Wednesday, March 19, 2008
[ Rich Murray: Although initially we seemed firmly on opposite poles
the aspartame toxicity issue, John E. Garth and I have evolved a
collaboration, exchanging many valuable ideas and references.
On March 5, I was delighted to be totally scooped by a private post
from him that presented breakthrough insights -- since folic acid
to help most people safely and usefully metabolize methanol, avoiding
the production of toxic formaldehyde and formic acid, then about
5 mg folic acid daily may suffice to prevent most symptoms of
aspartame toxicity in most people, and, also, renders lacking much
research since 1972, which has sadly neglected this essential
Train wrecks happen in science, which end up with clearing the tracks,
raising fresh questions and leading to multiple, rapid advances.
For instance, folic acid deficiency causes the build up of toxic
of indigenous methanol in normal metabolism and from ordinary
foods and beverages, leading to cancers, birth defects, and
Additionally, we may have a very valuable preventative for alcohol
hangovers, a billion dollar scourge, and for toxicity from many
At a two-for-one sale at CVS Pharmacy, 5 mg folic acid costs
2.5 cents for the 2-mg pills.
Anyone concerned about methanol toxicity, from dark wines and
liquors, or from aspartame, is free to experiment immediately. ]
An abstract for the 47th Annual Meeting of the Society of Toxicology
March 16-20, 2008, Seattle, Washington
The abstract will be provided to this website soon,
I am giving you a short time to post the abstract if you wish first.
Well the information I have promised for weeks was coming
is now openly available.
Sorry for the delay, but it could not be released
until after my presentation.
And I have just concluded presenting my discovery
this morning at a platform session on
"Health risks and food safety" at the
(National and International) Society of Toxicology 2008 meeting,
currently ongoing in Seattle.
This organization is the premier group of toxicologists
from all around the world.
Anyway, now my discovery can be made public to all.
(FYI, toxicology is the science of poisons.)
The title of my presentation was
CRITICAL FOLATE PROBLEM WITH "LIFETIME"
ASPARTAME AND RELATED STUDIES
Soffritti's two "lifetime" studies are simply invalid.
His results are likely to be absolutely correct,
but his conclusions are absolutely biased,
but so are virtually all other studies of aspartame all the way back
and including the original Searle work.
Here is why: it is a simple error of design
that even a high school science fair student would understand.
All studies of aspartame to date have used a common simple
The experimental design used by all these papers
(regardless of rat species
and that goes for the "my-aspartame-experiment" too)
is a simple control versus treated design,
where aspartame was provided in the food at dosages
from zero through various dosages to high values.
Zero dosing served as the control,
whereas the various doses served as the treated animals.
Most of you readers are aware that methanol
(and its oxidation products formaldehyde and formic acid)
seem(s) to be the issue most frequently raised about aspartame.
And that actually is why these studies are invalid.
Methanol, like ethanol (very well-known fact),
alters the disposition of the vitamin folate. [folic acid]
Amongst the many ways they work,
one is to enhance excretion of folate and hence deplete it over time.
That makes the treated animals very susceptible
to diseases of folate deficiency.
Hence, as aspartame hydrolyzes to methanol,
that methanol acts in a variety of ways to directly deplete
and to otherwise also diminish availability of this critical vitamin.
But this depletion and likely reduction of availability
of other folate molecules occurs just in the treated group,
not at all in the control group.
So the design is imbalanced, and hence invalid.
In the case of "my-aspartame-experiment",
folate deficiency was likely in her rats,
as it was just in the treatment group
that methanol-induced folate deficiency arose.
Actually, her discovery of tumors would be expected.
Moreover, unrealized by Soffritti et al
is that folate deficiency likely induced in his treated rats
likely is responsible for the semi-dose dependent relationship,
because folate deficiency, not aspartame per se.
causes leukemia, lymphoma, and mammary cancer.
Actually folate deficiency is linked to development of cervix,
colorectal, lung, esophagus. brain, pancreas, leukemia, lymphoma,
and breast (mammary) tumors.
Many other of the 20+ purported "aspartame diseases"
are either part of this group or are related to folate processing
in some way (methionine, homocysteine issues).
But you must understand aspartame is not toxic;
folate is depleted by many other substances,
including ethanol and even antibiotics.
That is why it is a vitamin,
and why vitamin means "amine required for life";
those who fail to take daily supplements of folate are susceptible
to many food and environmental substances --
aspartame is just one of many,
but you must realize there are now no studies
suggesting any harm from aspartame.
No drug alone can be deemed responsible for tumors,
if the user fails to consume daily multiple vitamins;
that is their responsibility.
But that wasn't the only Soffritti issue.
Two other fatal experimental issues were neglected
by Soffritti et al too.
Those are that
(1) Sprague-Dawley rats are highly susceptible to folate insufficiency
as they age (a fact scientifically evident even
at less than 12 months of age for a "lifetime" study), and
(2) that the rat leukemia virus is endemic
in this Sprague-Dawley strain of rat,
making their use unsuitable for any leukemia research, too.
Searle can be easily forgiven this design error,
because their work was conducted over 20 years ago,
before much of this was even known,
but the Soffritti papers are less easily forgiven,
since the methanol depletion of folate was discovered
and reported in 1981.
In fact the readers should note that as important as folate is
in metabolizing the methanol-formaldehyde produced formate,
this vitamin went totally unmentioned in the Soffritti papers.
In this day and age to not know how important folate is
for metabolism of methanol is a serious error in and of itself.
But to Soffritti et al's credit is
that no one else caught this fatal error either.
But more important to the safety issues for aspartame critics
is that perhaps the biggest objection to aspartame,
the so-called Bressler report, stems from the Searle work.
Let me point out that if the Searle work was in retrospect
conducted improperly, the Bressler report and all the other criticism
of it stemming from the Searle studies are also NULL & VOID too.
Consequently all the scientific work suggesting any harm from
aspartame is now dismissable, including all the claims
of Martini, Blaylock and Roberts;
all are based on the original and now invalid studies.
Most of the other arguments against aspartame are also invalid,
because they fail to note the role of folate too.
Suffice it to say, if anyone suffers any reaction to aspartame,
there is a very high likelihood that they are either
directly folate deficient
or have some other biochemical issue with the folate system.
The latter is actually not uncommon.
In fact one paper suggests only one in five women
take vitamin supplements effectively.
Folate was added to grain products (flour, etc) in 1998.
Before that many Americans had folate deficiency
as indicated by the marked (>30%) reduction seen in
neural tube disorders, which that supplementation improved.
It is possible that some folate deficient people may respond
with tumors, but not just from aspartame,
but equally if not more so from ethanol
and a whole variety of commonly used drugs
that also deplete or affect folate.
That said, many people are still folate deficient,
and perhaps another round of folate supplementation is warranted;
this matter it is being investigated right now.
Much more could be said, but the take home message
is simply that "aspartame is perfectly safe, used as directed,
in healthy people, but many people are simply folate deficient
or have their own issues with folate and may be termed unhealthy."
Very few of these folate issues cannot be overcome
by proper daily folate supplementation as is available
to all in multiple vitamins.
John E. Garst, Ph.D.
(Medicinal Chemistry, Pharmacology, and Toxicology)
"The Bressler Report" by Jerome Bressler
(Note: This is the text of an FDA report on Searle)
EIR 4/25/77 to 8/4/77 Searle Laboratories
JSA/DME/JT/LF Div. G.D. Searle & Co.
4901 Searle Parkway, Skokie, Illinois 60076
essential protective role of folic acid? re: prodrug releases of
formaldehyde and formic acid are "minute"? Sundeep S Dhareshwar,
Valentino J Stella, U. Kansas, J Pharm Sci 2008.02 20:
J Pharm Sci. 2008 Feb 20 [Epub ahead of print]
Your prodrug releases formaldehyde: Should you be concerned? No!
Sundeep S. Dhareshwar, Valentino J. Stella * ste...@ku.edu;
Department of Pharmaceutical Chemistry, The University of Kansas,
2095 Constant Avenue, Lawrence, Kansas 66047.
Published Online: 20 Feb 2008 Copyright © 2008 Wiley-Liss, Inc.
The title of this commentary contains a frequently asked question
whenever someone presents or proposes a prodrug strategy that
as a result of bioconversion of a prodrug to parent drug.
Formaldehyde, a highly water-soluble one-carbon molecule,
is endogenous to cells, tissues, and body fluids.
Although formaldehyde is generated and incorporated into essential
metabolic processes by the human body, exposure to large amounts
of formaldehyde vapor
can irritate the nasal mucosa and may potentially be carcinogenic.
It also gives a positive Ames test.
Metabolism of both endogenous and exogenous formaldehyde
involves rapid oxidation to formic acid catalyzed
by glutathione dependent and independent dehydrogenases
in the liver and erythrocytes [red blood cells].
Balancing this rapid detoxification pathway is endogenous formation
from normal metabolic processes and exogenous formaldehyde input,
resulting in approximately 0.1 mM systemic levels.
The possibility that formaldehyde released upon bioconversion of
prodrugs might induce toxicity has been repeatedly stated,
but no convincing evidence for this perceived toxicity
has been documented in experimental studies.
Therefore, as pharmaceutical chemists and not as toxicologists,
we present our perspective on the apparent concern with release
of formaldehyde as a by-product of in vivo bioconversion
of selective prodrugs,
and suggest that in comparison to the total amount
of daily endogenous formaldehyde production from metabolism,
and exogenous exposure from food and the environment,
the amount generated by prodrugs is minute
and is unlikely to cause any systemic toxicity in humans.
Such an argument does not preclude formaldehyde-based toxicity
assessment of a prodrug.
