Dermatology 2009 Nov: Rich Murray 2010.09.27
http://rmforall.blogspot.com/2010_09_01_archive.htm
Monday, September 27, 2010
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1613
[you may have to Copy and Paste URLs into your browser]
_______________________________________________


http://onlinelibrary.wiley.com/doi/10.1111/j.1525-1470.2008.00855.x/abstract

Pediatr Dermatol. 2009 Nov-Dec;26(6):739-43.
Systematized contact dermatitis and montelukast in an atopic boy.
Castanedo-Tardan MP,
González ME,
Connelly EA,
Giordano K,
Jacob SE.
Mari Paz Castanedo-Tardan
Mercedes E. González
Elizabeth A. Connelly
Kelly Giordano
Sharon E. Jacob
University of Miami, Miller School of Medicine,
Department of Dermatology and Cutaneous Surgery,
Miami, Florida, USA.
Article first published online: 2 APR 2009
DOI: 10.1111/j.1525-1470.2008.00855.x
© 2009 Wiley Periodicals, Inc.

Abstract

Upon ingestion, the artificial sweetener, aspartame is metabolized to
formaldehyde in the body and has been reportedly associated with systemic
contact dermatitis in patients exquisitely sensitive to formaldehyde.
We present a case of a 9-year-old Caucasian boy with a history of mild
atopic dermatitis that experienced severe systematized dermatitis after
being started on montelukast chewable tablets containing aspartame.
Patch testing revealed multiple chemical sensitivities which included a
positive reaction to formaldehyde.
Notably, resolution of his systemic dermatitis only occurred with
discontinuation of the montelukast chewables.
PMID: 20199453

We present a case of a 9-year-old Caucasian boy with a history of mild
atopic dermatitis (stable on topical ta-crolimus ointment 0.03%), mild
intermittent asthma and known food and environmental allergies diagnosed by
prick testing (egg, soy, and peanut) at 3 years of age, and wheat ...


Montelukast Chewable Tablets
Pronunciation: mon-te-LOO-kast
Generic Name: Montelukast
Brand Name: Singulair

http://www.rxlist.com/singulair-drug.htm 13 pages

Copyright 1996-2009 Cerner Multum, Inc.
Version: 7.03. Revision date: 06/25/2009.

Phenylketonuria

Phenylketonuric patients should be informed that the 4-mg and 5-mg chewable
tablets contain phenylalanine (a component of aspartame), 0.674 and 0.842 mg
per 4-mg and 5-mg chewable tablet, respectively.

[ Since phenylalanine is 50% by weight of aspartame, the dose of aspartame
is 1.348 mg and 1.684 mg, releasing the very small dose of methanol, 11 %,
of 0.148 mg and 0.185 mg, of which about 30% remains in the body as
cumulative durable toxic reaction products, concentrated where the tissues
have high levels of the ADH enzyme, such as brain,  retina, skin, liver,
kidney, GI tract, and muscle -- the ADH enzyme turns methanol into
formaldehyde, part of which becomes another toxin, formic acid. ]
A 12-oz can of diet drink has 200 mg aspartame, releasing 22 mg methanol
into the body, resulting in about 7 mg retained toxic products of
formadehyde and formic acid in concentrated locations. ]

CONTRAINDICATIONS

Hypersensitivity to any component of this product.

Who should not take SINGULAIR?

Do not take SINGULAIR if you are allergic to any of its ingredients.

PRECAUTIONS

Use of this medication is not recommended in children less than 15 years
old.

PATIENT INFORMATION
What is Singulair?

What is the dose of SINGULAIR?

The dose of SINGULAIR prescribed for your or your child's condition is based
on age:

2 to 5 years: one 4-mg chewable tablet
6 to 14 years: one 5-mg chewable tablet.

The mean systemic exposure of the 4-mg chewable tablet in pediatric patients
2 to 5 years of age and the 5-mg chewable tablets in pediatric patients 6 to
14 years of age is similar to the mean systemic exposure of the 10-mg
film-coated tablet in adults.

The 5-mg chewable tablet should be used in pediatric patients 6 to 14 years
of age
and the 4-mg chewable tablet should be used in pediatric patients 2 to 5
years of age.

Montelukast sodium, the active ingredient in SINGULAIR, is a selective and
orally active leukotriene receptor antagonist that inhibits the cysteinyl
leukotriene CysLT1 receptor.

Each 4-mg and 5-mg chewable SINGULAIR tablet contains 4.2 and 5.2 mg
montelukast sodium, respectively, which are equivalent to 4 and 5 mg of
montelukast, respectively.

Both chewable tablets contain the following inactive ingredients: mannitol,
microcrystalline cellulose, hydroxypropyl cellulose, red ferric oxide,
croscarmellose sodium, cherry flavor, aspartame, and magnesium stearate.

Asthma
SINGULAIR is indicated for the prophylaxis and chronic treatment of asthma
in adults and pediatric patients 12 months of age and older.

Exercise-Induced Bronchoconstriction
SINGULAIR is indicated for prevention of exercise-induced
bronchoconstriction (EIB) in patients 15 years of age and older.

Allergic Rhinitis
SINGULAIR is indicated for the relief of symptoms of seasonal allergic
rhinitis in patients 2 years of age and older and perennial allergic
rhinitis in patients 6 months of age and older.


four Murray AspartameNM reviews in SE Jacob & SA
Stechschulte debate with EG Abegaz & RG Bursey of
Ajinomoto re migraines from formaldehyde from aspartame,
Dermatitis 2009 May: TE Hugli -- folic acid with V-C
protects: Rich Murray 2009.08.12
http://rmforall.blogspot.com/2009_08_01_archive.htm
Wednesday, August 12, 2009
http://groups.yahoo.com/group/aspartameNM/message/1582
[ extracts ]

Formaldehyde, aspartame, migraines: a possible connection.
Abegaz EG, Bursey RG.
Dermatitis. 2009 May-Jun;20(3):176-7; author reply 177-9.
No abstract available. PMID: 19470307

Eyassu G. Abegaz *
Robert G. Bursey
Ajinomoto Corporate Services LLC, Scientific & Regulatory
Affairs, 1120 Connecticut Ave., N.W., Suite 1010,
Washington, DC 20036
* Corresponding author. Tel.: +1 202 457 0284;
fax: +1 202 457 0107.
abegazee@... (E.G. Abegaz),
burseyb@... (R.G. Bursey)

"For example, fruit juices, coffee, and alcoholic beverages
produce significantly greater quantities of formaldehyde than
aspartame-containing products. [6]"

"[6] Magnuson BA, Burdock GA, Doull J, et al. Aspartame:
a safety evaluation based on current use levels, regulations,
and toxicological and epidemiological studies.
Crit Rev Toxicol 2007;37:629-727"

[ 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." ]


http://www.medscape.com/viewarticle/579335

Dermatitis. 2008; 19(3): E10-E11.
© 2008  American Contact Dermatitis Society
Formaldehyde, Aspartame, and Migraines:
A Possible Connection
Sharon E. Jacob; Sarah Stechschulte
Published: 09/17/2008
[ Extract ]

Abstract

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.

Case Series

Six patients (ages 16 to 75 years) were referred for evaluation
of recalcitrant dermatitis. By history, five of the patients were
noted  to have developed migraines following aspartame
consumption; the sixth reported dermatitis flares associated
with diet cola consumption of >2 liters/day.

All six patients had current environmental exposures to
formaldehyde or formaldehyde-releasing preservatives in
their personal hygiene products and/or regular consumption
of "sugar-free food" artificially sweetened with aspartame.

Based on their histories and clinical presentations, these
patients were patch-tested with the North American Contact
Dermatitis Group 65-allergen Standard Screening Series and
selected chemicals from the University of Miami vehicle,
fragrance, bakery, and textile trays.

All six patients had positive reactions to formaldehyde, and
four had additional positive reactions to
formaldehyde-releasing preservatives (FRPs).
Expert counseling on allergen avoidance (including avoidance
of formaldehyde, FRPs, and aspartame) and alternative
product recommendations were provided to the patients.

At their follow-up appointments (between 8 and 12 weeks),
all the patients showed clearance of their dermatitis. Four
patients (two inadvertently) resumed their consumption of
aspartame and subsequently returned for an additional
follow-up visit. Three of the first five patients had recurrences
of both their migraines and their dermatitis; the sixth patient
(who had no migraines) had a positive rechallenge dermatitis.
These four patients were again counseled on avoidance
regimen.


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


http://www.skinandaging.com/article/5158
Skin & 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.

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



http://www.safecosmetics.org/downloads/Formaldehyde-allergic-reactions_SJacob_Pe\
diatricAnnalsJan07.pdf

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

"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


www.eczemacenter.org/eczema_center/meetfacultystaff.htm

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@...;
Sarah A. Stechschulte, BA  sstechschulte@...


http://groups.yahoo.com/group/aspartameNM/message/846
aspartame in Merck Maxalt-MLT worsens migraine,
AstraZeneca Zomig, Eli Lilly Zyprexa,
J&J Merck Pepcid AC (Famotidine 10mg) Chewable Tab,
Pfizer Cool Mint Listerine Pocketpaks: Murray 2002.07.16

Migraine MLT-Down: an unusual presentation of migraine
in patients with aspartame-triggered headaches.
Newman LC, Lipton RB Headache 2001 Oct; 41(9): 899-901.
[ Merck 10-mg Maxalt-MLT, for migraine, has 3.75 mg aspartame,
while 12 oz diet soda has 200 mg. ]
Headache Institute, St. Lukes-Roosevelt Hospital Center,
New York, NY
Department of Neurology newmanache@...
Albert Einstein College of Medicine, Bronx, NY
Innovative Medical Research RLipton@...


http://groups.yahoo.com/group/aspartameNM/message/855
Blumenthall & Vance: aspartame chewing gum headaches
Nov 1997: Murray 2002.07.28

Harvey J. Blumenthal, MD, Dwight A Vance, RPh
Chewing Gum Headaches. Headache 1997 Nov; 37(10): 665-6.
Department of Neurology, University of Oklahoma College of
Medicine, Tulsa, USA. neurotulsa@...
Aspartame, a popular dietetic sweetener, may provoke headache in
some susceptible individuals. Herein, we describe three cases of
young women with migraine who reported their headaches could be
provoked by chewing gum sweetened with aspartame.
[ 6-8 mg aspartame per stick chewing gum ]


methanol (11% of aspartame), made by body into
formaldehyde in many vulnerable tissues, causes modern
diseases of civilization, summary of a century of research,
Woodrow C Monte PhD, Medical Hypotheses journal:
Rich Murray 2009.11.15
http://rmforall.blogspot.com/2009_11_01_archive.htm
Sunday, November 15, 2009
http://groups.yahoo.com/group/aspartameNM/message/1589


Woodrow C Monte, PhD, Emiritus Prof. Nutrition gives
many PDFs of reseach -- methanol (11% of aspartame)
puts formaldehyde into brain and body --  multiple
sclerosis, Alzheimer's, cancers, birth defects, headaches:
Rich Murray 2010.05.13
http://rmforall.blogspot.com/2010_05_01_archive.htm
Thursday, May 13, 2010
http://groups.yahoo.com/group/aspartameNM/message/1601

[ Other formaldehyde sources include alcohol drinks and
tobacco and wood smoke,
while adequate folic acid levels protect most people,
but not for brain and retina harm.

See also:

sweeteners (aspartame), methanol (becomes formaldehyde),
and premature babies in Denmark, TI Halldorsson et al
2010.06.30 AmJClinNutr: Erik Millstone: Betty Martini:
Rich Murray 2010.07.08
http://rmforall.blogspot.com/2010_07_01_archive.htm
Thursday, July 8, 2010
http://groups.yahoo.com/group/aspartameNM/message/1609 ]

http://whilesciencesleeps.com/references

589 references -- click on each title for free pdf of
abstracts or full texts of most of the reports.

Article 2 http://www.thetruthaboutstuff.com/review2.html

Selection from Article 2, Fitness Life, December 2007.

Here is his very practical advice for diet:

http://whilesciencesleeps.com/montediet

Methanol: Where Is It Found? How Can It Be Avoided?

AVOID the following, ranked in order of greatest danger:

1. Cigarettes.
2. Diet foods and drinks with aspartame.
3. Fruit and vegetable products and their juices in bottles,
cans, or pouches.
4. Jellies, jams, and marmalades not made fresh and kept
refrigerated.
5. Black currant and tomato juice products, fresh or
processed.
6. Tomato sauces, unless first simmered at least 3 hours
with an open lid.
7. Smoked food of any kind, particularly fish and meat.
8. Sugar-free chewing gum.
9. Slivovitz: You can consume one alcoholic drink a day
on this diet -- no more! [ no fruit brandies ]
10. Overly ripe or near rotting fruits or vegetables.
_______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298  rmforall@...

http://groups.yahoo.com/group/AstroDeep/messages

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 148 members, 1,613 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1215 members, 24,105 posts in a public archive

http://groups.yahoo.com/group/rmforall/messages

participant, Santa Fe Complex www.sfcomplex.org
_______________________________________________

re GC Ebers study, females harmed more by body making methanol into
formaldehyde in brain via ADH enzyme: 589 references, WC Monte,
retired Prof. Nutrition: Rich Murray 2011.01.08
http://rmforall.blogspot.com/2011_01_01_archive.htm
Saturday, January 8, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1614
[you may have to Copy and Paste URLs into your browser]
_______________________________________________


Woodrow C Monte, PhD, Emiritus Prof. Nutrition gives many PDFs of
reseach -- methanol (11% of aspartame) puts formaldehyde into brain
and body -- multiple sclerosis, Alzheimer's, cancers, birth defects,
headaches: Rich Murray 2010.05.13
http://rmforall.blogspot.com/2010_05_01_archive.htm
Thursday, May 13, 2010
http://groups.yahoo.com/group/aspartameNM/message/1601

[ Other formaldehyde sources include alcohol drinks and
tobacco and wood smoke,
while adequate folic acid levels protect most people. ]

http://whilesciencesleeps.com/about

589 references, many abstracts and full texts

Methanol: Where Is It Found? How Can It Be Avoided?

AVOID the following, ranked in order of greatest danger:

1. Cigarettes.
2. Diet foods and drinks with aspartame.
3. Fruit and vegetable products and their juices in bottles,
cans, or pouches.
4. Jellies, jams, and marmalades not made fresh and kept
refrigerated.
5. Black currant and tomato juice products, fresh or
processed.
6. Tomato sauces, unless first simmered at least 3 hours
with an open lid.
7. Smoked food of any kind, particularly fish and meat.
8. Sugar-free chewing gum.
9. Slivovitz: You can consume one alcoholic drink a day
on this diet -- no more! [ no fruit brandies ]
10. Overly ripe or near rotting fruits or vegetables.

Selection from Article 2, Fitness Life, December 2007, and
well discussed in the DVD video:

"Identical Symptoms of MS, Methanol Poisoning
and Aspartame Toxicity

The symptoms of multiple sclerosis (44, 83, 85, 169), chronic
and acute methanol poisoning (13, 144, 189), and Aspartame
toxicity (54, 58, 93, 181), are in all ways identical.

There is nothing that happens to the human body from the
toxic effect of methanol that has not been expressed during
the course of MS... nothing (143, 144).

This generalization extends even to the remarkable
opthomological conditions common to both: transitory optic
neuritis and retrolaminar demyelinating optic neuropathy with
scotoma of the central visual field (which occasionally
manifests as unilateral temporary blindness (85, 138, 163).

In fact, these opthomological symptoms have been thought of
for years in their respective literatures to be "tell tale"
indications for the differential diagnosis for each of these
maladies independently (85, 138, 148, 163, 169).

The common symptoms of
headache (13, 83, 181, 189),
nervousness (13, 83, 181),
depression (58, 83, 189, 181),
memory loss (18, 147, 85, 169, 181),
tingling sensations (13, 85, 168, 138, 169),
pain in the extremities (13, 85, 169),
optic neuritis (85, 138, 148, 163, 169),
bright lights in the visual field (139, 83),
seizures (21, 83, 160),
inability to urinate or to keep from urinating (139, 146, 167)
are all shared by each of these conditions and shared yet
again by complaints from aspartame poisoning
(54, 58, 93, 181).

I take these strikingly similar symptom patterns as evidence
that these disorders act on identical components of the
central nervous system and in the same way.

The "Miracle" that MS shares with Methanol poisoning

In the early stages of MS, or when a non-lethal dose of
methanol has been administered, complete recovery is a
possibility.

The only two afflictions for which such dramatic "remissions"
are reported from identical neuromuscular and opthomological
damage, even "blindness" is relapsing-remitting multiple
sclerosis (85) and methyl alcohol poisoning (138, 163).

The pathology of the two maladies is in may ways identical,
particularly when it comes to destruction of the myelin
sheath with no harm to the axon itself (18, 148, 176).

Sex Ratios for MS and Aspartame Reactions

Women bear the brunt of multiple sclerosis (91a-c) and lupus
(SLE)(73) with fully three-fold representations in infliction
numbers over men for both diseases.

This is exactly the proportion represented by adverse
reactors to Aspartame reported by the US Center for
Disease Control in their study of 1984 (58).

The Center found three women to every man whose
Aspartame consumption complaints were serious enough
to warrant investigation (93).

Although the female/male ratio for those stricken with MS has
always been high, recent estimates place it at over 3 to 1
(91, 91a, 91c).

What might account for the difference across sexes in
incidence?

A study published in the New England Journal of Medicine
(94) reports biopsies of the gastric lining of men and women.

A result was that the concentration of ADH in the
gastric lining of men was much higher than for woman.

Men have the advantage of removing methanol from the
bloodstream four times faster on an equal-body-size basis
than women.

Thus, for men, methanol is more likely to be removed from the
blood before it reaches the brain.

The brain is spared but the methanol removed would still be
metabolized to formaldehyde in the gut where it would reap
its havoc on a more forgiving organ.

This may help explain why men have more gastrointestinal
complaints from both methanol and Aspartame consumption
(93, 99).

On the other hand, women's complaints from both more
frequently involve serious neurological complications."...

methanol (11% of aspartame), made by body into
formaldehyde in many vulnerable tissues, causes modern
diseases of civilization, summary of a century of research,
Woodrow C Monte PhD, Medical Hypotheses journal:
Rich Murray 2009.11.15
http://rmforall.blogspot.com/2009_11_01_archive.htm
Sunday, November 15, 2009
http://groups.yahoo.com/group/aspartameNM/message/1589

formaldehyde from 0.2 mg daily methanol from aspartame in Singulair
(montelukast) chewable asthma medicine causes severe allergic dermatitis in
boy, SE Jacob et al, Pediatric Dermatology 2009 Nov: Rich Murray 2010.09.27
http://rmforall.blogspot.com/2010_09_01_archive.htm
Monday, September 27, 2010
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1613
[you may have to Copy and Paste URLs into your browser]


http://www.medpagetoday.com/clinical-context/MultipleSclerosis/24207

Gene Study Suggests Why MS Is Women's Disease

This report is part of a 12-month Clinical Context series.
By John Gever, Senior Editor, MedPage Today
Published: January 06, 2011
Reviewed by Michael J. Olek, DO; Director, Newport Doctors Multiple
Sclerosis Clinic and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner
Earn CME/CE credit for reading medical news

Action Points
Explain to interested patients that this study shows there may be a
genetic cause for female predominance in multiple sclerosis.
The mystery of why multiple sclerosis predominantly strikes women may
have been unraveled a bit, thanks to a new genetic study.
Polymorphisms in major histocompatibility complex (MHC) genes and
their associated DNA methylation patterns may combine with
environmental influences in ways that promote greater susceptibility
to the disease in women than in men, according to George C. Ebers, MD,
FMedSci, of John Radcliffe Hospital in Oxford, England, and
colleagues.

Published online in Neurology, their findings were based on genomic
analyses of more than 7,000 members of 1,055 families affected by MS.

Ebers and colleagues noted that, 100 years ago, MS was reported to
affect men and women about equally.

However, in their sample, of the more than 2,100 individuals who had
MS, 73% were female.
They noted that published reports from around the world point to an
approximate 2:1 ratio of female versus male MS patients.

MS risk is believed to have a strong heritable component centered on
MHC genes, but the reason for the female predominance has been
unclear.
Previous studies have ruled out genes carried on the X chromosome as
contributing significantly to MS.

Consequently, Ebers and colleagues sought to identify genetic or
epigenetic factors related to MHC genes elsewhere in the genome that
might also have discrepant associations with gender.

The study showed that, depending on how the family members were
related, and on the genotype for a particular MS-associated MHC gene,
the female-to-male ratio of those with the disease differed markedly.

The female predominance was particularly great when affected members
of families had the HLA-DRB1*15 genotype.

There were also considerable differences in transmission of the
genotype from one generation to the next according to the
relationships between affected members.

When member pairs were related more directly -- parent-child or
sibling-sibling -- the odds of transmission across generations
appeared lower than when the family structure was "collateral,"
related as aunts-uncles-nieces-nephews or as cousins.

Within nuclear families, the odds ratio for HLA-DRB1*15 transmission
was 2.12, compared with 3.35 for the collateral families (P=0.0046 for
the comparison).

The odds of transmission also were greatest in both family types when
affected relative pairs were both female.

The findings, according to Ebers and colleagues, suggest that
"differential transmission of the same haplotype in families with
affected first-degree relatives versus those consisting of second- and
third-degree relatives reflects the inheritance of putative epigenetic
marks."

The researchers suggested that DNA methylation -- which can be
affected by environmental factors and is heritable -- could be the
"epigenetic mark" responsible for these effects, although they
acknowledged that supporting experimental data were still lacking.

In an accompanying editorial, a Mayo Clinic researcher pointed out
that epigenetics provide the only plausible mechanism that could
account for the onset of female predominance in MS.

"Given the rapidity of increase in the sex ratio, there does not seem
to be enough evolutionary time to spread a purely genetic risk, and
therefore [genomic-environmental interaction] seems to be the more
likely explanation," wrote Orhun Kantarci, MD, of Mayo's branch in
Rochester, Minn.

Ebers and colleagues noted that MHC genes are believed to be the
primary genetic drivers of other autoimmune diseases, such as systemic
lupus erythematosus and rheumatoid arthritis, that also affect far
more women than men.

Primary source: Neurology
Source reference:
Chao M, et al "MHC transmission: Insights into gender bias in MS
susceptibility" Neurology 2011; 76: 242–46.

Neurology. 2011 Jan 5. [Epub ahead of print]
MHC transmission: Insights into gender bias in MS susceptibility.
Chao MJ,
Ramagopalan SV,
Herrera BM,
Orton SM,
Handunnetthi L,
Lincoln MR,
Dyment DA,
Sadovnick AD,
Ebers GC.
From the Department of Clinical Neurology (M.J.C., S.V.R., B.M.H.,
S.M.O., L.H., M.R.L., D.A.D., G.C.E.), University of Oxford, John
Radcliffe Hospital, Oxford, UK; and Department of Medical Genetics and
Faculty of Medicine (A.D.S.), Division of Neurology, University of
British Columbia, Vancouver, Canada.

Abstract
OBJECTIVE:
Major histocompatibility complex (MHC) genes dominate genetic
susceptibility factors in multiple sclerosis (MS).
Given the general consensus that incidence and prevalence of MS has
been rising and specifically in women, we evaluated MHC-gender
interactions.

METHODS:
In a large family-based cohort consisting of 7,093 individuals (2,127
affected individuals) from 1,055 MS families, we examined MHC
transmission by family structure and gender stratified by genetic
distance of affected relatives from the MS proband.

RESULTS:
We found that affected individuals with HLA-DRB1*15-positive genotypes
have higher female-to-male ratios as compared with affected
individuals with HLA-DRB1*15-negative genotypes (χ(2) = 9.97, p =
0.0015) with the exception of multiplex families with 3 or more
affected across 2 generations.
Transmission disequilibrium test results show that HLA-DRB1*15
transmission was more distorted in collateral families vs nuclear
families (χ(2) = 8.030, p = 0.0046), exclusively in affected
female-female pairs (χ(2) = 7.81, p = 0.0051), but not in mixed gender
pairs (χ(2) = 1.58, p = 0.21) or matched male pairs (Fisher p = 0.21).

CONCLUSIONS:
These observations implicate the MHC as the site of interactions and
modifications mediating the female-to-male gender ratio in MS and its
progressive increase.
They further suggest this occurs via gene-environment interactions and
epigenetic modifications in this region.
The difference between collateral and nuclear families provides some
insight into the inheritance, decay, and gender specificity of
putative epigenetic marks.

PMID: 21209377

Additional source: Neurology
Source reference:
Kantarci O, "Sex-stratified inheritance of MS: New horizons from
studies in MHC region" Neurology 2011; 76: 210-12.

Neurology. 2011 Jan 5. [Epub ahead of print]
Sex-stratified inheritance of MS: New horizons from studies in MHC region.
Kantarci OH. kantarci.orhun@...
http://www.mayoclinic.org/bio/12971634.html
http://mayoresearch.mayo.edu/mayo/research/staff/Kantarci_OH.cfm
From the Department of Neurology, Mayo Clinic College of Medicine,
Rochester, MN.
PMID: 21209375
Orhun H. Kantarci, MD

The study was funded by the Multiple Sclerosis Society of Canada and
the Multiple Sclerosis Society of the United Kingdom.

Ebers reported relationships with Roche, UCB, and Bayer Schering.
Another author reported relationships with Bayer Canada, Teva, EMD
Serono, and Biogen Idec.
Other authors indicated they had no financial relationships with
commercial entities.

Kantarci reported research support from the Hilton Foundation and
other nonprofit organizations.


Congenital abnormalities and multiple sclerosis.
Ramagopalan SV,
Guimond C,
Criscuoli M,
Dyment DA,
Orton SM,
Yee IM,
Ebers GC,
Sadovnick D.
BMC Neurol. 2010 Nov 16;10:115.
PMID: 21080921 [PubMed - in process] Free Article

BMC Neurol. 2010 Nov 16;10:115.
Congenital abnormalities and multiple sclerosis.
Ramagopalan SV, Guimond C, Criscuoli M, Dyment DA, Orton SM, Yee IM,
Ebers GC, Sadovnick D.
Wellcome Trust Centre for Human Genetics, University of Oxford,
Oxford, OX3 7BN, UK.

Abstract

BACKGROUND:
There is a strong maternal parent-of-origin effect in determining
susceptibility to multiple sclerosis (MS).
One hypothesis is that an abnormal intrauterine milieu leading to
impaired fetal development could plausibly also result in increased
susceptibility to MS.
A possible marker for this intrauterine insult is the presence of a
non-fatal congenital anomaly.

METHODS:
We investigated whether or not congenital anomalies are associated
with MS in a population-based cohort.
We identified 7063 MS index cases and 2655 spousal controls with
congenital anomaly information from the Canadian Collaborative Project
on Genetic Susceptibility to MS (CCPGSMS).

RESULTS:
The frequency of congenital anomalies were compared between index
cases and controls.
No significant differences were found.

CONCLUSIONS:
Congenital anomalies thus do not appear to be associated with MS.
However, we did not have complete data on types and severity of
congenital anomalies or on maternal birth history and thus this study
should be regarded as preliminary.

