http://groups.yahoo.com/group/aspartameNM/message/974
ADHD kids & sleep deprivation, aspartame, MSG & NMDA receptors?:
O'Brien & Gozal, March 2003: Murray 3.5.3 rmforall

Ritalin, aspartame, and MSG can cause insomnia and sleep disturbances.
All three components of the aspartame molecule are genotoxic:
aspartate (40%), phenylalanine 50%), and methanol (10%, which quickly
becomes formaldehyde and then formic acid).
Pall (2002) gives a general theory of MCS type diseases, involving NMDA
receptor disorders-- formaldehyde is discussed as a major instigator.
David Gozal's team could apply their functional magnetic resonance
imaging of respiratory control brain sites in humans to the effects of
Ritalin, aspartame, MSG, and other drugs.

Confirming evidence and a general theory are given by Pall (2002):
http://groups.yahoo.com/group/aspartameNM/message/909
testable theory of MCS type diseases, vicious cycle of nitric oxide &
peroxynitrite: MSG: formaldehyde-methanol-aspartame:
Martin L. Pall: Murray: 12.9.2 rmforall
***********************************************************************

Pediatrics 2003 Mar; 111(3): 554-63
Sleep and neurobehavioral characteristics of 5- to 7-year-old children
with parentally reported symptoms of attention-deficit/hyperactivity
disorder.
O'Brien LM, Holbrook CR, Mervis CB, Klaus CJ, Bruner JL, Raffield TJ,
Rutherford J, Mehl RC, Wang M, Tuell A, Hume BC, Gozal D.
David Gozal cbmervis@...
Kosair Children's Hospital Research Institute, and Division of Pediatric
Sleep Medicine, Department of Pediatrics. Department of Pychological and
Brain Sciences, University of Louisville, Louisville, Kentucky.

OBJECTIVES: This study examined the hypothesis that domains of
neurobehavioral function would be selectively affected by
sleep-disordered breathing (SDB). Therefore, we assessed potential
relationships between objectively measured sleep disturbances
and neurobehavioral function in children with reported symptoms of
attention-deficit/hyperactivity disorder (ADHD) and also
determined the incidence of snoring and other sleep problems in 5- to
7-year-old children in the local community and potential
relationships to parental snoring and passive smoking. METHODS: Parents
of 5- to 7-year-old children in public schools were surveyed about their
child's sleeping habits using a validated questionnaire. The
questionnaire also asked whether they believed their child to be
hyperactive or have ADHD. Children with reported symptoms of ADHD and
control children were randomly selected and invited to the Sleep
Medicine Center for an overnight polysomnographic assessment and a
battery of neurocognitive tests.

RESULTS: The questionnaire response rate was 47.6% (n = 5728). Frequent
and loud snoring was reported for 673 children (11.7%). Similarly,
418 (7.3%) children were reported to have hyperactivity/ADHD, 313
(76.5%) of which were boys. Eighty-three children with parentally
reported symptoms of ADHD were invited for full evaluation at the Sleep
Medicine Center together with 34 control children. After assessment with
the Conners' Parent Rating Scale, 44 children were designated as having
"significant" symptoms of ADHD, 27 as "mild," and 39 designated as
"none" (controls). Overnight polysomnography indicated that obstructive
sleep apnea was present in 5% of those with significant ADHD symptoms,
26% of those with mild symptoms, and 5% of those with no symptoms. In
the cohort, no sleep variable accounted for more than a negligible
proportion of the variance in domains of neurobehavioral function.