Instead, it reduces the risk that in vivo liberation of formaldehyde
will cause undue toxicity. PMID: 18288723
(c) 2008 Wiley-Liss, Inc. and the American Pharmacists Association
J Pharm Sci.
*Correspondence to Valentino J. Stella,
Department of Pharmaceutical Chemistry, The University of Kansas,
2095 Constant Avenue, Lawrence, Kansas 66047.
Telephone: 785-864-3755; Fax: 785-864-5736.
prodrugs . formaldehyde release . apparent toxicity .
in vivo metabolism
30 female pet store rats drinking lifelong 13.5 mg aspartame,
1/3 packet of Equal, had 33% with obvious tumors -- also bulging,
sick, and missing eyes, paralysis, obesity, skin sores -- agrees with
Ramazzini Foundation results, Victoria Inness-Brown:
Friday, February 15, 2008
Folic acid protects against aspartame (methanol, formaldehyde,
formic acid) toxicity in many users -- however, many will also still
have problems from aspartic acid, phenylalanine, and DKP --
some recent teams have explored the roles of all three
components of aspartame:
Direct and indirect cellular effects of aspartame on the brain,
Humphries P, Pretorius E, Naude H, U. Pretoria, South Africa,
Eur J Clin Nutr. 2007 Aug 8: Murray 2007.08.12
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
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
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
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
aspartame (aspartic acid, phenylalanine) binding to DNA:
Karikas July 1998: Murray 2003.01.05 rmforall
Karikas GA, Schulpis KH, Reclos GJ, Kokotos G
Measurement of molecular interaction of aspartame and
its metabolites with DNA. Clin Biochem 1998 Jul; 31(5): 405-7.
Dept. of Chemistry, University of Athens, Greece
K.H. Schulpis inch...@otenet.gr ; G.J. Reclos rek...@otenet.gr
5 recent aspartame reports by S Tsakiris, KH Schulpis, I Simintzi,
with responses to critiques by AG Renwick and
by EB Abegaz, RG Bursey, 2005-2008 2008.03.05
Pharmacological Research 57 (2008) 89-90
Letter to the Editor
Answer to Letter sent to the Editor by
Drs. E. Abegaz and R. Bursey
(Ajinomoto Corporate Services LLC, Washington, USA)
related to Simintzi et al. report published in
Pharmacol Res 2007; 56: 155-9
Letter to the Editor / Pharmacological Research 57 (2008) 89-90
Stylianos Tsakiris a,? sts...@cc.uoa.gr;
Kleopatra H. Schulpis b inch...@otenet.gr;
a Department of Experimental Physiology, Medical School,
Athens University, P.O. Box 65257, GR-15401 Athens, Greece
b Inborn Errors of Metabolism Department, Institute of Child
Health, Research Center, Greece
? Corresponding author.
S. Tsakiris sts...@cc.uoa.gr;
K.H. Schulpis inch...@otenet.gr;
Pharmacological Research 57 (2008) 87-88
Response to "The effect of aspartame on the acetylcholinesterase
activity in hippocampal homogenates of suckling rats"
by Simintzi et al.
Eyassu G. Abegaz ?
Robert G. Bursey
Ajinomoto Corporate Services LLC,
Scientific & Regulatory Affairs,
1120 Connecticut Ave., N.W., Suite 1010, Washington, DC 20036,
? Corresponding author. Tel.: +1 202 457 0284;
fax: +1 202 457 0107.
E-mail addresses: abeg...@ajiusa.com; (E.G. Abegaz),
bur...@ajiusa.com; (R.G. Bursey)
Aspartame; Aspartate; Phenylalanine; Methanol; AChE activity
Tsakiris S, Schulpis KH.
Answer to letter sent by Professor A.G. Renwick
(University of Southampton, UK)
related to Simintzi et al. report published in Food and Chemical
Toxicology 2007; 45(12): 2397-401.
Food Chem Toxicol. 2008 Mar; 46(3): 1208-9.
Epub 2007 Oct 25. No abstract available. PMID: 18054419
Copyright © 2007 Elsevier Ltd All rights reserved.
The effect of aspartame metabolites on the suckling rat frontal cortex
acetylcholinesterase. An in vitro study. By I. Simintzi, K.H.
P. Angelogianni, C. Liapi and S. Tsakiris.
Food Chem Toxicol. 2008 Mar; 46(3): 1206-7.
Epub 2007 Oct 26. No abstract available. PMID: 18061330
1: Simintzi I, Schulpis KH, Angelogianni P, Liapi C, Tsakiris S.
The effect of aspartame metabolites on the suckling rat frontal cortex
acetylcholinesterase. An in vitro study.
Food Chem Toxicol. 2007 Dec;45(12):2397-401.
Epub 2007 Jun 16. PMID: 17673349
2: Simintzi I, Schulpis KH, Angelogianni P, Liapi C, Tsakiris S.
L-Cysteine and glutathione restore the reduction of rat
hippocampal Na+, K+-ATPase activity
induced by aspartame metabolites.
Toxicology. 2007 Jul 31;237(1-3):177-83.
Epub 2007 May 18. PMID: 17602817
3: Simintzi I, Schulpis KH, Angelogianni P, Liapi C, Tsakiris S.
The effect of aspartame on acetylcholinesterase activity in
hippocampal homogenates of suckling rats.
Pharmacol Res. 2007 Aug;56(2):155-9.
Epub 2007 May 13. PMID: 17580119
4: Schulpis KH, Papassotiriou I, Parthimos T, Tsakiris T, Tsakiris S.
The effect of L-cysteine and glutathione
on inhibition of Na+, K+-ATPase activity by aspartame metabolites
in human erythrocyte membrane.
Eur J Clin Nutr. 2006 May;60(5):593-7. PMID: 16391576
5: Tsakiris S, Giannoulia-Karantana A, Simintzi I, Schulpis KH.
The effect of aspartame metabolites on human erythrocyte membrane
Pharmacol Res. 2006 Jan;53(1):1-5.
Epub 2005 Aug 29. PMID: 16129618
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
Thursday, January 10, 2008
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.:
Wednesday, November 27, 2007
methanol impurity in alcohol drinks [ and aspartame ] is turned into
neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol
Syndrome, BM Kapur, DC Lehotay, PL Carlen at U. Toronto,
Alc Clin Exp Res 2007 Dec. plain text: detailed biochemistry,
CL Nie et al. 2007.07.18: Rich Murray 2008.02.24
Sunday, February 24, 2008
[ Rich Murray comments: As a medical layman volunteer information
activist for aspartame and related toxicity issues since January 1999,
I note with appreciation the remarkable exponential progress on all
fronts, including a rapidly emerging consensus about the primary
importance of all toxicity challenges for our world.
This lengthy review features in detail two quite different,
contributions, from Canada, and England and China.
It is indicative of our times that the CL Nie et al. study, 2007
appears in a free, open access journal -- indeed, as all life and
death information must.
Following rather vigorously, indeed blindly, the imperatives of
single-minded, profit-driven capitalist competition -- manipulating
adroitly research, education, media, citizens, governments -- many
great global corporations have inevitably created results that
oppose the common good. Alcohol and tobacco are well known.
Realistically, any further manipulations can only lead to inevitable
and even sudden corporate meltdowns, in the context of an
unfettered, cooperative, democratic global information forum,
Now, it is as easy and cheap to compose and instantly post a
30-page review as 3 pages a decade ago -- and such reviews
are archived forever in multiple collections, open via global search
engines to a billion Net citizens.
Perforce, and increasingly happily, all societal entities will have to
operate by high and shared voluntary universal standards
for the common good. ]
Alcoholism: Clinical and Experimental Research
Volume 31 Issue 12 Page 2114-2120, December 2007
Bhushan M. Kapur, b.k...@utoronto.ca;
Arthur C. Vandenbroucke, PhD, FCACB
Denis C. Lehotay, dleh...@health.gov.sk.ca;
Peter L. Carlen car...@uhnres.utoronto.ca;
(2007) Formic Acid, a Novel Metabolite of Chronic Ethanol
Abuse, Causes Neurotoxicity, Which Is Prevented by Folic Acid
Alcoholism: Clinical and Experimental Research 31 (12), 2114-2120.
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.
To determine if FA levels are higher in the alcohol-drinking
population and to assess its neurotoxicity in organotypic
hippocampal rat brain slice cultures.
Serum and CSF FA was measured in samples from both ethanol
abusing and control patients, who presented to a hospital emergency
department. [ CSF = Cerebral Spinal Fluid ]
FA's neurotoxicity and its reversibility by folic acid were assessed
using organotypic rat brain hippocampal slice cultures using
Serum FA levels in the alcoholics
(mean ± SE: 0.416 +- 0.093 mmol/l, n = 23)
were significantly higher than in controls
(mean ± SE: 0.154 +- 0.009 mmol/l, n = 82) (p < 0.0002).
FA was not detected in the controls' CSF (n = 20),
whereas it was >0.15 mmol/l in CSF of 3 of the 4 alcoholic cases.
Low doses of FA from 1 to 5 mmol/l added for 24, 48 or 72 hours
to the rat brain slice cultures caused neuronal death as measured by
propidium iodide staining.
When folic acid (1 umol/l) was added with the FA,
neuronal death was prevented. [ umol = micromole ]
Formic acid may be a significant factor in the neurotoxicity of
This neurotoxicity can be mitigated by folic acid administration
at a clinically relevant dose.
Formic Acid, Folic Acid, Methanol, Neurotoxicity, Alcoholism.
Int J Dev Neurosci. 2007 Dec; 25(8): 545-52. Epub 2007 Oct 7.
