| Rich Murray 2004-10-23, 10:08 pm |
|
http://groups.yahoo.com/group/aspartameNM/message/1128
hangover symptoms from methanol from dark wines and liquors or 11% methanol
part of aspartame, review of research: Jones AW 1988: Murray 2004.10.23
rmforall
" But higher blood-methanol concentrations are definitely associated with
higher blood-ethanol in this sample of Swedish drinking drivers.
Frequent exposure to methanol and its toxic products of metabolism,
formaldehyde and formic acid, might constitute an additional health risk
associated with heavy drinking in predisposed individuals. " Jones AW 1988
2004.10.23 Hi Paul Lee and Jeff Utz, Once again your pointed, fair
critical questions have galvanized me into rewarding explorations. For the
record, the end of this post gives our previous discussions.
In summary, I quote many abstracts here from the mainstream scientific
literature by qualified researchers that show that it is a scientific truism
that methanol ( wood alcohol ), whether as a one part in ten thousand
impurity in dark wines and liquors, or as the readily released 11% methanol
component of the aspartame molecule, is largely converted in the human body
into formaldehyde, and thence largely into formic acid -- both potent,
cumulative toxins that affect every cell and tissue, and are reasonably
asserted to be the major cause of hangovers in vulnerable people.
In mutual service, Rich Murray
Rich Murray, MA Room For All rmforall@comcast.net
1943 Otowi Road, Santa Fe, New Mexico 87505 USA 505-501-2298
http://groups.yahoo.com/group/aspartameNM/messages
142 members, 1,128 posts in a public searchable archive also Co-Moderator
****************************************************************
The 1,120 mg of aspartame in 2 liters ( 2 quarts == half-gallon ) diet
soda,
5.6 12-oz cans, gives 123 mg methanol (wood alcohol), about half the
methanol
from red wine: 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%,
o
ne part in ten thousand).
I apologize for my use of the phrase, which I can not so far buttress with
any references, "cheap red wine" -- which was a cheap PR shot, much like the
aspartame industry's wholesale dismissals of case reports as "anecdotal
complaints". Properly, I should have said, "red wine".
I had a bad few minutes when I was unable on PubMed
[ http://www.ncbi.nlm.nih.gov/PubMed ] to find a key reference from
Monte WC 1984 ( itself not in PubMed ) -- a prescient comprehensive review
( full text below ):
30. Lee, C.Y., Acree, T.E. and Butts, R.M.,
Determination of Methyl Alcohol in Wine by Gas Chromatography.
Anal. Chem., 47(4): 747-748 (1975).
But, as usual, Google saved the day with a search on the title
(which often brings up free full texts ):
http://www.nysaes.cornell.edu/fst/f...e/acreelit.html
For adequate sepn. of MeOH from other low mol. wt. compds. in alc.
beverages, an ethylvinylbenzene polymer (Porapak) was employed.
Thus, a 2 m Porapak QS column gave good sepn. and resolution of MeOH, AcH,
EtOH, and EtOAc.
By use of this method, the MeOH contents of 20 com. wines was 50-325 ppm.
I am of course happy to report that Terry E. Acree has published mnay papers
from 1965 to 1999.
http://www.nysaes.cornell.edu/fst/faculty/index.html
Flavor chemistry. Isolation and identification of the odor active compounds
present in fruits and vegetables. Utilization of Charm AnalysisTM, a
bio-assay, to characterize the response of humans to odors.
Terry E. Acree - Professor of Biochemistry
Department of Food Science & Technology - Geneva, NY 14456
116 Food Research Laboratory, 315-787-2240, e-mail: tea2@cornell.edu
Teaching & Research Activities - Terry Acree and the scientists working in
his laboratory study the perception of food flavor and its modulation by
chemical composition and human diversity. The work involves the isolation
and characterization of semiochemicals in fruits and vegetables that
contribute to the human smell response and the agricultural and industrial
practices that moderate them. Over the years Terry and his students have
developed a selective and sensitive bio-assay for smell based on gas
chromatography - olfactometry (GCO) called CharmAnalysis. In addition to the
development and application of GCO technologies his laboratory uses
chromatography, spectrometry, and sensory analysis to enhance food quality.