CONCLUSIONS:An unusually high prevalence of snoring was identified among
a group of children designated as showing mild symptoms of ADHD based on
the Conners' ADHD index identified from a community sample. However,
whereas SDB is not more likely to occur among children with significant
ADHD symptoms, it is significantly highly prevalent among children with
mild hyperactive behaviors. Sleep studies further revealed that rapid
eye movement disturbances are more likely to occur in children with
significant symptoms, and they seem to impose significant but mild
effects on daytime neurobehavioral functioning. We conclude that in
children with significant symptoms of ADHD, the prevalence of SDB is not
different from that of the general pediatric population and that rapid
eye movement sleep in these children is disturbed and may contribute to
the severity of their behavioral manifestations. Furthermore, SDB can
lead to mild ADHD-like behaviors that can be readily misperceived and
potentially delay the diagnosis and appropriate treatment.
PMID: 12612236
************************************************************************

Sleep Breath 2001; 5(1): 35-42
Morbidity of obstructive sleep apnea in children: facts and theory.
Gozal D. d0goza01@...
Department of Pediatrics, Kosair Children's Hospital Sleep Medicine and
Apnea Center, University of Louisville School of Medicine,
Louisville, Kentucky 40202, USA. d0goza01@...

Sleep-disordered breathing (SDB) is a frequent, albeit underdiagnosed,
problem in children. If left untreated, SDB may lead to substantial
morbidities affecting multiple target organs and systems. This review
provides a detailed and current description of the current status of our
understanding of SDB-associated morbidity in children, and provides
recommendations of future research directions necessary for increasing
our knowledge and awareness on the short- and long-term consequences of
SDB during childhood.
Publication Types: Review Review, Tutorial PMID: 11868138
************************************************************************

http://newsbreak.louisville.edu/010601/gozal.html

Researcher links snoring with behavior problems

Research conducted by a U of L physician may offer hope to
parents whose children have behavioral problems.

David Gozal, who holds a chair in the U of L department of
pediatrics, has been researching obstructive apnea, or childhood
sleep disorders in relation to snoring. He has found that snoring
is a major cause of disruptive sleep for children. In many cases, it
can lead to behavioral problems such as hypertension, or it can
contribute to learning deficiencies.

Gozal's research team elicited 5,156 responses to a detailed
questionnaire on frequent and loud snoring in 6-year-old children
who attended the first grade in a Kentucky county public school
system.

Of that group, 378 children had attention-deficit-hyperactivity
disorder (ADHD). Some 577 children (11.2 percent) had snoring
scores greater than four points on a zero-to-eight scale, which
indicates both frequent (more than three times per week) and
loud snoring.

Eighty-seven children with ADHD were frequent and loud snorers.

Gozal found no differences in snoring between boys and girls or
between white and African-American children.

The study did find an increased risk of a child snoring when one
or both parents snore or smoke. It also showed a correlation
between snoring and having tonsils.

Gozal's study and findings recently were featured on the
television show "48 Hours" and by Reuters news service and
several radio networks. He also presented them at the American
Thoracic Society's international conference in May.

The "48 Hours" segment drew considerable interest from parents
and the medical community. The show highlighted the story of a
small boy who was exhibiting severe behavioral problems when he was
brought to Gozal's clinic. After undergoing a tonsillectomy, the boy's
behavior and schoolwork drastically improved.

More than 40 telephone calls poured in to the "48 Hours" switchboard
following the segment. Some came from parents wanting to enroll their
children in the study; others came from medical professionals wanting
more information.

But Gozal is cautious.

"This is not a miracle cure," he said. "There are a lot of gray areas
that remain in the study. The television show might have given the
impression that a tonsillectomy could guarantee instant success. We wish
that were true, but it's not."

Gozal's research is being undertaken through U of L and the Kosair
Children's Hospital Research Institute. He said he hopes to expand it by
looking further into mood disorders among children and into sleep apnea
in premature babies.
************************************************************************

http://www.kosairchildrens.com/
Kosair Children's Hospital 502 629-6000
231 East Chestnut Louisville, KY 40202

http://pediatrics.louisville.edu/
Phone 502-852-8600 fax 502-852-8603

David Gozal, MD
Kosair Children's Hospital Research Institute
University of Louisville School of Medicine
Louisville, KY 40202-1788
502-852-2322 david.gozal@...