Concurrent folate treatment prevents Na+,K+-ATPase activity
inhibition and memory impairments caused by chronic
hyperhomocysteinemia during rat development.
Departamento de Bioquímica, ICBS,
Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcelos,
2600-Anexo, CEP 90035-003, Porto Alegre, RS, Brazil.
We investigated the hypothesis that folate administration would
prevent hyperhomocysteinemia-induced memory deficits
and Na(+),K(+)-ATPase activity inhibition.
Chronic hyperhomocysteinemia was induced
from the 6th to the 28th day of life
by subcutaneous injection of homocysteine
(0.3-0.6 micromol/g), twice a day;
control Wistar rats received
the same volume of saline solution (0.9% NaCl).
Half of the homocysteine- and saline-treated groups also received
intraperitoneal administration of folate (0.011 micromol/g)
from the 6th to the 28th day of life.
A group of animals was killed 12 h after the last injection,
plasma and parietal cortex were collected for biochemical analysis.
Another group stayed at Central Animal House until 60th day of life,
when the rats were submitted to behavioral testing in water maze
or were killed for evaluation of cortical Na(+),K(+)-ATPase activity.
Results showed that hyperhomocysteinemia
impaired reference memory for platform location,
as assessed by fewer crossings to the platform place
and increased latency for the first crossing,
when compared to controls.
In the working memory task homocysteine-treated animals
also needed more time to find the platform.
We also observed that Na(+),K(+)-ATPase activity
was reduced in parietal cortex of hyperhomocysteinemic rats
sacrificed 12h after the last injection of homocysteine
In contrast, this enzyme was not altered when the rats were
sacrificed 31 days after the treatment (60-day-old rats).
Hyperhomocysteinemic rats treated with folate had all those
impairments prevented, an effect probably related to folate
antioxidant properties. PMID: 18023318
Ned Tijdschr Geneeskd. 2008 Jan 26; 152(4): 185-6.
[Fortification of food with folic acid
diminishes the number of neural tube defects]
[Article in Dutch]
Vrije Universiteit, Instituut voor Gezondheidswetenschappen, afd.
Voeding en Gezondheid, De Boelelaan 0085, 1081 HV Amsterdam
A recent study from a research group from Quebec showed a
strong decrease in the number of births affected by a neural tube
defect since folic acid fortification was introduced in Canada.
The prevalence decreased from
1.58 neural tube defects per 1000 births
before the introduction of folic acid fortification to
0.86 per 1000 births in the period of complete fortification.
Although folic acid fortification of staple food is probably the most
effective way to decrease the incidence of neural tube defects, more
knowledge about possible health risks should be obtained before
fortification is introduced.
More research is needed to determine which population groups are
at risk of possible negative effects of folic acid fortification
and at which level of fortification.
Until then, it is important to generate more attention and publicity
order to increase awareness and knowledge concerning folic acid
and to promote its use before and after conception.
"It is still unclear whether homocysteine is genuinely genotoxic
or simply a biomarker of folate deficiency,
a known cause of genetic damage (Crott and Fenech, 2001 Go)."
"Thus folate deficiency may play a critical role by amplifying the
of other risk factors, such as elevated homocysteine
or variant MTHFR genotype, especially in subjects
with high cardiovascular risk."
"Our RC group was recruited as apparently healthy
from a rural area.
In this group we can expect higher white wine consumption,
as a result of following a traditional lifestyle
and living in a wine producing area (Smolková et al., 2004Go).
Surprisingly, we found a higher proportion of the variant MTHFR
genotype in this group compared with our earlier findings
for a healthy population (Raslová et al., 2000Go, 2001Go).
The frequencies in the RC group are similar to those found by
Andreassi et al. (2003)Go for coronary artery disease patients.
Multifactorial analysis did not show a significant effect of smoking
habit on the parameters studied
(MN frequency, homocysteine or folate levels).
Therefore, we did not exclude smokers from analysis
although the ratio of smokers in the RC group was higher.
A lower frequency of MN among smokers before supplementation
(data not shown) is in accordance with many reports
(see for example Bonassi et al., 2003Go).
They found a higher frequency of MN only in
smoking over 30 cigarettes/day.
In our study we analysed the relationship between smoking
over 20 cigarettes/day and MN because we had only
two subjects who smoked over 30 cigarettes/day."
[In winter there is more formaldehyde from wood
and probably coal smoke.
White wine can have high methanol levels.
Tobacco is a main indoor formaldehyde source.
Farmers are also exposed to pesticides.
Indoor air polution increases in closed up homes during winter,
with far less fruits and vegetables. ]
free full texts
[ Extracts ]
* Oxford Journals
* Life Sciences
* Volume 19, Number 6
* Pp. 469-476
Mutagenesis 2004 19(6):469-476; doi:10.1093/mutage/geh059
Mutagenesis vol. 19 no. 6
© UK Environmental Mutagen Society 2004; all rights reserved.
Folate levels determine effect of antioxidant supplementation
on micronuclei in subjects with cardiovascular risk
B. Smolková 1,
M. Dusinská 1,3,
K. Raslová 1,
M. Barancoková 1,
A. Kazimírová 1,
A. Horská 1,
V. Spustová 1
and A. Collins 2
1 Research Base of Slovak Medical University,
Institute of Preventive and Clinical Medicine,
Limbová 1 2, Bratislava 83303, Slovakia
and 2 Institute for Nutrition Research, University of Oslo,
PO Box 1046, Blindern, 0316 Oslo, Norway
We have investigated the effect of modest supplementation with
(alpha)-tocopherol (100 mg/day),
B-carotene (6 mg/day),
vitamin C (100 mg/day)
and selenium (50 µg/day) on oxidative stress and chromosomal
damage, and the influence of
methylenetetrahydrofolate reductase (MTHFR) genotype
on these end-points.
Subjects were two groups of middle-aged men differing
in cardiovascular risk;
46 survivors of myocardial infarction before age 50
and 60 healthy controls.
They were randomly divided into equal groups to receive
antioxidants or placebo for 12 weeks.
Twenty-eight patients and 58 controls completed the intervention.
Micronucleus levels in peripheral lymphocytes
and changes seen after intervention were studied in relation to the
MTHFR C677T genotype,
and plasma folate levels.
Ferric reducing ability of plasma and concentration
malondialdehyde were measured to assess the antioxidant effect
There was no association of micronuclei with folate,
homocysteine or malondialdehyde levels before supplementation.
Micronucleus frequencies and plasma folate levels did not vary
significantly with MTHFR genotype.
Homocysteine levels in subjects with the TT variant genotype
were significantly higher compared with CT or CC (P = 0.001),
especially in subjects with low folate (P = 0.012).
In the placebo control group an increase in micronuclei (P = 0.04)
was detected at the end of the intervention period.
This effect was not seen in the supplemented group.
In antioxidant-supplemented myocardial infarction survivors
we found an increase in the ferric reducing ability of plasma
(P 0.001) and a decrease in malondialdehyde (P = 0.001).
Micronucleus frequency showed a decrease,
strongest in subjects with normal folate levels (P = 0.015).
In subjects with low folate levels, a high correlation was found
between micronuclei after supplementation and homocysteine,
both before (r = 0.979, P = 0.002)
and after supplementation (r = 0.922, P = 0.009).
Thus, folate deficiency may amplify the effect of other risk factors
such as elevated homocysteine levels or variant MTHFR genotype,
as well as influencing the ability of antioxidant supplementation
to protect against genetic damage.
RM Pitkin reviews how neural tube defects have been reduced in the
offspring of folate deficient mothers by folate supplements.
http://www.ajcn.org/cgi/content/full/85/1/285S html full text
Ray M Pitkin 4 page AJCN 2007
RM Pitkin, 78900 Rancho La Quinta Drive, La Quinta, CA 92253.
American Journal of Clinical Nutrition,
Vol. 85, No. 1, 285S-288S, January 2007
© 2007 American Society for Nutrition
What is the Efficacy of Single Vitamin and Mineral Supplement Use
in Chronic Disease Prevention?
Folate and neural tube defects 1,2
Roy M Pitkin
1 From the UCLA School of Medicine, Los Angeles, CA
2 Presented at the conference "Multivitamin/Mineral Supplements
and Chronic Disease Prevention," held at the
National Institutes of Health, Bethesda, MD, May 15-17, 2006
A protective effect of folate against the development of
neural tube defects (NTDs), specifically, anencephaly and spina
bifida, is now well recognized, having been established by a chain
of clinical research studies over the past half century.
This article summarizes the more important of these studies,
which have led to the current situation in which all women
capable of becoming pregnant are
to ingest folic acid regularly.
The recommended intakes are 4 mg/d for those at high risk
(by virtue of a previous NTD pregnancy outcome)
and 0.4 mg/d for all others.
However, a reduction in NTD births did not follow promulgation
of these recommendations, and so folic acid fortification
mandated in the United States and some other countries.
Although some controversy remains about the adequacy of
fortification levels, the process was followed by significant
improvement in folate indexes and a reduction of
25-30% in NTD frequency (about one-half of the proportion of
cases assumed to be responsive to folate).
The folate-NTD relation represents the only instance in which a
congenital malformation can be prevented simply and consistently.
Nevertheless, several research gaps remain:
identification of the mechanism by which the defect occurs
and how folate ameliorates it;
characterization of the relative efficacy of food folate,
folic acid added to foods, and folic acid by itself;
delineation of the dose-response relations of folate
and NTD prevention;
and more precise quantification of the dose needed
to prevent recurrences.
Key Words: Folate . folic acid . neural tube defect . spina bifida .
anencephaly . congenital malformations . birth defects .