And, as a bonus:
http://www.nysaes.cornell.edu/fst/faculty/lee/
Chang Yong (Cy) Lee (Ph.D. Utah State)
Department Chairman / Professor
315 787-2271 Email: CYL1@cornell.edu
Biochemistry of fruits and vegetables as related to quality and processing.
Chemistry of provitamin A carotenoids, enzymes associated with sensory and
nutritional quality, enzymatic browning reaction, minimal processing, and
bioactive polyphenols of fresh and processed fruits and vegetables.
http://www.nysaes.cornell.edu/fst/faculty/lee/cv.pdf 26 pages, complete
bibliography
I'm hoping these two good men will be able to zerox the specifics on 20
wines
from their voluminous files.
I am obliged to share with you that A. Wayne Jones has 341 items in PubMed,
from 1950 to 2004, including 187 on alcohol, 19 on methanol, and 3 on
hangover:
1: Bendtsen P, Jones AW, Helander A.
Urinary excretion of methanol and 5-hydroxytryptophol as biochemical markers
of recent drinking in the hangover state. wayne.jones@RMV.se
Alcohol Alcohol. 1998 Jul-Aug; 33(4): 431-8. PMID: 9719404
Department of Forensic Toxicology
Department of Clinical Neuroscience, Karolinska Institutet & Hospital,
Stockholm, Sweden. Anders.Helander@cns.ki.se ; anders.helander@spo.sll.se ;
preben.bendtsen@lio.se ; university Hospital, SE-581 85 Linkoping, Sweden.
2: Jones AW.
Elimination half-life of methanol during hangover.
Pharmacol Toxicol. 1987 Mar; 60(3): 217-20. PMID: 3588516
3: Hogman B, Bergman H, Borg S, Eriksson T, Goldberg L, Jones AW, Linde CJ,
Tengroth B.
Readaptation time after photo stress. Alcohol-induced acute and post-alcohol
'hangover' changes in ocular readaptation time.
Psychopharmacology (Berl). 1977 Jul 18; 53(2): 165-7. PMID: 408841
4: Jones AW, Helander A.
Changes in the concentrations of ethanol, methanol and metabolites of
serotonin in two successive urinary voids from drinking drivers.
Forensic Sci Int. 1998 May 11; 93(2-3): 127-34. PMID: 9717263
5: Helander A, Beck O, Jones AW.
Laboratory testing for recent alcohol consumption: comparison of ethanol,
methanol, and 5-hydroxytryptophol.
Clin Chem. 1996 Apr; 42(4): 618-24. PMID: 8605681
8: Jones AW, Sternebring B.
Kinetics of ethanol and methanol in alcoholics during detoxification.
Alcohol Alcohol. 1992 Nov; 27(6): 641-7. PMID: 1292437
Jones AW, Helander A.
Time course and reproducibility of urinary excretion profiles of ethanol,
methanol, and the ratio of serotonin metabolites after intravenous infusion
of ethanol.
Alcohol Clin Exp Res. 1999 Dec; 23(12): 1921-6. PMID: 10630611
Bendtsen P, Jones AW, Helander A.
Urinary excretion of methanol and 5-hydroxytryptophol as biochemical markers
of recent drinking in the hangover state.
Alcohol Alcohol. 1998 Jul-Aug; 33(4): 431-8. PMID: 9719404
Bendtsen P, Jones AW, Helander A.
Urinary excretion of methanol and 5-hydroxytryptophol as biochemical markers
of recent drinking in the hangover state.
Alcohol Alcohol. 1998 Jul-Aug; 33(4): 431-8. PMID: 9719404
Jones AW, Helander A.
Changes in the concentrations of ethanol, methanol and metabolites of
serotonin in two successive urinary voids from drinking drivers.