PMID: 2108092

http://www.biomedcentral.com/1471-2377/10/115  free full text

Sreeram V Ramagopalan 1,2 ,  sreeramr@...
Colleen Guimond 3 ,
Maria Criscuoli 3 ,
David A Dyment 1,2 ,
Sarah-Michelle Orton 1,2 , ortons@...
Irene M Yee 3 ,
George C Ebers 1,2

http://www.well.ox.ac.uk/ebers/groupmembers.shtml
http://www.well.ox.ac.uk/ebers/  info@...
http://www.neuroscience.ox.ac.uk/directory/george-ebers
neuroscience@...
A. Dessa Sadovnick 3,4  sadovnik@...
http://www.labome.org/expert/dessa/a-dessa-sadovnick-362731.html
1  Wellcome Trust Centre for Human Genetics, University of Oxford,
Oxford, OX3 7BN, UK
2  Department of Clinical Neurology, University of Oxford, The West
Wing, The John Radcliffe Hospital, Oxford, OX3 9DU, UK
3  Department of Medical Genetics, University of British Columbia,
G920, Detwiller Pavilion, VCHA - UBC Hospital, 2211 Wesbrook Mall,
Vancouver, British Columbia, V6T 2B5, Canada
4  Faculty of Medicine, Division of Neurology, University of British
Columbia, G920, Detwiller Pavilion, VCHA - UBC Hospital, 2211 Wesbrook
Mall, Vancouver, British Columbia, V6T 2B5, Canada
_______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-819-7388 rmforall@...

http://groups.yahoo.com/group/AstroDeep/messages

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 119 members, 1,614 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1226 members, 24,225 posts in a public archive

http://groups.yahoo.com/group/rmforall/messages

participant, Santa Fe Complex www.sfcomplex.org
_______________________________________________

Perhaps instead of using the message that diet coke is unhealthy,
the message that it makes you fat would be better received: Allan Rydberg
2011.01.11

http://groups.yahoo.com/group/aspartameNM/message/1616

Here are 2 links to that effect:

http://www.ncbi.nlm.nih.gov/pubmed/20589192

http://www.ncbi.nlm.nih.gov/pubmed/21138816

Al

Paris aspartame conference 16 p in French 2011.01.21: Rich Murray 2011.01.22
http://rmforall.blogspot.com/2011_01_01_archive.htm
Saturday, January 22, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1615
[you may have to Copy and Paste URLs into your browser]
_______________________________________________


http://www.reseau-environnement-sante.fr/images/Conf/conference_aspartame.pdf

16 p in French 2011.01.21

Reseau-environnement-sante.fr

Pauline Berthellemy pberthellemy.res@...
06 11 41 13 54

Soleane Duplan res.contact@...
06 70 07 84 87
09 54 05 24 11


http://www.docteurlaurentchevallier.fr/
Dr. Laurent Chevallier
04 67 02 49 04
Clinique du Parc
Chemin des Guilhems
34171 Castelnau Le Lez
Paris, FR


http://fr.wikipedia.org/wiki/Andr%C3%A9_Cicolella
Andre Ciolella

Ann N Y Acad Sci. 2006 Sep;1076:784-9.
Glycol ethers: a ubiquitous family of toxic chemicals: a plea for
REACH regulation.
Cicolella A.
Health Risk Assessment Unit,
National Institute of Risks and Industrial Environment, INERIS
BP N 2, 60550 Verneuil-en-Halatte, France. andre.cicolella@...

Abstract
Glycol ethers (GE) are chemicals used since the 1930s as solvents in
paints, inks, varnishes, and cleaning agents, mainly in water-based
products, cosmetics, and drugs.
World production approximates 1 million tons.
Nineteen GE are produced or imported each year;
over 1000 tons in European Union (EU) have been classified as high
production volume chemicals (HPVCs).
First animal data were published in 1971 and 1979 showing severe
reprotoxicity for some GE.
Two alerts were launched in the United States in 1982 and 1983, but
the first partial GE regulation only occurred in 1993 in the EU.
Although these chemicals may expose a very large population, basic
toxicity data, more especially carcinogenicity, are still lacking
(3/32 GE).
However, experimental data were sufficient to lead developmental
toxicity risk assessment since the early 1980s.
Risk indices over 1000 have been calculated for consumers and workers
exposed to reprotoxic GE in domestic and industrial activities.
The first ban was decided in 1999 in France, but was only for drugs
and cosmetics.
Not surprisingly, since the late 1980s, human studies have found
results similar to those in animal data: spontaneous abortions,
malformations, testicular toxicity, and hematotoxicity.
Despite this highly coherent set of data, and although substitution
products are available, reprotoxic GE have been and still remain
widely used in the world.
The case of GE shows the failure of the present system based on a
posteriori risk assessment.
This pleads for the change of paradigm through the European REACH
regulation based on the "No data, no market" principle. Ethics in
REACH management should also be considered.
PMID: 17119255


Pierre Meneton pierre.meneton@...

Physiol Rev. 2005 Apr;85(2):679-715.
Links between dietary salt intake, renal salt handling, blood
pressure, and cardiovascular diseases.
Meneton P, Jeunemaitre X, de Wardener HE, MacGregor GA.
Institut National de la Santé et de la Recherche Médicale U367,
Département de Santé Publique et d'Informatique Médicale,
Faculté de Médecine Broussais Hôtel Dieu, Paris, France. pmeneton@...

Abstract
Epidemiological, migration, intervention, and genetic studies in
humans and animals provide very strong evidence of a causal link
between high salt intake and high blood pressure.
The mechanisms by which dietary salt increases arterial pressure are
not fully understood, but they seem related to the inability of the
kidneys to excrete large amounts of salt.
From an evolutionary viewpoint, the human species is adapted to ingest
and excrete <1 g of salt per day, at least 10 times less than the
average values currently observed in industrialized and urbanized
countries.
Independent of the rise in blood pressure, dietary salt also increases
cardiac left ventricular mass, arterial thickness and stiffness, the
incidence of strokes, and the severity of cardiac failure.
Thus chronic exposure to a high-salt diet appears to be a major factor
involved in the frequent occurrence of hypertension and cardiovascular
diseases in human populations.
PMID: 1578870


Generations-Futures.fr

http://www.menustoxiques.fr/

Francois Veillerette mdrgf@...

Nadine Lauverjat  mdrdf2@...


rutube.ru/tracks/3030623.html?v=0cafadccbd7419eb9726f63db7e4732b
news video in French 2010.03.14 4:20 19.72 MB


Claude Rene Lambre  claude.lambre@...
+33 1 40 56 79 29
http://ec.europa.eu/health/ph_risk/committees/sct/documents/cv_lambre_en.pdf


Andre Aschieri
http://fr.wikipedia.org/wiki/Andr%C3%A9_Aschieri

Woodrow Monte <woodymonte@...>,
andre.cicolella@..., pierre.meneton@...,
pberthellemy.res@..., res.contact@..., pierre.meneton@...,
mdrgf@...,
mdrgf2@..., claude.lambre@...,
_______________________________________________


re GC Ebers study, females harmed more by body making methanol into
formaldehyde in brain via ADH enzyme: 589 references, WC Monte,
retired Prof. Nutrition: Rich Murray 2011.01.08
http://rmforall.blogspot.com/2011_01_01_archive.htm
Saturday, January 8, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1614
[you may have to Copy and Paste URLs into your browser]
_______________________________________________


Woodrow C Monte, PhD, Emiritus Prof. Nutrition gives many PDFs of
reseach -- methanol (11% of aspartame) puts formaldehyde into brain
and body -- multiple sclerosis, Alzheimer's, cancers, birth defects,
headaches: Rich Murray 2010.05.13
http://rmforall.blogspot.com/2010_05_01_archive.htm
Thursday, May 13, 2010
http://groups.yahoo.com/group/aspartameNM/message/1601

[ Other formaldehyde sources include alcohol drinks and
tobacco and wood smoke,
while adequate folic acid levels protect most people. ]

http://whilesciencesleeps.com/about

589 references, many abstracts and full texts

Methanol: Where Is It Found? How Can It Be Avoided?

AVOID the following, ranked in order of greatest danger:

1. Cigarettes.
2. Diet foods and drinks with aspartame.
3. Fruit and vegetable products and their juices in bottles,
cans, or pouches.
4. Jellies, jams, and marmalades not made fresh and kept
refrigerated.
5. Black currant and tomato juice products, fresh or
processed.
6. Tomato sauces, unless first simmered at least 3 hours
with an open lid.
7. Smoked food of any kind, particularly fish and meat.
8. Sugar-free chewing gum.
9. Slivovitz: You can consume one alcoholic drink a day
on this diet -- no more! [ no fruit brandies ]
10. Overly ripe or near rotting fruits or vegetables.

Selection from Article 2, Fitness Life, December 2007, and
well discussed in the DVD video:

"Identical Symptoms of MS, Methanol Poisoning
and Aspartame Toxicity

The symptoms of multiple sclerosis (44, 83, 85, 169), chronic
and acute methanol poisoning (13, 144, 189), and Aspartame
toxicity (54, 58, 93, 181), are in all ways identical.

There is nothing that happens to the human body from the
toxic effect of methanol that has not been expressed during
the course of MS... nothing (143, 144).

This generalization extends even to the remarkable
opthomological conditions common to both: transitory optic
neuritis and retrolaminar demyelinating optic neuropathy with
scotoma of the central visual field (which occasionally
manifests as unilateral temporary blindness (85, 138, 163).

In fact, these opthomological symptoms have been thought of
for years in their respective literatures to be "tell tale"
indications for the differential diagnosis for each of these
maladies independently (85, 138, 148, 163, 169).

The common symptoms of
headache (13, 83, 181, 189),
nervousness (13, 83, 181),
depression (58, 83, 189, 181),
memory loss (18, 147, 85, 169, 181),
tingling sensations (13, 85, 168, 138, 169),
pain in the extremities (13, 85, 169),
optic neuritis (85, 138, 148, 163, 169),
bright lights in the visual field (139, 83),
seizures (21, 83, 160),
inability to urinate or to keep from urinating (139, 146, 167)
are all shared by each of these conditions and shared yet
again by complaints from aspartame poisoning
(54, 58, 93, 181).

I take these strikingly similar symptom patterns as evidence
that these disorders act on identical components of the
central nervous system and in the same way.

The "Miracle" that MS shares with Methanol poisoning

In the early stages of MS, or when a non-lethal dose of
methanol has been administered, complete recovery is a
possibility.

The only two afflictions for which such dramatic "remissions"
are reported from identical neuromuscular and opthomological
damage, even "blindness" is relapsing-remitting multiple
sclerosis (85) and methyl alcohol poisoning (138, 163).

The pathology of the two maladies is in may ways identical,
particularly when it comes to destruction of the myelin
sheath with no harm to the axon itself (18, 148, 176).

Sex Ratios for MS and Aspartame Reactions

Women bear the brunt of multiple sclerosis (91a-c) and lupus
(SLE)(73) with fully three-fold representations in infliction
numbers over men for both diseases.

This is exactly the proportion represented by adverse
reactors to Aspartame reported by the US Center for
Disease Control in their study of 1984 (58).

The Center found three women to every man whose
Aspartame consumption complaints were serious enough
to warrant investigation (93).

Although the female/male ratio for those stricken with MS has
always been high, recent estimates place it at over 3 to 1
(91, 91a, 91c).

What might account for the difference across sexes in
incidence?

A study published in the New England Journal of Medicine
(94) reports biopsies of the gastric lining of men and women.

A result was that the concentration of ADH in the
gastric lining of men was much higher than for woman.

Men have the advantage of removing methanol from the
bloodstream four times faster on an equal-body-size basis
than women.

Thus, for men, methanol is more likely to be removed from the
blood before it reaches the brain.

The brain is spared but the methanol removed would still be
metabolized to formaldehyde in the gut where it would reap
its havoc on a more forgiving organ.

This may help explain why men have more gastrointestinal
complaints from both methanol and Aspartame consumption
(93, 99).

On the other hand, women's complaints from both more
frequently involve serious neurological complications."...
_______________________________________________


methanol (11% of aspartame), made by body into
formaldehyde in many vulnerable tissues, causes modern
diseases of civilization, summary of a century of research,
Woodrow C Monte PhD, Medical Hypotheses journal:
Rich Murray 2009.11.15
http://rmforall.blogspot.com/2009_11_01_archive.htm
Sunday, November 15, 2009
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1589
[you may have to Copy and Paste URLs into your browser]


formaldehyde from 0.2 mg daily methanol from aspartame in Singulair
(montelukast) chewable asthma medicine causes severe allergic dermatitis in
boy, SE Jacob et al, Pediatric Dermatology 2009 Nov: Rich Murray 2010.09.27
http://rmforall.blogspot.com/2010_09_01_archive.htm
Monday, September 27, 2010
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1613
[you may have to Copy and Paste URLs into your browser]
_______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-819-7388 rmforall@...

http://groups.yahoo.com/group/AstroDeep/messages

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 119 members, 1,615 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1225 members, 24,246 posts in a public archive

http://groups.yahoo.com/group/rmforall/messages

participant, Santa Fe Complex www.sfcomplex.org
_______________________________________________

aspartame abstinance cures fibromyalgia chronic pain in 2 French
adults: R Ciappuccini et al, Clin Exp Rheumatol 2010 Nov: Rich Murray
2011.02.19
http://rmforall.blogspot.com/2011_02_01_archive.htm
Saturday, February 19, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1617
[you may have to Copy and Paste URLs into your browser]
_______________________________________________



Clin Exp Rheumatol. 2010 Nov-Dec;28(6 Suppl 63):S131-3. Epub 2010 Dec 22.
Aspartame-induced fibromyalgia, an unusual but curable cause of chronic pain.
Ciappuccini R,
Ansemant T,
Maillefert JF, <jean-francis.maillefert@...>,
Tavernier C,
Ornetti P.  <paul.ornetti@...>,
Department of Rheumatology, Dijon University Hospital,
Burgundy University, Faculty of Medicine, Dijon, France.
http://www.u-bourgogne.fr/

Abstract

We report for the first time an unusual musculoskeletal adverse effect
of aspartame in two patients.
A 50-year-old woman had been suffering from widespread pain and
fatigue for more than 10 years leading to the diagnosis of
fibromyalgia.
During a vacation in a foreign country, she did not suffer from
painful symptoms since she had forgotten to take her aspartame.
All of the symptoms reappeared in the days following her return when
she reintroduced aspartame into her daily diet.
Thus, aspartame was definitively excluded from her diet, resulting in
a complete regression of the fibromyalgia symptoms.

A 43-year-old man consulted for a 3-year history of bilateral forearm,
wrist, and hand and cervical pain with various unsuccessful
treatments.
A detailed questioning allowed to find out that he had been taking
aspartame for three years.
The removal of aspartame was followed by a complete regression of
pain, without recurrence.
We believe that these patients' chronic pain was due to the ingestion
of aspartame, a potent flavouring agent, widely used in food as a
calorie-saver.
The benefit/ risk ratio of considering the diagnosis of
aspartame-induced chronic pain is obvious:
the potential benefit is to cure a disabling chronic disease,
to spare numerous laboratory and imaging investigations, and
to avoid potentially harmful therapies;
the potential risk is to temporarily change the patient's diet.

Thus, practitioners should ask patients suffering from fibromyalgia
about their intake of aspartame.
In some cases, this simple question might lead to the resolution of a
disabling chronic disease.
PMID: 21176433
_______________________________________________


Paris aspartame conference 16 p in French 2011.01.21: Rich Murray 2011.01.22
http://rmforall.blogspot.com/2011_01_01_archive.htm
Saturday, January 22, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1615
[you may have to Copy and Paste URLs into your browser]


http://www.reseau-environnement-sante.fr/images/Conf/conference_aspartame.pdf

16 p in French 2011.01.21

Reseau-environnement-sante.fr

Pauline Berthellemy pberthellemy.res@...
06 11 41 13 54

Soleane Duplan res.contact@...
06 70 07 84 87
09 54 05 24 11


http://www.docteurlaurentchevallier.fr/
Dr. Laurent Chevallier
04 67 02 49 04
Clinique du Parc
Chemin des Guilhems
34171 Castelnau Le Lez
Paris, FR


http://fr.wikipedia.org/wiki/Andr%C3%A9_Cicolella
Andre Ciolella

Ann N Y Acad Sci. 2006 Sep;1076:784-9.
Glycol ethers: a ubiquitous family of toxic chemicals: a plea for
REACH regulation.
Cicolella A.
Health Risk Assessment Unit,
National Institute of Risks and Industrial Environment, INERIS
BP N 2, 60550 Verneuil-en-Halatte, France. andre.cicolella@...

Abstract
Glycol ethers (GE) are chemicals used since the 1930s as solvents in
paints, inks, varnishes, and cleaning agents, mainly in water-based
products, cosmetics, and drugs.
World production approximates 1 million tons.
Nineteen GE are produced or imported each year;
over 1000 tons in European Union (EU) have been classified as high
production volume chemicals (HPVCs).
First animal data were published in 1971 and 1979 showing severe
reprotoxicity for some GE.
Two alerts were launched in the United States in 1982 and 1983, but
the first partial GE regulation only occurred in 1993 in the EU.
Although these chemicals may expose a very large population, basic
toxicity data, more especially carcinogenicity, are still lacking
(3/32 GE).
However, experimental data were sufficient to lead developmental
toxicity risk assessment since the early 1980s.
Risk indices over 1000 have been calculated for consumers and workers
exposed to reprotoxic GE in domestic and industrial activities.
The first ban was decided in 1999 in France, but was only for drugs
and cosmetics.
Not surprisingly, since the late 1980s, human studies have found
results similar to those in animal data: spontaneous abortions,
malformations, testicular toxicity, and hematotoxicity.
Despite this highly coherent set of data, and although substitution
products are available, reprotoxic GE have been and still remain
widely used in the world.
The case of GE shows the failure of the present system based on a
posteriori risk assessment.
This pleads for the change of paradigm through the European REACH
regulation based on the "No data, no market" principle. Ethics in
REACH management should also be considered.
PMID: 17119255


Pierre Meneton pierre.meneton@...

Physiol Rev. 2005 Apr;85(2):679-715.
Links between dietary salt intake, renal salt handling, blood
pressure, and cardiovascular diseases.
Meneton P, Jeunemaitre X, de Wardener HE, MacGregor GA.
Institut National de la Santé et de la Recherche Médicale U367,
Département de Santé Publique et d'Informatique Médicale,
Faculté de Médecine Broussais Hôtel Dieu, Paris, France. pmeneton@...

Abstract
Epidemiological, migration, intervention, and genetic studies in
humans and animals provide very strong evidence of a causal link
between high salt intake and high blood pressure.
The mechanisms by which dietary salt increases arterial pressure are
not fully understood, but they seem related to the inability of the
kidneys to excrete large amounts of salt.
From an evolutionary viewpoint, the human species is adapted to ingest
and excrete <1 g of salt per day, at least 10 times less than the
average values currently observed in industrialized and urbanized
countries.
Independent of the rise in blood pressure, dietary salt also increases
cardiac left ventricular mass, arterial thickness and stiffness, the
incidence of strokes, and the severity of cardiac failure.
Thus chronic exposure to a high-salt diet appears to be a major factor
involved in the frequent occurrence of hypertension and cardiovascular
diseases in human populations.
PMID: 1578870


Generations-Futures.fr

http://www.menustoxiques.fr/

Francois Veillerette mdrgf@...

Nadine Lauverjat  mdrdf2@...


rutube.ru/tracks/3030623.html?v=0cafadccbd7419eb9726f63db7e4732b
news video in French 2010.03.14 4:20 19.72 MB


Claude Rene Lambre  claude.lambre@...
+33 1 40 56 79 29
http://ec.europa.eu/health/ph_risk/committees/sct/documents/cv_lambre_en.pdf


Andre Aschieri
http://fr.wikipedia.org/wiki/Andr%C3%A9_Aschieri

Woodrow Monte ,
andre.cicolella@..., pierre.meneton@...,
pmenetone@...,  pberthellemy.res@...,
res.contact@..., pierre.meneton@..., mdrgf@...,
mdrgf2@..., claude.lambre@...,
_______________________________________________


re GC Ebers study, females harmed more by body making methanol into
formaldehyde in brain via ADH enzyme: 589 references, WC Monte,
retired Prof. Nutrition: Rich Murray 2011.01.08
http://rmforall.blogspot.com/2011_01_01_archive.htm
Saturday, January 8, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1614
[you may have to Copy and Paste URLs into your browser]
_______________________________________________


Woodrow C Monte, PhD, Emiritus Prof. Nutrition gives many PDFs of
reseach -- methanol (11% of aspartame) puts formaldehyde into brain
and body -- multiple sclerosis, Alzheimer's, cancers, birth defects,
headaches: Rich Murray 2010.05.13
http://rmforall.blogspot.com/2010_05_01_archive.htm
Thursday, May 13, 2010
http://groups.yahoo.com/group/aspartameNM/message/1601

[ Other formaldehyde sources include alcohol drinks and
tobacco and wood smoke,
while adequate folic acid levels protect most people. ]

http://whilesciencesleeps.com/about

589 references, many abstracts and full texts

Methanol: Where Is It Found? How Can It Be Avoided?

AVOID the following, ranked in order of greatest danger:

1. Cigarettes.
2. Diet foods and drinks with aspartame.
3. Fruit and vegetable products and their juices in bottles,
cans, or pouches.
4. Jellies, jams, and marmalades not made fresh and kept
refrigerated.
5. Black currant and tomato juice products, fresh or
processed.
6. Tomato sauces, unless first simmered at least 3 hours
with an open lid.
7. Smoked food of any kind, particularly fish and meat.
8. Sugar-free chewing gum.
9. Slivovitz: You can consume one alcoholic drink a day
on this diet -- no more! [ no fruit brandies ]
10. Overly ripe or near rotting fruits or vegetables.

Selection from Article 2, Fitness Life, December 2007, and
well discussed in the DVD video:

"Identical Symptoms of MS, Methanol Poisoning
and Aspartame Toxicity

The symptoms of multiple sclerosis (44, 83, 85, 169), chronic
and acute methanol poisoning (13, 144, 189), and Aspartame
toxicity (54, 58, 93, 181), are in all ways identical.

There is nothing that happens to the human body from the
toxic effect of methanol that has not been expressed during
the course of MS... nothing (143, 144).

This generalization extends even to the remarkable
opthomological conditions common to both: transitory optic
neuritis and retrolaminar demyelinating optic neuropathy with
scotoma of the central visual field (which occasionally
manifests as unilateral temporary blindness (85, 138, 163).

In fact, these opthomological symptoms have been thought of
for years in their respective literatures to be "tell tale"
indications for the differential diagnosis for each of these
maladies independently (85, 138, 148, 163, 169).

The common symptoms of
headache (13, 83, 181, 189),
nervousness (13, 83, 181),
depression (58, 83, 189, 181),
memory loss (18, 147, 85, 169, 181),
tingling sensations (13, 85, 168, 138, 169),
pain in the extremities (13, 85, 169),
optic neuritis (85, 138, 148, 163, 169),
bright lights in the visual field (139, 83),
seizures (21, 83, 160),
inability to urinate or to keep from urinating (139, 146, 167)
are all shared by each of these conditions and shared yet
again by complaints from aspartame poisoning
(54, 58, 93, 181).

I take these strikingly similar symptom patterns as evidence
that these disorders act on identical components of the
central nervous system and in the same way.

The "Miracle" that MS shares with Methanol poisoning

In the early stages of MS, or when a non-lethal dose of
methanol has been administered, complete recovery is a
possibility.

The only two afflictions for which such dramatic "remissions"
are reported from identical neuromuscular and opthomological
damage, even "blindness" is relapsing-remitting multiple
sclerosis (85) and methyl alcohol poisoning (138, 163).

The pathology of the two maladies is in may ways identical,
particularly when it comes to destruction of the myelin
sheath with no harm to the axon itself (18, 148, 176).

Sex Ratios for MS and Aspartame Reactions

Women bear the brunt of multiple sclerosis (91a-c) and lupus
(SLE)(73) with fully three-fold representations in infliction
numbers over men for both diseases.

This is exactly the proportion represented by adverse
reactors to Aspartame reported by the US Center for
Disease Control in their study of 1984 (58).

The Center found three women to every man whose
Aspartame consumption complaints were serious enough
to warrant investigation (93).

Although the female/male ratio for those stricken with MS has
always been high, recent estimates place it at over 3 to 1
(91, 91a, 91c).

What might account for the difference across sexes in
incidence?

A study published in the New England Journal of Medicine
(94) reports biopsies of the gastric lining of men and women.

A result was that the concentration of ADH in the
gastric lining of men was much higher than for woman.

Men have the advantage of removing methanol from the
bloodstream four times faster on an equal-body-size basis
than women.

Thus, for men, methanol is more likely to be removed from the
blood before it reaches the brain.

The brain is spared but the methanol removed would still be
metabolized to formaldehyde in the gut where it would reap
its havoc on a more forgiving organ.

This may help explain why men have more gastrointestinal
complaints from both methanol and Aspartame consumption
(93, 99).

On the other hand, women's complaints from both more
frequently involve serious neurological complications."...
_______________________________________________


methanol (11% of aspartame), made by body into
formaldehyde in many vulnerable tissues, causes modern
diseases of civilization, summary of a century of research,
Woodrow C Monte PhD, Medical Hypotheses journal:
Rich Murray 2009.11.15
http://rmforall.blogspot.com/2009_11_01_archive.htm
Sunday, November 15, 2009
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1589
[you may have to Copy and Paste URLs into your browser]


formaldehyde from 0.2 mg daily methanol from aspartame in Singulair
(montelukast) chewable asthma medicine causes severe allergic dermatitis in
boy, SE Jacob et al, Pediatric Dermatology 2009 Nov: Rich Murray 2010.09.27
http://rmforall.blogspot.com/2010_09_01_archive.htm
Monday, September 27, 2010
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1613
[you may have to Copy and Paste URLs into your browser]
_______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-819-7388 rmforall@...

http://groups.yahoo.com/group/AstroDeep/messages

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 118 members, 1,617 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1226 members, 24,279 posts in a public archive

http://groups.yahoo.com/group/rmforall/messages

participant, Santa Fe Complex www.sfcomplex.org
_______________________________________________

Chemico-Biological Interactions, JA Bond, MA Medinsky, can share WC
Monte paradigm re harm by formaldehyde via ADH enzyme & methanol in
blood capillaries --  tobacco, wood smoke; dark wines, liquors;
aspartame; canned tomatoes: Rich Murray 2011.02.21
http://rmforall.blogspot.com/2011_02_01_archive.htm
Monday, February 21, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1618
[you may have to Copy and Paste URLs into your browser]
_______________________________________________


This would meet an urgent need to inform, heal, and protect people worldwide.

http://whilesciencesleeps.com/about  WC Monte paradigm

http://ees.elsevier.com/chembioint/
CBI private journal, Santa Fe, NM

http://www.santafenewmexican.com/Opinion/Their-View--James-A--Bond-and-Michele-A\
--Medinsky-Remember--the

Remember, the dose makes the poison The New Mexican
Posted: Saturday, February 19, 2011 [ standard aspartame PR... ]

[ More info from these sources is given at the end of this post. ]


aspartame abstinance cures fibromyalgia chronic pain in 2 French
adults: R Ciappuccini et al, Clin Exp Rheumatol 2010 Nov: Rich Murray
2011.02.19
http://rmforall.blogspot.com/2011_02_01_archive.htm
Saturday, February 19, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1617
[you may have to Copy and Paste URLs into your browser]


Clin Exp Rheumatol. 2010 Nov-Dec;28(6 Suppl 63):S131-3. Epub 2010 Dec
22.
Aspartame-induced fibromyalgia, an unusual but curable cause of
chronic pain.
Ciappuccini R,
Ansemant T,
Maillefert JF, <jean-francis.maillefert@...>,
Tavernier C,
Ornetti P.  <paul.ornetti@...>,
Department of Rheumatology, Dijon University Hospital,
Burgundy University, Faculty of Medicine, Dijon, France.
http://www.u-bourgogne.fr/

Abstract

We report for the first time an unusual musculoskeletal adverse effect
of aspartame in two patients.
A 50-year-old woman had been suffering from widespread pain and
fatigue for more than 10 years leading to the diagnosis of
fibromyalgia.
During a vacation in a foreign country, she did not suffer from
painful symptoms since she had forgotten to take her aspartame.
All of the symptoms reappeared in the days following her return when
she reintroduced aspartame into her daily diet.
Thus, aspartame was definitively excluded from her diet, resulting in
a complete regression of the fibromyalgia symptoms.

