Re: confounding variable is formaldehyde from methanol from aspartame, smoke, wines and liquors, pectins in fruits and vegetables: Murray 2005.06.02


"Sbharris[atsign]ix.netcom.com" <sbharris@xxxxxxxxxxxxx> wrote in message
news:1117759013.008962.291490@xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
>>>In humans, ingested or inhaled methanol is always quickly largely
>>>converted
> into formaldehyde and thence largely into formic acid.
> These are both potent cumulative toxins that must affect every cell
> type, thus aggravating every disease process. <<
>
>
> COMMENT:
>
> Boloney, boloney, boloney. If this statement above was anywhere close
> to being true, then mortality among chronic formaldehyde workers would
> be vastly higher from every disease you can think of. They aren't.
> Studies have really not been able to find any bad effects in particular
> from the stuff.
**************************************************************


Rich Murray rmforall@xxxxxxxxxxx 505-501-2298 replies:

Baloney, baloney, baloney... I had to check my dictionary to be sure of
the spelling.


"These data provide little evidence that mortality from cancer is associated
with formaldehyde exposure at levels experienced by workers in this study."

Note the final qualifier, "...at levels experienced by workers in this
study."

J Natl Cancer Inst. 1986 Jun; 76(6): 1071-84.
Comment in:
J Natl Cancer Inst. 1994 Oct 19;86(20):1556-8.
Mortality among industrial workers exposed to formaldehyde.
Blair A, Stewart P, O'Berg M, Gaffey W, Walrath J, Ward J, Bales R, Kaplan
S, Cubit D.

A historical cohort study evaluated the mortality experience of 26,561
workers employed in 10 formaldehyde-producing or -using facilities.
Approximately 600,000 person-years of follow-up accrued as workers were
followed to January 1, 1980.
Estimates of historical exposure to formaldehyde by job were developed by
project industrial hygienists using monitoring data available from
participating plants, comments from long-term workers, and comprehensive
monitoring data specifically collected for this study.
Mortality from all causes combined was about as expected [standardized
mortality ratio (SMR) = 96] based on mortality rates of the general U.S.
population.
Significantly fewer deaths occurred from infective and parasitic diseases
(SMR = 51) and from accidents (SMR = 72) than expected.
Cancer overall was not related to formaldehyde exposure.
Workers exposed to formaldehyde had slight excesses for Hodgkin's disease
and cancers of the lung and prostate gland, but these excesses were not
consistently related to duration of or average, cumulative, or peak
formaldehyde exposure levels.
Recent animal studies found nasal cancer among rats exposed to formaldehyde,
but no excess of this tumor occurred in this study.
Mortality from brain cancer and leukemia among these industrial workers was
not excessive in contrast to reported excesses among professional groups
(e.g., anatomists, embalmers, and pathologists) with exposure to
formaldehyde. Although there was a deficit for cancer of the buccal cavity
and pharynx, mortality from certain subsites, i.e., the nasopharynx and
oropharynx, was elevated.
These subsites did not, however, show a consistently rising risk with level
of exposure.
These data provide little evidence that mortality from cancer is associated
with formaldehyde exposure at levels experienced by workers in this study.
PMID: 3458945


However, one of these researchers, Walrath J:

'Formaldehyde-related occupations in printing appeared to be associated with
any type of nasal cancer (either SNC or NPC). "

J Natl Cancer Inst. 1987 Dec; 79(6): 1221-4.
Nasopharyngeal cancer, sinonasal cancer, and occupations related to
formaldehyde: a case-control study.
Roush GC, Walrath J, Stayner LT, Kaplan SA, Flannery JT, Blair A.
Department of Epidemiology and Public Health, Yale University School of
Medicine, New Haven, CT 06510.