Forensic Sci Int. 1998 May 11;93(2-3):127-34. PMID: 9717263
" But higher blood-methanol concentrations are definitely associated with
higher blood-ethanol in this sample of Swedish drinking drivers.
Frequent exposure to methanol and its toxic products of metabolism,
formaldehyde and formic acid, might constitute an additional health risk
associated with heavy drinking in predisposed individuals. "
Forensic Sci Int. 1988 Jun; 37(4): 277-85.
Relationship between the concentration of ethanol and methanol in blood
samples from Swedish drinking drivers.
Jones AW, Lowinger H.
Department of Alcohol Toxicology, university Hospital, Linkoping, Sweden.
Headspace gas chromatography was used to determine the concentration of
ethanol and methanol in blood samples from 519 individuals suspected of
drinking and driving in Sweden where the legal alcohol limit is 0.50 mg/g in
whole blood (11 mmol/l).
The concentration of ethanol in blood ranged from 0.01 to 3.52 mg/g with a
mean of 1.83 +/- 0.82 mg/g (+/- S.D.).
The frequency distribution was symmetrical about the mean but deviated from
normality.
A plot of the same data on normal probability paper indicated that it might
be composed of two subpopulations (bimodal).
The concentration of methanol in the same blood specimens ranged from 1 to
23 mg/l with a mean of 7.3 +/- 3.6 mg/l (+/- S.D.) and this distribution was
markedly skew (+).
The concentration of ethanol (x) and methanol (y) were positively correlated
(r == 0.47, P less than 0.001) and implies that 22% (r2) of the variance in
blood-methanol can be attributed to its linear regression on blood-ethanol.
The regression equation was y == 3.6 + 2.1 x and the standard error estimate
was 0.32 mg/l.
This large scatter precludes making reliable estimates of blood-methanol
concentration from measurements of blood-ethanol concentration and the
regression equation.
But higher blood-methanol concentrations are definitely associated with
higher blood-ethanol in this sample of Swedish drinking drivers.
Frequent exposure to methanol and its toxic products of metabolism,
formaldehyde and formic acid, might constitute an additional health risk
associated with heavy drinking in predisposed individuals.
The determination of methanol in blood of drinking drivers in addition to
ethanol could indicate long-standing ethanol intoxication and therefore
potential problem drinkers or alcoholics. PMID: 3410397
****************************************************************
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 2004.09.11 rmforall
http://bmj.bmjjournals.com/search.dtl search to get free full text
British Medical Journal 1997 (4 January); 314(7073): 2.
Ian Calder, F.R.C.A. [ Tel/Fax: 0171 720 9279 Consultant Anaesthetist at
the National Hospital for Neurology and Neurosurgery,
London WCIN 3BG, UK ]
Editorials Hangovers: Not the ethanol - perhaps the methanol
"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."
6. Pawan GL.
Alcoholic drinks and hangover effects.
Proc Nutr Soc 1973 May; 32: 15A. PMID: 4760771
****************************************************************
Jeff, thanks for http://www.annals.org/cgi/content/full/132/11/897 free
full text
http://my.webmd.com/content/Article/35/1728_58194.htm long article
Checking out this article and its references, I notice that indeed they do
not mention methanol, although two references are:
39. Pawan GL. Alcoholic drinks and hangover effects [Abstract]. Proc Nutr
Soc. 1973; 32: 15-A.
41. Chapman LF. Experimental induction of hangover. Q J Stud Alcohol. 1970;
5(suppl 5): 67-86.[Medline]
They do not cite Jones AW or Lee CY at all -- methanol is simply not
discussed in their text.
Hangovers More of a Headache Than You Think
By Sean Swint WebMD Medical News
June 5, 2000 - Everyone has his or her own hangover remedy. Ancient Romans
said eat fried canaries. Modern Greeks in college fraternities say drink
more "hair of the dog that bit you" -- meaning more alcohol. But although
many people swear by their personal hangover cure, a review of more than 100
studies finds that, other than time, only a few things may actually help.