NEJM Volume 327: 1832-1835; December 24, 1992 Number 26
Prevention of the first occurrence of neural-tube defects
by periconceptional vitamin supplementation
AE Czeizel, and I Dudas
The risk of recurrent neural-tube defects is decreased in women
who take folic acid or multivitamins containing such
during the periconceptional period.
The extent to which folic acid supplementation can reduce
the first occurrence of defects is not known.
We conducted a randomized, controlled trial of periconceptional
multivitamin supplementation to test the efficacy of this treatment
in reducing the incidence of a first occurrence of neural-tube
Women planning a pregnancy (in most cases their first)
were randomly assigned to receive a single tablet of a
vitamin supplement (containing 12 vitamins, including
0.8 mg of folic acid; 4 minerals; and 3 trace elements)
or a trace-element supplement (containing copper, manganese, zinc,
and a very low dose of vitamin C) daily for at least one month
before conception and until the date of the second missed menstrual
period or later.
Pregnancy was confirmed in 4753 women.
The outcome of the pregnancy (whether the fetus or infant had
a neural-tube defect or congenital malformation) was known in
2104 women who received the vitamin supplement and in
2052 who received the trace-element supplement.
Congenital malformations were significantly more prevalent
in the group receiving the trace-element supplement
than in the vitamin-supplement group
(22.9 per 1000 vs. 13.3 per 1000, P = 0.02).
There were six cases of neural-tube defects in the group
receiving the trace-element supplement, as compared with
none in the vitamin-supplement group (P = 0.029).
The prevalence of cleft lip with or without cleft palate
was not reduced by periconceptional vitamin supplementation.
Periconceptional vitamin use decreases the incidence of a
first occurrence of neural-tube defects.
Department of Human Genetics and Teratology,
National Institute of Hygiene, Budapest, Hungary.
free full text
Obstetrics & Gynecology 2003;102:1255-1261
© 2003 by The American College
of Obstetricians and Gynecologists
Periconceptional Multivitamin Supplementation
and Multimalformed Offspring
Andrew E. Czeizel, MD, DSc and Erika Medveczky, MD
From the Foundation for the Community Control
of Hereditary Diseases, Budapest, Hungary.
Address reprint requests to:
Andrew E. Czeizel, MD, DSc, Törökvész lejtö 32,
026 Budapest, Hungary; E-mail: cze...@interware.hu;
26. Wald NJ. Folic acid and the prevention of neural tube defects.
N Engl J Med 2004.01.08; 350: 101-3.
free full text Nicholas J. Wald n.j....@qmul.ac.uk;
Wolfson Institute of Preventive Medicine, Barts
and the London School of Medicine and Dentistry,
Queen Mary University of London, Charterhouse Square,
London EC1M 6BQ, UK
" According to the model, folic acid at a dose of about 5 mg per day
is expected to decrease the risk of a neural-tube defect by an
estimated 85 percent in women with a background serum folate
level of 5 ng per milliliter, which is typical in many Western
(see Table). Little is gained with higher doses. " ]
"As noted earlier, all clinical trials but one assessed recurrence,
whereas primary occurrence accounts for the most NTD cases
and is therefore the more important public health problem. The
only reported trial aimed at occurrence was reported by Czeizel
and Dudas in 1992 (13). The subjects were Hungarian women
planning pregnancy who were randomly assigned to a supplement
of 0.8 mg folic acid plus multivitamins or a supplement of
trace elements. No NTD cases occurred in 2104 supplemented
women compared with 6 cases among 2052 unsupplemented
women, a statistically significant difference (P under 0.029)."
[ probably high use of liquor -- so this small dose of folic acid must
be equally protective against similar levels of methanol intake for
heavy users of aspartame, above 6 cans daily. ]
"Finally, the dose recommended for women who have previously
had an NTD pregnancy, 4 mg, needs to be examined. This
level was based on the MRC study, which tested only that dose
because it had been reported previously to be effective. The
problem with the dose is that the largest folic acid tablet
manufactured is 1 mg, and thus women must take 4 tablets daily,
which may impair compliance. Furthermore, 4 mg is 4 times the
Tolerable Upper Intake Level for adults. Therefore, it is important
to know whether recurrent NTDs can be prevented with under 4
During 2004 and 2005, Roy M Pitkin was a member of the scientific
advisory board of Herbalife International of America Inc."
"The highest rates, at least in the Western world, are found
in Ireland and Scotland, where the frequency approaches 10 per
1000 births. US figures overall are much lower, although considerable
geographic variation exists, with levels highest in the Southeast."
Here's much of what I've noted about folic acid since 1999:
methanol in blood during experimental alcohol hangover,
YS Woo et al, 2005 Dec, Addict Biol: related studies:
aspartame, an equal methanol source: Murray 2006.12.29
" Reprod Toxicol. 1996 Nov-Dec; 10(6): 455-63.
Influence of dietary folic acid on the developmental toxicity of
methanol and the frequency of chromosomal breakage in the
Fu SS, Sakanashi TM, Rogers JM, Hong KH, Keen CL.
Department of Nutrition, University of California, Davis 95616 "
ban aspartame speech, Roger Williams MP, UK Parliament
2005.12.14: www.TheyWorkForYou.com: Murray 2006.02.20
" Folic acid, from fruits and vegetables, plays a role by powerfully
protecting against methanol (formaldehyde) toxicity.
Many common drugs, such as aspirin, interfere with folic acid,
as do some mutations in relevant enzymes. "
formaldehyde & formic acid from 11% methanol in aspartame:
This study admitted one datum that showed accumulation of
formaldehyde in the midbrain from an acute toxicity dose
methanol, and widespread accumulation of formic acid
in five tissues.
Biochemical Pharmcacology 1979: 28; 645-649.
Lack of a role for formaldehyde in methanol poisoning in the monkey.
Kenneth E. McMartin, Gladys Martin-Amat, Patricia E. Noker
and Thomas R. Tephly
The Toxicology Center, Dept. of Pharmacology,
University of Iowa, Iowa City, Iowa 52242
Abstract [not given in PubMed]:
[My comments are in square braclets.]
Methanol was administered [by nasogastric tube] either to untreated
cynomolgus monkeys [2-3.5 kg]
or to a folate-deficient cynomolgus monkey which exhibits
exceptional sensitivity to the toxic effects of methanol.
Marked formic acid accumulation in the blood and in body fluids and
tissues was observed.
No formaldehyde accumulation was observed in the blood and no
formaldehyde was detected in the urine, cerebrospinal fluid, vitreous
humor, liver, kidney, optic nerve, and brain in these monkeys at a
when marked metabolic acidosis and other characteristics of methanol
poisoning were observed.
Following intravenous infusion into the monkey, formaldehyde was
rapidly eliminated from the blood with a half-life of about 1.5 min
formic acid levels promptly increased in the blood.
Since formic acid accumulation accounted for the metabolic acidosis
and since ocular toxicity essentially identical to that produced in
methanol poisoning has been described after formate treatment, the
predominant role of formic acid as the major metabolic agent for
methanol toxicity is certified.
Also, results suggest that formaldehyde is not a major factor in the
toxic syndrome produced by methanol in the monkey.
Monkey A was folate-deficient and thus highly vulnerable to
methanol toxicity. This means that the large number of people who
are folate-deficient will also be more vulnerable.
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.
" The high ethanol/methanol ration of alcoholic beverages
must have a very significant protective effect,
though enzyme kinetics mandate some constant but low level of
One could speculate that the delicate balance which
maintains this defense might be jeopardized by the general nutrition
neglect and specifically the folic acid deficiency (21) associated
the meager food intake of some alcoholics.
[ 21. Holvey, D.N., the Merck Manual. 12th ed Rahway, New Jersey:
Merck and Company (1972). ]
Alcoholics have a much higher incidence of cancer and other
degenerative diseases, none of which
can be attributed to ethanol alone (56).
[56. U.S. Department of Health and Human Services. Alcohol and
Health., Fourth Special Report to the U.S. Congress. DeLuca, J.R., ed.
January 1981. ] "
Gold: Tephly: re Trocho: aspartame critique: Murray 1999.11.11
Life Sci 1991; 48(11): 1031-41
The toxicity of methanol.
Tephly TR. [a notable pro-aspartame scientist]
Department of Pharmacology, University of Iowa, Iowa City 52242.
Methanol toxicity in humans and monkeys is characterized by a latent
period of many hours followed by a metabolic acidosis and
This is not observed in most lower animals.
The metabolic acidosis and blindness is apparently due to formic acid
accumulation in humans and monkeys, a feature not seen in lower
The accumulation of formate is due to a deficiency in
formate metabolism which is, in turn, related, in part, to low hepatic
tetrahydrofolate (H4 folate).
An excellent correlation between
hepatic H4 folate and formate oxidation rates has been shown within
and across species.
Thus, humans and monkeys possess
low hepatic H4 folate levels, low rates of formate oxidation
and accumulation of formate after methanol.
Formate, itself, produces
blindness in monkeys in the absence of metabolic acidosis.
In addition to low hepatic H4 folate concentrations,
monkeys and humans
also have low hepatic 10-formyl H4 folate dehydrogenase levels,
the enzyme which is the ultimate catalyst for conversion of formate
to carbon dioxide.
This review presents the basis for the role of
folic acid-dependent reactions in the regulation of methanol toxicity.