A 43-year-old man consulted for a 3-year history of bilateral forearm,
wrist, and hand and cervical pain with various unsuccessful
treatments.
A detailed questioning allowed to find out that he had been taking
aspartame for three years.
The removal of aspartame was followed by a complete regression of
pain, without recurrence.
We believe that these patients' chronic pain was due to the ingestion
of aspartame, a potent flavouring agent, widely used in food as a
calorie-saver.
The benefit/ risk ratio of considering the diagnosis of
aspartame-induced chronic pain is obvious:
the potential benefit is to cure a disabling chronic disease,
to spare numerous laboratory and imaging investigations, and
to avoid potentially harmful therapies;
the potential risk is to temporarily change the patient's diet.

Thus, practitioners should ask patients suffering from fibromyalgia
about their intake of aspartame.
In some cases, this simple question might lead to the resolution of a
disabling chronic disease.
PMID: 21176433
_______________________________________________


Paris aspartame conference 16 p in French 2011.01.21: Rich Murray
2011.01.22
http://rmforall.blogspot.com/2011_01_01_archive.htm
Saturday, January 22, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1615
[you may have to Copy and Paste URLs into your browser]


http://www.reseau-environnement-sante.fr/images/Conf/conference_aspartame.pdf

16 p in French 2011.01.21

Reseau-environnement-sante.fr

Pauline Berthellemy pberthellemy.res@...
06 11 41 13 54

Soleane Duplan res.contact@...
06 70 07 84 87
09 54 05 24 11


http://www.docteurlaurentchevallier.fr/
Dr. Laurent Chevallier
04 67 02 49 04
Clinique du Parc
Chemin des Guilhems
34171 Castelnau Le Lez
Paris, FR


http://fr.wikipedia.org/wiki/Andr%C3%A9_Cicolella
Andre Ciolella

Ann N Y Acad Sci. 2006 Sep;1076:784-9.
Glycol ethers: a ubiquitous family of toxic chemicals: a plea for
REACH regulation.
Cicolella A.
Health Risk Assessment Unit,
National Institute of Risks and Industrial Environment, INERIS
BP N 2, 60550 Verneuil-en-Halatte, France. andre.cicolella@...

Abstract
Glycol ethers (GE) are chemicals used since the 1930s as solvents in
paints, inks, varnishes, and cleaning agents, mainly in water-based
products, cosmetics, and drugs.
World production approximates 1 million tons.
Nineteen GE are produced or imported each year;
over 1000 tons in European Union (EU) have been classified as high
production volume chemicals (HPVCs).
First animal data were published in 1971 and 1979 showing severe
reprotoxicity for some GE.
Two alerts were launched in the United States in 1982 and 1983, but
the first partial GE regulation only occurred in 1993 in the EU.
Although these chemicals may expose a very large population, basic
toxicity data, more especially carcinogenicity, are still lacking
(3/32 GE).
However, experimental data were sufficient to lead developmental
toxicity risk assessment since the early 1980s.
Risk indices over 1000 have been calculated for consumers and workers
exposed to reprotoxic GE in domestic and industrial activities.
The first ban was decided in 1999 in France, but was only for drugs
and cosmetics.
Not surprisingly, since the late 1980s, human studies have found
results similar to those in animal data: spontaneous abortions,
malformations, testicular toxicity, and hematotoxicity.
Despite this highly coherent set of data, and although substitution
products are available, reprotoxic GE have been and still remain
widely used in the world.
The case of GE shows the failure of the present system based on a
posteriori risk assessment.
This pleads for the change of paradigm through the European REACH
regulation based on the "No data, no market" principle. Ethics in
REACH management should also be considered.
PMID: 17119255


Pierre Meneton pierre.meneton@...

Physiol Rev. 2005 Apr;85(2):679-715.
Links between dietary salt intake, renal salt handling, blood
pressure, and cardiovascular diseases.
Meneton P, Jeunemaitre X, de Wardener HE, MacGregor GA.
Institut National de la Santé et de la Recherche Médicale U367,
Département de Santé Publique et d'Informatique Médicale,
Faculté de Médecine Broussais Hôtel Dieu, Paris, France.
pmeneton@...

Abstract
Epidemiological, migration, intervention, and genetic studies in
humans and animals provide very strong evidence of a causal link
between high salt intake and high blood pressure.
The mechanisms by which dietary salt increases arterial pressure are
not fully understood, but they seem related to the inability of the
kidneys to excrete large amounts of salt.
From an evolutionary viewpoint, the human species is adapted to ingest
and excrete <1 g of salt per day, at least 10 times less than the
average values currently observed in industrialized and urbanized
countries.
Independent of the rise in blood pressure, dietary salt also increases
cardiac left ventricular mass, arterial thickness and stiffness, the
incidence of strokes, and the severity of cardiac failure.
Thus chronic exposure to a high-salt diet appears to be a major factor
involved in the frequent occurrence of hypertension and cardiovascular
diseases in human populations.
PMID: 1578870


Generations-Futures.fr

http://www.menustoxiques.fr/

Francois Veillerette mdrgf@...

Nadine Lauverjat  mdrdf2@...


rutube.ru/tracks/3030623.html?v=0cafadccbd7419eb9726f63db7e4732b
news video in French 2010.03.14 4:20 19.72 MB


Claude Rene Lambre  claude.lambre@...
+33 1 40 56 79 29
http://ec.europa.eu/health/ph_risk/committees/sct/documents/cv_lambre_en.pdf


Andre Aschieri
http://fr.wikipedia.org/wiki/Andr%C3%A9_Aschieri

"Woodrow C. Monte" <woodymonte@...>,
andre.cicolella@..., pierre.meneton@...,
pmenetone@...,  pberthellemy.res@...,
res.contact@..., pierre.meneton@..., mdrgf@...,
mdrgf2@..., claude.lambre@...,


re GC Ebers study, females harmed more by body making methanol into
formaldehyde in brain via ADH enzyme: 589 references, WC Monte,
retired Prof. Nutrition: Rich Murray 2011.01.08
http://rmforall.blogspot.com/2011_01_01_archive.htm
Saturday, January 8, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1614
[you may have to Copy and Paste URLs into your browser]


Woodrow C Monte, PhD, Emiritus Prof. Nutrition gives many PDFs of
reseach -- methanol (11% of aspartame) puts formaldehyde into brain
and body -- multiple sclerosis, Alzheimer's, cancers, birth defects,
headaches: Rich Murray 2010.05.13
http://rmforall.blogspot.com/2010_05_01_archive.htm
Thursday, May 13, 2010
http://groups.yahoo.com/group/aspartameNM/message/1601

[ Other formaldehyde sources include alcohol drinks and
tobacco and wood smoke,
while adequate folic acid levels protect most people. ]

http://whilesciencesleeps.com/about

http://while-science-sleeps.com/references/pdf/586
[ summary, not peer reviewed ]
Monte WC.
Methanol: A chemical Trojan horse as the root of the inscrutable U.
Medical Hypotheses 2010;74(3):493-6
DOI 2010.10.16

Monte WC.
Bittersweet: Aspartame Breast Cancer Link.
Fitness Life 2008 Jan. 34: 32-36

Monte WC.
A Deadly Experiment. Methanol and MS,
Fitness Life 2007 Dec. 34: 36-41

Monte WC.
Sickly Sweet: Is your Diet Sweetener killing you?
Fitness Life 2007 Nov. 33: 31-33

http://whilesciencesleeps.com/references
589 references for above articles and upcoming book

http://whilesciencesleeps.com/montediet
[ and Fitness Life 2007 Dec. 34: 36-41 ]

Methanol: Where Is It Found? How Can It Be Avoided?

AVOID the following, ranked in order of greatest danger:

1. Cigarettes.
2. Diet foods and drinks with aspartame.
3. Fruit and vegetable products and their juices in bottles,
cans, or pouches.
4. Jellies, jams, and marmalades not made fresh and kept
refrigerated.
5. Black currant and tomato juice products, fresh or
processed.
6. Tomato sauces, unless first simmered at least 3 hours
with an open lid.
7. Smoked food of any kind, particularly fish and meat.
8. Sugar-free chewing gum.
9. Slivovitz: You can consume one alcoholic drink a day
on this diet -- no more! [ no fruit brandies ]
10. Overly ripe or near rotting fruits or vegetables.

Selection from Article 2, Fitness Life, December 2007, and
well discussed in the DVD video:

"Identical Symptoms of MS, Methanol Poisoning
and Aspartame Toxicity

The symptoms of multiple sclerosis (44, 83, 85, 169), chronic
and acute methanol poisoning (13, 144, 189), and Aspartame
toxicity (54, 58, 93, 181), are in all ways identical.

There is nothing that happens to the human body from the
toxic effect of methanol that has not been expressed during
the course of MS... nothing (143, 144).

This generalization extends even to the remarkable
opthomological conditions common to both: transitory optic
neuritis and retrolaminar demyelinating optic neuropathy with
scotoma of the central visual field (which occasionally
manifests as unilateral temporary blindness (85, 138, 163).

In fact, these opthomological symptoms have been thought of
for years in their respective literatures to be "tell tale"
indications for the differential diagnosis for each of these
maladies independently (85, 138, 148, 163, 169).

The common symptoms of
headache (13, 83, 181, 189),
nervousness (13, 83, 181),
depression (58, 83, 189, 181),
memory loss (18, 147, 85, 169, 181),
tingling sensations (13, 85, 168, 138, 169),
pain in the extremities (13, 85, 169),
optic neuritis (85, 138, 148, 163, 169),
bright lights in the visual field (139, 83),
seizures (21, 83, 160),
inability to urinate or to keep from urinating (139, 146, 167)
are all shared by each of these conditions and shared yet
again by complaints from aspartame poisoning
(54, 58, 93, 181).

I take these strikingly similar symptom patterns as evidence
that these disorders act on identical components of the
central nervous system and in the same way.

The "Miracle" that MS shares with Methanol poisoning

In the early stages of MS, or when a non-lethal dose of
methanol has been administered, complete recovery is a
possibility.

The only two afflictions for which such dramatic "remissions"
are reported from identical neuromuscular and opthomological
damage, even "blindness" is relapsing-remitting multiple
sclerosis (85) and methyl alcohol poisoning (138, 163).

The pathology of the two maladies is in may ways identical,
particularly when it comes to destruction of the myelin
sheath with no harm to the axon itself (18, 148, 176).

Sex Ratios for MS and Aspartame Reactions

Women bear the brunt of multiple sclerosis (91a-c) and lupus
(SLE)(73) with fully three-fold representations in infliction
numbers over men for both diseases.

This is exactly the proportion represented by adverse
reactors to Aspartame reported by the US Center for
Disease Control in their study of 1984 (58).

The Center found three women to every man whose
Aspartame consumption complaints were serious enough
to warrant investigation (93).

Although the female/male ratio for those stricken with MS has
always been high, recent estimates place it at over 3 to 1
(91, 91a, 91c).

What might account for the difference across sexes in
incidence?

A study published in the New England Journal of Medicine
(94) reports biopsies of the gastric lining of men and women.

A result was that the concentration of ADH in the
gastric lining of men was much higher than for woman.

Men have the advantage of removing methanol from the
bloodstream four times faster on an equal-body-size basis
than women.

Thus, for men, methanol is more likely to be removed from the
blood before it reaches the brain.

The brain is spared but the methanol removed would still be
metabolized to formaldehyde in the gut where it would reap
its havoc on a more forgiving organ.

This may help explain why men have more gastrointestinal
complaints from both methanol and Aspartame consumption
(93, 99).

On the other hand, women's complaints from both more
frequently involve serious neurological complications."...
_______________________________________________


methanol (11% of aspartame), made by body into
formaldehyde in many vulnerable tissues, causes modern
diseases of civilization, summary of a century of research,
Woodrow C Monte PhD, Medical Hypotheses journal:
Rich Murray 2009.11.15
http://rmforall.blogspot.com/2009_11_01_archive.htm
Sunday, November 15, 2009
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1589
[you may have to Copy and Paste URLs into your browser]


formaldehyde from 0.2 mg daily methanol from aspartame in Singulair
(montelukast) chewable asthma medicine causes severe allergic
dermatitis in boy, SE Jacob et al, Pediatric Dermatology 2009 Nov:
Rich Murray 2010.09.27
http://rmforall.blogspot.com/2010_09_01_archive.htm
Monday, September 27, 2010
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1613
[you may have to Copy and Paste URLs into your browser]


http://old.library.georgetown.edu/newjour/c/msg03216.html

Chemico-Biological Interactions

Cynde Reid Gustafson wrote:
From: "Cynde Reid Gustafson" <nj@...>
Subject: Chemico-Biological Interactions
Date: Mon, 5 Nov 2001 19:43:12 -0500

Chemico-Biological Interactions
http://www.elsevier.com/locate/chembioint
Content available at:
http://www.sciencedirect.com/science/journal/00092797

Chemico-Biological Interactions publishes research reports and review
articles that examine the molecular, cellular, and/or biochemical basis of
toxicologically relevant outcomes.
Special emphasis is placed on mechanisms associated
with interactions between chemicals and biological systems.
Outcomes may include all traditional endpoints caused by synthetic or
naturally occurring chemicals, both in vivo and in vitro.
Endpoints of interest include, but are not limited to, carcinogenesis,
mutagenesis, respiratory toxicology, neurotoxicology,
reproductive and developmental toxicology, and immunotoxicology.

Subscribers have access to full-text articles.

Editor: James A. Bond, Ph.D.
Email: toxcon@...


http://www.santafenewmexican.com/Opinion/Their-View--James-A--Bond-and-Michele-A\
--Medinsky-Remember--the

Remember, the dose makes the poison The New Mexican
Posted: Saturday, February 19, 2011 - 2/20/11
0 Comments and 0 Reactions
        Email Share

In 1933, at his first inauguration, President Franklin D. Roosevelt
famously stated, "The only thing we have to fear is fear itself."
Although this statement was made in response to a bank panic in the
midst of the Great Depression, the same sentiment can describe what is
an overreaction to the common artificial sweetener, aspartame, which
was relayed in the Feb. 13 My View, "Gov. Martínez, take a stand for
consumer protection," by Stephen Fox.

Mr. Fox suggests that Gov. Martinez "might take further protective
actions about the terrible effects of aspartame."
We could not disagree more with this recommendation because it strikes
fear in the minds of people regarding the use of aspartame in consumer
products including soft drinks, Jell-O and gum.
As board-certified toxicologists, we consider the statements in the
article regarding aspartame toxicity such as, "aspartame ... a
poisonous substance," "terrible effects of aspartame" and "neurotoxic,
carcinogenic artificial sweetener" misleading and without scientific
basis.

We have no financial or other interest in aspartame.
Our interest derives from the desire to advise others against making
statements regarding the toxicity of materials, including aspartame,
without using sound scientific and toxicological principles.

The fundamental principle in the science of toxicology is "the dose
makes the poison." This principle was articulated by Paracelsus, a
15th-century physician, who stated "What is there that is not poison?"
What we find lacking in Mr. Fox's view is a discussion regarding dose.
Instead, there is the implicit assumption that any intake of
aspartame, however small, will have adverse health effects, including
cancer and neurological disorders.
Nothing could be further from the truth.

Aspartame is composed of two common amino acids, aspartic acid and
phenylalanine. Amino acids are the building blocks for proteins.
After ingestion, aspartame is broken down into these two amino acids
with the release of methanol.
Methanol is further transformed by the body into formaldehyde and formate.
The amount of methanol (and thus formaldehyde and formate) produced by
the breakdown of aspartame is less than what is in fruit or fruit
juices, where methanol occurs naturally.
It is true that at high doses methanol can cause blindness or even
death, but the levels of methanol that are produced after consuming
aspartame are hundreds of times lower than the doses of methanol that
cause toxicity.
High doses, poisonous; low doses, not poisonous.

Numerous regulatory agencies, including the FDA, have reviewed the
toxicological data on aspartame collected in laboratory animals and
people and have concluded that aspartame is not carcinogenic and is
safe at the Accepted Daily Intake level.
This is the amount of a substance that can be consumed every day over
a lifetime without any adverse effects.
The ADI for aspartame is 50 milligrams/kilogram of body weight, or the
equivalent of drinking 21 cans of diet soda daily for an average
adult.
The FDA also reviewed reports suggesting that aspartame is neurotoxic
and found them to be without merit.
We say to Gov. Martínez, yes, take a stand for consumer protection,
but focus on facts, not fear.

James A. Bond, Ph.D., and Michele A. Medinsky, Ph.D. are toxicology
consultants in Santa Fe.


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http://groups.yahoo.com/group/aspartameNM/message/846
aspartame in Merck Maxalt-MLT worsens migraine,
AstraZeneca Zomig, Eli Lilly Zyprexa,
J&J Merck Pepcid AC (Famotidine 10mg) Chewable Tab,
Pfizer Cool Mint Listerine Pocketpaks: Murray 2002.07.16

Migraine MLT-Down: an unusual presentation of migraine
in patients with aspartame-triggered headaches.
Newman LC, Lipton RB Headache 2001 Oct; 41(9): 899-901.
[ Merck 10-mg Maxalt-MLT, for migraine, has 3.75 mg aspartame,
giving 0.4 mg methanol,
while 12 oz diet soda has 200 mg, methanol 22 mg. ]
Headache Institute, St. Lukes-Roosevelt Hospital Center,
New York, NY
Department of Neurology newmanache@...
Albert Einstein College of Medicine, Bronx, NY
Innovative Medical Research RLipton@...


http://groups.yahoo.com/group/aspartameNM/message/855
Blumenthall & Vance: aspartame chewing gum headaches
Nov 1997: Murray 2002.07.28

Harvey J. Blumenthal, MD, Dwight A Vance, RPh
Chewing Gum Headaches. Headache 1997 Nov; 37(10): 665-6.
Department of Neurology, University of Oklahoma College of
Medicine, Tulsa, USA. neurotulsa@...
Aspartame, a popular dietetic sweetener, may provoke headache in
some susceptible individuals. Herein, we describe three cases of
young women with migraine who reported their headaches could be
provoked by chewing gum sweetened with aspartame.
[ 6-8 mg aspartame per stick chewing gum ]



older women drinking over 2 aspartame beverages weekly had 30% decline
kidney function in 11 years, Nurses Health Study, Julie Lin, Gary C Curhan,
Brigham and Women's Hospital, Boston: Rich Murray 2009.11.02
http://rmforall.blogspot.com/2009_11_01_archive.htm
Monday, November 2, 2009
http://groups.yahoo.com/group/aspartameNM/message/1588

[ over 400 mg aspartame/7 days = over 57 mg aspartame/day,
over 6 mg methanol/day ]

"Lin's team looked at the cumulative average beverage intake,
derived from food questionnaires completed in 1984, 1986,
and 1990.
The women replied whether they drank the beverages less than
once a month, one to four times a month, two to six times weekly,
once daily but less than twice, or twice a day or more often."

[ Aspartame, approved in the USA for beverages in July, 1983,
was by far the dominant artificial sweetener in beverages
in 1984 to 1990. ]

3,267 women, median age 67 in 2000, in Nurses Health Study:

"When the researchers compared kidney function of the women
in 1989 and 2000, they found that 11.4% or 372 women
had a kidney function decline of 30% or more.
When they looked at the diet information, they found that the 30%
decline in kidney function was associated with drinking two or more
artificially sweetened sodas a day.
This was true even after taking into account factors such as age,
high blood pressure, diabetes, and physical activity."... [ more ]



http://ees.elsevier.com/chembioint/

Editor-in-Chief

James A. Bond, Ph.D., DABT
25 Rabbitbrush Road, Santa Fe, NM 87506-7782, USA,
Fax: +1 505 988 1298, Tel: +1 505 988 1298,
Email: toxcon@...,
[ M. Medinski has the same phone number ]

Section Editors:

Enrique Cadenas
Department of Molecular Toxicology, School of Pharmacy, University of
Southern California (USC), 1985 Zonal Avenue- PSC 616, Los Angeles,
95616-8501, USA, Fax: +1 323 224 7473, Tel: +1 323 442 1418, Email:
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8701 Watertown Plank Road, Milwaukee, WI 53226, USA, Fax: +1 414 955
6651, Tel: +1 414 456 4322, Email: rhines@...

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In Vitro ADMET Laboratories LLC, Advanced Pharmaceutical Sciences,
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Inst. of Environmental Medicine, Division of Biochemical Toxicology,
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343849, Tel: +46 8 524 87574, Email: Ralf.Morgenstern@...

Minireviews Editor:

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Assistant Professor of Pharmacology, John A. Burns School of Medicine,
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Honolulu, HI 96813, USA, Fax: +1 808 692 1777, Tel: +1 808 692 1613,
Email: acollier@...


http://groups.yahoo.com/group/aspartameNM/message/1143
antiseptic? antifungal? antiviral? 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 rmforall

http://www.toxsci.oupjournals.org/cgi/content/full/64/2/169
free full text

A Biologically Based Dynamic Model for Predicting the Disposition
of Methanol and Its Metabolites in Animals and Humans.
Michèle Bouchard,
Robert C. Brunet,
Pierre-Olivier Droz,
and Gaétan Carrier.
Toxicological Sciences 64, 169-184 (2001)
Copyright © 2001 by the Society of Toxicology
[ extracts ]

"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).
[ It's unusual for a mainstream journal article to mention "fruits, fruit
juices, certain vegetables, aspartame sweetener" and "alcoholic
beverages" to be methanol sources.]
... little is known about the chronic effects of low exposure doses...
Systemic methanol is extensively metabolized by liver alcohol
dehydrogenase [ ADH ] and catalase-peroxidase enzymes to
formaldehyde, which is in turn rapidly oxidized to formic acid by
formaldehyde dehydrogenase enzymes...
Formaldehyde, as it is highly reactive, forms relatively stable adducts
with cellular constituents...
Primates and humans appear to be more susceptible to the acute
toxicity of methanol than rodents...
Although methanol has been reported to be metabolized mainly in
the liver, pulmonary metabolism is also likely to occur. Indeed,
the catalase-peroxidase system responsible for a major fraction of
methanol metabolism in rats is widely distributed in mammalian
tissues...
The model included a constant background whole body methanol
burden of 2.133 mmol, which corresponds to the mean blood
concentration of 0.5 mg/L of methanol measured by Osterloh et al.
(1996) in control subjects at the end of an 8-h frequent blood
sampling period...
... 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; Roe,
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...
Experimental studies on the detailed time profiles following
controlled repeated exposures to methanol are lacking...
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."

If we assume 30% retention of durable cumulative toxic products of
formaldehyde and formic acid, then a 12-oz can diet drink gives 200
mg aspartame, 22 mg methanol, and 7 mg formaldehyde and formic
acid at 30% cumulative retention. We may add that well known
sources of formaldehyde include both wood and tobacco smoke,
and, notoriously, mobile homes. Two teams give evidence that
formaldehyde and formic acid from methanol in ethanol drinks
(often far above the 100 mg/L methanol in red wines, two times the
level in aspartame drinks) are the main cause of the many symptoms
of "morning after" hangovers.

http://groups.yahoo.com/group/aspartameNM/message/1495
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

Furthermore, BM Kapur et al, 2007 give evidence that formic acid
from methanol in ethanol drinks is a major cause of Fetal Alcohol
Syndrome, readily preventable by adequate levels of folic acid,
which expedites the safe metabolism of formaldehyde, in most
people.
"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." ...
"MeOH concentrations between 4 and 4500 mg/l can be present
in various alcoholic beverages (Sprung et al., 1988)."


A variety of mutations, as well as aspirin and many painkillers,
impede folic acid. However, fruits and vegetables give enough folic
acid to mitigate harm from their methanol. Then again, formaldehyde
may in many people treat infections by fungi, bacteria, and virusus.
All these unexamined co-factors have confused attempts to study
aspartame toxicity for three decades.


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.


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

A widely proclaimed NIH-AARP mass survey by U Lim et al. 2006,
while failing to show specific cancers with feeble diet drink
consumption data for a year for seniors, did find that 4% of a
half-million seniors drank 3 and more cans daily diet soda
[ 12-oz can gives 200 mg aspartame, 22 mg methanol,
7 mg formaldehyde and formic acid at 30% cumulative retention ]

aspartame mg/d
0 ---- under 100 - 100-200 - 200-400 - 400-600 - 600-1200 -
cohort %
46 ------- 25 ------ 13 ------- 7 --------- 5 ------ about 3 ----

over 1200 mg/d
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.

The highest level 3400 mg aspartame [ 17 12-oz cans ] gives
11% = 374 mg methanol, 48 times the recommended daily limit of
consumption of 7.8 mg as recommended by the
Environmental Protection Agency (EPA).3

At 30% retention of cumulative toxic products of formaldehyde and
formic acid, these would be 125 mg, 60 times higher than the 1999
EPA alarm level for formaldehyde in daily drinking water of
1 ppm = 2 mg for average daily drinking water of 2 L daily.

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
40 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
______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-819-7388 rmforall@...

http://groups.yahoo.com/group/AstroDeep/messages

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 118 members, 1,618 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1226 members, 24,280 posts in a public archive

http://groups.yahoo.com/group/rmforall/messages

participant, Santa Fe Complex www.sfcomplex.org
______________________________________________

careful expert lifetime study on mice shows liver and lung cancers
from aspartame, M Soffritti et al, Ramazzini Institute, Italy, checked
by US National Toxicology Program experts, confirms many previous
studies from 2001 on: Rich Murray 2011.02.27
http://rmforall.blogspot.com/2011_02_01_archive.htm
Sunday, February 27, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1619
[you may have to Copy and Paste URLs into your browser]
_______________________________________________


"CONCLUSIONS

The present study demonstrates for the �rst time that APM administered
in feed to Swiss mice at doses of 32,000, 16,000, 8,000, 2,000, or 0
ppm, starting the dietary exposure on day 12 of gestation and lasting
until death, induces signi�cant dose-related increases of
hepatocellular carcinomas (P<0.01) and of alveolar/bronchiolar
carcinomas (P<0.05) in males.
In particular, the signi�cant increased incidences of hepatocellular
carcinomas were observed at the dietary levels of 32,000 ppm (P<0.01)
and 16,000 ppm (P<0.05) and of lung alveolar/bronchiolar carcinomas at
32,000 ppm (P<0.05).
HCA and HCC (combined) resulted signi�cantly increased (P<0.05) in the
male group treated at 16,000 ppm.
A/BA and A/BC (combined) resulted signi�cantly increased (P<0.05) in
the male group treated at 32,000 ppm.
A signi�cant dose-related trend (P<0.05) was also observed.