Hangovers may actually be more of a headache than previously thought,
according to Jeffrey G. Wiese, MD. Medical problems associated with
hangovers can be severe for some people. People with heart problems can be
at greater risk for heart attacks, says Wiese, because hangovers put people
in a situation "that is very similar to high stress, and that is an increase
in blood pressure, a high heart rate."
He adds that there is some evidence that blood cells involved in clotting
called platelets become "stickier," thus making blood clots more likely.
Other studies have shown that thinking and performance can be impaired.
Wiese and colleagues from the General Internal Medicine Section of the
Veterans Affairs Medical Center in San Francisco reviewed more than 4,700
medical journal articles written about alcohol intoxication since 1965, and
found 108 that addressed the hangover. Their findings were published in a
recent issue of the journal Annals of Internal Medicine.
"It's something that here and there, people toyed with, but nobody ever
really got around to saying how big of a problem this is," Wiese tells
WebMD, adding many people simply view the hangover as penance, nothing more,
nothing less.
One "big purpose" of the review, says Wiese, was to not only alert the
public to the problem of hangovers, but also to raise awareness among
physicians that this is something worth asking your patients about "to try
to assess those who might be at greater risk for alcoholism.
"We need to get over the social sentiment, 'well, that's what you deserve,'
if this is really putting people at risk, and do a better job of raising
awareness so people know that this can cause medical problems," Wiese tells
WebMD.
But more common than potential medical problems is the muddleheaded feeling
the day after. Robert Cloninger, MD, a well-known researcher in alcohol
studies, defines a hangover quite simply as "feeling bad after drinking."
But it does go beyond just that, Cloninger tells WebMD.
"You don't think as well; you're achy; you're slower; you're really not
functioning a 100%," he says. Cloninger is a professor of psychiatry,
genetics, and psychology at Washington university in St. Louis, Mo.
Wiese writes about the common symptoms of hangovers, predominantly a
headache, then a poor sense of overall well-being, diarrhea, loss of
appetite, shakiness, fatigue, and nausea. The alcohol causes the bad
feelings because it leaves a person dehydrated and malnourished. One
debatable theory, Wiese writes, is that a hangover is the first stage of
alcohol withdrawal.
Wiese affirms Cloninger's definition, saying multiple studies show decreased
reaction times, less ability to concentrate, lower managerial skills, and
increased risk for injury, even after some of the more obvious hangover
symptoms are gone and alcohol can no longer be detected in the blood.
Wiese describes one study looking at airline pilots, where pilots drank
enough one night to meet the criteria for having a hangover the next day.
The pilots followed an eight-hour "bottle to throttle" standard before
entering a flight simulator. Wiese says even though half of the pilots
didn't feel like they had a hangover, their thought, or cognitive, functions
were clearly reduced.
"The point being is that many people see being hungover as having a headache
or just not feeling great, but don't recognize that their cognitive function
is actually impaired," says Wiese, "and that may have implications for
whether people decide to work with heavy machinery, decide to drive, or
operate aircraft, for example. People should be aware that their cognitive
function may not be optimal, even though they may not be feeling the most
severe symptoms."
Wiese says 75% of all drinkers will have a hangover in a year, and 15% will
have a hangover at least monthly, which has a large economic impact. "You're
talking about a big part of the American workforce, and if each of those
[people] misses work one or two times a year, and then if you toss on the
decreased productivity from the cognitive decline ... it starts to become a
fairly large opportunity cost, a large loss in productivity," Wiese says.
Some studies have put the annual cost in the U.S. at a whopping $148 billion
per year, while another researcher estimated the average annual loss to be
about $2,000 per working adult, Wiese writes. Light-to-moderate drinkers
cause 87% of all alcohol-related problems in the workplace and,
paradoxically, this same group suffers more hangovers than heavier drinkers.
So, the million-dollar question is, what can be done about hangovers?
Humorist and writer Robert Benchley said, "there is no cure for the
hangover, save death." He was close. Wiese says "prevention" is the only
surefire hangover cure, followed closely by moderation and not drinking on
an empty stomach.