Publication Types: Review Review, Academic PMID: 1997785
Here's a quite different assessment:
Folic Acid Supplements are a Health Hazard, John McDougall, MD:
The McDougall Newsletter, October 2005, Vol. 4, No. 10
Folic Acid Supplements are a Health Hazard
Stop Folic Acid Pills Now
Limit Your Intake of Fortified Flour Products (in the USA)
Don't Lower Your Homocysteine Levels with Supplements
Taking supplements with as little as 0.8 mg/day of folic acid
has been shown to increase your risk of dying of heart disease
according to the results of the first large randomized treatment trial
to carefully examine this issue. 1 [ 0.8 mg = 800 micrograms ]
The Norwegian Vitamin Trial (NORVIT) of 3,749 patients,
who were followed for 3.5 years was designed to show the benefits
of taking supplements -- but the results were contrary to
Folic acid supplementation was found to lower homocysteine levels
by 28%, but to increase relative risks of heart attack, stroke, and
death by 20%, along with a more than a 30% increase in cancer.
Those with the highest baseline homocysteine levels
(13 umol/L or greater) suffered the most harm
from taking supplements of folic acid.
Homocysteine Is Only a Risk Factor
Elevated levels of the amino acid homocysteine, found with a blood
test, have been associated with many common diseases, including
heart disease, strokes, venous thrombosis, dementia, and Alzheimer's
disease. The commonly made, but incorrect, assumption is that these
diseases are caused by elevated homocysteine in the body and
the solution is to give medications (vitamin pills) to fix the
However, homocysteine is not the problem.
Elevated homocysteine is only a sign that the body is becoming
diseased and at risk of a tragedy. We call this type of sign a
"risk factor" -- it predicts future risk, but it is not a disease in
itself -- no one dies of an elevated homocysteine level --
most commonly, clogged heart arteries are the actual cause of death
for those people showing this sign.
So what is the real meaning of this risk factor?
Homocysteine levels increase when people eat more meat and
These same dietary habits cause other signs (risk factors) --
indicating a higher chance of death and disability -- to rise;
like cholesterol, triglycerides, uric acid, blood sugar,
lipoprotein a, C-reactive protein, blood pressure, and body weight.
Fortunately, correcting the poor diet heals the underlying disease,
and at the same time the risk factors show improvement.
Folic Acid Supplements Overload the Body
Consuming more than 0.2 mg of folic acid daily floods the
bloodstream with this vitamin, overloading the metabolic capacities
of the body, causing imbalances that increase the risk of heart
disease and cancer. 2
Folic acid is a synthetic version of the natural vitamin, folate,
found in plant foods. Folate from food is essential for good health.
Folic acid sold in capsules is a medication at best and a toxin at
When given in doses of 0.8 mg it will lower homocysteine by about
30% (3 to 4 umol/L). 3 Higher doses then 0.08 mg have no greater
benefit for lowering blood levels of homocysteine.
Folic Acid Mandated for U.S. Cereal Products
January 1998 was the mandatory deadline for the fortification of
grain products with folic acid in the United States.
Folic acid was added to flours used to make bread, rolls, and
crackers. Another hefty source of this supplement comes from
enriched (vitamin-added) "ready-to-eat cereals."
Since 1998, folic acid intake has increased significantly in every
segment of the U.S. population with the
average additional intake of 0.22 mg/day. 3,4
Remember, as little is 0.2 mg causes overloads and imbalances
with an increased risk of illness.
A significant segment of the USA population is now consuming
over 1 mg/day of folic acid daily -- an amount found by the
NORVIT study to increase the risk of heart disease and cancer.
Doctors Harm Patients with Supplements
Cardiologists are fond of recommending vitamin pills to treat elevated
homocysteine in hopes of preventing further heart disease in their
patients. One of the most commonly prescribed preparations is
called Foltx -- a combination of 2.5 mg of folic Acid,
25 mg of vitamin B6, and 2 mg of vitamin B12.
A recent study showed a similar preparation
reduced the homocysteine levels of patients with a history of stroke
by 2 units (umol/L), but found no difference in risk of future
heart attacks, or death compared to a control group. 5
Another recent study showing folic acid actually causes the heart
arteries to close should cause doctors to mend their prescribing
practices. After six months of supplementation in 636 heart patients
with stents (stents are wire-mesh supports placed in the coronary
arteries during angioplasty), the Folate After Coronary Intervention
Trial found those patients taking folic acid had significantly more
narrowing of the arteries, more artery closure (restenosis),
and more major adverse cardiac events
compared to those taking placebo -- the exact opposite of what
investigators had expected to find. 6,7 As expected, the
homocysteine blood levels were reduced by the above treatment.
The authors recommended that the routine administration of folate
treatment not be advocated at the present time.
Even with all this condemning evidence, you can easily find experts
(many working with vitamin companies) trying to convince the
unaware buyer that high-dose folic acid supplementation -- as much
as 5 mg/day -- will be good for their heart and blood vessels. 8
Appropriate Response to Homocysteine in Your Blood
The main motivation behind fortification of flours and taking
supplemental vitamins has been to reduce the occurrence of serious
birth defects, especially the occurrence of neural tube defects
(NTDs). The effort seems to be working a little -- since the onset of
fortification there has been a 19% decrease in the incidence of NTDs.
Unfortunately, these same widespread recommendations to take folic
acid may be causing more heart disease and cancer. So, what to do?
All that money and effort now spent on supplementation with the hope
of reducing birth defects, heart disease, and cancer should be
towards educational programs to teach people to eat more legumes,
vegetables, and fruits -- the plentiful and safe sources of folic
(The name folic comes from the word foliage, which refers to plants.)
When packaged in the plant, folic acid is never harmful and always
beneficial. Further efforts should be made towards making sure
all people have ready access to plant-foods.
Because of the overwhelming evidence that the vitamin supplements
people are buying are a serious health hazard, I propose these
products be labeled with bold warnings like:
"Taking Vitamin E can raise your risk of dying,"
"Vitamin A (retinol) can damage your bones and cause birth defects,"
"Beta carotene may raise your risk of cancer," and
"Folic acid causes heart disease."
All supplement packages should also tell people that vitamins and
other nutrients are best obtained from healthy vegetable foods.
For more information on the hazards of supplementation,
please read from my newsletter archives the following:
August 2003: Plants, not Pills, for Vitamins and Minerals:
November 2004: Vitamins Do Not Prevent Cancer and May Increase
Likelihood of Death: How Supplements Can Make You Sicker
July 2005: Neither Aspirin Nor Vitamin E Will Save Women
February 2004: Treating Homocysteine with Vitamins Fails
1) Bonaa KH.
NORVIT: Randomized trial of homocysteine-lowering
with B-vitamins for secondary prevention of cardiovascular disease
after acute myocardial infarction.
Program and Abstracts from the
European Society of Cardiology Congress 2005;
September 3-7, 2005; Stockholm, Sweden. Hot Line II.
2) Quinlivan EP, Gregory JF 3rd.
Effect of food fortification on folic acid
intake in the United States.
Am J Clin Nutr. 2003 Jan; 77(1): 221-5.
3) Homocysteine Lowering Trailists Collaboration.
Dose-dependent effects of folic acid on blood concentrations
of homocysteine: a meta-analysis of the randomized trials.
Am J Clin Nutr. 2005 Oct; 82(4): 806-812.
4) Choumenkovitch SF, Selhub J, Wilson PW, Rader JI,
Rosenberg IH, Jacques PF.
Folic acid intake from fortification in United States
J Nutr. 2002 Sep; 132(9): 2792-8.
5) Toole JF .
Lowering homocysteine in patients with ischemic stroke
to prevent recurrent stroke, myocardial infarction, and death:
the Vitamin Intervention for Stroke Prevention (VISP)
randomized controlled trial.
JAMA. 2004 Feb 4; 291(5): 565-75.
6) Lange H.
Folate After Coronary Intervention Trial" (FACIT).
The folate after coronary intervention trial (FACIT).
Scientific presentation at the 52nd Annual Scientific Sessions
of the American College of Cardiology, Chicago, March 30th, 2003.
7) Schnyder G, Roffi M, Flammer Y, et al.
Effects of homocysteine-lowering therapy on restenosis
after percutaneous coronary intervention for narrowings
in small coronary arteries.
Am J Cardiol 2003; 91: 1265-1269.
You may subscribe to this free McDougall Newsletter at
2005 John McDougall All Rights Reserved
BJOG: An International Journal of Obstetrics and Gynaecology
2007 Jun; 114(6): 778-9; author reply 779.
Comment on: BJOG. 2007 Mar; 114(3): 243-52.
Low levels of prenatal alcohol exposure can cause fetal damage.
D Black, Fetal Alcohol Syndrome Foundation of the Netherlands,
Uithuizen, the Netherlands
JM Cobben, Emma Kinderziekenhuis, Amsterdam Medical Center,
Amsterdam, the Netherlands
R Didden, Department of Special Education, Radboud University,
Nijmegen, the Netherlands
D Lindhout, University Medical Center Utrecht,
Utrecht, the Netherlands
RR Pereira, Netherlands Organisation for Applied Scientific Research,
Leiden, the Netherlands &
H van Wieringen, Mesos Medical Center, Utrecht, the Netherlands
In BJOG 114:3, Henderson et al. review studies on the effects
of low to moderate prenatal alcohol exposure. 1
Their stated goal was to review human studies
tallying the following outcomes:
intrauterine growth restriction,
small for gestational age at birth
and birth defects including fetal alcohol syndrome'
The authors drew the conclusion that there is
'no convincing evidence of adverse effects of prenatal alcohol
exposure at low to moderate levels of exposure'.
This broad conclusion is, in our opinion, misleading.