Formaldehyde vapor induces cancer of the nasal passages in laboratory
animals. In this case-control epidemiologic study, occupational information
was obtained for 198 persons with sinonasal cancer (SNC), for 173 with
nasopharyngeal cancer (NPC) identified as incident cases by the Connecticut
Tumor Registry over 41 years among Connecticut males dying of any cause, and
for 605 controls sampled from Connecticut death certificates.
City directories and death certificates provided information on job,
industry, employer, and year of employment for exposure classification.
Without knowledge as to case-control status, an industrial hygienist
particularly experienced in epidemiologic studies of formaldehyde classified
each study subject with respect to probability and degree of formaldehyde
exposure.
For those with probable exposure to the high level 20+ years prior to death
the odds ratio for NPC was 2.3 [95% confidence limits (CL): 0.9, 6.0], and
for those with this same risk factor among men dying at age 68+ (the median
study age at death or older) the odds ratio was 4.0 [95% CL: 1.3, 12.0--with
two-sided P = .015, unadjusted for multiple significance tests, and with
two-sided P = .129 in testing for interaction between this risk factor
(never any exposure vs. probable exposure to high level 20+ years prior to
death) and age (age less than 68 yr vs. age 68+ yr)].
Odds ratios were close to unity for 9 of 13 industries. Formaldehyde-related
occupations in printing appeared to be associated with any type of nasal
cancer (either SNC or NPC). PMID: 3480373

"Mortality was significantly elevated for total cancer, arteriosclerotic
heart disease, and suicide, whereas significant deficits were noted in
mortality from diseases of the respiratory and genitourinary systems.
Deaths from cancers of the brain, colon, and prostate and leukemia were
significantly higher than expected."

Cancer Res. 1984 Oct; 44(10): 4638-41.
Cancer and other causes of death among embalmers.
Walrath J, Fraumeni JF Jr.

To evaluate the potential carcinogenic effects of formaldehyde, we examined
the proportionate mortality experience of embalmers licensed to practice in
California.
Mortality was significantly elevated for total cancer, arteriosclerotic
heart disease, and suicide, whereas significant deficits were noted in
mortality from diseases of the respiratory and genitourinary systems.
Deaths from cancers of the brain, colon, and prostate and leukemia were
significantly higher than expected.
No increased mortality was seen for cancers of the respiratory tract,
including the nasal passages, where an effect might be expected based on
animal studies. A parallel mortality survey of embalmers from New York State
showed similar findings, with excesses of brain tumors, leukemia, colon
cancer, arteriosclerotic heart disease, and cirrhosis.
Further investigation is needed to determine whether any of these outcomes
is related to formaldehyde exposure. PMID: 6467219


"Mortality was significantly elevated for cancers of the skin and colon and
for arteriosclerotic heart disease, whereas significant deficits were seen
in mortality from respiratory diseases and accidents.
....Mortality was significantly elevated for cancers of the skin, kidney, and
brain among those licensed only as embalmers, whereas mortality patterns
were unremarkable among those licensed also as funeral directors (and
presumably less exposed to formaldehyde)."

Int J Cancer. 1983 Apr 15; 31(4): 407-11.
Mortality patterns among embalmers.
Walrath J, Fraumeni JF Jr.

In view of recent findings of nasal cancer in rats exposed to formaldehyde
vapors, we investigated the proportionate mortality experience of embalmers
licensed to practice in New York State.
Mortality was significantly elevated for cancers of the skin and colon and
for arteriosclerotic heart disease, whereas significant deficits were seen
in mortality from respiratory diseases and accidents.
Respiratory cancer mortality was not excessive and no deaths were attributed
to nasal cancer.
Mortality was significantly elevated for cancers of the skin, kidney, and
brain among those licensed only as embalmers, whereas mortality patterns
were unremarkable among those licensed also as funeral directors (and
presumably less exposed to formaldehyde).
These preliminary results indicate the need for occupational cohort studies
to clarify the carcinogenic potential of formaldehyde.
Publication Types: Case Reports PMID: 6832852



http://groups.yahoo.com/group/aspartameNM/message/1071
research on aspartame (methanol, formaldehyde, formic acid) toxicity: Murray
2004.04.29 rmforall

http://groups.yahoo.com/group/aspartameNM/message/1108
faults in 1999 July EPA 468-page formaldehyde profile:
Elzbieta Skrzydlewska PhD, Assc. Prof., Medical U. of Bialystok, Poland,
abstracts -- ethanol, methanol, formaldehyde, formic acid, acetaldehyde,
lipid peroxidation, green tea, aging, Lyme disease:
Murray 2004.08.08 rmforall