Faculty of the Department of Pharmacology and Toxicology
http://www.louisville.edu/medschool/pharmacology/dgozal.html
http://www.louisville.edu/medschool/pharmacology/dgozalres.html

Current Research Interests
My laboratory has been interested in translational research particularly
as it relates to ventilatory response to hypoxia in the developing
mammal and human infant and child. Over the years we have uncovered a
variety of neurotransmitters and intracellular signaling pathways which
are immediately relevant to the acute hypoxic response. More recently,
we have shifted our interest to later stages in the temporal domain of
hypoxia as they relate to mechanisms underlying functional adaptation,
programmed cell death, and cellular survival. The major topics currently
undergoing active research in the lab include the following:

Obstructive sleep apnea in children.
Signal transduction mechanisms underlying ventilatory response to
hypoxia.
Sudden Infant Death Syndrome.
Neuronal adaptations to intermittent hypoxia: growth factors,
intracellular signaling, and genomic implications.
Maturation of neural mechanisms underlying gasping mechanisms.
Platelet activating factor and respiratory control.
Functional magnetic resonance imaging of respiratory control brain sites
in humans.
************************************************************************

Pediatrics 2002 Nov; 110(5): 884-8
Effect of supplemental oxygen on sleep architecture and
cardiorespiratory events in preterm infants.
Simakajornboon N, Beckerman RC, Mack C, Sharon D, Gozal D.
Constance S. Kaufman Pediatric Pulmonary Research Laboratory, Department
of Pediatrics, Tulane University School of Medicine,
New Orleans, Louisiana 70112, USA. nsimaka@...
nsimaka@...
************************************************************************

Am J Respir Crit Care Med 2000 Sep; 162(3 Pt 1): 1140-7
N-Methyl-D-aspartate [NMDA] receptor expression in the nucleus tractus
solitarii and maturation of hypoxic ventilatory response in the rat.
Ohtake PJ, Simakajornboon N, Fehniger MD, Xue YD, Gozal D.
Department of Physical Therapy, Exercise and Nutrition Sciences, State
University of New York at Buffalo, Buffalo, New York,
ohtake@...

Ventilatory responses to hypoxia are critically dependent on the
activation of N-methyl-D-aspartate (NMDA) glutamate receptors in
adult rats. To investigate the role of NMDA receptors during
development, we measured minute ventilation (V E) in 5-d, 10-d, and
15-d-old intact, freely behaving rat pups, using whole-body
plethysmography during breathing of room air (RA), during hypoxia (10%
O(2)), and during hypercapnia (5% CO(2)), both before and after
administration of the NMDA receptor antagonist MK-801 (1 mg/kg
intraperitoneally). MK-801 did not affect V E in RA in the younger
animals, but increased both V E and respiratory frequency in the 15-d-
old rats. Similarly, V E responses to hypoxia were unchanged from
control values in young animals, whereas V E respones in 15-d-old rats
showed significant attenuation under hypoxic conditions. In contrast,
hypercapnic ventilatory responses were not altered by administration of
MK-801 to rats at any age. To further examine the topographic
distribution patterns of NMDA receptor-positive neurons in the caudal
brainstem and their recruitment during hypoxia, we performed
immunostaining for NMDA receptor subunit NR1 and c-fos after exposing
rat pups at postnatal ages of 2 d, 5 d, 10 d, and 20 d and adult rats to
either RA or 10% O(2) for 3 h. With advancing postnatal age, NR1
expression increased in the nucleus tractus solitarii (nTS), whereas it
decreased in the hypoglossal nucleus. Hypoxic exposure was associated
with increased c-fos expression in the nTS at all postnatal ages, with a
marked increase occurring in >/= 10-d-old animals. Similarly, the
density of c-fos-NR1 double-labeled neurons during hypoxia
progressively increased with maturation. We conclude that NMDA glutamate
receptor expression in the caudal brainstem undergoes postnatal
maturation that closely parallels the development of the hypoxic
ventilatory response in the rat. PMID: 10988143
************************************************************************

Neurosci Lett 2000 Jan 7; 278(1-2): 17-20
Hypoxia induces activation of a N-methyl-D-aspartate glutamate
receptor-protein kinase C pathway in the dorsocaudal brainstem of the
conscious rat.
Simakajornboon N, Gozal E, Gozal YM, Gozal D.
Department of Pediatrics, Constance S. Kaufman Pediatric Pulmonary
Research Laboratory, Tulane University School of Medicine,
New Orleans, LA 70112, USA.