First, Henderson et al. 1 did not include studies examining cognitive
or neurological effects of prenatal alcohol exposure, sequelae
to be more common than the full fetal alcohol syndrome. 2
Second, animal studies have shown that even transient, low levels
of alcohol exposure can cause negative neurological effects. 3
The only conclusion justified by the current scientific evidence is
that pregnant women should be advised against drinking during
pregnancy, a position supported by the
Health Council of the Netherlands after weighing all the evidence,
including animal studies. 4
1 Henderson J, Gray R, Brocklehurst P.
Systematic review of effects of low-moderate prenatal alcohol
exposure on pregnancy outcome.
BJOG 2007; 114: 243-52.
Synergy, Medline, ISI, Chemport
2 Willford JA, Richardson GA, Leech SL, Day NL.
Verbal and visuospatial learning and memory function in children
with moderate prenatal alcohol exposure.
Alcohol Clin Exp Res 2004; 28: 497-507.
Synergy, Medline, ISI
3 Young C, Olney JW.
Neuroapoptosis in the infant mouse brain triggered by a transient
small increase in blood alcohol concentration.
Neurobiol Dis 2006; 22: 548-54.
CrossRef, Medline, ISI, Chemport
4 Health Council of the Netherlands.
Risks of Alcohol Consumption Related to Conception,
Pregnancy and Breastfeeding.
Hague, The Netherlands:
Health Council of the Netherlands, 2005; publication no. 2004/22.
R Gray, J Henderson, P Brocklehurst (20070
National Perinatal Epidemiology Unit, University of Oxford, Oxford, UK
Authors response to:
Low levels of prenatal alcohol exposure can cause fetal damage
BJOG: An International Journal of Obstetrics and Gynaecology
114 (6) , 779-779 doi:10.1111/j.1471-0528.2007.01350.x
We would like to thank Black et al. for their comments. 1
However, we would also like to point out that our paper specifically
reviewed human studies only, addressed low-to-moderate
and not moderate prenatal alcohol consumption
and focused on the outcome of pregnancy
but not cognitive or neurological effects in the child.
We have discussed the findings from animal experiments
and reviewed neurobehavioural effects in the child elsewhere. 2
In our conclusions, we note that
'although there was no consistent evidence of adverse effect,
this does not mean that it is safe for women to drink at these levels
during pregnancy; the existing evidence is inconclusive'.
1 Black D, Cobben JM, Didden R, Lindhout D,
Pereira RR, van Wieringen H.
Low levels of prenatal alcohol exposure can cause fetal damage.
BJOG 2007; 114: 778.
Synergy, Medline, Chemport
2 Gray R, Henderson J.
Review of the Fetal Effects of Prenatal Alcohol Exposure.
Report to the Department of Health. Oxford, UK:
National Perinatal Epidemiology Unit, 2006
www.npeu.ox.ac.uk/alcoholreport Accessed 6 March 2007.
Note: many recent aspartame bans.....
ASDA (unit of Wal-Mart Stores WMT.N) and Marks & Spencer
will join Tesco and also Sainsbury to ban and limit aspartame,
MSG, artificial flavors dyes preservatives additives, trans fats, salt
"nasties" to protect kids from ADHD: leading UK media:
Artificial sweeteners (aspartame, sucralose) and coloring agents
will be banned from use in newly-born and baby foods,
the European Parliament decided: Latvia ban in schools 2006:
Connecticut bans artificial sweeteners in schools, Nancy Barnes,
New Milford Times: Murray 2006.05.25
Bristol, Connecticut, schools join state program to limit artificial
sweeteners, sugar, fats for 8800 students, Johnny J Burnham,
The Bristol Press: Murray 2006.09.22
Aspartame and Manufacturer-Funded Scientific Reviews
Mark D. Gold critique of GA Burdock et al., 2007 Sept.
bias, omissions, incuriosity = opportunity, aspartame safety
evaluation, Magnuson BA, Burdock GA, Williams GM, 7 more,
2007 Sept, Ajinomoto funded 98 pages html [ $ 32 pdf ]:
Saturday, September 15, 2007
industry scientists praise aspartame safety and benefits in Paris on
2006.05.30, Herve Nordmann, Andrew G. Renwick,
Carlo La Vecchia, Tommy Visscher, Jaap Seidell, France Bellisle,
Adam Drewnowski, Margaret Ashwell, Anne de la Hunty,
Sigrid A. Gibson, Alan R. Boobis: Murray 2007.11.18
critique of aspartame review, French Food Safety Agency AFSSA
2002.05.07 aspartamgb.pdf (18 pages, in English), Martin Hirsch:
safety of aspartame Part 1/2 12.4.2: EC HCPD-G SCF:
Murray 2003.01.12 EU Scientific Committee on Food, a whitewash
Mark Gold exhaustively critiques European Commission Scientific
Committee on Food re aspartame ( 2002.12.04 ):
59 pages, 230 references
J Am Diet Assoc. 2004 Feb; 104(2): 255-75.
Position of the American Dietetic Association: use of nutritive and
nonnutritive sweeteners. American Dietetic Association.
critique of aspartame review
by American Dietetic Association Feb 2004,
Valerie B. Duffy & Madeleine J. Sigman-Grant: Murray 2004.05.14
aspartame expose 96K Oct 1987 Part 1/3: Gregory Gordon,
UPI reporter: Murray 2000.07.10
aspartame history Part 1/4 1964-1976: Gold: Murray 1999.11.06
Donald Rumsfeld, 1977 head of Searle Corp.,
got aspartame FDA approval: Turner: Murray 2002.12.23
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:
revolving door, Monsanto, FDA, EPA: NGIN: Murray 2002.12.23
Samuels: Strong: Roberts: Gold: flaws in double-blind studies re
aspartame and MSG toxicity: Murray 2002.08.01
"Survey of aspartame studies: correlation of outcome and funding
sources," 1998, unpublished: http://www.dorway.com/peerrev.html
Walton found 166 separate published studies in the peer reviewed
medical literature, which had relevance for questions of human safety.
The 74 studies funded by industry all (100 %) attested to aspartame's
safety, whereas of the 92 non-industry funded studies, 84 (91 %)
identified a problem. Six of the seven non-industry funded studies
that were favorable to aspartame safety were from the FDA, which
has a public record that shows a strong pro-industry bias.
Ralph G. Walton, MD, Prof. of Clinical Psychology, Northeastern
Ohio Universities, College of Medicine, Dept. of Psychiatry,
Youngstown, OH 44501,
Chairman, The Center for Behavioral Medicine,
Northside Medical Center, 500 Gypsy Lane, P.O. Box 240
Youngstown, OH 44501 330-740-3621 rwalt...@aol.com;
Aspartame Controversy, in Wikipedia democratic
encyclopedia, 72 references (including AspartameNM # 864
and 1173 by Murray, brief fair summary of much more research:
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?:
"But the one-third who ate the most fried food increased their risk
by 25 percent, compared with the one-third who ate the least, and
surprisingly, the risk of developing metabolic syndrome was 34
percent higher among those who drank one can of diet soda a day
compared with those who drank none.
"This is interesting," said Lyn M. Steffen, an associate professor of
epidemiology at the University of Minnesota and a co-author of the
paper, which was posted online in the journal Circulation on Jan. 22.
"Why is it happening? Is it some kind of chemical in the diet soda,
or something about the behavior of diet soda drinkers?""
"The diet soda association was not hypothesized
and deserves further study."
methanol (formaldehyde, formic acid) disposition:
Bouchard M et al, full plain text, 2001:
substantial sources are degradation
of fruit pectins, liquors, aspartame, smoke:
vinyl acetate, ethyl alcohol, or aspartame in womb increases later
cancers in adults with lifetime exposure in many studies, M Soffritti
et al, Ramazzini Foundation, Basic Clin. Pharm. Toxicol. 2008 Feb.:
Rich Murray 2008.02.07
President Bush & formaldehyde (aspartame) toxicity:
Ramazzini Foundation carcinogenicity results Dec 2002:
Soffritti: Murray 2003.08.03 rmforall
p. 88 "The sweetening agent aspartame hydrolyzes in the
gastrointestinal tract to become free methyl alcohol,
which is metabolized in the liver
to formaldehyde, formic acid, and CO2. (11)"
Medinsky MA & Dorman DC. 1994;
Assessing risks of low-level methanol exposure.
CIIT Act. 14: 1-7.
Souring on fake sugar (aspartame), Jennifer Couzin,
Science 2007.07.06: 4 page letter to FDA from 12 eminent
USA toxicologists re two Ramazzini Foundation cancer studies
2007.06.25: Murray 2007.07.18
30 female pet store rats drinking lifelong 13.5 mg aspartame,
1/3 packet of Equal, had 33% with obvious tumors -- also bulging,
sick, and missing eyes, paralysis, obesity, skin sores -- agrees with
Ramazzini Foundation results, Victoria Inness-Brown:
Friday, February 15, 2008
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
aspartame groups and books:
updated research review of 2004.07.16: Murray 2006.05.11
old tiger roars -- Woodrow C Monte, PhD -- aspartame causes
many breast cancers, as ADH enzyme in breasts makes methanol
from diet soda into carcinogenic formaldehyde -- same in dark
wines and liquors, Fitness Life 2008 Jan.: Murray 2008.02.11
Monday, February 11, 2008
"Alcohol dehydrogenase ADH is required for the conversion of
methanol to formaldehyde (112).
ADH is not a common enzyme in the human body -- not many cells
in the human body contain this enzyme.
The human breast is one of the few organs in the body with a high
concentration of ADH (190b), and it is found there exclusively in the
mammary epithelial cells, the very cells known to transform into
adenocarcinoma (190c) (breast cancer).