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

http://groups.yahoo.com/group/aspartameNM/message/1070
critique of aspartame review, French Food Safety Agency AFSSA 2002.05.07
aspartamgb.pdf (18 pages, in English), Martin Hirsch:
Murray 2004.04.13

http://groups.yahoo.com/group/aspartameNM/message/957
safety of aspartame Part 1/2 12.4.2: EC HCPD-G SCF:
Murray 2003.01.12 rmforall EU Scientific Committee on Food, a whitewash

http://groups.yahoo.com/group/aspartameNM/message/1045
http://www.holisticmed.com/aspartame/scf2002-response.htm
Mark Gold exhaustively critiques European Commission Scientific
Committee on Food re aspartame ( 2002.12.04 ): 59 pages, 230 references

http://groups.yahoo.com/group/aspartameNM/message/989 On 2003.04.10
the European Union Parliament voted 440 to 20 to approve sucralose,
limit cyclamates & reevaluate aspartame & stevia: Murray 2003.04.12 rmforall

http://www.eatright.org/Nutritive(1).pdf
J Am Diet Assoc. 2004 Feb; 104(2): 255-75.
Position of the American Dietetic Association: use of nutritive and
nonnutritive sweeteners. American Dietetic Association.

http://groups.yahoo.com/group/aspartameNM/message/1068
critique of aspartame review by American Dietetic Association Feb 2004,
Valerie B. Duffy & Madeleine J. Sigman-Grant: Murray 2004.04.03 rmforall


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--
unlike the large levels of methanol locked up in complex molecules inside
many fruits and vegetables.
Within hours, the liver turns much of the methanol into formaldehyde, and
then much of that into formic acid, both of which in time are partially
eliminated as carbon dioxide and water.

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

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

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

http://groups.yahoo.com/group/aspartameNM/message/835
ATSDR: EPA limit 1 ppm formaldehyde in drinking water July 1999:
Murray 2002.05.30 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, rashes, and leading to vision and eye
problems, and even seizures. In many cases there is addiction. Probably
there are immune system disorders, with a hypersensitivity to these toxins
and other chemicals.

J. Nutrition 1973 Oct; 103(10): 1454-1459.
Metabolism of aspartame in monkeys.
Oppermann JA, Muldoon E, Ranney RE.
Dept. of Biochemistry, Searle Laboratories,
Division of G.D. Searle and Co. Box 5110, Chicago, IL 60680
They found that about 70% of the radioactive methanol in aspartame put into
the stomachs of 3 to 7 kg monkeys was eliminated within 8 hours, with little
additional elimination, as carbon dioxide in exhaled air and as water in
the urine.
They did not mention that this meant that about 30% of the methanol must
transform into formaldehyde and then into formic acid, both of which must
remain as toxic products in all parts of the body.
They did not report any studies on the distribution of radioactivity in body
tissues, except that blood plasma proteins after 4 days held 4% of the
initial methanol.
This study did not monitor long-term use of aspartame.

http://groups.yahoo.com/group/aspartameNM/message/915
formaldehyde toxicity: Thrasher & Kilburn: Shaham: EPA: Gold:
Wilson: CIIN: Murray 2002.12.12 rmforall

Thrasher (2001): "The major difference is that the Japanese demonstrated
the incorporation of FA and its metabolites into the placenta and fetus.
The quantity of radioactivity remaining in maternal and fetal tissues
at 48 hours was 26.9% of the administered dose." [ Ref. 14-16 ]