Some studies also have found the only other effective remedies are drinking
plenty of nonalcoholic fluids to rehydrate you, vitamin B6, and
prostaglandin inhibitors -- the class of anti-inflammatory drugs that
include ibuprofen and aspirin, according to Wiese. These should be taken at
the time you drink the alcohol for a small effect in reducing hangover
severity.
There was one study of an herbal preparation called Liv.52 that was shown to
reduce hangover symptoms, but Wiese writes the results are suspect because
of the way the study was conducted and because the manufacturer sponsored
the study.
Wiese also points out that darker drinks, such as red wine or scotch,
contain more impurities, called congeners, thereby increasing the frequency
and severity of hangovers. And as for "hair of the dog," well, that hangover
you are trying to avoid is going to still bite you sooner or later.
"Nobody has a cure for hangover. These are completely symptomatic
treatments, much like taking over-the-counter drugs for a flu and a cold.
You know, it's very questionable whether it really does anything," Cloninger
tells WebMD.
Overall, Cloninger says the findings in Wiese's review are "not novel,"
since they are based on published studies, but the findings are
"well-appreciated and well-recognized." Cloninger took issue with the cost
figures because they "are based on a world where no one's going to drink at
all, and that's not going to happen." He also says it's difficult to
pigeonhole people, because every one reacts to alcohol differently, and not
uniformly.
"Obviously, we're not going to go back to prohibition, but look what's
happening with cigarette smoking. ... We may be attacking some of the wrong
things, because there's certainly a lot of [death] associated with alcohol
on roads, and so on, comparable to what you get with cigarettes," Cloninger
tells WebMD. "So we need to maybe have a more balanced approach."
Vital Information:
People have been dealing with hangovers throughout history, but doctors
haven't done much to research the medical issues they raise.
From the research that is available, experts say hangovers impair thinking
and performance, in addition to making sufferers feel terrible. Overall,
loss of productivity has economic effects on society as well.
There isn't a cure for a hangover, but severity may be lessened by using
ibuprofen or aspirin and drinking plain water while you are drinking
alcohol. Also, doctors should be asking patients about hangover frequency,
which hints at one's risk of alcoholism. ©
http://www.dbbs.wustl.edu/DBBS/webs.../rib/cloningerr
C. Robert Cloninger, M.D. Wallace Renard Professor clon@wupsych.wustl.edu
Psychiatry
Genetics
Psychology
Evolution, Ecology and Population Biology Program
Neurosciences Program
Quantitative Human and Statistical Genetics Program
FAX: 314-362-5594 Box: 8134 Lab Address: 3308 Renard Hospital
Email: Keywords: substance abuse; genetics; genome analysis; psychoses;
personality
Research in my laboratory is focused on the causes of individual differences
in personality development and the genetic epidemiology of psychiatric
disorders.
The goal is to integrate psychometric, developmental and neurogenetic
analyses of complex phenotypes related to health and disorder in the general
population and in families.
Current work involves longitudinal and family studies of normal and abnormal
personality, alcoholism, schizophrenia and related traits.
The relations of personality to psychopathology are being studied in terms
of the non-linear dynamics of complex adaptive systems.
Quantitative genetic analysis is conducted to characterize the transmission
of psychiatric disorders.
Genome screens and candidate gene analysis are underway for schizophrenia,
alcoholism and personality traits.
Cloninger, C. Robert. Feeling good: The science of well-being. New York:
Oxford university Press; 2004. 374 p.
Cloninger, C. Robert. The discovery of susceptibility genes for mental
disorders. Proc Natl Acad Sci USA 2002; 99(21): 13365-13367.
Cloninger CR. Biology of personality dimensions. Curr Opin Psychiatry 2000;
13: 611-616.
Cloninger CR, Svrakic DM, Przybeck TR. A psychobiological model of
temperament and character. Arch Gen Psychiatry 1993; 50: 975-990.
204 PubMed items, 39 on alcohol, 0 on methanol, 0 on hangover.
Am J Med Genet. 2004 Jan 1; 124A(1): 19-27.