Given that APM is completely metabolized in the gastrointestinal tract
to phenylalanine, aspartic acid, and methanol, it may be concluded
that the observed carcinogenic effects were caused not by APM itself
but rather by its metabolites.

In particular, it cannot be disregarded that the conversion of APM
methanol into formaldehyde in the liver may result in a generation of
formaldehyde adducts [Trocho et al., 1998], which could explain the
plausibility of hepatocarcinogenic effects of APM in male mice.

The fact that females did not develop a signi�cantly increased
incidence of liver tumors may be explained by the gender resistance,
as already reported.

On the basis of these results, together with previous carcinogenicity
bioassays conducted on rats in our laboratories, APM should be
considered a multiple site, transspecies carcinogenic agent.

A re-evaluation of the current regulations on APM remains, in our
opinion, urgent.

ACKNOWLEDGMENTS

This research was supported entirely by the Ramazzini Institute.
The authors declare that they have no competing �nancial interests.
The authors thank Dr. David Hoel for his great support in the
statistical evaluation of the results.
A special thanks to the U.S. National Toxicology Program for having
organized a meeting of a group of pathologists at NIEHS in order to
provide a second opinion regarding the pathological lesions observed
in the APM Swiss mice study.
Ten pathologists participated in the NTP histopathology review.
The number of slides reviewed was 100 of which 26 were the subject of
discussion.
In the remaining cases, the original Ramazzini Institute diagnoses
were con�rmed.
The lesions reviewed were liver adenomas/carcinomas and angiosarcomas;
lung adenomas/carcinomas; lymphomas; skin �brosarcomas; and a few
miscellaneous lesions.

With regard to the data presented in this manuscript (liver and lung
tumors) there were no discrepancies between NTP and RI pathology
evaluation."


http://www.ncbi.nlm.nih.gov/pubmed/20886530

Am J Ind Med. 2010 Sep 30. [Epub ahead of print]
Aspartame administered in feed, beginning prenatally through life span,
induces cancers of the liver and lung in male Swiss mice.
Soffritti M, Belpoggi F, Manservigi M, Tibaldi E, Lauriola M, Falcioni L, Bua L.
Cesare Maltoni Cancer Research Center, Ramazzini Institute,
Bentivoglio, Bologna, Italy.
Morando Soffritti MD,
Fiorella Belpoggi DBS,
Marco Manservigi DBS,
Eva Tibaldi DBS,
Michelina Lauriola PhD,
Laura Falcioni DVM,
Luciano Bua MD
Article first published online: 30 SEP 2010
DOI: 10.1002/ajim.20896
Copyright © 2010 Wiley-Liss, Inc.

Abstract

BACKGROUND:
Aspartame (APM) is a well-known intense artificial sweetener used in more
than 6,000 products.
Among the major users of aspartame are children and women of childbearing
age.
In previous lifespan experiments conducted on Sprague-Dawley rats we have
shown that APM is a carcinogenic agent in multiple sites and that its
effects are increased when exposure starts from prenatal life.
OBJECTIVE:
The aim of this study is to evaluate the potential of APM to induce
carcinogenic effects in mice.
METHODS:
Six groups of 62-122 male and female Swiss mice were treated with APM in
feed at doses of 32,000, 16,000, 8,000, 2,000, or 0 ppm from prenatal life
(12 days of gestation) until death.
At death each animal underwent complete necropsy and all tissues and organs
of all animals in the experiment were microscopically examined.
RESULTS:
APM in our experimental conditions induces in males a significant
dose-related increased incidence of hepatocellular carcinomas (P<0.01),
and a significant increase at the dose levels of 32,000 ppm (P<0.01) and
16,000 ppm (P<0.05).
Moreover, the results show a significant dose-related increased incidence of
alveolar/bronchiolar carcinomas in males (P<0.05),
and a significant increase at 32,000 ppm (P<0.05).
CONCLUSIONS:
The results of the present study confirm that APM is a carcinogenic agent in
multiple sites in rodents,
and that this effect is induced in two species,
rats (males and females) and mice (males).
No carcinogenic effects were observed in female mice.
Am. J. Ind. Med. © 2010 Wiley-Liss, Inc.
PMID: 20886530

American Journal of Industrial Medicine
Copyright © 2010 Wiley-Liss, Inc., A Wiley Company
Edited by: Steven B. Markowitz
Impact Factor: 1.721
ISI Journal Citation Reports © Ranking: 2009: 59/122 (Public Environmental &
Occupational Health)
Online ISSN: 1097-0274

Recently Published Issues
Current Issue: November 2010  Volume 53, Issue 11
October 2010  Volume 53, Issue 10
September 2010 Volume 53, Issue 9

Abbreviations:
APM, aspartame;
CMCRC/RI, Cesare Maltoni Cancer Research Center/Ramazzini Institute;
EFSA, European Food Safety Authority;
EU, European Union;
FDA, Food and Drug Administration.

Cesare Maltoni Cancer Research Center, Ramazzini Institute,
Bentivoglio, Bologna, Italy
Contract grant sponsor: Ramazzini Institute.
*Correspondence to: Morando Soffritti, Cesare Maltoni Cancer Research
Center, Ramazzini Institute, Castello di Bentivoglio,Via Saliceto, 3,
40010 Bentivoglio, Bologna, Italy. E-mail: soffrittim@...
Accepted 30 July 2010
DOI 10.1002/ajim.20896.
Published online 30 September 2010 in Wiley Online Library
(wileyonlinelibrary.com)

...APM is metabolized in the gastrointestinal tract by esterases and
peptidases into three components: the amino acids phenylanine and
aspartic acid, and methanol [Ranney et al., 1976].

APM can be also absorbed into the mucosal cells prior to hydrolysis
and then metabolized within the cell to its three components which
then enter circulation [Mattews, 1984].

Methanol is not subject to metabolism within the enterocyte and
rapidly enters the portal circulation and is oxidized in the liver to
formaldehyde, an highly reactive chemical which strongly binds to
proteins [Haschemeyer and Haschemeyer, 1973] and nucleic acids
[Metzler, 1977] forming formaldehyde adducts.

In a study, in which APM, 14 C-labeled in the methanol carbon, was
given orally to adult male Wistar rats for 10 days, it was shown that
the carbon adducts of protein and DNA could have been generated only
from formaldehyde derived from APM methanol.
Moreover, it was suggested that the amount of formaldehyde adducts may
be cumulative [Trocho et al., 1998].

Several reviews conclude that APM is digested in all species in the
same way [Ranney et al., 1976].
Since APM is metabolized before entering the blood stream, there is no
distribution of APM outside the gastrointestinal tract.

Epidemiological studies conducted among users of arti�cial sweeteners
(including APM) did not show an increased carcinogenic risk, except in
one study which postulated an association of increased risk of brain
cancer and use of APM [Olney et al., 1996].

Studies performed by the US National ToxicologyProgram (NTP) in which
groups of 15 males and 15 females of transgenic mice, p53
haploinsuf�cient strain (p53) and Tg.AC homozygous strain (Tg.AC)
dermal exposure model were treated with diets containing 0, 3, 125,
6,250, 12,500, 25,000, or 50,000 ppm of APM for 40 weeks and then
sacri�ced did not show any carcinogenic responses [NTP, 2005].
Overall there was no evidence of a positive response for tumors in
animals treated with APM in feed up to 50,000 ppm.
Although the studies did not show carcinogenic response, it should be
noted that altered genetic mice were evaluated by NTP with the intent
to develop faster, less costly and more predictive in vivo models for
identifying potential chemical carcinogenic agents and that APM was
selected as a presumed non-carcinogen.
Pritchard et al. [2003] evaluated the NTP �ndings regarding the
potential of transgenic mouse models to identify carcinogenic agents.
The authors concluded that the Tg.AC dermal exposure model and p53
oral exposure model had an overall accuracy of 74% in correctly
predicting chemicals that are listed by the International Agency for
Research on Cancer (IARC) and/or NTP in their respective lists of
chemicals classi�ed carcinogenic or probably carcinogenic in humans.
The study concluded that the transgenic mouse models missed a number
of known or probable human carcinogens, whereas long-term rodent
bioassays missed none of these chemicals.

Indeed, the authors of the studies performed by NTP concluded that the
negative �ndings were of uncertain value:
‘‘because this is a new model, there is uncertainty whether the
(aspartame) study possessed suf�cient sensitivity to detect a
carcinogenic effect’’ [NTP, 2005].
In fact the P53 de�cient transgenic model does not respond to
non-genotoxic carcinogenic chemicals, and hence choosing that model
con�rmed this fact with APM.
The NTP has since virtually discontinued the use of genetically
modi�ed models for identifying carcinogens.

Long-term carcinogenicity bioassays performed on rats and mice in the
early 1970s by industry did not show any carcinogenic effects.
In female p53 haploinsuf�cient mice, the results of the micronucleus
test were judged to be positive, based on a signi�cant trend test and
a small but statistically signi�cant increased frequency of
micronucleated erythrocytes in the 50,000 ppm group
(P=0.028) [NTP, 2005].

A detailed review and comments on the genotoxicity, long-term
carcinogenicity studies in rodents and epidemiological studies
available today on APM has been reported previously [Soffritti et al.,
2005, 2006, 2007].
Overall, we believe that the potential long-term toxic effects of APM,
and in particular the carcinogenic effects, had not been adequately
demonstrated by the long-term bioassays on rats and mice, mainly
because of the small number of animals used per sex per group and the
duration of the experiments (in which rodents were sacri�ced at 110
weeks of age, corresponding to the two-thirds of the lifespan).

For these reasons we started a project encompassing several
experiments on rats and mice in which APM was administered in feed at
various doses to a large number of rats or mice per group per sex.
Treatment started at different ages and lasted for different periods;
rodents were always kept under observation until natural death to
allow APM to express all its full carcinogenic potential.

In the �rst experiment we demonstrated that APM, administered from 8
weeks of age for the lifespan to Sprague–Dawley rats, induced a
signi�cantly increased incidence of lymphomas/leukemias and of
neoplastic lesions of the renal pelvis and ureter in females, and a
signi�cantly increased incidence of malignant Schwannomas of the
peripheral nerves in males [Soffritti et al., 2006].

In a second experiment we showed that APM, administered from fetal
life until natural death, caused lymphomas/leukemias in male and
female rats and, for the �rst time, cancers of the mammary glands in
females [Soffritti et al., 2007].
Furthermore, this study demonstrated that when lifespan exposure
starts during fetal life, the incidences of lymphomas/leukemias were
increased in comparison to the treatment starting postnatally.
Neither cranial Schwannomas nor neoplasms of the renal pelvis and
ureter were observed in the second experiment.
This result may be explained by the fact that the number of rats per
sex per group in this study was lower and therefore the sensitivity of
the study for this type of tumors may have been reduced....

.... APM was pulverized in a standard pelleted diet at concentrations of
0, 2,000, 8,000, 16,000, or 32,000
to simulate an assumed daily APM intake of
0, 250, 1,000, 2,000, and 4,000 mg/kg b.w.,
and was administered to groups of 62–122 male and female Swiss mice
from the 12th day of fetal life until death.
The dose levels of APM were chosen on the basis of available data
reported in the literature.
The standard ‘‘Corticella diet’’ was provided by Laboratorio Dottori
Piccioni, Milan, Italy;
the same diet used for more than 30 years at the laboratory of the
Cesare Maltoni Cancer Research Center (CMCRC).
Fresh tap water was provided daily.
The major constituents of the diet were: water 12%; raw protein 24%;
raw fat 3.50%; raw �bers 5.50%; ashes 10.50%; non-nitrogenous extracts
56.50%.
The diet was analyzed for nutritional components, microorganisms, and
possible contaminants (pesticides, metals, estrogen activity,
nitrosamines, and aflatoxins) every 6 months, and disposed of if older
than 3 months from the date of manufacture.
The diet was formulated every 40–50 days.
At room temperature APM is stable in food and liquid.
The stability of APM in the feed was analyzed periodically during the
experiment.
Feed and water were supplied ad libitum.....

...DISCUSSION
The present study, in which APM was administered in feed at the dose
levels of 0, 2,000, 8,000, 16,000, or 32,000 ppm to Swiss mice from
prenatal life until death, further con�rms that APM induces
carcinogenic effects in rodents.
The study shows:
(a) signi�cant dose-related increase of hepatocellular carcinomas in
males (P<0.01).
Incidences were also signi�cantly increased at the two top dietary
concentrations of 32,000 ppm (P<0.01) and 16,000 ppm (P<0.05);
(b) a signi�cant dose-related increase of the incidence of lung
alveolar/bronchiolar carcinomas (P<0.01), and at 32,000 ppm (P<0.05).
Since the survival of the males was not affected by APM exposure, we
used logistic analysis to evaluate the combined adenoma/carcinoma
results of the liver and of the lung.
The incidence of HCA and HCC combined resulted signi�cantly increased
(P<0.05) in the group treated at 16,000 ppm.
No signi�cant dose–response was observed.
The reason for the lack of signi�cance is that the dose–response is
flat over the exposure groups while the controls are lower (i.e., 12.8,
21.4, 21.0, 25.0, and 20.5).
It is noticeable that until 98 weeks of age 8/55 deceased males
(14.6%) treated at 32,000 ppm had HCC and no HCA.
On the contrary, three HCA and no HCC were observed among the 60
controls deceased in the same period.
This may depend on a more rapid progression of preneoplastic lesions to HCC.
However, others suggest that the response to carcinogens differ, and
that both HCA and HCC may develop de novo, without going through the
stage of foci of cellular alterations [Frith et al., 1979].
A signi�cant dose-related trend (P<0.05) of A/BA and A/BC combined
was observed among males.
Moreover, the incidence of A/BA plus A/BC in males treated at 32,000
ppm was signi�cantly increased (P<0.05) compared to controls.

Both liver and lung carcinomas in all exposure groups of males were
within the historical control range of these neoplasms in the CMCRC
laboratory.

Concerning the HCC, the concurrent control (5.1%) falls within the
lower range of our historical controls (0–26.3%) and because the
incidences of HCC in the groups treated at 32,000 (18.1%) and 16,000
(15.6%) were over three and two times the concurrent control, we
considered this effect related to the treatment.

Concerning A/BC, the concurrent  control (6.0%) falls also within the
lower range of our
historical controls (0–14.3%) and because the incidence observed at
the highest dose was more than double the concurrent control we
considered these effects to be related
to APM exposure [Haseman et al., 1984; Haseman, 1992, 1995].

No differences were observed in the incidences of liver and lung
tumors among the females of treated and control groups.
It has been reported that both spontaneously occurring and treatment
induced hepatocellular tumors occur with signi�cantly greater
frequency and multiplicity in males
than in females even though occasionally exceptions do occur [Maronpot, 2009].
Male mice are also more susceptible to develop A/BA and A/BC than
females [Hahn et al., 2007; Dixon et al., 2008].

The carcinogenic effects observed in our mouse bioassay do not support
the negative outcome obtained with the CD-1 mouse study performed at
the Searle Laboratory in 1974 [Molinary, 1984].
In that experiment one group of 72 male and female CD-1 mice (control)
and three groups of 32 males and 32 females were treated,
respectively, with APM in feed at the dose levels of 0, 1, 2, 4 g/kg
from prenatal life for 2 years.
These studies are not comparable for two reasons:
(a) the number of the treated animals per sex per group is smaller in
comparison to the number in our experiment and to the number requested
by the current standard for carcinogenic bioassays (at least 50
animals per sex per group) used by NTP
and most others and
(b) the length of observation is much shorter (110 weeks compared to
130 weeks).
Both of these factors result in a loss of sensitivity for detecting a
carcinogenic effect.

As already reported [Soffritti et al., 1999; Haseman et al., 2001;
Huff et al., 2008; Soffritti et al., 2008], in longterm
carcinogenicity bioassays the number of animals per sex/group and life
span observation are critical points for identi�cation and assessment
of diffuse carcinogenic risks, de�ned as the exposure to a single or
multiple agents or to mixtures that are expected to have limited
carcinogenic potential because of the agent type (weak carcinogen)
and/or dose/concentration (low), but that involve large group of the
population (as is the case with APM).

Concerning the prolonged (over 110 weeks of age) or lifespan duration
of the experiment, we must consider that neoplastic response depends
not only on the chemical–physical characteristics of the agent and its
toxicological properties, the mode of exposure, and the type of
animals, but also, to a greater extent, on the latency of the tumor
which varies and may be very long.
Truncating an experiment after 2 years (more or less two-thirds of the
natural life of rodents) as requested by several regulatory agencies
(and as practiced by NTP), may mask a possible carcinogenic response.
This has been shown by us in experiments on benzene, Mancozeb (a
widely used fungicide), vinyl acetate, toluene, and xylenes [Soffritti
et al., 2002].
It should be noted that in the experiment on toluene and xylenes
performed by NTP, in which the rats were sacri�ced after 104 weeks of
treatment, no carcinogenic effects were found [Huff, 2002, 2003; Huff
et al., 2010], whereas lifetime studies conducted in the CMCRC showed
unequivocal carcinogenicity after 104 weeks [Maltoni et al., 1997;
Soffritti et al., 2004].
These two factors in our opinion makes the Searle study less sensitive
than ours.

Overall, the results of our integrated project of lifespan
carcinogenic bioassays on APM conducted on Sprague–Dawley rats and
Swiss mice are consistent in showing that under our experimental
conditions APM must be considered a trans-species carcinogenic agent
in multiple sites (Table V), inducing a signi�cantly increased
incidence of malignant tumors in:
(a) multiple tissues in male and female rats;
(b) multiple organs in male mice;
(c) an earlier occurrence in treated animals and an higher incidence
and an anticipated onset of cancers when the treatment starts from
fetal life [Soffritti et al., 2007].

Finally, the carcinogenic effects of APM in rats were shown also at
dose levels of 100 and 20 mg/kg b.w. to which humans could be exposed
[Soffritti et al., 2006, 2007].

CONCLUSIONS

The present study demonstrates for the �rst time that APM administered
in feed to Swiss mice at doses of 32,000, 16,000, 8,000, 2,000, or 0
ppm, starting the dietary exposure on day 12 of gestation and lasting
until death, induces signi�cant dose-related increases of
hepatocellular carcinomas (P<0.01) and of alveolar/bronchiolar
carcinomas (P<0.05) in males.
In particular, the signi�cant increased incidences of hepatocellular
carcinomas were observed at the dietary levels of 32,000 ppm (P<0.01)
and 16,000 ppm (P<0.05) and of lung alveolar/bronchiolar carcinomas at
32,000 ppm (P<0.05).
HCA and HCC (combined) resulted signi�cantly increased (P<0.05) in the
male group treated at 16,000 ppm.
A/BA and A/BC (combined) resulted signi�cantly increased (P<0.05) in
the male group treated at 32,000 ppm.
A signi�cant dose-related trend (P<0.05) was also observed.

Given that APM is completely metabolized in the gastrointestinal tract
to phenylalanine, aspartic acid, and methanol, it may be concluded
that the observed carcinogenic effects were caused not by APM itself
but rather by its metabolites.

In particular, it cannot be disregarded that the conversion of APM
methanol into formaldehyde in the liver may result in a generation of
formaldehyde adducts [Trocho et al., 1998], which could explain the
plausibility of hepatocarcinogenic effects of APM in male mice.

The fact that females did not develop a signi�cantly increased
incidence of liver tumors may be explained by the gender resistance,
as already reported.

On the basis of these results, together with previous carcinogenicity
bioassays conducted on rats in our laboratories, APM should be
considered a multiple site, transspecies carcinogenic agent.

A re-evaluation of the current regulations on APM remains, in our
opinion, urgent.

ACKNOWLEDGMENTS

This research was supported entirely by the Ramazzini Institute.
The authors declare that they have no competing �nancial interests.
The authors thank Dr. David Hoel for his great support in the
statistical evaluation of the results.
A special thanks to the U.S. National Toxicology Program for having
organized a meeting of a group of pathologists at NIEHS in order to
provide a second opinion regarding the pathological lesions observed
in the APM Swiss mice study.
Ten pathologists participated in the NTP histopathology review.
The number of slides reviewed was 100 of which 26 were the subject of
discussion.
In the remaining cases, the original Ramazzini Institute diagnoses
were con�rmed.
The lesions reviewed were liver adenomas/carcinomas and angiosarcomas;
lung adenomas/carcinomas; lymphomas; skin �brosarcomas; and a few
miscellaneous lesions.

With regard to the data presented in this manuscript (liver and lung
tumors) there were no discrepancies between NTP and RI pathology
evaluation.

A special thanks to Luana De Angelis and to all the CRCCM staff who
were involved in the study.

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_______________________________________________


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
[ Extract ]

... 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.....


http://www.ramazzini.it/ricerca/blogDetail.asp?id=31

April 02, 2009
Hazard Assessment deadline for science re aspartame (methanol,
formaldehyde, formic acid) toxicity California Office of Environmental
Health Hazard Assessment deadline May 5 for science re aspartame
(methanol, formaldehyde, formic acid) toxicity --  folic acid protects:
Stephen Fox: Rich Murray 2009.03.24
http://rmforall.blogspot.com/2009_03_01_archive.htm
Tuesday, March 24, 2009
http://groups.yahoo.com/group/aspartameNM/message/1571

http://www.opednews.com/populum/diarypage.php?did=12485#

March 11, 2009 at 23:10:52

California Opens Proposition 65 File, Could Lead to aspartame State
Suits re: Carcinogenic Properties

Diary Entry by Stephen Fox.....

http://www.ramazzini.it/ricerca/newsDetail.asp?id=25

news archive|archivio notizie
overview/sommario
November 15, 2008
EHP: limits of bioassay exposure regimens
EHP commentary argues the limits of 2-year bioassay exposure regimens:
Ramazzini lifespan studies aspartame and toluene cited.

In a recent commentary entitled "The limits of 2-Year Bioassay
Exposure Regimens for Identifying Chemical Carcinogens"Environ Health
Perspect 116:11, 2008, authors James Huff, Devra Davis and Michael
Jacobson argue that the sensitivity of chemical carcinogenesis
bioassays would be enhanced by exposing rodents beginning in utero and
continuing for 30 months (130 weeks) or until their natural deaths at
up to about 3 years.
Citing lifespan studies conducted by the European Ramazzini Foundation on
aspartame and toluene the authors conclude that observing rodents
until their natural deaths (i.e the Ramazzini lifespan model)
increases the sensitivity of bioassays, avoids false-negative results,
and strengthens the value and validity of results for regulatory
agencies.


http://www.ramazzini.it/istituto/staff.asp

http://www.ramazzini.it/centro_di_saggio/aboutus.asp

About us

The EEL of the Ramazzini Institute is a Contract Research Organisation
specialized in non-clinical toxicological studies required for international
Drug Registration and Notification of Chemical Substances, founded in 2009,
sited in Bentivoglio (Bologna), Italy.

Since 2009, the EEL has been subject to regular GLP inspection by Italian
authorities and on February 2010 received the certificate of working in
compliance with the GLP standards.

Research Expertise:

Repeated Dose Toxicity Studies
Chronic Toxicity and Carcinogenicity Studies
Toxicokinetics Studies (only the in vivo phase)
Expertise Services:
Biophase (in vivo phase)
Pathology: Gross Necropsy, Histopathology and Peer Review
Consultancy Services
Bibliographic Services
Archive: Data Storage
The research team of EEL supplies the highest level of scientific knowledge,
quality standards and regulatory competence to their customer's requests,
whether for routine studies or specific complex and innovative projects.

Staff members are:

Director of the EEL
Fiorella Belpoggi, DBS

Quality Assurance
Lucia Bortoluzzi, DBS
Daniela Chiozzotto, PHD

Head of Archives
Luana de Angelis, High School Diploma, Chemistry

Head of Unit
Luciano Bua, MD
Laura Falcioni, DVM
Michelina Lauriola, PHD
Eva Tibaldi, DBS

Researchers
Damiano Accurso, DVM
Marco Manservigi, DBS
Fabiana Manservisi, DBS

Animal care and health
Giovanni Vecchi, DVM

http://www.ramazzini.it/istituto/contatti.asp

tel 051.302252  fax 051.302245 info@...;

DIREZIONE SCIENTIFICA
tel 051.6640460 int. 1 crcdir@...;

CENTRO DI RICERCA SUL CANCRO "CESARE MALTONI"
Castello di Bentivoglio, via Saliceto, 3 - 40010 Bentivoglio (BO)
tel 051.6640460  fax 051.6640223

Direzione belpoggif@...;

Servizi e laboratorio BPL servizi@...;

Ufficio Stampa ed Eventi events@...;

Invio curriculum lauriolam@...;

Centro di Ricerche Epidemiologiche crcre@...;

POLIAMBULATORIO ONCOLOGICO
Via Libia, 13/a 40138 Bologna
tel. 051-302252  fax 051-302245 info@...;


http://www.collegiumramazzini.org/executivecouncil.asp

Executive Council

President: Philip J. Landrigan, MD, MSc, DIH
Professor and Chairman, Department of Community and Preventive Medicine,
The Mount Sinai School of Medicine,
New York, NY, USA.

Secretary General: Morando Soffritti, MD
Scientific Director,
Ramazzini Institute,
Bologna, Italy.

Treasurer: Nachman Brautbar, MD
University of California School of Medicine,
Los Angeles, CA, USA.

Councilors: Henry Anderson, MD
Wisconsin Department of Health and Social Services,
Madison, WI, USA.

Fiorella Belpoggi
Director, Cesare Maltoni Cancer Research Center,
Ramazzini Institute, Bologna, Italy.

Massimo Crespi, MD
Director Emeritus, Istituto Regina Elena,
Rome, Italy.

Philippe Grandjean, PhD
Department of Environmental Medicine, Institute of Public Health, University
of Southern Denmark,
Odense, Denmark.

James M. Melius, MD, Dr.P.H.
Director, New York State Laborers' Health and Safety Trust Fund,
Albany, NY, USA.