Arch Environ Health 2001 Jul-Aug; 56(4): 300-11.
Embryo toxicity and teratogenicity of formaldehyde. [100 references]
Thrasher JD, Kilburn KH. toxicology@xxxxxxxxxxxxxx
Sam-1 Trust, Alto, New Mexico, USA.
http://www.drthrasher.org/formaldehyde_embryo_toxicity.html full text

http://www.drthrasher.org/formaldehyde_1990.html full text Jack Dwayne
Thrasher, Alan Broughton, Roberta Madison. Immune activation and
autoantibodies in humans with long-term inhalation exposure to formaldehyde.
Archives of Environmental Health. 1990; 45: 217-223. "Immune activation,
autoantibodies, and anti-HCHO-HSA antibodies are associated with long-term
formaldehyde inhalation." PMID: 2400243


http://groups.yahoo.com/group/aspartameNM/message/1016
President Bush & formaldehyde (aspartame) toxicity: Ramazzini Foundation
carcinogenicity results Dec 2002: Soffritti: Murray 2003.08.03 rmforall

p. 88 "The sweetening agent aspartame hydrolyzes in the gastrointestinal
tract to become free methyl alcohol, which is metabolized in the liver
to formaldehyde, formic acid, and CO2. (11)"
Medinsky MA & Dorman DC. 1994; Assessing risks of low-level
methanol exposure. CIIT Act. 14: 1-7.

Ann N Y Acad Sci. 2002 Dec; 982: 87-105.
Results of long-term experimental studies on the carcinogenicity of
formaldehyde and acetaldehyde in rats.
Soffritti M, Belpoggi F, Lambertin L, Lauriola M, Padovani M, Maltoni C.
Cancer Research Center, European Ramazzini Foundation for Oncology and
Environmental Sciences, Bologna, Italy. crcfr@xxxxxx

Formaldehyde was administered for 104 weeks in drinking water supplied
ad libitum at concentrations of 1500, 1000, 500, 100, 50, 10, or 0 mg/L
to groups of 50 male and 50 female Sprague-Dawley rats beginning at
seven weeks of age.
Control animals (100 males and 100 females) received tap water only.
Acetaldehyde was administered to 50 male and 50 female Sprague-Dawley
rats beginning at six weeks of age at concentrations of 2,500, 1,500,
500, 250, 50, or 0 mg/L.
Animals were kept under observation until spontaneous death.
Formaldehyde and acetaldehyde were found to produce an increase in total
malignant tumors in the treated groups and showed specific carcinogenic
effects on various organs and tissues. PMID: 12562630

Ann N Y Acad Sci. 2002 Dec; 982: 46-69.
Results of long-term experimental studies on the carcinogenicity of
methyl alcohol and ethyl alcohol in rats.
Soffritti M, Belpoggi F, Cevolani D, Guarino M, Padovani M, Maltoni C.
Cancer Research Center, European Ramazzini Foundation for Oncology and
Environmental Sciences, Bologna, Italy. crcfr@xxxxxx

Methyl alcohol was administered in drinking water supplied ad libitum at
doses of 20,000, 5,000, 500, or 0 ppm to groups of male and female
Sprague-Dawley rats 8 weeks old at the start of the experiment.
Animals were kept under observation until spontaneous death.
Ethyl alcohol was administered by ingestion in drinking water at a
concentration of 10% or 0% supplied ad libitum to groups of male and
female Sprague-Dawley rats; breeders and offspring were included in the
experiment.
Treatment started at 39 weeks of age (breeders), 7 days before mating,
or from embryo life (offspring) and lasted until their spontaneous death.
Under tested experimental conditions, methyl alcohol and ethyl alcohol
were demonstrated to be carcinogenic for various organs and tissues.
They must also be considered multipotential carcinogenic agents.
In addition to causing other tumors, ethyl alcohol induced malignant
tumors of the oral cavity, tongue, and lips.
These sites have been shown to be target organs in man by epidemiologic
studies. Publication Types: Review Review, Tutorial PMID: 12562628

Surely the authors deliberately emphasized that aspartame is well-known
to be a source of formaldehyde, which is an extremely potent, cumulative
toxin, with complex, multiple effects on all tissues and organs.