The most recent breast cancer scientific literature implicates ADH
as perhaps having a pivotal role in the formation of breast cancer,
indicating a greater incidence of the disease in those
with higher levels of ADH activity in their breasts (190a)."
role of formaldehyde, made by body from methanol from foods
and aspartame, in steep increases in fetal alcohol syndrome, autism,
multiple sclerosis, lupus, teen suicide, breast cancer, Nutrition
Prof. Woodrow C. Monte, retired, Arizona State U., two reviews,
190 references supplied, Fitness Life, New Zealand
2007 Nov, Dec: Murray 2007.12.26
Wednesday, December 26 2007
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.
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:
DMDC: Dimethyl dicarbonate 200mg/L in drinks
adds methanol 98 mg/L ( becomes formaldehyde in body ):
EU Scientific Committee on Foods 2001.07.12: Murray 2004.01.22
"...DMDC was evaluated by the SCF in 1990
and considered acceptable for
the cold sterilization of soft drinks and fruit juices at levels of
addition up to 250 mg/L (1)
...DMDC decomposes primarily to CO2 and methanol ...
[ Note: Sterilization of bacteria and fungi is a toxic process,
probably due to the inevitable conversion in the body of methanol
into highly toxic formaldehyde and then formic acid. ]
The use of 200 mg DMDC per liter would add 98 mg/L of methanol
to wine which already contains an average of about 140 mg/L
from natural sources.
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:
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.
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...@RMV.se;
Department of Forensic Toxicology,
University Hospital, SE-581 85 Linkoping, Sweden.
This paper reports the elimination half-life of methanol in human
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
Avoiding Hangover Hell 2003.12.31 Mark Sherman, AP writer:
Robert Swift, MD [ formaldehyde from methanol in aspartame ]:
hangovers from formaldehyde from methanol (aspartame?):
Schwarcz: Linsley: Murray 2004.01.18
Thrasher (2001): "The major difference is that the Japanese
demonstrated the incorporation of FA and its metabolites
into the placenta and fetus.
The quantity of radioactivity remaining in maternal and fetal tissues
at 48 hours was 26.9 % of the administered dose." [ Ref. 14-16 ]
Arch Environ Health 2001 Jul-Aug; 56(4): 300-11.
Embryo toxicity and teratogenicity of formaldehyde. [100 references]
Thrasher JD, Kilburn KH. toxic...@drthrasher.org
Sam-1 Trust, Alto, New Mexico, USA.
www.drthrasher.org/formaldehyde_embryo_toxicity.html full text
http://www.drthrasher.org/formaldehyde_1990.html full text
Jack Dwayne Thrasher, Alan Broughton, Roberta Madison.
Immune activation and autoantibodies in humans
with long-term inhalation exposure to formaldehyde.
Archives of Environmental Health. 1990; 45: 217-223.
"Immune activation, autoantibodies, and anti-HCHO-HSA antibodies
are associated with long-term formaldehyde inhalation."
formaldehyde in FEMA trailers and other sources (aspartame,
dark wines and liquors, tobacco smoke): Murray 2008.01.30
Wednesday, January 30, 2008
The FEMA trailers give about the same amount of formaldehyde
daily as from a quart of dark wine or liquor, or two quarts
(6 12-oz cans) of aspartame diet soda, from their over 1 tenth gram
methanol impurity (one part in 10,000),
which the body quickly makes into formaldehyde -- enough
to be the major cause of "morning after" alcohol hangovers.
Methanol and formaldehyde also result from many fruits and
vegetables, tobacco and wood smoke, heater and vehicle exhaust,
household chemicals and cleaners, cosmetics, and new cars, drapes,
carpets, furniture, particleboard, mobile homes, buildings,
so all these sources add up and interact
with many other toxic chemicals.
BN Ames and LS Gold, 1998, have presented detailed information
that there is no increase in recent decades for most cancers,
and that common carcinogens do not result in significant exposures
to the average human population.
However, individuals are not average -- each person has a unique
genetic makeup, resulting in a huge range of variation of
to specific chemicals, as is well evidenced in the case of methanol,
formaldehyde, and formic acid, especially with regard
to behavioral effects.
Each is subject to very wide ranges of exposure levels.
Many are in especially vulnerable groups, depending on diet, obesity,
sex, exercise, life stress, age from conception to very old, unusually
severe toxic exposures, injuries, and diseases.
It is clear that a variety of multiple chemical sensitivity syndromes
exist, often with remarkable hypersensitivity.
Methanol, formaldehyde, and formic acid toxicity are unusual, in that
humans are far more vulnerable than any other mammal, as much as
ten to sixty-fold, which complicates the utility of animal data.
The unusally long human life span also increases the role of long-term
chronic low-level exposure.
FEMA slow to safety test Katrina toxic trailers, Charles Babington,
Associated Press -- 1 ppm formaldehyde in air is about half the daily
dose from 3 cans aspartame diet soda and ten times the 1999 EPA
alarm level for drinking water: Murray 2007.07.23
50% UK baby food is now organic - aspartame or MSG
with food dyes harm nerve cells, CV Howard 3 year study
funded by Lizzy Vann, CEO, Organix Brands,
Children's Food Advisory Service: Murray 2006.01.13
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
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
C. Trocho (1998):
"In all, the rats retained, 6 hours after administration, about 5 % of
label, half of it in the liver."
They used a very low level of aspartame ingestion, 10 mg/kg, for rats,
which have a much greater tolerance for aspartame than humans.
So, the corresponding level for humans would be about 1 or 2 mg/kg.
Many headache studies in humans used doses of about 30 mg/kg daily.
aspartame puts formaldehyde adducts into tissues, Part 1/2
full text, Trocho & Alemany 1998.06.26: Murray 2002.12.22
http://ww.presidiotex.com/barcelona/index.html full text
Formaldehyde derived from dietary aspartame
binds to tissue components in vivo.
Life Sci June 26 1998; 63(5): 337-49.
Departament de Bioquimica i Biologia Molecular,
Facultat de Biologia, Universitat de Barcelona, Spain.
http://www.bq.ub.es/cindex.html Línies de Recerca: Toxicitat de
Sra. Carme Trocho, Sra. Rosario Pardo, Dra. Immaculada Rafecas,
Sr. Jordi Virgili, Dr. Xavier Remesar, Dr. Jose Antonio
Fernandez-Lopez, Dr. Mari? Alemany [male]
Fac. Biologia Tel.: (93)4021521, FAX: (93)4021559
Sra. Carme Trocho "Trok-ho" Fac. Biologia Tel.: (93)4021544,
FAX: (93)4021559 ale...@porthos.bio.ub.es;
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
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
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
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
been considered carcinogenic (34,47).
The repeated occurrence of claims that aspartame
produces headache and other neurological and psychological
secondary effects --
more often than not challenged by careful analysis --
(5, 9, 10, 15, 48)
may eventually find at least a partial explanation in the permanence
of the formaldehyde label,
since formaldehyde intoxication can induce similar effects (49).
The cumulative effects derived from the incorporation of label in the
chronic administration model suggests that regular intake of aspartame
may result in the progressive accumulation of formaldehyde adducts.
It may be further speculated that the formation of adducts can help to
explain the chronic effects aspartame consumption may induce on
sensitive tissues such as brain (6, 9, 19, 50).
In any case, the possible negative effects that the accumulation of
formaldehyde adducts can induce is, obviously, long-term.
The alteration of protein integrity and function may needs some time
to induce substantial effects.
The damage to nucleic acids, mainly to DNA,
may eventually induce cell death and/or mutations.
The results presented suggest that the conversion of aspartame
methanol into formaldehyde adducts in significant amounts in vivo
should to be taken into account because of the widespread utilization
of this sweetener.
Further epidemiological and long-term studies are needed to
determine the extent of the hazard that aspartame consumption
poses for humans."
Many scientific studies and case histories report: * headaches
* many body and joint pains (or burning, tingling, tremors, twitching,
spasms, cramps, stiffness, numbness, difficulty swallowing)
* fever, fatigue, swollen glands * "mind fog", "feel unreal",
poor memory, confusion, anxiety, irritability, depression, mania,
insomnia, dizziness, slurred speech, sexual problems,
poor vision, hearing (deafness, tinnitus), or taste
* red face, itching, rashes, allergic dermatitis, hair loss,
burning eyes or throat, dry eyes or mouth, mouth sores,
burning tongue * obesity, bloating, edema, anorexia,
poor appetite or excessive hunger or thirst
* breathing problems, shortness of breath
* nausea, diarrhea or constipation * coldness * sweating
* racing heart, low or high blood pressure, erratic blood sugar levels
* hypothryroidism or hyperthyroidism * seizures * birth defects
* brain cancers * addiction * aggrivates diabetes, autism, allergies,
lupus, ADHD, fibromyalgia, chronic fatigue syndrome,
multiple chemical sensitivity, multiple sclerosis, pseudotumor cerebri
and interstitial cystitis (bladder pain).
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
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
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 184.108.40.206.),
formyl-tetrahydrofolate synthetase (EC 220.127.116.11.) (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
ethyl alcohol is more toxic than methanol to these test animals (43)."
Recent research [see links at end of post] supports his focus on the
methanol to formaldehyde toxic process:
"The United States Environmental Protection Agency in their
Multimedia Environmental Goals for Environmental Assessment
recommends a minimum acute toxicity concentration
of methanol in drinking water at 3.9 parts per million,
with a recommended limit of consumption below 7.8 mg/day (8).
This report clearly indicates that methanol:
"...is considered a cumulative poison due to the low rate of excretion
once it is absorbed. In the body, methanol is oxidized to formaldehyde
and formic acid; both of these metabolites are toxic." (8)...
Recently the toxic role of formaldehyde (in methanol toxicity) has
No skeptic can overlook the fact that, metabolically, formaldehyde
must be formed as an intermediate to formic acid production (54).