A genomic scan for habitual smoking in families of alcoholics: common and
specific genetic factors in substance dependence.
Bierut LJ, Rice JP, Goate A, Hinrichs AL, Saccone NL, Foroud T, Edenberg HJ,
Cloninger CR, Begleiter H, Conneally PM, Crowe RR, Hesselbrock V, Li TK,
Nurnberger JI Jr, Porjesz B, Schuckit MA, Reich T.
School of Medicine, Washington university School of Medicine, 4940
Children's Place, St. Louis, MO 63110, USA. bierutl@psychiatry.wustl.edu
http://groups.yahoo.com/group/aspartameNM/message/1055
hormesis: possible benefits of low-level aspartame (methanol, formaldehyde)
use: Calabrese: Soffritti: Murray 2004.03.11 rmforall
http://groups.yahoo.com/group/aspartameNM/message/1056
disorders of NMDA glutamate receptors in brain range from high activity
(MCS, CF, PTSD, FM, from carbon monoxide or formaldehyde (methanol,
aspartame)-- Pall)
to low activity (schizophrenia-- Coyle, Goff, Javitts):
Murray 2004.03.13 rmforall
http://www.infectionspotlight.com/EditorialCouncil.jsp
Jeffrey G. Wiese, MD
Assistant Professor of Medicine
Tulane university Medical Center
Chief of Medicine
The Medical Center of Louisiana New Orleans
New Orleans, LA
Jeffrey G. Wiese, MD, is Assistant Professor of Medicine at Tulane
University Medical Center and Chief of Medicine at The Medical Center of
Louisiana in New Orleans, LA. He is also Program Director of the Tulane
Internal Medicine program. He has served on numerous clinical and
administrative university committees.
Dr. Wiese devotes much of his time to teaching and educational research,
some of which incorporates evolving technologies. The recipient of many
academic, athletic, and teaching awards, Dr. Wiese was named the Tulane
Attending Physician of the Year in 2001. A diplomat of the American Board of
Internal Medicine, Dr. Wiese is also certified by the National Board of
Medical Examiners. He belongs to several professional societies, including
the American college of Physician Executives, American Program Directors in
Internal Medicine, National Association of Inpatient Physicians, and Society
of General Internal Medicine. Dr. Wiese has written approximately 30
articles, books, or book chapters and has made numerous presentations to
national and international audiences. He is a reviewer for the American
Journal of Medicine and Internal Medicine Alert and serves on the editorial
board of American Health Consultants.
Dr. Wiese attended Johns Hopkins School of Medicine, where he received his
medical degree in 1995. He completed his residency training in internal
medicine at the university of California at San Francisco.
http://www.som.tulane.edu/pr/releases/02-16Wie.htm
Tulane university HEALTH SCIENCES CENTER
Office of Public Relations SL26 1430 Tulane Avenue
New Orleans, Louisiana 70112-2699 (504) 588-5221 FAX (504) 585-6019
FOR IMMEDIATE RELEASE: February 16, 2001 CONTACT: Fran Simon
PHONE NUMBER: 504-584-3663 http://www.som.tulane.edu/pr/
Internist Joins Tulane Faculty
Dr. Jeffrey G. Wiese has joined the Tulane university Health Sciences Center
as an assistant professor of medicine.
He specializes in general internal medicine.
Wiese serves as associate chairman of the Department of Medicine at Tulane
as well as Chief of Medicine at the Medical Center of Louisiana at New
Orleans.
Wiese received his medical degree from the Johns Hopkins School of Medicine
in 1995.
He completed his residency training in internal medicine at the University
of California - San Francisco, where he was chief resident and then on the
faculty.
At UCSF he received the 2000 Teacher of the Year Award on the Clinical
Faculty and an Alpha Omega Alpha Teaching Award.