This is even more significant, considering that they have already tested
aspartame, but not yet released the results:

p. 29-32 Table 1: The Ramazzinni Foundation Cancer Program
Project of [200] Long-Term Carcinogenicity Bioassays: Agents Studied

No. No. of Bioassays Species No. Route of Exposure
108. "Coca-Cola" 4 Rat 1,999 Ingestion, Transplantal Route
109. "Pepsi-Cola" 1 Rat 400 Ingestion
110. Sucrose 1 Rat 400 Ingestion
111. Caffeine 1 Rat 800 Ingestion
112. Aspartame 1 Rat 1,800 Ingestion

http://members.nyas.org/events/conference/conf_02_0429.html
Soffritti said that Coca-Cola showed no carcinogenicity.

It may be time to disclose these important aspartame results.

Finally, an intripid and much published team in Japan has found DNA damage
in 8 tissues from single non-lethal doses of aspartame (near-significant
high levels of DNA damage in 5 tissues) and many other additives in groups
of just 4 mice:

Mutat Res 2002 Aug 26; 519(1-2): 103-19
The comet assay with 8 mouse organs: results with 39 currently used food
additives.
Sasaki YF, Kawaguchi S, Kamaya A, Ohshita M, Kabasawa K, Iwama K,
Taniguchi K, Tsuda S.
Laboratory of Genotoxicity, Faculty of Chemical and Biological
Engineering, Hachinohe National College of Technology,
Tamonoki Uwanotai 16-1, Aomori 039-1192, Japan.
yfsasaki-c@xxxxxxxxxxxxxxxxxx s.tsuda@xxxxxxxxxxxxx

We determined the genotoxicity of 39 chemicals currently in use as food
additives.
They fell into six categories-dyes, color fixatives and
preservatives, preservatives, antioxidants, fungicides, and sweeteners.

We tested groups of four male ddY mice once orally with each additive at
up to 0.5xLD(50) or the limit dose (2000mg/kg) and performed the comet
assay on the glandular stomach, colon, liver, kidney, urinary bladder, lung,
brain, and bone marrow 3 and 24 h after treatment.

Of all the additives, dyes were the most genotoxic.
Amaranth, Allura Red, New Coccine, Tartrazine, Erythrosine, Phloxine, and
Rose Bengal induced dose-related DNA damage in the glandular stomach, colon,
and/or urinary bladder.
All seven dyes induced DNA damage in the gastrointestinal organs at a
low dose (10 or 100mg/kg).

Among them, Amaranth, Allura Red, New Coccine, and Tartrazine induced
DNA damage in the colon at close to the acceptable daily intakes (ADIs).

Two antioxidants (butylated hydroxyanisole (BHA) and butylated
hydroxytoluene (BHT)), three fungicides (biphenyl, sodium
o-phenylphenol, and thiabendazole), and four sweeteners (sodium
cyclamate, saccharin, sodium saccharin, and sucralose) also induced DNA
damage in gastrointestinal organs.

Based on these results, we believe that more extensive assessment of
food additives in current use is warranted. PMID: 12160896

http://groups.yahoo.com/group/aspartameNM/message/934
24 recent formaldehyde toxicity [Comet assay] reports:
Murray 2002.12.31 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 2003.01.01 rmforall
[ Also borderline evidence, in this pilot study of 39 food additives,
using test groups of 4 mice, for DNA damage from for stomach, colon,
liver, bladder, and lung 3 hr after oral dose of 2000 mg/kg aspartame--
a very high dose.]