To study in vivo phosphorylation of N-methyl-D-aspartate (NMDA)
glutamate receptors and the recruitment of protein kinase C isoforms
during acute hypoxia, dorsocaudal brainstem lysates were harvested from
conscious rats exposed to either room air or hypoxia (10% O2 for 5 and
15 min). Increased phosphorylation of the NR-1 subunit at serine residue
896 occurred during hypoxia and was blocked by pre-treatment with
MK-801. Immunoblots of soluble and particulate fractions revealed
subcellular translocation for PKC-beta, -gamma, -delta, -epsilon, and
-iota during hypoxia with no changes in PKC-alpha, -mu, and -zeta.
Translocation of PKC-beta, -delta and -epsilon was selectively
attenuated following MK-801. We demonstrate that hypoxia leads to
PKC-mediated activation of NMDA receptors in the brainstem, and that
PKC-beta, -delta and -epsilon are the most likely candidates for NR-1
phosphorylation. PMID: 10643790
************************************************************************

RESPIRATORY RESEARCH GROUP MEMBER
SHABIH U. HASAN, MD (Karachi, Pakistan), DCH (University of Dublin,
Ireland), FRCPC hasans@...
Associate Professor, Department of Paediatrics, Faculty of Medicine,
University of Calgary Staff Neonatologist, Calgary Regional Health
Authority: Foothills Hospital Consulting Staff, Alberta Children's
Hospital, Peter Lougheed Centre, Rockyview Hospital
************************************************************************

http://groups.yahoo.com/group/aspartameNM/message/959
aspartame review: methanol, formaldehyde, formic acid toxicity:
Murray 3.3.3 rmforall

Rich Murray, MA Room For All rmforall@...
1943 Otowi Road, Santa Fe, New Mexico 87505 USA 505-986-9103

http://groups.yahoo.com/group/aspartameNM/messages
for 974 posts in a public searchable archive

http://groups.yahoo.com/group/aspartame/ 615 member group

http://groups.yahoo.com/group/aspartameNM/message/968
EU MEPs vote to re-evaluate aspartame and stevia:
Martini: Murray 2.21.3 rmforall

http://www.holisticmed.com/aspartame/scf2002-response.htm
Mark Gold exhaustively critiques European Commission Scientific
Committee on Food re aspartame (12.4.2): 59 pages, 230 references

http://groups.yahoo.com/group/aspartameNM/message/910
formaldehyde & formic acid from methanol in aspartame:
Murray: 12.9.2 rmforall

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, since 11% of aspartame (1,120 mg in 2L diet soda, 5.6 12-oz
cans) is 123 mg methanol (wood alcohol), immediately released into the
body after drinking (unlike the large levels of methanol locked up in
molecules inside many fruits), then quickly transformed into
formaldehyde, which in turn becomes formic acid, both of which in
time become carbon dioxide and water-- however, about 30% of the
methanol remains in the body as cumulative durable toxic metabolites of
formaldehyde and formic acid-- 37 mg daily, a gram every month.
If 10% of the methanol is retained as formaldehyde, that would give 12
mg daily formaldehyde accumulation, about 60 times more than the 0.2 mg
from 10% retention of the 2 mg EPA daily limit for formaldehyde in
drinking water.