Karel Van Damme, PhD
Center for Human Genetics, University of Leuven,
Leuven- Heverlee, Belgium.

http://www.collegiumramazzini.org/fellows.asp

over 200 experts listed

Fellows:

Ahlbom Anders
Albin Maria
Anderson Henry A.
Andrews John S. Jr.
Anwar Wagida A.
Aragon Aurora
Araki Shunichi
Ashford Nicolas A.
Au William W.
Basaran Ayse Nursen
Belpoggi Fiorella
Berlin Maths
Bertollini Roberto
Bingham Eula
Birnbaum Linda
Blair Aaron Earl
Boden Leslie
Brautbar Nachman
Bucher John
Bulat Petar
Casteleyn Ludwine
Castleman Barry
Cheong Hae Kwan
Cherniack Martin G.
Christiani David C.
Claudio Luz
Cogliano Vincent James
Comba Pietro
Cordier Sylvaine
Corra Lilian A.
Cranor Carl F.
Crespi Massimo
Davis Devra Lee
De Rosa Christopher T.
Dement John M.
Dobbin R. Denny
Donnelly Thomas P.
Duffy Richard M.
Ehrlich Rodney
Ellingsen Dag G.
Englund Anders
Falk Henry
Finkelman Jacobo
Foà Vito
Forastiere Francesco
Franco Giuliano
Frank Arthur
Froines John
Froneberg Brigitte
Frumkin Howard
Fucic Aleksandra
Gee David
Giannasi Fernanda
Gochfeld Michael
Goldman Lynn
Goldstein Bernard D.
Grandjean Philippe
Graziano Joseph H.
Greenberg Morris
Groth David H.
Guo Yue-Liang Leon
Gut Ivan
Ha Eun-Hee
Harari Raul
Hardell Lennart
Hay Alastair
Heinzow Birger G.J.
Hermanus Mavis A.
Hoel David G.
Howard Charles Vyvyan
Hryhorczuk Daniel
Huff James
Husgafvel-Pursiainen Kirsti
Infante Peter F.
Jackson Richard J.
Jakubowski Marek
Jarvholm Bengt
Jensen Tina Kold
Joshi Tushar Kant
Katsouyanni Klea
Kelsey Karl T.
Kilburn Kaye H.
Kogevinas Manolis
Kogi Kazutaka
Koh David S.Q.
Landrigan Philip
Langard Sverre
Lanphear Bruce P.
Lemen Richard A.
Lerman Yehuda
Levin Stephen M.
Li Guilan
Lioy Paul J.
London Leslie
Lucchini Roberto G.
Lynge Elsebeth
Markowitz Steven B.
McDiarmid Melissa A.
Mehlman Myron A.
Melius James M.
Melnick Ronald L.
Minardi Franco
Mirer Franklin E.
Misra Usha Kant
Moccaldi Antonio
Myers Jonathan E.
Natali Pier Giorgio
Needleman Herbert L.
Newman Lee S.
Ngowi Aiwerasia Vera Festo
Niemeier Richard W.
Nordberg Gunnar
Nuwayhid Iman A.
Okubo Toshiteru
Olden Kenneth
Oliver L. Christine
Omenn Gilbert S.
Ozonoff David M.
Paek Domyung
Pelclova Daniela
Pershagen Goran
Poje Gerald V.
Rantanen Jorma
Rest Kathleen M.
Ribak Joseph
Rice Carol H.
Richter Elihu D.
Ringen Knut
Rinsky Robert A.
Ritz Beate
Rogan Walter J.
Rosenman Kenneth D.
Rosenstock Linda
Ruchirawat Mathuros
Rydzynski Konrad J.
Santos-Burgoa Carlos
Sardas Semra
Sasco Annie Jeanne
Sass Jennifer
Silbergeld Ellen K.
Sly Peter D.
Soffritti Morando
Songnian Yin
Sorsa Marja
Soskolne Colin L.
Straif Kurt
Suk William A.
Takahashi Ken
Takala Jukka
Tarkowski Stanislaw
Taskinen Helena
Teitelbaum Daniel T.
Thorborg Marina
Tompa Anna
Toren Kjell O.
Vainio Harri
Van Damme Karel
Vineis Paolo
Wagner Gregory R.
Wang Jung-Der
Wardenbach Peter
Watterson Andrew
Wedeen Richard P.
Wegman David H.
Wesseling Catharina
White Roberta F.
Wolff Mary S.
Xia Zhao-Lin
Xintaras Charles
Yano Eiji

Emeritus Fellows:

Bailar III John C.
Barrett J. Carl
Beliczky Louis S.
Chiriboga Jorge
Dooge James C.I.
Fischbein S. Alf
Fraumeni Joseph F. Jr.
Harington John S.
Hogstedt Christer
Holmberg Bo E.G.
Izmerov Nikolai F.
Johnson Barry L.
Kelman Howard R.
LaDou Joseph
Levy Barry S.
Lucier George W.
McCloskey Michael J.
McGlashan Neil D.
Merchant James A.
Milham, Samuel
Miller Albert
Muir David C.F.
Nefedov Oleg M.
Noweir Madbuli H.
Paladini Giuseppe
Pott Friedrich
Rappe Christoffer
Samuels Sheldon
Sugimura Takashi
Suzuki Yasunosuke
Upton Arthur C.
Westerholm Peter J.M.
Woitowitz Hans-Joachim
Zampi Giancarlo


Contact

The International Headquarters of the Collegium Ramazzini have been provided
by the town of Carpi in honor of its famous son, and are located in the
Castle of Pio, home of the Princes of Carpi.

The General Secretariat of the Collegium is located in the Castle of
Bentivoglio near Bologna, Italy.
Since the early 1970s the Castle has also been home to the Cesare Maltoni
Cancer Research Center of the European Foundation of Oncology and
Environmental Sciences "B. Ramazzini", established by Collegium Ramazzini
co-founder, Professor Cesare Maltoni.

General Secretariat
Castello di Bentivoglio
Via Saliceto, 3
40010 Bentivoglio, Bologna, Italy

General Secretary
Dr. Morando Soffritti, M.D

Executive Secretary
Kathryn Knowles
skype: kathrynknowles collegium@...;

Ramazzini Days
Federica Scagliarini
Tel. +39 051.6640460 Fax. +39 051.6640223 events@...;


http://www.unboundmedicine.com/medline/ebm/research/aspartame

Zygler A, Wasik A, Namiesnik J
Retention behaviour of some high-intensity sweeteners on different SPE
sorbents. [Journal Article]
Talanta 2010 Oct 15; 82(5):1742-8.

Alleva R, Borghi B, Santarelli L, et al.
In vitro effect of aspartame in angiogenesis induction. [JOURNAL ARTICLE]
Toxicol In Vitro 2010 Sep 10.

Cabaniols C, Giorgi R, Chinot O, et al.
Links between private habits, psychological stress and brain cancer: a
case-control pilot study in France. [JOURNAL ARTICLE]
J Neurooncol 2010 Sep 11.

Fernández-Maestre R, Hill HH
Ion mobility spectrometry for the rapid analysis of over-the-counter
drugs and beverages. [JOURNAL ARTICLE]
Int J Ion Mobil Spectrom 2009 Aug; 12(3):91-102.

Schoeb TR, McConnell EE
Commentary: Further Comments on Mycoplasma pulmonis and Lymphoma in
Bioassays of Rats. [JOURNAL ARTICLE]
Vet Pathol 2010 Aug 17.

Alsuhaibani ES
In vivo cytogenetic studies on aspartame. [Journal Article] Comp Funct
Genomics 2010.

Yang Q
Gain weight by "going diet?" Artificial sweeteners and the
neurobiology of sugar cravings: Neuroscience 2010. [Journal Article]
Yale J Biol Med 2010 Jun; 83(2):101-8.

Nseir W, Nassar F, Assy N
Soft drinks consumption and nonalcoholic fatty liver disease. [Editorial]
World J Gastroenterol 2010 Jun 7; 16(21):2579-88.

Anton SD, Martin CK, Han H, et al.
Effects of stevia, aspartame, and sucrose on food intake, satiety, and
postprandial glucose and insulin levels. [Journal Article, Research
Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't]
Appetite 2010 Aug; 55(1):37-43.
_______________________________________________


re GC Ebers study, females harmed more by body making methanol into
formaldehyde in brain via ADH enzyme: 589 references, WC Monte,
retired Prof. Nutrition: Rich Murray 2011.01.08
http://rmforall.blogspot.com/2011_01_01_archive.htm
Saturday, January 8, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1614
[you may have to Copy and Paste URLs into your browser]


Woodrow C Monte, PhD, Emiritus Prof. Nutrition gives many PDFs of
reseach -- methanol (11% of aspartame) puts formaldehyde into brain
and body -- multiple sclerosis, Alzheimer's, cancers, birth defects,
headaches: Rich Murray 2010.05.13
http://rmforall.blogspot.com/2010_05_01_archive.htm
Thursday, May 13, 2010
http://groups.yahoo.com/group/aspartameNM/message/1601

[ Other formaldehyde sources include alcohol drinks and
tobacco and wood smoke,
while adequate folic acid levels protect most people. ]

http://whilesciencesleeps.com/about

http://while-science-sleeps.com/references/pdf/586
[ summary, not peer reviewed ]
Monte WC.
Methanol: A chemical Trojan horse as the root of the inscrutable U.
Medical Hypotheses 2010;74(3):493-6
DOI 2010.10.16

Monte WC.
Bittersweet: Aspartame Breast Cancer Link.
Fitness Life 2008 Jan. 34: 32-36

Monte WC.
A Deadly Experiment. Methanol and MS,
Fitness Life 2007 Dec. 34: 36-41

Monte WC.
Sickly Sweet: Is your Diet Sweetener killing you?
Fitness Life 2007 Nov. 33: 31-33

http://whilesciencesleeps.com/references
589 references for above articles and upcoming book

http://whilesciencesleeps.com/montediet
[ and Fitness Life 2007 Dec. 34: 36-41 ]

Methanol: Where Is It Found? How Can It Be Avoided?

AVOID the following, ranked in order of greatest danger:

1. Cigarettes.
2. Diet foods and drinks with aspartame.
3. Fruit and vegetable products and their juices in bottles,
cans, or pouches.
4. Jellies, jams, and marmalades not made fresh and kept
refrigerated.
5. Black currant and tomato juice products, fresh or
processed.
6. Tomato sauces, unless first simmered at least 3 hours
with an open lid.
7. Smoked food of any kind, particularly fish and meat.
8. Sugar-free chewing gum.
9. Slivovitz: You can consume one alcoholic drink a day
on this diet -- no more! [ no fruit brandies ]
10. Overly ripe or near rotting fruits or vegetables.

Selection from Article 2, Fitness Life, December 2007, and
well discussed in the DVD video:

"Identical Symptoms of MS, Methanol Poisoning
and Aspartame Toxicity

The symptoms of multiple sclerosis (44, 83, 85, 169), chronic
and acute methanol poisoning (13, 144, 189), and Aspartame
toxicity (54, 58, 93, 181), are in all ways identical.

There is nothing that happens to the human body from the
toxic effect of methanol that has not been expressed during
the course of MS... nothing (143, 144).

This generalization extends even to the remarkable
opthomological conditions common to both: transitory optic
neuritis and retrolaminar demyelinating optic neuropathy with
scotoma of the central visual field (which occasionally
manifests as unilateral temporary blindness (85, 138, 163).

In fact, these opthomological symptoms have been thought of
for years in their respective literatures to be "tell tale"
indications for the differential diagnosis for each of these
maladies independently (85, 138, 148, 163, 169).

The common symptoms of
headache (13, 83, 181, 189),
nervousness (13, 83, 181),
depression (58, 83, 189, 181),
memory loss (18, 147, 85, 169, 181),
tingling sensations (13, 85, 168, 138, 169),
pain in the extremities (13, 85, 169),
optic neuritis (85, 138, 148, 163, 169),
bright lights in the visual field (139, 83),
seizures (21, 83, 160),
inability to urinate or to keep from urinating (139, 146, 167)
are all shared by each of these conditions and shared yet
again by complaints from aspartame poisoning
(54, 58, 93, 181).

I take these strikingly similar symptom patterns as evidence
that these disorders act on identical components of the
central nervous system and in the same way.

The "Miracle" that MS shares with Methanol poisoning

In the early stages of MS, or when a non-lethal dose of
methanol has been administered, complete recovery is a
possibility.

The only two afflictions for which such dramatic "remissions"
are reported from identical neuromuscular and opthomological
damage, even "blindness" is relapsing-remitting multiple
sclerosis (85) and methyl alcohol poisoning (138, 163).

The pathology of the two maladies is in may ways identical,
particularly when it comes to destruction of the myelin
sheath with no harm to the axon itself (18, 148, 176).

Sex Ratios for MS and Aspartame Reactions

Women bear the brunt of multiple sclerosis (91a-c) and lupus
(SLE)(73) with fully three-fold representations in infliction
numbers over men for both diseases.

This is exactly the proportion represented by adverse
reactors to Aspartame reported by the US Center for
Disease Control in their study of 1984 (58).

The Center found three women to every man whose
Aspartame consumption complaints were serious enough
to warrant investigation (93).

Although the female/male ratio for those stricken with MS has
always been high, recent estimates place it at over 3 to 1
(91, 91a, 91c).

What might account for the difference across sexes in
incidence?

A study published in the New England Journal of Medicine
(94) reports biopsies of the gastric lining of men and women.

A result was that the concentration of ADH in the
gastric lining of men was much higher than for woman.

Men have the advantage of removing methanol from the
bloodstream four times faster on an equal-body-size basis
than women.

Thus, for men, methanol is more likely to be removed from the
blood before it reaches the brain.

The brain is spared but the methanol removed would still be
metabolized to formaldehyde in the gut where it would reap
its havoc on a more forgiving organ.

This may help explain why men have more gastrointestinal
complaints from both methanol and Aspartame consumption
(93, 99).

On the other hand, women's complaints from both more
frequently involve serious neurological complications."...
______________________________________________


Chemico-Biological Interactions, JA Bond, MA Medinsky, can share WC
Monte paradigm re harm by formaldehyde via ADH enzyme & methanol in
blood capillaries -- tobacco, wood smoke; dark wines, liquors;
aspartame; canned tomatoes: Rich Murray 2011.02.21
http://rmforall.blogspot.com/2011_02_01_archive.htm
Monday, February 21, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1618
[you may have to Copy and Paste URLs into your browser]

methanol (11% of aspartame), made by body into
formaldehyde in many vulnerable tissues, causes modern
diseases of civilization, summary of a century of research,
Woodrow C Monte PhD, Medical Hypotheses journal:
Rich Murray 2009.11.15
http://rmforall.blogspot.com/2009_11_01_archive.htm
Sunday, November 15, 2009
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1589
[you may have to Copy and Paste URLs into your browser]

aspartame abstinance cures fibromyalgia chronic pain in 2 French
adults: R Ciappuccini et al, Clin Exp Rheumatol 2010 Nov: Rich Murray
2010.02.19
http://rmforall.blogspot.com/2011_02_01_archive.htm
Saturday, February 19, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1617
[you may have to Copy and Paste URLs into your browser]

formaldehyde from 0.2 mg daily methanol from aspartame in Singulair
(montelukast) chewable asthma medicine causes severe allergic
dermatitis in boy, SE Jacob et al, Pediatric Dermatology 2009 Nov:
Rich Murray 2010.09.27
http://rmforall.blogspot.com/2010_09_01_archive.htm
Monday, September 27, 2010
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1613
[you may have to Copy and Paste URLs into your browser]
______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-819-7388 rmforall@...

http://groups.yahoo.com/group/AstroDeep/messages

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 118 members, 1,619 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1226 members, 24,283 posts in a public archive

http://groups.yahoo.com/group/rmforall/messages

participant, Santa Fe Complex www.sfcomplex.org
______________________________________________

aspartame water in rats for 6 months causes liver harm, RH Nair et al,
Mahatma Gandhi U, Food Chem Toxicol 2011.03.02: Rich Murray 2011.03.12
http://rmforall.blogspot.com/2011_03_01_archive.htm
Saturday, March 12, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1620
[you may have to Copy and Paste URLs into your browser]


http://www.ncbi.nlm.nih.gov/pubmed/21376768

Food Chem Toxicol. 2011 Mar 2. [Epub ahead of print]
Effect of long term intake of aspartame on antioxidant defense status in liver.
Abhilash M, Paul MV, Varghese MV, Nair RH.
School of Biosciences, Mahatma Gandhi University,
Kottayam, Kerala, India, 686560.
harikumarannair@..., harinair@...,

Abstract

The present study evaluates the effect of long term intake of
aspartame, the artificial sweetener, on liver antioxidant system and
hepatocellular injury in animal model.
Eighteen adult male Wistar rats, weighing 150 - 175 g, were randomly
divided into three groups as follows:
first group was given aspartame dissolved in water in a dose of 500 mg/kg.b.wt;
the second group was given a dose of 1000 mg/kg.b.wt;
and controls were given water freely.
Rats that had received aspartame (1000 mg/kg.b.wt) in the drinking
water for 180 days showed a significant increase in activities of
alanine aminotransferase (ALT),
aspartate aminotransferase (AST),
alkaline phosphatase (ALP) and
y-glutamyl transferase (GGT).
The concentration of reduced glutathione (GSH)
and the activity of glutathione peroxidase (GPx), and
glutathione reductase (GR)
were significantly reduced in the liver of rats that had received
aspartame (1000 mg/kg.b.wt).
Glutathione was significantly decreased in both the experimental groups.
Histopathological examination revealed leukocyte infiltration in
aspartame-treated rats (1000 mg/kg.b.wt).
It can be concluded from these observations that long term consumption
of aspartame leads to hepatocellular injury and alterations in liver
antioxidant status mainly through glutathione dependent system.
Copyright 2011. Published by Elsevier Ltd. PMID: 21376768

Souganth Paul, MV - Research Fellow

Abhilash, M - Research Fellow

Mathews V Varghese - Research Fellow

http://www.mgu.ac.in/index.php?option=com_content&view=article&id=493&Itemid=96

School of Bio-Sciences  Teacher Profiles [photo]

Name: Dr. R. Harikumaran Nair
Designation: Assistant Professor
Address: Room No. 5
School of Biosciences,
Mahatma Gandhi University
Priyadarshini Hills. P O., Kottayam-686 560
Kerala, India
Phone: +91-481-2731035 Extension: 16
Mobile Phone: +91-94472 60362
Email: harikumarannair@..., harinair@...
Home page: www.biophysiol.org

Research Interest

In our laboratory, we study the effect of food additives such as
monosodium glutamate, aspartame, drug component arsenic trioxide and
other toxins like organic solvents on different physiological
mechanisms in rats and tissue culture model systems.
Another area of interest is environmental and occupational stress.

Academic Profile

Ph. D - Physiology (2001), School of Biosciences,
Mahatma Gandhi University, Kottayam, Kerala, India
M. Sc - Zoology (1994)
University of Kerala, Thiruvananthapuram, Kerala, India,
B. Sc - Zoology (1992)
University of Kerala, Thiruvananthapuram, Kerala, India,

Professional Experience:

*Lecturer in Physiology (Permanent service) -
School of Biosciences, Mahatma Gandhi
University, Kerala, India. 22nd May 2006 to present
*Lecturer in Physiology (contract service) -
School of Biosciences, Mahatma Gandhi University, Kerala, India. 20th
November 2003 to 21st May 2006
*Postdoctoral Research fellow -
Dept. of Physiology, St. John's Medical College, Bangalore, India.
01st March 2002 to 15th July 2002
*Research Fellow -
School of Biosciences, Mahatma Gandhi University, Kottayam, Kerala,
India. October 1995 to April 2001

Group Members

Sagi, TM - Research Fellow
Souganth Paul, MV - Research Fellow
Abhilash, M - Research Fellow
Mathews V Varghese - Research Fellow
Manju Alex - Research Fellow

Publications:

Scientific Proceedings

1. Abhilash M, Shashidhar S, Harikumaran Nair R,
The role of electrolytes in cataractogenesis and modulation by silver
nitrate in albino rats.
22nd Kerala Science Congress. 28-31 January 2010. KFRI, Peechi,
Thrissur, Kerala, India

2. Sauganth Paul, Harikumaran Nair R, Shashidhar S,
Lipid peroxidation and antioxidant activities in hypertensive subjects
of different age groups.
Indian Science Congress, Medical Sciences section. 03.01.2010 to 07.01.2010,
University of Kerala, Kerala, India

Publications

1. Ajitha Kumari R, Shashidhar S and Harikumaran Nair R,
Oxidative stress and lung functions in diabetic mellitus.
Biomedicine. 2010 (accepted)

2. Pankajam K, Harikumaran Nair R, Kesavachandran C, Rethamma KV, and
Shashidhar S,
Effects of Automobile exhaust pollution on the pulmonary functions in
shopkeepers.
Pollution Research. 2005; 24(1): 51-56.

3. Kesavachandran C, Harikumaran Nair R. and Shashidhar S.
Pulmonary function studies in Kalarypayathu Practitioners.
Ind. J. Physiol. Pharmacol., 2004; 48(2), 235-240.

4. Geetha B., Harikumaran Nair R, Kesavachandran C, Susan Chandy and
Shashidhar S,
Pulmonary functions in workers of fertilizer and chemical Industry.
Ind.J.Physiol.Pharmacol. 2001; 45(2):215-221.

5. Geetha B., Harikumaran Nair R, Kesavachandran, C and Shashidhar S,
Respiratory Function Studies in Rare Earth Factory Workers.
Pollution Research 2001; 20(1):115-119.

6. Kesavachandran C, Harikumaran Nair R, and Shashidhar S,
Lung Volume in Swimmers performing different strokes.
Ind.J.Med.Sci. 2001; 55(12):669-676.

7. Reethamma KV, Harikumaran Nair R, Kesavachandran C and Shashidhar S,
Effect of Wood Dust on Lung Functions.
Pollution Research 2000; 19(4):693-699.

8. Harikumaran Nair R, Kesavachandran C and Shashidhar S,
Spirometric Impairments in Undernourished Children.
Ind.J.Physiol.Pharmacol.1999; 43(4):467-473.

9. Harikumaran Nair R, Kesavachandran C, Sanil R, Sreekumar R and Shashidhar S,
Prediction Equation for Lung Functions in South Indian Children.
Ind.J.Physiol.Pharmacol.1997; 41(4):390-396.

10. Kesavachandran C., Sanil R, Harikumaran Nair R, Arun A Rauf and
Shashidhar S,
Pulmonary Function Studies in Rowers.
Ind.J.Physiol.Pharmacol.1997; 41(1):29-34.

11. Bindu K Pazhur, Susan Chandy, Harikumaran Nair R, and Shadhidhar S,
Effect of Domestic Cooking Fuels on Lung Function in Women.
Pollution Research 1997;16(3):149-154.

Scientific Papers in International Conference:

1. Geetha B, Harikumaran Nair R, Kesavachandran C and Shashidhar S,
Respiratory Function Studies on Newsprint Factory workers.
International Conference on Health, Occupation and Environment in
Unorganized Sector - Problems and Road Maps (ICHOE 2004). November
1-3, 2004, Industrial Toxicology Research Centre (ITRC, CSIR),
Lucknow, INDIA.

2. Rethamma KV, Harikumaran Nair R, Kesavachandran C and Shashidhar S,
Pulmonary function status among Wood workers.
International Conference on Health, Occupation and Environment in
Unorganized Sector - Problems and Road Maps (ICHOE 2004). November
1-3, 2004, Industrial Toxicology Research Centre
(ITRC, CSIR), Lucknow, INDIA.

Academic & Administrative Duties

* Chairman, B Sc Biophysics Board of Examinations,
University of Calicut, Kerala, India
* Convenor & Member, Institutional Animal Ethics Committee,
Mahatma Gandhi University, Kerala, India
* Member Secretary, Institutional Human Ethics Committee,
Mahatma Gandhi University, Kerala, India
* External Examiner in Fundamentals of Physiology,
School of Medical Education,
Mahatma Gandhi University, Kerala, India
* Member, Campus Development Committee,
Mahatma Gandhi University, Kerala, India

Training undertaken: ( 2007 Onwards)

* Refresher Course in Lifesciences. 08.12.2009 to 29.12.2009
UGC Academic Staff College, University of Kerala, Kerala
* University workshop on Research Projects, 02.04.2009
Mahatma Gandhi University, Kerala
* UGC sponsored short term course for Research Guides. 23.03.2009 to
28.03.2009
UGC Academic Staff College, University of Kerala, Kerala.
* Workshop on Curriculum Design for B.Sc. Biophysics Course,
Kerala State Higher Education Council and
the University of Calicut, Kerala, 24.02.2009 to 28.02.2009

Research Collaborations
IITR - Lucknow,UP, India
NIIST - Thiruvananthapuram, Kerala, India

Copyright 2010 MG University, All Rights Reserved. Content by PRD.
Supported by System Administration Team, M.G. University
_______________________________________________


careful expert lifetime study on mice shows liver and lung cancers
from aspartame, M Soffritti et al, Ramazzini Institute, Italy, checked
by US National Toxicology Program experts, confirms many previous
studies from 2001 on: Rich Murray 2011.02.27
http://rmforall.blogspot.com/2011_02_01_archive.htm
Sunday, February 27, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1619
[you may have to Copy and Paste URLs into your browser]

re GC Ebers study, females harmed more by body making methanol into
formaldehyde in brain via ADH enzyme: 589 references, WC Monte,
retired Prof. Nutrition: Rich Murray 2011.01.08
http://rmforall.blogspot.com/2011_01_01_archive.htm
Saturday, January 8, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1614
[you may have to Copy and Paste URLs into your browser]

Woodrow C Monte, PhD, Emiritus Prof. Nutrition gives many PDFs of
reseach -- methanol (11% of aspartame) puts formaldehyde into brain
and body -- multiple sclerosis, Alzheimer's, cancers, birth defects,
headaches: Rich Murray 2010.05.13
http://rmforall.blogspot.com/2010_05_01_archive.htm
Thursday, May 13, 2010
http://groups.yahoo.com/group/aspartameNM/message/1601

[ Other formaldehyde sources include alcohol drinks and
tobacco and wood smoke,
while adequate folic acid levels protect most people. ]

http://whilesciencesleeps.com/about

http://while-science-sleeps.com/references/pdf/586
[ summary, not peer reviewed ]
Monte WC.
Methanol: A chemical Trojan horse as the root of the inscrutable U.
Medical Hypotheses 2010;74(3):493-6
DOI 2010.10.16

Monte WC.
Bittersweet: Aspartame Breast Cancer Link.
Fitness Life 2008 Jan. 34: 32-36

Monte WC.
A Deadly Experiment. Methanol and MS,
Fitness Life 2007 Dec. 34: 36-41

Monte WC.
Sickly Sweet: Is your Diet Sweetener killing you?
Fitness Life 2007 Nov. 33: 31-33

http://whilesciencesleeps.com/references
589 references for above articles and upcoming book

http://whilesciencesleeps.com/montediet
[ and Fitness Life 2007 Dec. 34: 36-41 ]

Methanol: Where Is It Found? How Can It Be Avoided?

AVOID the following, ranked in order of greatest danger:

1. Cigarettes.
2. Diet foods and drinks with aspartame.
3. Fruit and vegetable products and their juices in bottles,
cans, or pouches.
4. Jellies, jams, and marmalades not made fresh and kept
refrigerated.
5. Black currant and tomato juice products, fresh or
processed.
6. Tomato sauces, unless first simmered at least 3 hours
with an open lid.
7. Smoked food of any kind, particularly fish and meat.
8. Sugar-free chewing gum.
9. Slivovitz: You can consume one alcoholic drink a day
on this diet -- no more! [ no fruit brandies ]
10. Overly ripe or near rotting fruits or vegetables.

Selection from Article 2, Fitness Life, December 2007, and
well discussed in the DVD video:

"Identical Symptoms of MS, Methanol Poisoning
and Aspartame Toxicity

The symptoms of multiple sclerosis (44, 83, 85, 169), chronic
and acute methanol poisoning (13, 144, 189), and Aspartame
toxicity (54, 58, 93, 181), are in all ways identical.

There is nothing that happens to the human body from the
toxic effect of methanol that has not been expressed during
the course of MS... nothing (143, 144).

This generalization extends even to the remarkable
opthomological conditions common to both: transitory optic
neuritis and retrolaminar demyelinating optic neuropathy with
scotoma of the central visual field (which occasionally
manifests as unilateral temporary blindness (85, 138, 163).