Formaldehyde has a high reactivity which may be why it has not been
found in humans or other primates during methanol poisoning (59)....
If formaldehyde is produced from methanol and does have a
reasonable half life within certain cells in the poisoned organism
he chronic toxicological ramifications could be grave.
Formaldehyde is a known carcinogen (57) producing squanous-cell
carcinomas by inhalation exposure in experimental animals (22).
The available epidemiological studies do not provide adequate data
for assessing the carcinogenicity of formaldehyde in man (22, 24, 57).
However, reaction of formaldehyde with deoxyribonucleic acid
(DNA) has resulted in irreversible denaturation that could interfere
with DNA replication and result in mutation (37)..."
It is certain that high levels of aspartame use,
above 2 liters daily for months and years,
must lead to chronic formaldehyde-formic acid toxicity.
Fully 11 % of aspartame is methanol -- 1,120 mg aspartame
in 2 L diet soda, almost six 12-oz cans, gives 123 mg methanol
(wood alcohol). The methanol is immediately released
into the body after drinking .
Within hours, the liver turns much of the methanol into formaldehyde,
and then much of that into formic acid, both of which in time
are partially eliminated as carbon dioxide and water.
However, about 30 % of the methanol remains in the body
as cumulative durable toxic metabolites of formaldehyde
and formic acid -- 37 mg daily,
a gram every month, accumulating in and affecting every tissue.
If only 10 % of the methanol is retained daily as formaldehyde,
that would give 12 mg daily formaldehyde accumulation -- about
60 times more than the 0.2 mg from 10 % retention
of the 2 mg EPA daily limit for formaldehyde in drinking water.
Bear in mind that the EPA limit for formaldehyde in drinking water is
1 ppm, or 2 mg daily for a typical daily consumption of 2 L of water.
ATSDR: EPA limit 1 ppm formaldehyde in drinking water July 1999:
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
rashes, and leading to vision and eye problems, and even seizures.
In many cases there is addiction. Probably there are immune system
disorders, with a hypersensitivity to these toxins and other
J. Nutrition 1973 Oct; 103(10): 1454-1459.
Metabolism of aspartame in monkeys.
Oppermann JA, Muldoon E, Ranney RE.
Dept. of Biochemistry, Searle Laboratories,
Division of G.D. Searle and Co. Box 5110, Chicago, IL 60680
They found that about 70 % of the radioactive methanol in aspartame
put into the stomachs of 3 to 7 kg monkeys
was eliminated within 8 hours, with little additional elimination,
as carbon dioxide in exhaled air and as water in the urine.
They did not mention that this meant that about 30 % of the methanol
must transform into formaldehyde and then into formic acid,
both of which must remain as toxic products in all parts of the body.
They did not report any studies on the distribution of radioactivity
in body tissues, except that blood plasma proteins after 4 days
held 4 % of the initial methanol.
This study did not monitor long-term use of aspartame.
The low oral dose of aspartame and for methanol
was 0.068 mmol/kg, about 1 part per million [ppm]
of the acute toxicity level of 2,000 mg/kg, 67,000
mmol/kg, used by McMartin (1979).
Two L daily use of diet soda provides 123 mg methanol,
2 mg/kg for a 60 kg person, a dose of 67 mmole/kg,
a thousand times more than the dose in this study.
By eight hours excretion of the dose in air and urine had leveled off
67.1 +-2.1 % as CO2 in the exhaled air
and 1.57+-0.32 % in the urine, so 68.7 % was excreted,
and 31.3 % was retained.
This data is the average of 4 monkeys.
"...the 14C in the feces was negligible."
"That fraction not so excreted (about 31%) was converted to body
constituents through the one-carbon metabolic pool."
"All radioactivity measurements were counted to +-1 % accuracy..."
This indicates that the results could not be claimed to have a
of a tenth of a percent. OK, so this is a nit-pick -- but I believe
espousing spurious accuracy is a sign of scientific insecurity.
The abstract ends, "It was concluded that aspartame was digested to
its three constituents that were then absorbed
as natural constituents of the diet.
Thus, the concept is very subtly insinuated that methanol, as a
constituent of aspartame, is absorbed as a natural constituent
of the diet.
Nowhere in this report are mentioned the dread words,
"formaldehyde" and "formic acid".
Of course, methanol and formaldehyde toxicity studies are highly
relevant to the issue of aspartame toxicity.
[ Aspartame has to be turned into its toxic products,
formaldehyde and formic acid, in the body, before it is toxic,
so some pro-aspartame reseach studies test aspartame outside the
body, and then proclaim that they have proved that it is not toxic. ]
http://www.dorway.com/tldaddic.html 5-page review
Roberts HJ Aspartame (NutraSweet) addiction.
Townsend Letter 2000 Jan; HJRob...@aol.com
Sunshine Sentinel Press P.O.Box 17799
West Palm Beach, FL 33416
800-814-9800 561-588-7628 561-547-8008 fax
1038-page medical text "Aspartame Disease: An Ignored Epidemic"
published May 30 2001 $ 60.00 postpaid data from 1200 cases
available at http://www.amazon.com
over 600 references from standard medical research
Moseley: review Roberts "Aspartame Disease: An Ignored Epidemic":
Murray 2002.02.07 rmforall
Roberts, Hyman J., 1924- ,
Useful insights for diagnosis, treatment and public heath: an updated
anthology of original research, 2002, 798 pages,
aspartame disease, pages 627-685, 778-780
Roberts: the life work of a brilliant clinician: aspartame toxicity:
Murray 2002.08.02 rmforall
Russell L. Blaylock, MD 601-982-1175 Madison, Mississippi
"Excitotoxins: The Taste that Kills", 1977, 298 p., 493 references.
"Health and Nutrition Secrets that can save your life", 2002, 459 p.,
558 + 30 references, $ 30 http://www.russellblaylockmd.com/
aspartame, MSG, excitotoxins, NMDA glutamate receptors,
multiple sclerosis: Blaylock: Murray 2004.06.09
Lancet website aspartame letter 1999.07.29:
Excitotoxins 1999 Part 1/3 Blaylock: Murray 2000.01.14
The Medical Sentinel Journal 1999 Fall; (95 references)
Comet assay finds DNA damage from sucralose, cyclamate, saccharin
in mice: Sasaki YF & Tsuda S Aug 2002: Murray 2003.01.01
[ Also borderline evidence, in this pilot study of 39 food additives,
using test groups of 4 mice, for DNA damage from for stomach, colon,
liver, bladder, and lung 3 hr after oral dose of 2000 mg/kg
aspartame -- a very high dose. Methanol is the only component of
aspartame that can lead to DNA damage. ]
genotoxins, Comet assay in mice: Ace-K, stevia fine; aspartame poor;
sucralose, cyclamate, saccharin bad: Y.F. Sasaki Aug 2002:
Murray 2003.01.27 [A detailed look at the data] ]
MSG and Aspartame -- A Personal Story, TV health reporter
Dick Allgire (vegetarian) healed of migraines and panic attacks:
Tuesday, February 12, 2008
group with 1,080 members, 22,439 posts in a public archive
E. Bryant Holman bry...@presidiotex.com
Carol Guilford CarolG...@sbcglobal.net
Aspartame Toxicity Information Center Mark D. Gold
12 East Side Drive #2-18 Concord, NH 03301 603-225-2100
"Scientific Abuse in Aspartame Research"
http://health.groups.yahoo.com/group/GFCFKids/ an excellent group
Gluten Free Casein Free Kids
This list is unmoderated and unrestricted. The principle aim of this
is to provide a discussion forum for parents of children on the autism
spectrum who are avoiding gluten and casein and other substances
in their children's diets.
9,108 members, 234,968 posts in public archive since Dec. 1998
A very detailed, highly credible account of the dubious approval
process for aspartame in July, 1981 is part of the just released
two-hour documentary "Sweet Misery, A Poisoned World:
An Industry Case Study of a Food Supply In Crisis"
by Cori Brackett: co...@soundandfuryproductions.com;
2301 East Broadway, Suite 111 Tucson, AZ 85719
Mary Nash Stoddard
Toxicology Sourcebook: "Deadly Deception Story of Aspartame"
Aspartame Consumer Safety Network and Pilot Hotline [since 1987]
P.O. Box 2001 Frisco, Texas 75034 U.S. [ North of Dallas ]
Dr. Janet Starr Hull, PhD, CN jsh...@sweetpoison.com;
Splenda®: Is It Safe Or Not?
http://www.truthinlabeling.org/ Truth in Labeling Campaign [MSG]
Adrienne Samuels, PhD The toxicity/safety of processed
free glutamic acid (MSG): a study in suppression of information.
Accountability in Research 1999; 6: 259-310. 52-page review
P.O. Box 2532 Darien, Illinois 60561
http://www.fedupwithfoodadditives.info/ an excellent group
These web pages provide:
independent information about the effects of food on behaviour,
health and learning ability in both children and adults.
support for families using a low-chemical elimination diet free of
additives, low in salicylates, amines and flavour enhancers
(FAILSAFE) for health, behaviour and learning problems.
Food Intolerance Network, Sue Dengate sden...@ozemail.com.au;
"Of course, everyone chooses, as a natural priority, to enjoy
peace, joy, and love by helping to find, quickly share, and positively
act upon evidence about healthy and safe food, drink, and
Rich Murray, MA Room For All rmfo...@comcast.net
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505
http://RMForAll.blogspot.com new primary archive
group with 120 members, 1,528 posts in a public archive
"The blog you were looking for was not found."
It's not on The Wayback Machine, either. :-(
Marshall Price of Miami
Known to Yahoo as d021317c