His primary research areas of interest include clinical reasoning, the
physical examination, and the alcohol hangover.
http://www.annals.org/cgi/content/full/134/6/533-a
LETTER
The Alcohol Hangover
Jeff Becker, BA
20 March 2001 | Volume 134 Issue 6 | Pages 533-534
TO THE EDITOR:
Wiese and colleagues' statement that hangover-induced absenteeism and poor
job performance costs the U.S. economy $148 billion each year is incorrect,
as are the claims that the annual cost is $2000 per worker and that
light-to-moderate drinkers are the primary source of the problem (1).
The authors cite a report by Stockwell, but the $148 billion
lost-productivity estimate is not found in this source.
However, the National Institute on Drug Abuse and National Institute on
Alcohol Abuse and Alcoholism estimate that the total cost of alcohol abuse
in the United States is $148 billion (2).
Of note, the agencies' estimate includes all costs from alcohol-not simply
the costs of hangovers-and it has been criticized as seriously inflated,
with other published estimates running from $12 to $30 billion per year (3).
Furthermore, even though a significant part of the agencies' estimate is
from lost productivity, the loss comes entirely from alcohol abusers.
In contrast, many studies suggest that moderate drinkers, on average, have
higher wages than abstainers or abusers (4).
The authors' $2000-per-person cost figure is equally misleading.
This estimate comes from a telephone survey (n == 635) in which 22
respondents
reported alcohol-related problems for which costs could be estimated (5).
However, the author of that report specifically noted that the bulk of the
costs were attributed to people who drank five or more drinks every day or
every other day, not to light-to-moderate drinkers.
Effective programs, policies, and treatments require a broad and balanced
understanding of alcohol-related behaviors and problems.
Unfortunately, the suggestions that hangovers cost the United States $148
billion annually and that light-to-moderate drinkers are mostly to blame is
a misreading of the literature and a disservice to responsible consumers.
Author and Article Information
Beer Institute; Washington, DC 20001 (Becker)
1. Wiese JG, Shlipak MG, Browner WS. The alcohol hangover. [PMID:
0010836917] Ann Intern Med. 2000;132:897-902.[Abstract/Free Full Text]
2. Harwood H, Fountain D, Livermore G. The Economic Costs of Alcohol and
Drug Abuse in the United States, 1992. Rockville, MD: U.S. Department of
Health and Human Services, National Institutes of Health, National Institute
on Drug Abuse, Office of Science Policy and Communications, National
Institute on Alcohol Abuse and Alcoholism, Office of Policy Analysis; 1998.
NIH publication no. 98-4327.
3. Manning WG, Keeler EB, Newhouse JP, Sloss EM, Wasserman J. The taxes of
sin. Do smokers and drinkers pay their way? [PMID: 0002918654] JAMA.
1989; 261: 1604-9.[Abstract]
4. Zarkin GA, French MT, Mroz T, Bray JW. Alcohol use and wages: new results
from the National Household Survey on Drug Abuse. [PMID: 0010176315]
J Health Econ. 1998; 17: 53-68.[Medline]
5. Stockwell T. Towards guidelines for low-risk drinking: quantifying the
short- and long-term costs of hazardous alcohol consumption. [PMID:
0009603308] Alcohol Clin Exp Res. 1998; 22: 63S-69S.[Medline]
Ann Intern Med. 2000 Jun 6; 132(11): 897-902.
Comment in:
Ann Intern Med. 2001 Mar 20; 134(6): 533-4.
The alcohol hangover.
Wiese JG,
Shlipak MG,
Browner WS.
Veterans Affairs Medical Center and the university of California, San
Francisco 94121, USA.
PURPOSE: To review the cause, pathophysiologic characteristics, cost, and
treatment of alcohol-induced hangover.
DATA SOURCES: A MEDLINE search of English-language reports (1966 to 1999)
and a manual search of bibliographies of relevant papers.
STUDY SELECTION: Related experimental, clinical, and basic research studies.
DATA EXTRACTION: Data in relevant articles were reviewed, and relevant
clinical information was extracted.
DATA SYNTHESIS: The alcohol hangover is characterized by headache,
tremulousness, nausea, diarrhea, and fatigue combined with decreased
occupational, cognitive, or visual-spatial skill performance.