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

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

This long-term low-level chronic toxic exposure leads to typical
patterns of increasingly severe complex symptoms, starting with
headache, fatigue, joint pain, irritability, memory loss, and
leading to vision and eye problems and even seizures. In many cases
there is addiction. Probably there are immune system disorders, with a
hypersensitivity to these toxins and other chemicals.

Confirming evidence and a general theory are given by Pall (2002):
http://groups.yahoo.com/group/aspartameNM/message/909
testable theory of MCS type diseases, vicious cycle of nitric oxide &
peroxynitrite: MSG: formaldehyde-methanol-aspartame:
Martin L. Pall: Murray: 12.9.2 rmforall

http://groups.yahoo.com/group/aspartameNM/message/946
Functional Therapeutics in Neurodegenerative Disease Part 1/2:
Perlmutter 7.15.99: Murray 1.10.3 rmforall

http://groups.yahoo.com/group/aspartameNM/message/915
formaldehyde toxicity: Thrasher & Kilburn: Shaham: EPA: Gold: Murray:
Wilson: CIIN: 12.12.2 rmforall

http://groups.yahoo.com/group/aspartameNM/message/934
24 recent formaldehyde toxicity [Comet assay] reports:
Murray 12.31.2 rmforall

http://groups.yahoo.com/group/aspartameNM/message/935
comet assay finds DNA damage from sucralose, cyclamate, saccharin in
mice: Sasaki YF & Tsuda S Aug 2002: Murray 1.1.3 rmforall
[Also borderline evidence, in this pilot study of 39 food additives,
using a test group of 4 mice, for DNA damage from for stomach, colon,
liver, bladder, and lung 3 hr after oral dose of 2000 mg/kg aspartame--
a very high dose.]

http://groups.yahoo.com/group/aspartameNM/message/961
genotoxins, Comet assay in mice: Ace-K, stevia fine; aspartame poor;
sucralose, cyclamate, saccharin bad: Y.F. Sasaki Aug 2002:
Murray 1.27.3 rmforall [A detailed look at the data]

http://groups.yahoo.com/group/aspartameNM/message/939
aspartame (aspartic acid, phenylalanine) binding to DNA:
Karikas July 1998: Murray 1.5.3 rmforall
Karikas GA, Schulpis KH, Reclos GJ, Kokotos G
Measurement of molecular interaction of aspartame and
its metabolites with DNA. Clin Biochem 1998 Jul; 31(5): 405-7.
Dept. of Chemistry, University of Athens, Greece
http://www.chem.uoa.gr gkokotos@...

http://groups.yahoo.com/group/aspartameNM/message/960
aspartame & MSG: possible role in autoimmune hepatitis:
Prandota Jan 2003: Murray 1.15.3 rmforall

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

http://groups.yahoo.com/group/aspartameNM/message/669
1038-page medical text "Aspartame Disease: An Ignored Epidemic"
published May 30 2001 $ 85.00 postpaid data from 1200 cases
available at http://www.amazon.com
over 600 references from standard medical research

Roberts, Hyman J., 1924- ,
Useful insights for diagnosis, treatment and public heath: an updated
anthology of original research, 2002, 798 pages,
Palm Beach Institute for Medical Research, Inc.
P.O. Box 17799, West Palm Beach, FL 33416
fax 561-547-8008 dr.roberts@...
aspartame disease pages 627-685, 778-780

http://groups.yahoo.com/group/aspartameNM/message/859
RTM: Roberts: the life work of a brilliant clinician:
aspartame toxicity 8.2.2 rmforall

http://groups.yahoo.com/group/aspartameNM/message/790
RTM: Moseley:
review Roberts "Aspartame Disease: An Ignored Epidemic" 2.7.2 rmforall