In fact, these opthomological symptoms have been thought of
for years in their respective literatures to be "tell tale"
indications for the differential diagnosis for each of these
maladies independently (85, 138, 148, 163, 169).

The common symptoms of
headache (13, 83, 181, 189),
nervousness (13, 83, 181),
depression (58, 83, 189, 181),
memory loss (18, 147, 85, 169, 181),
tingling sensations (13, 85, 168, 138, 169),
pain in the extremities (13, 85, 169),
optic neuritis (85, 138, 148, 163, 169),
bright lights in the visual field (139, 83),
seizures (21, 83, 160),
inability to urinate or to keep from urinating (139, 146, 167)
are all shared by each of these conditions and shared yet
again by complaints from aspartame poisoning
(54, 58, 93, 181).

I take these strikingly similar symptom patterns as evidence
that these disorders act on identical components of the
central nervous system and in the same way.

The "Miracle" that MS shares with Methanol poisoning

In the early stages of MS, or when a non-lethal dose of
methanol has been administered, complete recovery is a
possibility.

The only two afflictions for which such dramatic "remissions"
are reported from identical neuromuscular and opthomological
damage, even "blindness" is relapsing-remitting multiple
sclerosis (85) and methyl alcohol poisoning (138, 163).

The pathology of the two maladies is in may ways identical,
particularly when it comes to destruction of the myelin
sheath with no harm to the axon itself (18, 148, 176).

Sex Ratios for MS and Aspartame Reactions

Women bear the brunt of multiple sclerosis (91a-c) and lupus
(SLE)(73) with fully three-fold representations in infliction
numbers over men for both diseases.

This is exactly the proportion represented by adverse
reactors to Aspartame reported by the US Center for
Disease Control in their study of 1984 (58).

The Center found three women to every man whose
Aspartame consumption complaints were serious enough
to warrant investigation (93).

Although the female/male ratio for those stricken with MS has
always been high, recent estimates place it at over 3 to 1
(91, 91a, 91c).

What might account for the difference across sexes in
incidence?

A study published in the New England Journal of Medicine
(94) reports biopsies of the gastric lining of men and women.

A result was that the concentration of ADH in the
gastric lining of men was much higher than for woman.

Men have the advantage of removing methanol from the
bloodstream four times faster on an equal-body-size basis
than women.

Thus, for men, methanol is more likely to be removed from the
blood before it reaches the brain.

The brain is spared but the methanol removed would still be
metabolized to formaldehyde in the gut where it would reap
its havoc on a more forgiving organ.

This may help explain why men have more gastrointestinal
complaints from both methanol and Aspartame consumption
(93, 99).

On the other hand, women's complaints from both more
frequently involve serious neurological complications."...
______________________________________________


methanol (11% of aspartame), made by body into
formaldehyde in many vulnerable tissues, causes modern
diseases of civilization, summary of a century of research,
Woodrow C Monte PhD, Medical Hypotheses journal:
Rich Murray 2009.11.15
http://rmforall.blogspot.com/2009_11_01_archive.htm
Sunday, November 15, 2009
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1589
[you may have to Copy and Paste URLs into your browser]

aspartame abstinance cures fibromyalgia chronic pain in 2 French
adults: R Ciappuccini et al, Clin Exp Rheumatol 2010 Nov: Rich Murray
2010.02.19
http://rmforall.blogspot.com/2011_02_01_archive.htm
Saturday, February 19, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1617
[you may have to Copy and Paste URLs into your browser]

formaldehyde from 0.2 mg daily methanol from aspartame in Singulair
(montelukast) chewable asthma medicine causes severe allergic
dermatitis in boy, SE Jacob et al, Pediatric Dermatology 2009 Nov:
Rich Murray 2010.09.27
http://rmforall.blogspot.com/2010_09_01_archive.htm
Monday, September 27, 2010
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1613
[you may have to Copy and Paste URLs into your browser]
______________________________________________

Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-819-7388 rmforall@...

http://groups.yahoo.com/group/AstroDeep/messages

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 118 members, 1,620 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1226 members, 24,284 posts in a public archive

http://groups.yahoo.com/group/rmforall/messages

participant, Santa Fe Complex www.sfcomplex.org
______________________________________________

aspartame doubts aired by EU MPs Corinne Lepage and Antonyia Parvanova
-- EFSA  National Experts agreed that "there should be more clarity
about the metabolism of aspartame": Rich Murray 2011.04.24
http://rmforall.blogspot.com/2011_04_01_archive.htm
Sunday, April 24, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1621
[ you may have to Copy and Paste URLs into your browser ]


http://www.laleva.org/eng/2011/04/aspartame_-_european_health_authorities_play_a\
_fools_game-print.html

Aspartame - European Health Authorities play a Fools' Game

Aspartame, the artificial sweetener, is made of two amino acids bound
together by a molecule of methanol. The white powder is sweeter than
sugar, and its purpose is to give you the sweet without the calories.
A great idea, but is it really?

There are many indications that aspartame is not as healthy an
alternative to sugar as its creators and vendors would have us
believe. The isolated amino acids excite neural activity leading to
effects on the brain and the methanol binder degrades into a nasty
poison in the bodies of consumers. Research to prove those effects
however is hard to come by. After all, the manufacturer has no reason
to provide evidence that would end a winning streak of profitability.

Dr. Morando Soffritti at the Italian Ramazzini Foundation fed
aspartame to mice and rats and found it had a multi-potential
carcinogenic effect.

An Icelandic university researcher found that the consumption of those
artificially sweetened soft drinks was associated with premature
termination of pregnancy in a study of Danish women.

Numerous "anecdotal" reports of effects on the brain and the nerves
have been compiled, but they are of course not scientific enough to
catch the attention of the health authorities. The FDA has stopped
accepting complaints and reports of aspartame related side effects
soon after it became clear that they would have to take action if
complaints continued to pile up.

The international committees in charge of evaluating additives have
"reviewed the evidence", meaning the studies that were sanitized and
provided to them by the manufacturers, and they cannot find anything
wrong.

And so we are left with a sweetener that is sold all over the world,
consumed by hundreds of millions of people. Its effects are
devastating to many, but there seems to be no way to make the health
authorities pay heed. Hundreds of complaints of those suffering
aspartame's effects have come to the attention of two members of the
European Parliament, Corinne Lepage and Antonyia Parvanova.

They organized a seminar to try and force action on the part of the
European Commission and the agencies responsible for health and
consumer protection.

Their frustration is palpable when they say that we are being taken
for a ride...


http://www.alde.eu/press/press-and-release-news/press-release/article/aspartame-\
the-european-health-authorities-play-a-fools-game-37287/

ASPARTAME: The European Health authorities play a fools game

Two members of the European Parliament organized a seminar on the
possible dangers of Aspartame, the controversal artificial sweetener
manufactured first by Searle and now by the Japanese Ajinomoto.
Aspartame is present in thousands of products, including a few hundred
medicines, particularly meds for children. Studies have shown it to be
associated with cancer and other deleterious health effects. Aspartame
consumers have told horror stories of its effects. Yet, our health
authorities show no will to warn consumers or even to pro-actively
look into aspartame's effects.

Corinne Lepage expressed her shock,
"by the failure to examine the subject more thoroughly, and the close
links that have been established between industry, the EFSA and the
Commission, each one passing the buck to the others. This attitude has
meant that looking at the health effects of aspartame is no longer
taken seriously."

For Antonyia Parvanova,
"Aspartame is a substance to which millions of consumers are exposed
on a daily basis. For this reason, and even if there is only a hint of
risk, the European health authorities should commit themselves
proactively to the gathering of data and the supervision of
complementary and independent studies, instead of being passive and
waiting for additional data to come to them".

In a more recent development, the European Parliament's Environment
Committee is now pushing for a warning label on aspartame.

The European Parliament's Environment committee is pushing for a
warning label on products containing aspartame stating that they may
not be suitable for pregnant women - despite opinions from EFSA and
the French food safety ANSES that scientific evidence does not warrant
a reconsideration of the sweetener's safety.

Video: Artificial sweeteners: Should we be afraid of Aspartame ?

This is a long video (one hour and 55 minutes) and it is the complete
record of a seminar organized by ALDE, the Alliance of Liberals and
Democrats for Europe, at the European Parliament on 16 March 2011. [
Wednesday 16 March 2011 13:00 to 15:00  Location: BE BRUSSELS A5G-2 ]

The first speaker is Dr Morando Soffritti of the Ramazzini Research
Foundation in Bologna, Italy, who presents experiments conducted at
the institute that showed aspartame to be associated with increased
incidence of certain cancers in laboratory animals.

Thorhallur Halldorsson of the University of Iceland relates of a study
that found a 30 to 80 % increase in pre-term delivery in pregnant
women in Denmark who consumed artificially sweetened soft drinks.

Hugues Kenigswald of the Unit supporting the scientific panel on Food
Additives and Nutrient Sources added to Foods - ANS, of the European
Food Safety Authority, explained how aspartame has been evaluated by
the EFSA and its predecessor, the Scientific Committee for Foods
(SCF), stating that "further studies are needed".

In the second part of the discussions the question is:
Should the precautionary principle be applied to aspartame use as an additive?

The tone is set by A.G. Renwick a scientist working for the
International Sweeteners Association who points to an "enormous and
comprehensive safety database on aspartame", and assures participants
that aspartame is one of the best evaluated and most studied
substances. He adds that the new studies - both of the Ramazzini
Institute and the Iceland University researchers - do not give any
reason to be preoccupied.

Lynn Insall of the CIAA (Food and Drink Industry Association) also
calls aspartame the "most studied food additive" used at safe levels,
and she adds that aspartame allows the drink industry to provide for
consumer choice.

Laurent Chevallier from France talks about risk/benefit analysis
saying aspartame is not effective in weight loss, and since there are
a lot of warning signs, EFSA should very well review and challenge the
early studies that were used to set the acceptable daily intake for
aspartame. He criticizes EFSA's handling of the controversal
sweetener.

[ http://www.docteurlaurentchevallier.fr/
Dr. Laurent Chevallier
04 67 02 49 04
Clinique du Parc
Chemin des Guilhems
34171 Castelnau Le Lez
Paris, FR ]

Katrien Renders of a Dutch consumer group does not add much to the
specific discussion of Aspartame. She makes it clear however that
there are strong feelings on the consumer side about the safety of
additives.

Concluding speaker is Michael Flueh, Head of the Chemicals,
contaminants and pesticides unit of the European Commission's Health
and Consumers Directory (SANCO). He states aspartame has been
re-evaluated various times, and that the Commission will continue to
monitor the scientific literature. He denies that there is a need to
intervene at the present time.

The discussion shows how, once an additive has been approved, it is
just about impossible to have it comprehensively re-considered, even
in the face of studies that show there are problems or in the face of
"anecdotal" evidence from doctors or the consuming public. The Members
of the EU Parliament who organized the seminar, Corinne Lepage of
France and Antonyia Parvanova of Bulgaria, do criticize the officials
present for not taking their part of responsibility for protecting the
public from possible damage. Their press release after the seminar
sums it up:

ASPARTAME: The European Health authorities play a fools game
"This is a long video (one hour and 55 minutes) and it is the complete
record of a seminar organized by ALDE, the Alliance of Liberals and
Democrats for Europe, at the European Parliament on 16 March 2011."
http://www.youtube.com/watch?v=n4mrBEaRMKU&feature=related
video 1:56:45
FULL VIDEO Event of the ALDE Seminar: Artificial sweeteners: Should we
be afraid of Aspartame ?

Photo Album: http://ow.ly/4fSqG

http://www.youtube.com/watch?v=pA8BNmS1b_I
video 2:57
Corinne Lepage cites need to use precautionary principle to warn
pregnant women about doubts

http://www.youtube.com/watch?v=rq-vzX-40OE&NR=1
video 3:56
Antonyia Parvanova reminds that medical science has known that food
affects health...

For more information
CORLETT Neil ( neil.corlett@... )
BRU: +32 (0)2 28.42077STR: +33 (0)3 88 1.74167MOBILE: +32 478 78 22 84

HAL'KO Norbert ( norbert.halko@... )
BRU: +32 (0)2 28.42602STR: +33 (0)3 88 1.76651


http://www.alde.eu/press/press-and-release-news/press-release/article/aspartame-\
the-european-health-authorities-play-a-fools-game-37287/

ASPARTAME: The European Health authorities play a fools game  17/03/2011

On Wednesday March 16th, 2011 ALDE MEPs Corinne Lepage (CAP 21,
France) and Antonyia Parvanova (NMSP, Bulgaria) organised a hearing in
the European Parliament to examine concerns about the health risks of
aspartame, an artificial sweetener used in products such as some soft
drinks.

This hearing brought together scientific authors of the most recent
studies on the health effects of aspartame, representatives of the
European Food Safety Authority, the European Commission, industry, and
NGOs.

Corinne Lepage expressed her shock,
"by the failure to examine the subject more thoroughly, and the close
links that have been established between industry, the EFSA and the
Commission, each one passing the buck to the others. This attitude has
meant that looking at the health effects of aspartame is no longer
taken seriously. It is inadmissible that the Acceptable Daily Intake
(ADI) for aspartame which was calculated in 1980 based on
non-independent studies which were supplied by the manufacturer and
were very questionable, still serve as the basis and that neither the
EFSA, nor the Commission are willing to re-open the discussion.

For Antonyia Parvanova,
"Aspartame is a substance to which millions of consumers are exposed
on a daily basis.  For this reason, and even if there is only a hint
of risk, the European health authorities should commit themselves
proactively to the gathering of data and the supervision of
complementary and independent studies, instead of being passive and
waiting for additional data to come to them".

Corinne Lepage and Antonyia Parvanova demand:

  * that the toxicology data on the Admissible Daily Intake (ADI) be
communicated to the scientific community and that the data be
recalculated based on studies that are independent from the
manufacturers, and guided according to the Good Laboratory Practice;

  * that the EFSA take position on the new studies which tend to show
the toxicity of aspartame, and that they do so quickly, in a
contradictory manner, and carefully avoiding all conflict of
interests.

  * that in applying the principle of precaution, which is a principle
of Community Law, public information be available on the uncertainties
concerning health implications, and that pregnant women be informed
about the potential danger to the foetus.


LEPAGE Corinne
Citoyenneté Action Participation pour le 21ème siècle

http://www.europarl.europa.eu/members/expert/committees/view.do?language=EN&id=9\
7076

Corinne LEPAGE
Group of the Alliance of Liberals and Democrats for Europe
Member France  corinne.lepage@...
Citoyenneté Action Participation pour le 21ème siècle
Born on 11 May 1951, Boulogne-Billancourt

Vice-Chair
Committee on the Environment, Public Health and Food Safety [See]

Member
Delegation for relations with the People's Republic of China [See]

Substitute
Committee on Industry, Research and Energy [See]
Delegation for relations with Japan [See]

Curriculum vitae
Graduate (cum laude) of the Paris Institute of Political Studies (1971).
Higher degree (DES) in public law (1974).
Awarded DES by the Paris Institute of Political Studies (1974).
Diploma to practise as a lawyer (1974).
Highest doctoral degree in public law, awarded summa cum laude (1982).
Lawyer (1975-1995 and since 1997).
Chair of CAP 21 (since 1996).
Chair of the European Parliament Intergroup on Seas and Coastal Affairs.
Deputy mayor of Cabourg (1998-2001).
Minister of the Environment (1995-1997).
President-in-office of the Council of European Ministers of the
Environment (French Presidency of the European Union) (1995).
Member of Global Environment Facility high-level advisory group.
Member of international Council on sustainable consumption.
Member of Millennium Ecosystem Assessment.
Chair of the Committee for independent research and information on
genetic engineering (CRIIGEN).
Chair of the Ecological Monitoring and Early Warning Centre (OVALE).
Former chair of national association of doctors of law.
Member of management board of Transparence International - France
(French branch of Transparency International).
Knight of the Legion of Honour.


PARVANOVA Antonyia
National Movement for Stability and Progress

http://www.europarl.europa.eu/members/public/inOut/viewOutgoing.do?language=EN&i\
d=34234
send a message

Antonyia Parvanova, MP, EU

http://parvanova.eu/index.php?lang=en   website

http://parvanova.eu/blog.php   blog

http://parvanova.eu/main.php?id=2   about

Born on 26 April 1962, Dobrich

Dr Antonyia Parvanova (1962), Bulgarian, Paediatrician and Public
Health policy expert, is currently Member of the European Parliament,
Vice-President of the Alliance of the Liberals and Democrats for
Europe (ALDE), and seats as a full Member of the Committee on the
Environment, Public Health and Food Safety. She is also the ALDE group
coordinator for the Committee on Women's Rights and Gender Equality.

Following her career as a clinician and researcher in Bulgaria and in
the UK, Dr Parvanova started her political career when elected Member
of the Bulgarian Parliament in 2001. There she was Vice-Chairperson of
the Committee on Public Health and worked actively on public health
and healthcare legislations at national level. In the European
Parliament she initiated several public health policy actions, notably
the campaign on patients' rights in Europe in 2007. At the same time,
she also took part in the debate on Combating HIV/AIDS in the European
Union, stressing on the need to combat the spread of the epidemic in
neighbouring countries from central Europe. She now continues being
actively involved in public health dossiers currently being discussed
in the European Parliament, such as the pharmaceutical package, the
communication on health inequalities or the proposal for a Directive
on Patients' rights in cross-border healthcare.

Throughout her professional and political activities, she has been
actively involved in the Women's Rights debate, looking most
particularly at societal and health related issues, at both national
and EU level. She focuses her action on sexual and reproductive health
issues, with a specific emphasis on the ones affecting women. Looking
at access to care and treatment, she notably initiated in Bulgaria the
establishment of a national fund facilitating and reimbursing In Vitro
Fertilisation treatments for women and couples affected by
reproductive disorders. In the European Parliament she managed to
include in the EP Resolution on the Stockholm programme a text urging
the Commission to propose a directive on elimination of violence
against women. She is also launching a project called "The other face
of Bulgaria" aiming to prevent the cases of violence against women by
disfiguring their faces with acid and to help the victims of these
crimes.

Dr. Parvanova is also actively working on the issues of children's
rights and child protection. She intends to launch a campaign in
Bulgaria and at European level for the protection of children against
violence, elimination of the discrimination of the state towards
children victims of such crimes and adopting harsher punishments for
the perpetrators.

http://parvanova.eu/main.php?id=32   Etienne MAURY

etienne.maury@...

Head of office and Parliamentary adviser

Etienne began his professional career in the field of media and
communication. He spent several months campaigning for Reporters
without Borders in Brussels, and has also worked at the Agence
France-Presse in Paris within the communication department.

He started working in the European Parliament in 2006, and already
joined Antonyia Parvanova's team when she became Member of European
Parliament in 2007.

After two years working as European affairs consultant in the field of
public health, Etienne came back at the beginning of this mandate to
be head of office and parliamentary adviser. He covers the
parliamentary and legislative work for the Committee on the
Environment, Public Health and Food Safety (ENVI) and the Committee on
the Internal Market and Consumer Protection (IMCO), focusing mainly on
issues related to public health and the healthcare sector.

As Head of office, Etienne follows Antonyia's work as Vice-President
of the ALDE Group. He is also coordinating Antonyia's calendar and is
in charge of her media relations.

Etienne has a background in political sciences, European affairs and
public relations. He has a master degree in Information and
Communication from the University of Paris-Sorbonne, and a master
degree in political sciences and European public policies from the
Strasbourg Institute of Political Studies. He is a lecturer at the
Institute of Political Studies (Lille University).

Etienne is a French native and is fluent in English and Spanish. He
just started to learn Bulgarian.


"There was discussion on the metabolism of aspartame and the
consideration of metabolites including methanol.
The National Experts agreed that there should be more clarity about
the metabolism of aspartame."

http://www.efsa.europa.eu/en/events/event/af091110-m.pdf

SCIENTIFIC COMMITTEE AND ADVISORY FORUM UNIT

European Food Safety Authority - Largo N. Palli 5/a, I - 43100 Parma

Tel: (+39) 0521 036 111 • Fax: (+39) 0521 036 110 •
afsecretariat@... • www.efsa.europa.eu

Parma, 7 January 2010

Minutes of the National Experts Meeting on Aspartame
Porto, Portugal, 10-11 November 2009
(Agreed on 19 January, 2010)

Participants

National Experts:
Hannu Raunio (FI),
Iona Pratt (IE),
Indre Karpoviene (LT),
Jacqueline J.M. Castenmiller (NL),
Andre H. Penninks* (NL),
Tor Øystein Fotland (NO),
Maria de Lourdes Bastos (PT),
Maria Conceiç�o Branco Montenegro* (PT),
Angelina Lopes Simões Pena* (PT),
Marica Theiszová* (SK),
Martina Valachovi�ová (SK),
Nils-Gunnar Ilbäck* (SE),
Stephen Atkin* (UK),
Natalie Thatcher* (UK)
(* Organising Team Member)

EFSA:
Gian Luca Bonduri,
Georgi Nikolaev Grigorov,
Miriam Jacobs,
Hugues Kenigswald,
Djien Liem,
Jeffrey Moon,
Torben Nilsson,
Karen Talbot.

1. Opening of the meeting

Djien Liem, Head of Scientific Committee and Advisory Forum Unit of
EFSA, welcomed
the National Experts to the meeting and invited them to introduce themselves.

Djien Liem provided an overview of the objectives for the meeting and
highlighted the
fact that the work on preparing a report was undertaken at the request
of the Advisory
Forum not because of new safety concerns, but to address remaining
public concerns.

Apologies were noted from representatives of
The Netherlands, Denmark, Finland, Cyprus, Ireland, Czech Republic and
Slovak Republic.

2. Adoption of the agenda
The Agenda was presented and adopted without changes.  No additional items were
raised.

3.  Declarations of interests
In accordance with EFSA’s Policy on Declarations of Interests, EFSA
screened the Annual Declaration of Interest filled in by the invited
experts.
No conflicts of interests related to the issues discussed in this
meeting have been identified during the screening
process.

Stephen Atkin declared that he was currently involved in undertaking a
pilot study of
clinical trials funded by the Food Standards Agency (FSA) UK.
Iona Pratt informed the meeting that she was also a member of
EFSA’s Panel on Food Additives and Nutrient Sources added to Food (ANS) .

These additional interests were not deemed to represent a conflict of interest.

4.  Introduction and background

The background to the work of the Organising Team was presented,
noting that since
the preliminary National Experts meeting in April, all the additional
identified publications
had been considered and a database of anecdotal case reports had been
established.

5.  Presentation and discussion/Anecdotal data analysis

Information on the establishment of a database and the subsequent
analysis of the anecdotal case information that had been carried out
was presented.
It was noted that in general the anecdotal information lacked
information on exposure, diet, health and other relevant factors which
prevents establishing cause and effect.
It was also noted that the large number of assumptions made about the
data and the limitations in the data made interpretation difficult and
that the data was not gathered within a proper framework for
scientific analysis.
The chairman summarised the discussion noting that there were
limitations in the anecdotal data which prevented conclusive
interpretation but the information and analysis could be useful as a
starting point for any further investigations.
The chairman considered it important to note in the report the
‘lessons learnt’ on the limitations of such information and what can
and can not be done with it.

6.  Presentation and discussion/Endpoint updates

Each of the experts of the Organising Team presented a short summary
on each endpoint considered by way of an update on the information
presented at the National Expert meeting held on 2-3 April, 2009.

The National Experts agreed that the consideration of satiation and
appetite needed clarification on the context in relation to aspartame
use.

There was discussion on the metabolism of aspartame and the
consideration of metabolites including methanol.
The National Experts agreed that there should be more clarity about
the metabolism of aspartame.

With regard to carcinogenicity, the National Experts noted the EFSA
Opinions on the studies carried out by the European Ramazzini
Foundation (ERF) and also other papers commenting on the protocols
used by the ERF.
Djien Liem noted that it was not possible to prepare conclusions and
recommendations
for the Advisory Forum until all the issues raised in the discussions
could be considered.

7. Summary of discussions and Next steps

Djien Liem briefly summarised the discussions, highlighting the areas
of concern for the
finalisation of the report, particularly in relation to the anecdotal
information and the conclusions.

The suggested timeframe for the completion of the report was no later
than January.

The report would then be prepared for consultation and forwarded to
the Advisory Forum for the February meeting.

Djien Liem thanked the participants for their contributions to the
meeting, the EFSA Staff
involved for their support and brought the meeting to a close.


http://www.youtube.com/watch?v=kTzOmk9S0P8&feature=related
video 1:29:55
After 7000 miles, and 25 hours of footage, "Sweet Misery" reveals one
of the most pervasive, insidious forms of corporate negligence in the
history of the industrial revolution.
The toxic long-term effects of aspartame are often dismissed as a
"hoax" by the sweetener industry and at least five other Internet
websites. The real footwork, however, unravels something less
comforting than a mere "Hoax." "Sweet Misery" is a documentary just
released by Sound and Fury Productions.
http://www.soundandfuryproductions.com/


http://www.youtube.com/watch?v=JkS1adbM8Po&feature=related
video 10:00  part 1 of 3  108,061 views
Uploaded by mercola on Jul 23, 2010
http://articles.mercola.com/sites/articles/archive/2010/07/31/aspartame-update.a\
spx
video Dr. Joseph Mercola, author of two New York Times best-sellers,
exposes the questionable history of aspartame and why you should stay
away from this dangerous artificial sweetener if you care for your
health. (Part 1 of 3)
Aspartame’s Dangers, Side Effects and FDA Approval Explained
Posted By Dr. Mercola | July 31 2010 | 364,457 views


aspartame water in rats for 6 months causes liver harm, RH Nair et al,
Mahatma Gandhi U, Food Chem Toxicol 2011.03.02: Rich Murray 2011.03.12
http://rmforall.blogspot.com/2011_03_01_archive.htm
Saturday, March 12, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1620
[ you may have to Copy and Paste URLs into your browser ]


http://www.ncbi.nlm.nih.gov/pubmed/21376768

Food Chem Toxicol. 2011 Mar 2. [Epub ahead of print]
Effect of long term intake of aspartame on antioxidant defense status in liver.
Abhilash M, Paul MV, Varghese MV, Nair RH.
School of Biosciences, Mahatma Gandhi University,
Kottayam, Kerala, India, 686560.
harikumarannair@..., harinair@...,


careful expert lifetime study on mice shows liver and lung cancers
from aspartame, M Soffritti et al, Ramazzini Institute, Italy, checked
by US National Toxicology Program experts, confirms many previous
studies from 2001 on: Rich Murray 2011.02.27
http://rmforall.blogspot.com/2011_02_01_archive.htm
Sunday, February 27, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1619
[you may have to Copy and Paste URLs into your browser]

re GC Ebers study, females harmed more by body making methanol into
formaldehyde in brain via ADH enzyme: 589 references, WC Monte,
retired Prof. Nutrition: Rich Murray 2011.01.08
http://rmforall.blogspot.com/2011_01_01_archive.htm
Saturday, January 8, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1614
[you may have to Copy and Paste URLs into your browser]

Woodrow C Monte, PhD, Emiritus Prof. Nutrition gives many PDFs of
reseach -- methanol (11% of aspartame) puts formaldehyde into brain
and body -- multiple sclerosis, Alzheimer's, cancers, birth defects,
headaches: Rich Murray 2010.05.13
http://rmforall.blogspot.com/2010_05_01_archive.htm
Thursday, May 13, 2010
http://groups.yahoo.com/group/aspartameNM/message/1601

[ Other formaldehyde sources include alcohol drinks and
tobacco and wood smoke,
while adequate folic acid levels protect most people. ]

http://whilesciencesleeps.com/about

http://while-science-sleeps.com/references/pdf/586
[ summary, not peer reviewed ]
Monte WC.
Methanol: A chemical Trojan horse as the root of the inscrutable U.
Medical Hypotheses 2010;74(3):493-6
DOI 2010.10.16

Monte WC.
Bittersweet: Aspartame Breast Cancer Link.
Fitness Life 2008 Jan. 34: 32-36

Monte WC.
A Deadly Experiment. Methanol and MS,
Fitness Life 2007 Dec. 34: 36-41

Monte WC.
Sickly Sweet: Is your Diet Sweetener killing you?
Fitness Life 2007 Nov. 33: 31-33

http://whilesciencesleeps.com/references
589 references for above articles and upcoming book

http://whilesciencesleeps.com/montediet
[ and Fitness Life 2007 Dec. 34: 36-41 ]

Methanol: Where Is It Found? How Can It Be Avoided?