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


Rich Murray, MA Room For All rmforall@xxxxxxxxxxx 505-501-2298
1943 Otowi Road Santa Fe, New Mexico 87505 USA
http://groups.yahoo.com/group/aspartameNM/messages
group with 184 members, 1,170 posts in a public, searchable archive
**************************************************************


http://groups.yahoo.com/group/aspartameNM/message/1106
hangover research relevant to toxicity of 11% methanol in aspartame
(formaldehyde, formic acid): Calder I (full text): Jones AW: also some
methanol from fruit pectin in colon: Murray 2004.09.05 rmforall

[ NutraSweet, Equal, Canderel, Benevia, E951 ]

Since no adaquate data has ever been published on the exact disposition of
the toxic metabolites, formaldehyde and formic acid, in specific tissues in
humans of the readily released 11% methanol component of aspartame, the many
studies on morning-after hangover from the methanol impurity in alcohol
drinks are the main available resource to date.

Jones AW (1987) found next-morning hangover from red wine with
100 to 150 mg methanol
(9.5% w/v ethanol; 100 mg/l methanol = 0.01%, one part in ten thousand).

The expert review by Monte WC (1984) states: "An alcoholic consuming 1500
calories a day from alcoholic sources alone may consume between 0 and 600 mg
of methanol each day depending on his choice of beverages (Table 1)...."
Table 1 lists red wine as having 128 mg/l methanol, about one part in ten
thousand.

Fully 11% of aspartame is methanol -- 1,120 mg aspartame in 2 L diet soda,
almost six 12-oz cans, gives 123 mg methanol (wood alcohol) -- the same
amount that produces hangover from red wine.

Other strong formaldehyde sources are tobacco and wood smoke, and the
particleboard and new furniture, carpet, and drapes especially concentrated
in mobile homes.

Similar potent levels of methanol, and its inevitable products in the human
body, formaldehyde and formic acid, can also ensue from degradation of
fruit pectins in the colon:

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

Alcohol Clin Exp Res. 1995 Oct; 19(5): 1147-50.
Methanol in human breath.
Taucher J, Lagg A, Hansel A, Vogel W, Lindinger W.
Institut fur Ionenphysik, Universitat Innsbruck, Austria.

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

http://groups.yahoo.com/group/aspartameNM/message/1109
Toxicological Profile for Formaldehyde 1/4 plain text, start to 111 of 468
pages USA DHHS PHS ATSDR 1999 July: Murray 2004.08.30 rmforall

An editorial review by Ian Calder, F.R.C.A., "Hangovers: not the ethanol--
perhaps the methanol", British Medical Journal 1997 Jan 4; 314(7073): 2
[ Tel/Fax: 0171 720 9279 Consultant Anaesthetist at the National Hospital
for Neurology and Neurosurgery, London WCIN 3BG, UK ]
http://bmj.bmjjournals.com/search.dtl search to get free full text ] ,
states:

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

"Between a quarter and a half of drinkers claim not to experience hangover
symptoms despite having been intoxicated. (three citations)"

The symptom list is similar to reports by aspartame reactors.

If only a fraction of aspartame users happen to be vulnerable to the
methanol, that would account well for the disbelief by those who are not
aspartame reactors, as well as the scientific difficulty in proving
aspartame toxicity in the general population.

Research can study whether the hangover prone are also vulnerable to
aspartame, methanol, formaldehyde, and formic acid, and determine the
specific biochemistry for different groups.

Hangover treatments may help aspartame reactors. For instance, adaquate
folic acid (folate) helps humans eliminate toxic products from methanol.

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 CD-1 mouse.
Fu SS, Sakanashi TM, Rogers JM, Hong KH, Keen CL.
Department of Nutrition, University of California, Davis 95616, USA.