http://groups.yahoo.com/group/aspartameNM/message/782
RTM: Smith, Terpening, Schmidt, Gums:
full text: aspartame, MSG, fibromyalgia 1.17.2 rmforall
Jerry D Smith, Chris M Terpening, Siegfried OF Schmidt, and John G Gums
Relief of Fibromyalgia Symptoms Following
Discontinuation of Dietary Excitotoxins.
The Annals of Pharmacotherapy 2001; 35(6): 702–706.
Malcolm Randall Veterans Affairs Medical Center, Gainesville, FL, USA.
BACKGROUND: Fibromyalgia is a common rheumatologic disorder that is
often difficult to treat effectively.
CASE SUMMARY: Four patients diagnosed with fibromyalgia syndrome
for two to 17 years are described.
All had undergone multiple treatment
modalities with limited success. All had complete, or nearly complete,
resolution of their symptoms within months after eliminating monosodium
glutamate (MSG) or MSG plus aspartame from their diet.
All patients were women with multiple comorbidities
prior to elimination of MSG.
All have had recurrence of symptoms whenever MSG is ingested.

Siegfried O. Schmidt, MD Asst. Clinical Prof. siggy@...
Community Health and Family Medicine, U. Florida, Gainesville, FL
Shands Hospital
West Oak Clinic Gainesville, FL 32608-3629 352-376-5071

Debbie J. Hypes painfreeliving@... 304-872-4141 (Case # 1 of 4)
P.O Box 25 Lookout, WV 25868-0025 She has about 1,000 on her local
mailing list, and has been a volunteer activist since 1997. Her guide
first came out in 1997: http://www.Pain-Free-Living.net
"The Food Plan: How To Do It" $ 5 by mail, free by email.
Her sister Darlene, now 47, cured her own severe fibromyalgia in 1995
by using an elimination diet, and then Debbie also cured herself by
1997. Their doctor, Siegfried Schmidt, paying attention, tried it on
two selected women, who got well, and are his third and fourth cases.

http://groups.yahoo.com/group/aspartameNM/message/846
RTM: 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 7.16.2 rmforall
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
RTM: Blumenthall & Vance:
aspartame chewing gum headaches Nov 1997 7.28.2 rmforall
Harvey J. Blumenthal, MD, Dwight A Vance, RPh
Chewing Gum Headaches.
Headache 1997 Nov-Dec; 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]

http://groups.yahoo.com/group/aspartameNM/message/925
aspartame puts formaldehyde adducts into tissues, Part 1/2
full text, Trocho & Alemany 6.26.98: Murray 12.22.2 rmforall

http://groups.yahoo.com/group/aspartameNM/message/926
aspartame puts formaldehyde adducts into tissues, Part 2/2
full text, Trocho & Alemany 6.26.98: Murray 12.22.2 rmforall

http://ww.presidiotex.com/barcelona/index.html
Trocho C, Pardo R, Rafecas I, Virgili J, Remesar X,
Fernandez-Lopez JA, Alemany M ["Trok-ho"]
Formaldehyde derived from dietary aspartame binds to tissue
components in vivo. Life Sci 1998 Jun 26; 63(5): 337-49.
Departament de Bioquimica i Biologia Molecular, Facultat de Biologia,
Universitat de Barcelona, Spain.
http://www.presidiotex.com/barcelona/index.html
Maria Alemany, PhD (male) alemany@...

http://groups.yahoo.com/group/aspartameNM/message/864
Murray: Butchko, Tephly, McMartin: Alemany: aspartame formaldehyde
adducts in rats 9.8.2 rmforall
Prof. Alemany vigorously affirms the validity of the Trocho study
against criticism:
Butchko, HH et al [24 authors], Aspartame: review of safety.
Regul. Toxicol. Pharmacol. 2002 April 1; 35 (2 Pt 2): S1-93, review
available for $35, [an industry paid organ]. Butchko:
"When all the research on aspartame, including evaluations in both the
premarketing and postmarketing periods, is examined as a whole, it is
clear that aspartame is safe, and there are no unresolved questions
regarding its safety under conditions of intended use."
[They repeatedly pass on the ageless industry deceit that the methanol
in fruits and vegetables is as as biochemically available as that in
aspartame-- see the 1984 rebuttal by Monte, below.]