AVOID the following, ranked in order of greatest danger:

1. Cigarettes.
2. Diet foods and drinks with aspartame.
3. Fruit and vegetable products and their juices in bottles,
cans, or pouches.
4. Jellies, jams, and marmalades not made fresh and kept
refrigerated.
5. Black currant and tomato juice products, fresh or
processed.
6. Tomato sauces, unless first simmered at least 3 hours
with an open lid.
7. Smoked food of any kind, particularly fish and meat.
8. Sugar-free chewing gum.
9. Slivovitz: You can consume one alcoholic drink a day
on this diet -- no more! [ no fruit brandies ]
10. Overly ripe or near rotting fruits or vegetables.

Selection from Article 2, Fitness Life, December 2007, and
well discussed in the DVD video:

"Identical Symptoms of MS, Methanol Poisoning
and Aspartame Toxicity

The symptoms of multiple sclerosis (44, 83, 85, 169), chronic
and acute methanol poisoning (13, 144, 189), and Aspartame
toxicity (54, 58, 93, 181), are in all ways identical.

There is nothing that happens to the human body from the
toxic effect of methanol that has not been expressed during
the course of MS... nothing (143, 144).

This generalization extends even to the remarkable
opthomological conditions common to both: transitory optic
neuritis and retrolaminar demyelinating optic neuropathy with
scotoma of the central visual field (which occasionally
manifests as unilateral temporary blindness (85, 138, 163).

In fact, these opthomological symptoms have been thought of
for years in their respective literatures to be "tell tale"
indications for the differential diagnosis for each of these
maladies independently (85, 138, 148, 163, 169).

The common symptoms of
headache (13, 83, 181, 189),
nervousness (13, 83, 181),
depression (58, 83, 189, 181),
memory loss (18, 147, 85, 169, 181),
tingling sensations (13, 85, 168, 138, 169),
pain in the extremities (13, 85, 169),
optic neuritis (85, 138, 148, 163, 169),
bright lights in the visual field (139, 83),
seizures (21, 83, 160),
inability to urinate or to keep from urinating (139, 146, 167)
are all shared by each of these conditions and shared yet
again by complaints from aspartame poisoning
(54, 58, 93, 181).

I take these strikingly similar symptom patterns as evidence
that these disorders act on identical components of the
central nervous system and in the same way.

The "Miracle" that MS shares with Methanol poisoning

In the early stages of MS, or when a non-lethal dose of
methanol has been administered, complete recovery is a
possibility.

The only two afflictions for which such dramatic "remissions"
are reported from identical neuromuscular and opthomological
damage, even "blindness" is relapsing-remitting multiple
sclerosis (85) and methyl alcohol poisoning (138, 163).

The pathology of the two maladies is in may ways identical,
particularly when it comes to destruction of the myelin
sheath with no harm to the axon itself (18, 148, 176).

Sex Ratios for MS and Aspartame Reactions

Women bear the brunt of multiple sclerosis (91a-c) and lupus
(SLE)(73) with fully three-fold representations in infliction
numbers over men for both diseases.

This is exactly the proportion represented by adverse
reactors to Aspartame reported by the US Center for
Disease Control in their study of 1984 (58).

The Center found three women to every man whose
Aspartame consumption complaints were serious enough
to warrant investigation (93).

Although the female/male ratio for those stricken with MS has
always been high, recent estimates place it at over 3 to 1
(91, 91a, 91c).

What might account for the difference across sexes in
incidence?

A study published in the New England Journal of Medicine
(94) reports biopsies of the gastric lining of men and women.

A result was that the concentration of ADH in the
gastric lining of men was much higher than for woman.

Men have the advantage of removing methanol from the
bloodstream four times faster on an equal-body-size basis
than women.

Thus, for men, methanol is more likely to be removed from the
blood before it reaches the brain.

The brain is spared but the methanol removed would still be
metabolized to formaldehyde in the gut where it would reap
its havoc on a more forgiving organ.

This may help explain why men have more gastrointestinal
complaints from both methanol and Aspartame consumption
(93, 99).

On the other hand, women's complaints from both more
frequently involve serious neurological complications."...
______________________________________________


methanol (11% of aspartame), made by body into
formaldehyde in many vulnerable tissues, causes modern
diseases of civilization, summary of a century of research,
Woodrow C Monte PhD, Medical Hypotheses journal:
Rich Murray 2009.11.15
http://rmforall.blogspot.com/2009_11_01_archive.htm
Sunday, November 15, 2009
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1589
[you may have to Copy and Paste URLs into your browser]

aspartame abstinance cures fibromyalgia chronic pain in 2 French
adults: R Ciappuccini et al, Clin Exp Rheumatol 2010 Nov: Rich Murray
2010.02.19
http://rmforall.blogspot.com/2011_02_01_archive.htm
Saturday, February 19, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1617
[you may have to Copy and Paste URLs into your browser]

formaldehyde from 0.2 mg daily methanol from aspartame in Singulair
(montelukast) chewable asthma medicine causes severe allergic
dermatitis in boy, SE Jacob et al, Pediatric Dermatology 2009 Nov:
Rich Murray 2010.09.27
http://rmforall.blogspot.com/2010_09_01_archive.htm
Monday, September 27, 2010
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1613
[you may have to Copy and Paste URLs into your browser]
______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-819-7388 rmforall@...

http://groups.yahoo.com/group/AstroDeep/messages

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 118 members, 1,621 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1225 members, 24,315 posts in a public archive

http://groups.yahoo.com/group/rmforall/messages

participant, Santa Fe Complex www.sfcomplex.org
______________________________________________

Merisant "Equal" aspartame USA sales still falling for years to 7%,
while stevia rises to 34%: Duane Stanford, Business Week: Rich Murray
2011.04.29
http://rmforall.blogspot.com/2011_04_01_archive.htm
Friday, April 29, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1622
[ you may have to Copy and Paste URLs into your browser ]
______________________________________________


"U.S. sugar substitute sales rose 3.7 percent in the last year, aided
by the rapid growth of all-natural sweeteners derived from leaves of
the stevia plant.
Sales of Splenda, Sweet'N Low, and Equal all declined."

http://www.businessweek.com/magazine/content/11_19/b4227017750321.htm

FOOD April 28, 2011, 5:00PM EST text size: TT
Ailing Merisant Looks for La Dolce Vita
The aspartame maker puts the Equal brand on other types of sweeteners

Illustrations by Al Murphy

By Duane Stanford
BW MAGAZINE
May 2, 2011

Early last year, Merisant Chief Executive Officer Paul Block found
himself in a sticky situation.
Recently emerged from bankruptcy, the sweetener maker relied on
aspartame -- an aging sugar substitute long dogged by concerns that
its use increased cancer risks -- for almost 90 percent of its
revenue.
Sales of Merisant's flagship Equal, whose blue packets were once as
ubiquitous as forks on restaurant tables, had been dissolving for
several years.

With less than $300 million in global sales and a balance sheet that
had been wrecked by the recession, Block knew Merisant was in no
position to develop a new patented sweetener of its own.
His solution: Reject the "one-brand, one sweetener" strategy the $2
billion industry had hewed to for decades.
Block decided to slap the Equal name on a range of popular sweetener
ingredients already sold by competitors and then try to out-market the
rivals.
"It's going from dogma to heresy," he says.

For much of the 1990s, Equal was the market leader.
Then in 1998 the Food & Drug Administration approved a sweetener
called sucralose.
Ingredient company Tate & Lyle, along with its retail marketing
partner Johnson & Johnson (JNJ), branded their tabletop version
Splenda and packaged it in bright yellow packets.
Unlike aspartame, however, sucralose didn't break down as easily when
heated and was ideal for baking.
Splenda's marketing also played off consumers' suspicions about aspartame.
By the mid-2000s, Splenda overtook Equal.

Splenda now holds 48 percent of the U.S. sugar substitute retail
market, excluding Wal-Mart Stores (WMT), according to researcher
SymphonyIRI Group.
Cumberland Packing's Sweet'N Low is a distant No. 2 with an 11 percent share,
while No. 5 Equal controls about 7 percent.
U.S. sugar substitute sales rose 3.7 percent in the last year, aided
by the rapid growth of all-natural sweeteners derived from leaves of
the stevia plant.
Sales of Splenda, Sweet'N Low, and Equal all declined.
[ Stevia is about 34 percent. ]

To counter Equal's 10 percent sales drop in the past year, Block has
introduced a new sucralose-based Equal in a yellow packet to take on
Splenda, whose patents recently expired.
New pink packets of a saccharin-based version of Equal this year will
go head-to-head with Sweet'N Low, years past its patent.
Green packets of stevia-based Equal are on the way as well.
Merisant is marketing sweetener caddies with all four colors to restaurants.
"We call it our rainbow strategy," Block says.

Block was named a Brandweek Marketer of the Year in 1998 after
launching Dannon Natural Spring Water for foodmaker Danone and turning
it into America's largest bottled-water brand within two years.
He did it by pulling a hodgepodge of regional spring waters, all
marketed separately, under a single brand.
Block says it won't be enough to merely copy other sweeteners and
group them under a single umbrella.
He says Merisant will have to make Equal a better value as well.

In the U.S., Equal Yellow costs about 20 percent less than Splenda.
James Targett, an analyst with Berenberg Bank in London, says Merisant
will have to undercut it more significantly to take meaningful share.
"Once people find a sweetener they think tastes good in their coffee
or on their breakfast cereal, they tend to stick with it," he says.

Rather than blanketing the market with brand advertising, Block is
counting on the Equal name to lure consumers once Merisant gets its
rainbow of sweeteners on as many store shelves and restaurant tables
as possible.
Block hopes to have blue, pink, and yellow versions of Equal in 70
percent of large U.S. grocers by yearend.

One big risk remains: Surging sales of all-natural, no-calorie
sweeteners could make artificial sweeteners less relevant.
Truvia, developed by Cargill from stevia leaves and marketed with help
from Coca-Cola (KO), grew 66 percent last year and is the
fourth-largest sugar substitute in the U.S.
Merisant, in partnership with PepsiCo (PEP), has its own stevia-based
sweetener called Pure Via.
Others are rushing in with similar concoctions.
Explains Block: "You can't patent a plant."

The bottom line: Merisant, maker of the flagging Equal brand of
aspartame, is slapping the Equal name on other more-popular
sweeteners.

Stanford is a reporter for Bloomberg News.  dstanford2@...
______________________________________________


aspartame doubts aired by EU MPs Corinne Lepage and Antonyia Parvanova
-- EFSA  National Experts agreed that "there should be more clarity
about the metabolism of aspartame": Rich Murray 2011.04.24
http://rmforall.blogspot.com/2011_04_01_archive.htm
Sunday, April 24, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1621
[ you may have to Copy and Paste URLs into your browser ]

methanol (11% of aspartame), made by body into
formaldehyde in many vulnerable tissues, causes modern
diseases of civilization, summary of a century of research,
Woodrow C Monte PhD, Medical Hypotheses journal:
Rich Murray 2009.11.15
http://rmforall.blogspot.com/2009_11_01_archive.htm
Sunday, November 15, 2009
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1589
[ you may have to Copy and Paste URLs into your browser ]

aspartame abstinance cures fibromyalgia chronic pain in 2 French
adults: R Ciappuccini et al, Clin Exp Rheumatol 2010 Nov: Rich Murray
2010.02.19
http://rmforall.blogspot.com/2011_02_01_archive.htm
Saturday, February 19, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1617
[ you may have to Copy and Paste URLs into your browser ]

formaldehyde from 0.2 mg daily methanol from aspartame in Singulair
(montelukast) chewable asthma medicine causes severe allergic
dermatitis in boy, SE Jacob et al, Pediatric Dermatology 2009 Nov:
Rich Murray 2010.09.27
http://rmforall.blogspot.com/2010_09_01_archive.htm
Monday, September 27, 2010
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1613
[ you may have to Copy and Paste URLs into your browser ]
______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298 rmforall@...

http://groups.yahoo.com/group/AstroDeep/messages

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 118 members, 1,622 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1226 members, 24,319 posts in a public archive

http://groups.yahoo.com/group/rmforall/messages

participant, Santa Fe Complex www.sfcomplex.org
_______________________________________________

Dr. Oz TV show -- organic low fat, low protein plant based diet
prevents and cures cancer, heart disease, hypertension, diabetes,
obesity... 7:29 video re new movie ForksOverKnives.com: Rich Murray
2011.05.01
http://rmforall.blogspot.com/2011_05_01_archive.htm
Sunday, May 1, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1623
[ you may have to Copy and Paste URLs into your browser ]
______________________________________________


Dr. Oz TV show Wednesday, April 27, 2011
re film "Forks Over Knives" --

http://www.vegsource.com/news/2011/04/forks-over-knives-on-dr-oz-video.html

ForksOverKnives.com

VegSource.com

DrMcDougall.com
______________________________________________


aspartame doubts aired by EU MPs Corinne Lepage and Antonyia Parvanova
-- EFSA  National Experts agreed that "there should be more clarity
about the metabolism of aspartame": Rich Murray 2011.04.24
http://rmforall.blogspot.com/2011_04_01_archive.htm
Sunday, April 24, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1621
[ you may have to Copy and Paste URLs into your browser ]

methanol (11% of aspartame), made by body into
formaldehyde in many vulnerable tissues, causes modern
diseases of civilization, summary of a century of research,
Woodrow C Monte PhD, Medical Hypotheses journal:
Rich Murray 2009.11.15
http://rmforall.blogspot.com/2009_11_01_archive.htm
Sunday, November 15, 2009
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1589
[ you may have to Copy and Paste URLs into your browser ]

aspartame abstinance cures fibromyalgia chronic pain in 2 French
adults: R Ciappuccini et al, Clin Exp Rheumatol 2010 Nov: Rich Murray
2010.02.19
http://rmforall.blogspot.com/2011_02_01_archive.htm
Saturday, February 19, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1617
[ you may have to Copy and Paste URLs into your browser ]

formaldehyde from 0.2 mg daily methanol from aspartame in Singulair
(montelukast) chewable asthma medicine causes severe allergic
dermatitis in boy, SE Jacob et al, Pediatric Dermatology 2009 Nov:
Rich Murray 2010.09.27
http://rmforall.blogspot.com/2010_09_01_archive.htm
Monday, September 27, 2010
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1613
[ you may have to Copy and Paste URLs into your browser ]
______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-819-7388  rmforall@...

http://groups.yahoo.com/group/AstroDeep/messages

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 118 members, 1,623 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1226 members, 24,320 posts in a public archive

http://groups.yahoo.com/group/rmforall/messages

participant, Santa Fe Complex www.sfcomplex.org
_______________________________________________

aspartame, acesulfame K, saccharin, fructose each "caused accelerated
senescence in human dermal fibroblasts" (re metabolic syndrome and
diabetes), Kyung-Hyun Cho et al, Yeungnam University, Korea, Mol
Cells. 2011 Apr 21: Rich Murray 2011.05.21
http://rmforall.blogspot.com/2011_05_01_archive.htm
Saturday, May 21, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1624
[ you may have to Copy and Paste URLs into your browser ]
______________________________________________


[ This research has to consider that the 11% methanol (wood alcohol)
part of aspartame in humans is converted into formaldehyde by the ADH
enzyme directly in tissues: liver, brain, retina, kidney, skin,
muscle, prostate, breast, womb, leading to cumulative localized
damage.  Prof. Woodrow C. Monte (retired) www.WhileScienceSleeps.com ]


"These results suggest that long-term consumption of AS [Artificial
Sweeteners] might accelerate atherosclerosis and senescence via
impairment of function and structure of apoA-I and HDL."

http://www.ncbi.nlm.nih.gov/pubmed/21533907

Mol Cells. 2011 Apr 21. [Epub ahead of print]
Modified apolipoprotein (apo) A-I by artificial sweetener causes
severe premature cellular senescence and atherosclerosis with
impairment of functional and structural properties of apoA-I in
lipid-free and lipid-bound state.
Jang W,
Jeoung NH,
Cho KH.
Source
School of Biotechnology, Yeungnam University, Gyeongsan, 712-749,
Korea.  chok@...

[ Correspondence to: Dr Kyung-Hyun Cho, School of Biotechnology,
Aging-associated Vascular Disease Research Center, Yeungnam
University, Gyeongsan, 712-749, Korea
E-mail: chok@... ]

Abstract

Long-term consumption of artificial sweeteners (AS) has been the
recent focus of safety concerns.

However, the potential risk of the AS in cardiovascular disease and
lipoprotein metabolism has not been investigated sufficiently.

We compared the influence of AS (aspartame, acesulfame K, and
saccharin) and fructose in terms of functional and structural
correlations of apolipoprotein (apo) A-I and high-density lipoproteins
(HDL), which have atheroprotective effects.

Long-term treatment of apoA-I with the sweetener at physiological
concentration (3 mM for 168 h) resulted in loss of antioxidant and
phospholipid binding activities with modification of secondary
structure.

The AS treated apoA-I exhibited proteolytic cleavage to produce 26 kDa-fragment.

They showed pro-atherogenic properties in acetylated LDL phagocytosis
of macrophages.

Each sweetener alone or sweetener-treated apoA-I caused accelerated
senescence in human dermal fibroblasts.

These results suggest that long-term consumption of AS might
accelerate atherosclerosis and senescence via impairment of function
and structure of apoA-I and HDL.

PMID: 21533907



Related Citations:

"Non-enzymatic glycation of serum apolipoproteins is a main feature of
diabetes mellitus under hyperglycemia.

Advanced glycation end products are implicated in the development of
aging and metabolic syndrome, including premature atherosclerosis in
diabetic subjects.

ApoA-I is the principal protein constituent of HDL."

2. http://www.ncbi.nlm.nih.gov/pubmed/20059975
Fructated apolipoprotein A-I showed severe structural modification and
loss of beneficial functions in lipid-free and lipid-bound state with
acceleration of atherosclerosis and senescence.
Park KH,
Jang W,
Kim KY,
Kim JR,
Cho KH.
Biochem Biophys Res Commun. 2010 Feb 12;392(3):295-300. Epub 2010 Jan 7.
PMID: 20059975 [PubMed - indexed for MEDLINE]

Source
Aging-associated Vascular Disease Research Center, Yeungnam
University, Gyeongsan 712-749, Republic of Korea.

Abstract

Non-enzymatic glycation of serum apolipoproteins is a main feature of
diabetes mellitus under hyperglycemia.

Advanced glycation end products are implicated in the development of
aging and metabolic syndrome, including premature atherosclerosis in
diabetic subjects.

ApoA-I is the principal protein constituent of HDL.

In this study, glycated human apoA-I (gA-I) by fructation was
characterized on functional and structural correlations in lipid-free
and lipid-bound states.

The gA-I showed more spontaneous multimeric band formation up to
pentamer and exhibited slower elution profile with more degraded
fragments from fast protein liquid chromatography.

The gA-I showed modified secondary structure from fluorescence and
circular dichroism analysis.

Reconstituted high-density lipoprotein (rHDL) containing the gA-I had
less content of phospholipid with a much smaller particle size than
those of rHDL-containing nA-I (nA-I-rHDL).

The rHDL containing gA-I (gA-I-rHDL) consisted of less molecular
number of apoA-I than nA-I-rHDL with decreased alpha-helical content.

Treatment of the gA-I-rHDL induced more atherogenic process in
macrophage cell and premature senescence in human dermal fibroblast
cell.

Conclusively, fructose-mediated apoA-I glycation resulted in severe
loss of several beneficial functions of apoA-I and HDL regarding
anti-senescence and anti-atherosclerosis activities due to a lack of
anti-oxidant activity with increased susceptibility of protein
degradation and structural modification.

PMID: 20059975 [PubMed - indexed for MEDLINE]


"The antiatherogenic properties of HDL can, however be compromised in
metabolic diseases associated with accelerated atherosclerosis.

Indeed, metabolic syndrome and type 2 diabetes are characterized not
only by elevated cardiovascular risk and by low HDL-cholesterol
(HDL-C) levels but also by defective HDL function."

4. http://www.ncbi.nlm.nih.gov/pubmed/16968945
Functionally defective high-density lipoprotein: a new therapeutic
target at the crossroads of dyslipidemia, inflammation, and
atherosclerosis.
Kontush A, Chapman MJ.
Pharmacol Rev. 2006 Sep;58(3):342-74. Review.
PMID: 16968945 [PubMed - indexed for MEDLINE]

Pharmacol Rev. 2006 Sep;58(3):342-74.
Functionally defective high-density lipoprotein: a new therapeutic
target at the crossroads of dyslipidemia, inflammation, and
atherosclerosis.
Kontush A, Chapman MJ.
Source
Dyslipoproteinemia and Atherosclerosis Research Unit, National
Institute for Health and Medical Research, Hôpital de la Pitié, 83
boulevard de l'Hôpital, 75651 Paris Cedex 13, France.
kontush@...

Abstract

High-density lipoproteins (HDL) possess key atheroprotective
biological properties, including cellular cholesterol efflux capacity,
and anti-oxidative and anti-inflammatory activities.

Plasma HDL particles are highly heterogeneous in physicochemical
properties, metabolism, and biological activity.

Within the circulating HDL particle population, small, dense HDL
particles display elevated cellular cholesterol efflux capacity,
afford potent protection of atherogenic low-density lipoprotein
against oxidative stress and attenuate inflammation.

The antiatherogenic properties of HDL can, however be compromised in
metabolic diseases associated with accelerated atherosclerosis.

Indeed, metabolic syndrome and type 2 diabetes are characterized not
only by elevated cardiovascular risk and by low HDL-cholesterol
(HDL-C) levels but also by defective HDL function.

Functional HDL deficiency is intimately associated with alterations in
intravascular HDL metabolism and structure.

Indeed, formation of HDL particles with attenuated antiatherogenic
activity is mechanistically related to core lipid enrichment in
triglycerides and cholesteryl ester depletion, altered apolipoprotein
A-I (apoA-I) conformation, replacement of apoA-I by serum amyloid A,
and covalent modification of HDL protein components by oxidation and
glycation.

Deficient HDL function and subnormal HDL-C levels may act
synergistically to accelerate atherosclerosis in metabolic disease.

Therapeutic normalization of attenuated antiatherogenic HDL function
in terms of both particle number and quality of HDL particles is the
target of innovative pharmacological approaches to HDL raising,
including inhibition of cholesteryl ester transfer protein, enhanced
lipidation of apoA-I with nicotinic acid and infusion of reconstituted
HDL or apoA-I mimetics.

A preferential increase in circulating concentrations of HDL particles
possessing normalized antiatherogenic activity is therefore a
promising therapeutic strategy for the treatment of common metabolic
diseases featuring dyslipidemia, inflammation, and premature
atherosclerosis.

PMID: 16968945


5. http://www.ncbi.nlm.nih.gov/pubmed/21415260
High-Density Lipoprotein (HDL) From Elderly and Reconstituted HDL
Containing Glycated Apolipoproteins A-I Share Proatherosclerotic and
Prosenescent Properties With Increased Cholesterol Influx.
Park KH,
Cho KH.
J Gerontol A Biol Sci Med Sci. 2011 May;66(5):511-20. Epub 2011 Mar 17.
PMID: 21415260 [PubMed - in process]

J Gerontol A Biol Sci Med Sci. 2011 May;66(5):511-20. Epub 2011 Mar 17.
High-Density Lipoprotein (HDL) From Elderly and Reconstituted HDL
Containing Glycated Apolipoproteins A-I Share Proatherosclerotic and
Prosenescent Properties With Increased Cholesterol Influx.
Park KH, Cho KH.
Source
School of Biotechnology, Yeungnam University, Gyeongsan, 712-749,
South Korea. chok@...

Abstract

High-density lipoprotein (HDL) is a strong antioxidant,
anti-inflammatory, and antisenescence molecule.

However, in the current study, HDL from the elderly group (E-HDL)
exhibited increased glycation with apolipoprotein (apo) A-I
multimerization and decreased phospholipid content.

Similarly, glycated apoA-I (gA-I) by fructosylation has a covalently
multimerized band without a crosslinker and impaired
phospholipid-binding ability.

Treatment of human dermal fibroblasts and macrophages with E-HDL and
gA-I caused more severe cellular senescence and foam cell formation,
respectively;

however, treatment with HDL from a young group (Y-HDL) and native
apoA-I (nA-I) suppressed senescence and atherosclerosis.

E-HDL(3) and reconstituted HDL (rHDL) containing gA-I showed enhanced
cholesterol influx into macrophages compared with Y-HDL(3) and
nA-I-rHDL.

In conclusion, E-HDL and gA-I-rHDL share similar physiologic
properties in macrophages and human dermal fibroblasts.

E-HDL and gA-I-rHDL exacerbated cellular senescence and
atherosclerosis with increased cellular cholesterol influx.

PMID: 21415260 [PubMed - in process]


http://www.spandidos-publications.com/ijmm/25/1/129  free full text pdf

The functional and compositional properties of lipoproteins are
altered in patients with metabolic syndrome with increased cholesteryl
ester transfer protein activity
Authors:
Ki-Hoon Park,
Dong-Gu Shin,
Jae-Ryong Kim,
Joo-Heon Hong,
Kyung-Hyun Cho
Affiliations: School of Biotechnology, Aging-associated Vascular
Disease Research Center, Yeungnam University, Gyeongsan, 712-749,
Korea
Doi: 10.3892/ijmm_00000322
Pages: 129-136
International Journal of Molecular Medicine
January 2010
Volume 25 Number 1


http://www.yu.ac.kr/_english/about/index.php?c=about_08_read&seq=80&page=7

YU   2010-04-20 17:16:49  824

Professor Cho, Kyung-Hyun's Team of the School of Biotechnology
Presents New Hope for Incurable Disease Treatment [80]

[ photo ]

"World's First" Gene Treatment Medicine Effect Improved by 10 Fold
Completed publication on SCI Journal and Patent Registration
[Jan 27, 2010]

Professor Cho, Kyung-Hyun explains the effects of the newly developed
gene treatment medicine [ photo ]

The effects of 'gene treatment medicine', which is treated as the
up-and-coming bio-engineering for treatment of incurable diseases such
as cancer, cardiovascular diseases, AIDS, rheumatism, and foot ulcers,
has been greatly improved by a research team of Korea.