"These results show that marginal folate deficiency in pregnant dams
significantly increases the teratogenicity of MeOH." PMID: 8946559

There are no reports of hangover from heavy use of orange juice, 34 mg/l
methanol, since the methanol in many fruits and vegetables is locked up in
complex pectin molecules, not released by human digestion. (Monte WC 1984)

I've never found any reports by aspartame reactors, who are often sensitive
even to a single breath mint or stick of chewing gum
(0.4 to 0.8 mg methanol),
of having the same symptoms from fruits or vegetables.

Pharmacol Toxicol. 1987 Mar; 60(3): 217-20.
Elimination half-life of methanol during hangover.
Jones AW.
Department of Forensic Toxicology, University Hospital, SE-581 85 Linkoping,
Sweden. wayne.jones@xxxxxx

This paper reports the elimination half-life of methanol in human
volunteers. Experiments were made during the morning after the subjects had
consumed 1000-1500 ml red wine (9.5% w/v ethanol, 100 mg/l methanol)
the previous evening. [ 100 to 150 mg methanol ]
The washout of methanol from the body coincided with the onset of hangover.
The concentrations of ethanol and methanol in blood were determined
indirectly by analysis of end-expired alveolar air.
In the morning when blood-ethanol dropped below the Km of liver alcohol
dehydrogenase (ADH) of about 100 mg/l (2.2 mM), the disappearance half-life
of ethanol was 21, 22, 18 and 15 min. in 4 test subjects respectively.
The corresponding elimination half-lives of methanol were 213, 110, 133 and
142 min. in these same individuals.
The experimental design outlined in this paper can be used to obtain useful
data on elimination kinetics of methanol in human volunteers without undue
ethical limitations.
Circumstantial evidence is presented to link methanol or its toxic metabolic
products, formaldehyde and formic acid, with the pathogenesis of hangover.
PMID: 3588516

http://groups.yahoo.com/group/aspartameNM/message/1047
Avoiding Hangover Hell 2003.12.31 Mark Sherman, AP writer:
Robert Swift, MD [ formaldehyde from methanol in aspartame ]:
Murray 2004.01.16 rmforall

http://groups.yahoo.com/group/aspartameNM/message/1048
hangovers from formaldehyde from methanol (aspartame?):
Schwarcz: Linsley: Murray 2004.01.18

http://groups.yahoo.com/group/aspartameNM/message/1099
Diagnose-Me.com: formaldehyde from 11 % methanol part of aspartame:
recent abstracts for methanol and hangovers: Murray 2004.07.10 rmforall

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

Editorials Hangovers: Not the ethanol - perhaps the methanol

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

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

In fact, ethanol itself may play only a minor part in producing the thirst,
headache, fatigue, nausea, sweating, tremor, remorse, and anxiety that
hangover sufferers report.
Hangover symptoms are worst at a time when almost all ethanol and its
metabolite acetaldehyde have been cleared from the blood, and peak blood
ethanol or acetaldehyde levels are not related to the severity of
hangover.(3 )

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

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

Chapman found that hangover symptoms were almost twice as common in
volunteers who drank 1.5 ml/kg [ body weight ] of bourbon whiskey - which
has methanol concentrations of 26 mg/l - as in those drinking the same dose
of vodka ( 3.9 mg of methanol per litre ). (5) [ For a 60 kg person, this
would be 90 mg bourbon, 0.09 l, giving 2.34 mg methanol, which led to twice
as many symptoms as the 0.35 mg methanol from vodka. The bourbon gave as
about as much methanol as an ounce of diet soda. ]

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

8. Peeke SC, Callaway E, Jones RT, Stone GC, Doyle J.
Combined effect of alcohol and sleep deprivation in normal young adults.
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9. Seppala T, Leino T, Linnoila M, Huttunen MO, Ylikahri RH.
Effects of hangover on psychomotor skills related to driving: modification
by fructose and glucose.
Acta Pharmacol Toxicol 1976; 38: 209-18.

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

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

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

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

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