http://groups.yahoo.com/group/aspartameNM/message/911
RTP ties to industry criticized by CSPI: Murray: 12.9.2 rmforall

http://groups.yahoo.com/group/aspartameNM/message/872
immune system reactions due to formaldehyde from the 11% methanol in
aspartame: Thrasher: Tephly: Monte: Murray 9.27.2 rmforall

J. Nutrition 1973 Oct; 103(10): 1454-1459.
Metabolism of aspartame in monkeys.
Oppermann JA, Muldoon E, Ranney RE.
Dept. of Biochemistry, Searle Laboratories,
Division of G.D. Searle and Co. Box 5110, Chicago, IL 60680
They found that about 70% of the radioactive methanol in aspartame put
into the stomachs of 3 to 7 kg monkeys was eliminated within a day as
carbon dioxide in exhaled air and as water in the urine. They did not
mention that this meant that about 30% of the methanol must transform
into formaldehyde and then into formic acid, much of which must remain
as toxic products in all parts of the body. They did not report any
studies on the distribution of radioactivity in body tissues, except
that blood plasma proteins after 4 days held 4% of the initial
methanol. This study did not monitor long-term use of aspartame.

http://groups.yahoo.com/group/aspartameNM/message/873
MCS, aspartame, formaldehyde, other toxicants: Kerns: Murray 9.27.2
rmforall [an excellent overview]

http://groups.yahoo.com/group/aspartameNM/message/628
Rich Murray: Professional House Doctors: Singer: EPA: CPSC:
formaldehyde toxicity 6.10.1 rmforall

http://groups.yahoo.com/group/aspartameNM/message/622
Rich Murray: Gold: Koehler: Walton: Van Den Eeden: Leon:
aspartame toxicity 6.4.1 rmforall

http://groups.yahoo.com/group/aspartameNM/message/623
Rich Murray: Simmons: Gold: Schiffman: Spiers:
aspartame toxicity 6.4.1 rmforall

http://groups.yahoo.com/group/aspartameNM/message/870
Aspartame: Methanol and the Public Interest 1984:
Monte: Murray 9.23.2 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
Director of the Food Science and Nutrition Laboratory
Arizona State University, Tempe, Arizona 85287
6411 South River Drive #61 Tempe, Arizona 85283-3337
602-965-6938 woody.monte@... [now retired in New Zealand]
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.)

"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 fruit and vegetable products
during canning (31, 33)."

Recent research [see links at end of post] supports his focus on the
methanol to formaldehyde toxic process:

"The United States Environmental Protection Agency in their Multimedia
Environmental Goals for Environmental Assessment recommends a minimum
acute toxicity concentration of methanol in drinking water at 3.9 parts
per million, with a recommended limit of consumption below 7.8 mg/day
(8). This report clearly indicates that methanol:

"is considered a cumulative poison
due to the low rate of excretion once it is absorbed.
In the body, methanol is oxidized to formaldehyde and
formic acid; both of these metabolites are toxic." (8)....

Recently the toxic role of formaldehyde (in methanol toxicity) has been
questioned (34). No skeptic can overlook the fact that, metabolically,
formaldehyde must be formed as an intermediate to formic acid
production (54).

Formaldehyde has a high reactivity which may be why it
has not been found in humans or other primates during methanol
poisioning (59)....

If formaldehyde is produced from methanol and does have a reasonable
half life within certain cells in the poisoned organism the chronic
toxicological ramifications could be grave.

Formaldehyde is a known
carcinogen (57) producing squamous-cell carcinomas by inhalation
exposure in experimental animals (22). The available epidemiological
studies do not provide adequate data for assessing the carcinogenicity
of formaldehyde in man (22, 24, 57).

However, reaction of formaldehyde
with deoxyribonucleic acid (DNA) has resulted in irreversible
denaturation that could interfere with DNA replication and result in
mutation (37)...."
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