Professor Cho, Kyung-Hyun (age 42, photo) of Yeungnam University
School of Biotechnology developed the methods to greatly improve the
delivery efficiency of the existing 'genetic treatment medicine' and
to sharply lower the financial burden while also enhancing the
distribution potential, for the first time in the world.

'Gene treatment medicine' is a method for supplying genes that have
been lost for effectively treating various diseases caused by damaged
or missing DNA. Thus, the key is on how outside genes can be
effectively delivered to the inside of the cell. Currently, the most
widely used method is gene transfer method using an 'adenovirus', but
because it is unstable in room temperature, it has short distribution
periods, and its problem with the gene delivery abilities weakened in
the blood makes it an obstacle in treating incurable diseases.

Thus, Professor Cho used nano bio-technologies to make proteoliposomes
with phospholipids and apolipoproteins, covering the adenovirus in
order to improve gene delivery efficiency by 10 folds, while doubling
the stability, proving it for the first time in the world in vertebrae
models.

The results of this study that was conducted for three years since
2007 receiving support by the Yeungnam University Aging-associated
Vascular Disease Research Center (director, Kim, Jae-ryong) and the
Ministry of Knowledge Economy (Minister Choi, Kyung-hwan) and it was
published in the January 2010 volume of <Human Gene Therapy>, which is
an SCI-level journal in the gene treatment sector. This journal, which
received an impact factor of 4.1 in the biology and medical sector,
was selected as "Top 100 influential journals in medicine and biology
for the past 100 years" by the 2009 World Library Association.

The results of the research of Professor Cho is expected to greatly
contribute to the improved delivery efficiency of adenoviruses, but
all other medicine delivery devices and genetic treatment medicines
such as RNA inhibitors, plasmid DNA, aptamer, etc. Thus, the research
team has registered relevant patents, and is currently negotiating
with domestic and foreign gene treatment medicine production companies
for technology transfer.

In particular, this research is expected to be a period of great
development in the recently rising 'bio-similar pharmaceutical
industry'. 'Bio-similar' refers to reproductive medicines related to
protein compounds among pharmaceuticals whose patents have expired.
When new medicines are developed, international patents usually last
20-25 years. Most original medicines being worth about 1 billion US $
have their patents expired between 2012 and 2013, and thus many
companies are preparing in the competition to develop bio-similars,
which are a type of reproductive generic medicine. The market scale is
estimated at approximately 30 billion US $. Thus, if the results of
this study is used for domestic bio-similar pharmaceutical industry,
it is expected to provide epochal improvements in its international
competitiveness.

Meanwhile, Professor Cho is furthering his studies on genetic
treatment medicine that could be used for not only killing cancer
cells, but utilizing it as the atherosclerosis and aging models based
on this research results.
______________________________________________


Re;  http://www.sweeteners.org/Pdf/conferenceBrochure.pdf

International Sweeteners Association
LOW CALORIE FOODS, BEVERAGES AND SWEETENERS
CAN THEY REALLY CONTRIBUTE TO A HEALTHIER FUTURE?
Bibliothèque Solvay, Brussels
19 May 2011 09.00 - 17.00


aspartame doubts aired by EU MPs Corinne Lepage and Antonyia Parvanova
-- EFSA  National Experts agreed that "there should be more clarity
about the metabolism of aspartame": Rich Murray 2011.04.24
http://rmforall.blogspot.com/2011_04_01_archive.htm
Sunday, April 24, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1621
[ you may have to Copy and Paste URLs into your browser ]


aspartame water in rats for 6 months causes liver harm, RH Nair et al,
Mahatma Gandhi U, Food Chem Toxicol 2011.03.02: Rich Murray 2011.03.12
http://rmforall.blogspot.com/2011_03_01_archive.htm
Saturday, March 12, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1620
[ you may have to Copy and Paste URLs into your browser ]


http://www.ncbi.nlm.nih.gov/pubmed/21376768

Food Chem Toxicol. 2011 Mar 2. [Epub ahead of print]
Effect of long term intake of aspartame on antioxidant defense status in liver.
Abhilash M, Paul MV, Varghese MV, Nair RH.
School of Biosciences, Mahatma Gandhi University,
Kottayam, Kerala, India, 686560.
harikumarannair@..., harinair@...,


careful expert lifetime study on mice shows liver and lung cancers
from aspartame, M Soffritti et al, Ramazzini Institute, Italy, checked
by US National Toxicology Program experts, confirms many previous
studies from 2001 on: Rich Murray 2011.02.27
http://rmforall.blogspot.com/2011_02_01_archive.htm
Sunday, February 27, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1619
[ you may have to Copy and Paste URLs into your browser ]


re GC Ebers study, females harmed more by body making methanol into
formaldehyde in brain via ADH enzyme: 589 references, WC Monte,
retired Prof. Nutrition: Rich Murray 2011.01.08
http://rmforall.blogspot.com/2011_01_01_archive.htm
Saturday, January 8, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1614
[ you may have to Copy and Paste URLs into your browser ]


Woodrow C Monte, PhD, Emiritus Prof. Nutrition gives many PDFs of
reseach -- methanol (11% of aspartame) puts formaldehyde into brain
and body -- multiple sclerosis, Alzheimer's, cancers, birth defects,
headaches: Rich Murray 2010.05.13
http://rmforall.blogspot.com/2010_05_01_archive.htm
Thursday, May 13, 2010
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1601
[ you may have to Copy and Paste URLs into your browser ]

[ Other formaldehyde sources include alcohol drinks and
tobacco and wood smoke,
while adequate folic acid levels protect most people. ]

http://whilesciencesleeps.com/about

http://while-science-sleeps.com/references/pdf/586
[ summary, not peer reviewed ]
Monte WC.
Methanol: A chemical Trojan horse as the root of the inscrutable U.
Medical Hypotheses 2010;74(3):493-6
DOI 2010.10.16

Monte WC.
Bittersweet: Aspartame Breast Cancer Link.
Fitness Life 2008 Jan. 34: 32-36

Monte WC.
A Deadly Experiment. Methanol and MS,
Fitness Life 2007 Dec. 34: 36-41

Monte WC.
Sickly Sweet: Is your Diet Sweetener killing you?
Fitness Life 2007 Nov. 33: 31-33

http://whilesciencesleeps.com/references
589 references for above articles and upcoming book

http://whilesciencesleeps.com/montediet
[ and Fitness Life 2007 Dec. 34: 36-41 ]

Methanol: Where Is It Found? How Can It Be Avoided?

AVOID the following, ranked in order of greatest danger:

1. Cigarettes.
2. Diet foods and drinks with aspartame.
3. Fruit and vegetable products and their juices in bottles,
cans, or pouches.
4. Jellies, jams, and marmalades not made fresh and kept
refrigerated.
5. Black currant and tomato juice products, fresh or
processed.
6. Tomato sauces, unless first simmered at least 3 hours
with an open lid.
7. Smoked food of any kind, particularly fish and meat.
8. Sugar-free chewing gum.
9. Slivovitz: You can consume one alcoholic drink a day
on this diet -- no more! [ no fruit brandies ]
10. Overly ripe or near rotting fruits or vegetables.

Selection from Article 2, Fitness Life, December 2007, and
well discussed in the DVD video:

"Identical Symptoms of MS, Methanol Poisoning
and Aspartame Toxicity

The symptoms of multiple sclerosis (44, 83, 85, 169), chronic
and acute methanol poisoning (13, 144, 189), and Aspartame
toxicity (54, 58, 93, 181), are in all ways identical.

There is nothing that happens to the human body from the
toxic effect of methanol that has not been expressed during
the course of MS... nothing (143, 144).

This generalization extends even to the remarkable
opthomological conditions common to both: transitory optic
neuritis and retrolaminar demyelinating optic neuropathy with
scotoma of the central visual field (which occasionally
manifests as unilateral temporary blindness (85, 138, 163).

In fact, these opthomological symptoms have been thought of
for years in their respective literatures to be "tell tale"
indications for the differential diagnosis for each of these
maladies independently (85, 138, 148, 163, 169).

The common symptoms of
headache (13, 83, 181, 189),
nervousness (13, 83, 181),
depression (58, 83, 189, 181),
memory loss (18, 147, 85, 169, 181),
tingling sensations (13, 85, 168, 138, 169),
pain in the extremities (13, 85, 169),
optic neuritis (85, 138, 148, 163, 169),
bright lights in the visual field (139, 83),
seizures (21, 83, 160),
inability to urinate or to keep from urinating (139, 146, 167)
are all shared by each of these conditions and shared yet
again by complaints from aspartame poisoning
(54, 58, 93, 181).

I take these strikingly similar symptom patterns as evidence
that these disorders act on identical components of the
central nervous system and in the same way.

The "Miracle" that MS shares with Methanol poisoning

In the early stages of MS, or when a non-lethal dose of
methanol has been administered, complete recovery is a
possibility.

The only two afflictions for which such dramatic "remissions"
are reported from identical neuromuscular and opthomological
damage, even "blindness" is relapsing-remitting multiple
sclerosis (85) and methyl alcohol poisoning (138, 163).

The pathology of the two maladies is in may ways identical,
particularly when it comes to destruction of the myelin
sheath with no harm to the axon itself (18, 148, 176).

Sex Ratios for MS and Aspartame Reactions

Women bear the brunt of multiple sclerosis (91a-c) and lupus
(SLE)(73) with fully three-fold representations in infliction
numbers over men for both diseases.

This is exactly the proportion represented by adverse
reactors to Aspartame reported by the US Center for
Disease Control in their study of 1984 (58).

The Center found three women to every man whose
Aspartame consumption complaints were serious enough
to warrant investigation (93).

Although the female/male ratio for those stricken with MS has
always been high, recent estimates place it at over 3 to 1
(91, 91a, 91c).

What might account for the difference across sexes in
incidence?

A study published in the New England Journal of Medicine
(94) reports biopsies of the gastric lining of men and women.

A result was that the concentration of ADH in the
gastric lining of men was much higher than for woman.

Men have the advantage of removing methanol from the
bloodstream four times faster on an equal-body-size basis
than women.

Thus, for men, methanol is more likely to be removed from the
blood before it reaches the brain.

The brain is spared but the methanol removed would still be
metabolized to formaldehyde in the gut where it would reap
its havoc on a more forgiving organ.

This may help explain why men have more gastrointestinal
complaints from both methanol and Aspartame consumption
(93, 99).

On the other hand, women's complaints from both more
frequently involve serious neurological complications."...
______________________________________________


methanol (11% of aspartame), made by body into
formaldehyde in many vulnerable tissues, causes modern
diseases of civilization, summary of a century of research,
Woodrow C Monte PhD, Medical Hypotheses journal:
Rich Murray 2009.11.15
http://rmforall.blogspot.com/2009_11_01_archive.htm
Sunday, November 15, 2009
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1589
[ you may have to Copy and Paste URLs into your browser ]


aspartame abstinance cures fibromyalgia chronic pain in 2 French
adults: R Ciappuccini et al, Clin Exp Rheumatol 2010 Nov: Rich Murray
2010.02.19
http://rmforall.blogspot.com/2011_02_01_archive.htm
Saturday, February 19, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1617
[ you may have to Copy and Paste URLs into your browser ]


formaldehyde from 0.2 mg daily methanol from aspartame in Singulair
(montelukast) chewable asthma medicine causes severe allergic
dermatitis in boy, SE Jacob et al, Pediatric Dermatology 2009 Nov:
Rich Murray 2010.09.27
http://rmforall.blogspot.com/2010_09_01_archive.htm
Monday, September 27, 2010
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1613
[ you may have to Copy and Paste URLs into your browser ]
______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-819-7388             rmforall@...

http://groups.yahoo.com/group/AstroDeep/messages

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

http://groups.yahoo.com/group/aspartameNM/messages
group with 118 members, 1,624 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1225 members, 24,336 posts in a public archive

http://groups.yahoo.com/group/rmforall/messages
______________________________________________

Amid health fears, Diet Coke sweetener [aspartame] in safety
spotlight, Sean Poulter, UK Daily Mail 2011.05.27, 141 comments: Rich
Murray 2011.05.30
http://rmforall.blogspot.com/2011_05_01_archive.htm
Monday, May 30, 2011
[ at end of each long page, click on Older Posts ]
http://groups.yahoo.com/group/aspartameNM/message/1625
[ you may have to Copy and Paste URLs into your browser ]
______________________________________________


http://www.dailymail.co.uk/health/article-1391395/Amid-health-fears-Diet-Coke-sw\
eetner-safety-spotlight.html

Amid health fears, Diet Coke sweetener in safety spotlight
By Sean Poulter
Last updated at 11:24 AM on 27th May 2011

A sweetener used in Diet Coke is to undergo a safety review over fears
that it has harmful effects on human health

An artificial sweetener used in Diet Coke is to undergo an urgent EU
safety review.

Aspartame is ingested every day by millions of people around the world
in more than 6,000 well-known brands of food, drink  and medicine.

However, it has been the subject of a number of studies that appear to
show harmful effects on human health.

One recent study linked diet drinks containing aspartame to premature
births, while another suggested it could cause cancer.

To date, health watchdogs, including the European Food Safety
Authority (EFSA) and the UK’s Food Standards Agency (FSA), have ruled
out any link to ill-health.

But after several MEPs asked for a new investigation following
pressure from European health campaigners, EU Commission officials
have now asked the EFSA to bring forward a review that had been
planned for 2020.

The concern about artificial sweeteners such as aspartame relates to
the fact that they contain methanol, a nerve toxin which can be
metabolised in the body to form two more nerve toxins: formic acid and
formaldehyde, the chemical used to preserve dead bodies.

Earlier this year, experts on Britain’s Committee on Toxicity(CoT)
ruled that ‘long-term exposure to methanol consumed through food,
including from aspartame, is unlikely to be harmful to health’.

The committee pointed out that methanol is also found in fruit and vegetables.

As a result of the experts’ conclusions, the FSA ruled the consumption
of aspartame ‘is not of concern at the current levels of use’.

Despite this verdict, the FSA is currently recruiting volunteers for
an investigation into anecdotal reports of ill health, including
headaches and stomach upsets, associated with aspartame.

The watchdog announced the research project in 2009, however it has
had difficulties recruiting volunteers who claim to suffer problems.

EFSA spokesman, Lucia De Luca, said: ‘Aspartame is one of hundreds of
flavourings. It is on the market because it has been assessed in the
past and considered safe.

‘We have received an official request for a complete re-evaluation of
the safety of aspartame.

‘The re-evaluation is scheduled for 2020 but the Commission asked us
to do this re-evaluation now in the light of recent events.

A study last year of 60,000 mothers-to be found a correlation between
the amount of diet drink consumed and an early birth
‘In the past year, there have been a couple of studies looking at
aspartame and concerns expressed by consumer groups and others.’

In July last year, EU-funded research by Danish scientists, which
looked at almost 60,000 mothers-to-be, found a correlation between the
amount of diet drink consumed and an early birth.

Previously, the Independent Ramazzini Foundation in Italy has
published research suggesting aspartame caused several types of cancer
in rats at doses very close to the current acceptable daily intake for
humans.

Both of these have been evaluated by EFSA experts, who have rejected
any risk to human health.

Aspartame is manufactured by Ajinomoto Sweeteners Europe. The firm
said it welcomes the decision to bring forward the safety evaluation.

A spokesman said: ‘EFSA reaffirmed the safety of aspartame in 2006,
2009 and 2010. In addition, recent allegations about the safety of
aspartame made in France and by a handful of MEPs have already been
dismissed by EFSA.

‘This review of the extensive body of science on aspartame will
provide additional confirmation of the ingredient’s safety.

‘By providing an excellent sweet taste, aspartame makes a useful
contribution to a healthy, calorie-controlled diet and can help people
to avoid overweight and obesity, and their associated diseases.’

Places:
United Kingdom,
France
Organisations:
Committee On Toxicity
Comments (141)

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Aspartame is indeed 11% methanol (wood alcohol), which the human body
quickly turns into formaldehyde via the ADH enzyme, concentrated in
many tissues: liver, kidney, brain, retina, skin, prostate, breast,
womb, muscle -- forming cumulative micro lesions and a wide variety of
symptoms. Other methanol (formaldehyde) sources include wood and
tobacco smoke, dark wines and liquors, fruits and vegetables heated in
sealed metal and glass containers, and aspartame, as well as a variety
of products ranging from medicines to new carpet, drapes, and
furniture to mobile homes. People vary enormously in individual
vulnerability. Folic acid can protect many people. See
while-science-sleeps.com/references/pdf/586 Prof. (retired) Woodrow C.
Monte

- Rich Murray, Santa Fe, New Mexico, USA, 30/5/2011 07:04

I thought this was common knowledge? It still shocks me to see the
amount of overweight kids drinking diet soft drink in the mistaken
idea that adding aspartame to their diet is preferable to more sugar -
doesn't help them lose weight though does it? Diet coke with their Big
Mac meal?

- kiwi abroad, Ireland, 28/5/2011 23:35

Watch "the Truth about Aspartame" by Dr Russell Blaylock.

- Alan, Durham, 28/5/2011 22:09

I know, I know, I wear a tin foil hat but any one noticing that
conspiracy theorists are being proved right more and more? Rumsfeld's
disease has been known about for years.That's why the food companies
changed the labelling to "natural flavors" I guess something produced
from e coli bacteria's excrement is natural. Btw DM, I'm intigued to
know why your article reporting that GMO toxins have been found in 93%
of unborns only stayed up for a couple of hours. Yes it is still
searchable on site, but you would only search for it if you knew it
was there.

- tom bowden, perth australia, 28/5/2011 17:36

It's a choice but the facts have been around for years, I would never
buy food that has any artificial ingredients in but it's up to the
individual.

- quarrybanksurfer, Scotland, 28/5/2011 15:13

'EFSA spokesman, Lucia De Luca, said: "Aspartame is one of hundreds of
flavourings. It is on the market because it has been assessed in the
past and considered safe".' We are dealing with some tricky little
monkeys are we not? It took them years in the US to have this
flavouring legalised and it was done in very murky circumstances with
the help of Donald Rumsfeld who, had an interest in the corporation
that used it. The FSA is not here to look after your health, it is
here to make sure corporations maintain and increase profit. It is
frustrating that we seem to take backward steps all the time on this
sort of issue, indecently propelled by the Agri-corp shill SSEFRA C
Spelman MP.

- Bob, Leeds UK, 28/5/2011 14:22

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do not necessarily reflect the views of MailOnline.
Published by Associated Newspapers Ltd
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______________________________________________


Re; http://www.sweeteners.org/Pdf/conferenceBrochure.pdf

International Sweeteners Association
LOW CALORIE FOODS, BEVERAGES AND SWEETENERS
CAN THEY REALLY CONTRIBUTE TO A HEALTHIER FUTURE?
Bibliothèque Solvay, Brussels
19 May 2011 09.00 - 17.00


aspartame, acesulfame K, saccharin, fructose each "caused accelerated
senescence in human dermal fibroblasts" (re metabolic syndrome and
diabetes), Kyung-Hyun Cho et al, Yeungnam University, Korea, Mol
Cells. 2011 Apr 21: Rich Murray 2011.05.21
http://rmforall.blogspot.com/2011_05_01_archive.htm
Saturday, May 21, 2011
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aspartame doubts aired by EU MPs Corinne Lepage and Antonyia Parvanova
-- EFSA National Experts agreed that "there should be more clarity
about the metabolism of aspartame": Rich Murray 2011.04.24
http://rmforall.blogspot.com/2011_04_01_archive.htm
Sunday, April 24, 2011
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aspartame water in rats for 6 months causes liver harm, RH Nair et al,
Mahatma Gandhi U, Food Chem Toxicol 2011.03.02: Rich Murray 2011.03.12
http://rmforall.blogspot.com/2011_03_01_archive.htm
Saturday, March 12, 2011
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http://www.ncbi.nlm.nih.gov/pubmed/21376768

Food Chem Toxicol. 2011 Mar 2. [Epub ahead of print]
Effect of long term intake of aspartame on antioxidant defense status in liver.
Abhilash M, Paul MV, Varghese MV, Nair RH.
School of Biosciences, Mahatma Gandhi University,
Kottayam, Kerala, India, 686560.
harikumarannair@..., harinair@...,


careful expert lifetime study on mice shows liver and lung cancers
from aspartame, M Soffritti et al, Ramazzini Institute, Italy, checked
by US National Toxicology Program experts, confirms many previous
studies from 2001 on: Rich Murray 2011.02.27
http://rmforall.blogspot.com/2011_02_01_archive.htm
Sunday, February 27, 2011
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re GC Ebers study, females harmed more by body making methanol into
formaldehyde in brain via ADH enzyme: 589 references, WC Monte,
retired Prof. Nutrition: Rich Murray 2011.01.08
http://rmforall.blogspot.com/2011_01_01_archive.htm
Saturday, January 8, 2011
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Woodrow C Monte, PhD, Emiritus Prof. Nutrition gives many PDFs of
reseach -- methanol (11% of aspartame) puts formaldehyde into brain
and body -- multiple sclerosis, Alzheimer's, cancers, birth defects,
headaches: Rich Murray 2010.05.13
http://rmforall.blogspot.com/2010_05_01_archive.htm
Thursday, May 13, 2010
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[ Other formaldehyde sources include alcohol drinks and
tobacco and wood smoke,
while adequate folic acid levels protect most people. ]

http://whilesciencesleeps.com/about

http://while-science-sleeps.com/references/pdf/586
[ summary, not peer reviewed ]
Monte WC.
Methanol: A chemical Trojan horse as the root of the inscrutable U.
Medical Hypotheses 2010;74(3):493-6
DOI 2010.10.16

Monte WC.
Bittersweet: Aspartame Breast Cancer Link.
Fitness Life 2008 Jan. 34: 32-36

Monte WC.
A Deadly Experiment. Methanol and MS,
Fitness Life 2007 Dec. 34: 36-41

Monte WC.
Sickly Sweet: Is your Diet Sweetener killing you?
Fitness Life 2007 Nov. 33: 31-33

http://whilesciencesleeps.com/references
589 references for above articles and upcoming book

http://whilesciencesleeps.com/montediet
[ and Fitness Life 2007 Dec. 34: 36-41 ]

Methanol: Where Is It Found? How Can It Be Avoided?

AVOID the following, ranked in order of greatest danger:

1. Cigarettes.
2. Diet foods and drinks with aspartame.
3. Fruit and vegetable products and their juices in bottles,
cans, or pouches.
4. Jellies, jams, and marmalades not made fresh and kept
refrigerated.
5. Black currant and tomato juice products, fresh or
processed.
6. Tomato sauces, unless first simmered at least 3 hours
with an open lid.
7. Smoked food of any kind, particularly fish and meat.
8. Sugar-free chewing gum.
9. Slivovitz: You can consume one alcoholic drink a day
on this diet -- no more! [ no fruit brandies ]
10. Overly ripe or near rotting fruits or vegetables.

Selection from Article 2, Fitness Life, December 2007, and
well discussed in the DVD video:

"Identical Symptoms of MS, Methanol Poisoning
and Aspartame Toxicity

The symptoms of multiple sclerosis (44, 83, 85, 169), chronic
and acute methanol poisoning (13, 144, 189), and Aspartame
toxicity (54, 58, 93, 181), are in all ways identical.

There is nothing that happens to the human body from the
toxic effect of methanol that has not been expressed during
the course of MS... nothing (143, 144).

This generalization extends even to the remarkable
opthomological conditions common to both: transitory optic
neuritis and retrolaminar demyelinating optic neuropathy with
scotoma of the central visual field (which occasionally
manifests as unilateral temporary blindness (85, 138, 163).

In fact, these opthomological symptoms have been thought of
for years in their respective literatures to be "tell tale"
indications for the differential diagnosis for each of these
maladies independently (85, 138, 148, 163, 169).

The common symptoms of
headache (13, 83, 181, 189),
nervousness (13, 83, 181),
depression (58, 83, 189, 181),
memory loss (18, 147, 85, 169, 181),
tingling sensations (13, 85, 168, 138, 169),
pain in the extremities (13, 85, 169),
optic neuritis (85, 138, 148, 163, 169),
bright lights in the visual field (139, 83),
seizures (21, 83, 160),
inability to urinate or to keep from urinating (139, 146, 167)
are all shared by each of these conditions and shared yet
again by complaints from aspartame poisoning
(54, 58, 93, 181).

I take these strikingly similar symptom patterns as evidence
that these disorders act on identical components of the
central nervous system and in the same way.

The "Miracle" that MS shares with Methanol poisoning

In the early stages of MS, or when a non-lethal dose of
methanol has been administered, complete recovery is a
possibility.

The only two afflictions for which such dramatic "remissions"
are reported from identical neuromuscular and opthomological
damage, even "blindness" is relapsing-remitting multiple
sclerosis (85) and methyl alcohol poisoning (138, 163).

The pathology of the two maladies is in may ways identical,
particularly when it comes to destruction of the myelin
sheath with no harm to the axon itself (18, 148, 176).

Sex Ratios for MS and Aspartame Reactions

Women bear the brunt of multiple sclerosis (91a-c) and lupus
(SLE)(73) with fully three-fold representations in infliction
numbers over men for both diseases.

This is exactly the proportion represented by adverse
reactors to Aspartame reported by the US Center for
Disease Control in their study of 1984 (58).

The Center found three women to every man whose
Aspartame consumption complaints were serious enough
to warrant investigation (93).

Although the female/male ratio for those stricken with MS has
always been high, recent estimates place it at over 3 to 1
(91, 91a, 91c).

What might account for the difference across sexes in
incidence?

A study published in the New England Journal of Medicine
(94) reports biopsies of the gastric lining of men and women.

A result was that the concentration of ADH in the
gastric lining of men was much higher than for woman.

Men have the advantage of removing methanol from the
bloodstream four times faster on an equal-body-size basis
than women.

Thus, for men, methanol is more likely to be removed from the
blood before it reaches the brain.

The brain is spared but the methanol removed would still be
metabolized to formaldehyde in the gut where it would reap
its havoc on a more forgiving organ.

This may help explain why men have more gastrointestinal
complaints from both methanol and Aspartame consumption
(93, 99).

On the other hand, women's complaints from both more
frequently involve serious neurological complications."...
______________________________________________


methanol (11% of aspartame), made by body into
formaldehyde in many vulnerable tissues, causes modern
diseases of civilization, summary of a century of research,
Woodrow C Monte PhD, Medical Hypotheses journal:
Rich Murray 2009.11.15
http://rmforall.blogspot.com/2009_11_01_archive.htm
Sunday, November 15, 2009
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aspartame abstinance cures fibromyalgia chronic pain in 2 French
adults: R Ciappuccini et al, Clin Exp Rheumatol 2010 Nov: Rich Murray
2010.02.19
http://rmforall.blogspot.com/2011_02_01_archive.htm
Saturday, February 19, 2011
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formaldehyde from 0.2 mg daily methanol from aspartame in Singulair
(montelukast) chewable asthma medicine causes severe allergic
dermatitis in boy, SE Jacob et al, Pediatric Dermatology 2009 Nov:
Rich Murray 2010.09.27
http://rmforall.blogspot.com/2010_09_01_archive.htm
Monday, September 27, 2010
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______________________________________________


Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-819-7388       rmforall@...

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