In the United States, related absenteeism and poor job performance cost $148
billion annually (average annual cost per working adult, $2000).
Although hangover is associated with alcoholism, most of its cost is
incurred by the light-to-moderate drinker.
Patients with hangover may pose substantial risk to themselves and others
despite having a normal blood alcohol level.
Hangover may also be an independent risk factor for cardiac death.
Symptoms of hangover seem to be caused by dehydration, hormonal alterations,
dysregulated cytokine pathways, and toxic effects of alcohol.
Physiologic characteristics include increased cardiac work with normal
peripheral resistance,
diffuse slowing on electroencephalography, and
increased levels of antidiuretic hormone.
Effective interventions include rehydration,
prostaglandin inhibitors, and vitamin B6.
Screening for hangover severity and frequency may help early detection of
alcohol dependency and substantially improve quality of life.
Recommended interventions include discussion of potential therapies and
reminders of the possibility for cognitive and visual-spatial impairment.
No evidence suggests that alleviation of hangover symptoms leads to further
alcohol consumption, and the discomfort caused by such symptoms may do so.
Therefore, treatment seems warranted.
CONCLUSIONS: Hangover, a common disorder, has substantial morbidity and
societal cost.
Appropriate management may relieve symptoms in many patients.
Publication Types: Review Review, Tutorial PMID: 10836917
Jeffrey G. Wiese, MD; jwiese@tulane.edu
Michael G. Shlipak, MD, MPH; shlip@itsa.ucsf.edu
General Internal Medicine Section, San Francisco Veterans Affairs Medical
Center, San Francisco, CA 94121, USA.
and Warren S. Browner, MD, MPH
39. Pawan GL. Alcoholic drinks and hangover effects [Abstract]. Proc Nutr
Soc. 1973; 32: 15-A.
40. Damrau F, Liddy E. Hangovers and whisky congeners: comparison of whisky
with vodka. Journal of the National Medical Association. 1960; 52:
262-4.[Medline]
41. Chapman LF. Experimental induction of hangover. Q J Stud Alcohol. 1970;
5(suppl 5): 67-86.[Medline]
Damrau F has 26 items in PubMed, from 1959 to 1971.
9: DAMRAU F, LIDDY E, DAMRAU AM.
Value of stout as a sedative and relaxing soporific.
J Am Geriatr Soc. 1963 Mar; 11: 238-41. No abstract available.
PMID: 14024841
10: DAMRAU F, LIDDY E.
The use of vodka in geriatrics.
Ind Med Surg. 1962 Oct; 31: 463-4. No abstract available. PMID: 13883327
11: DAMRAU F, LIDDY E.The whisky congeners. Comparison of whisky with vodka
as to toxic effects.
Curr Ther Res Clin Exp. 1960 Sep; 2: 453-7. No abstract available.
PMID: 13813916
12: DAMRAU F, LIDDY E.Hangovers and whiskey congeners. Comparison of whisky
with vodka.
J Natl Med Assoc. 1960 Jul; 52: 262-5. No abstract available. PMID: 13813915
13: DAMRAU F, LIDDY E.
A psychological study of moderate social drinkers; organoleptic responses
and motivation field survey.
Exp Med Surg. 1959; 17: 291-6. No abstract available. PMID: 13813914
Arch Intern Med. 2004 Jun 28; 164(12): 1334-40.
Effect of Opuntia ficus indica on symptoms of the alcohol hangover.
Wiese J, McPherson S, Odden MC, Shlipak MG.
General Internal Medicine Section and Department of Medicine, Tulane Health
Sciences Center, New Orleans, LA, USA. jwiese@tulane.edu
BACKGROUND: The severity of the alcohol hangover may be related to
inflammation induced by impurities in the alcohol beverage and byproducts of
alcohol metabolism.
An extract of the Opuntia ficus indica (OFI) plant diminishes the
inflammatory response to stressful stimuli.
METHODS: In this double-blind, placebo-controlled, crossover trial, 64
healthy, young adult volunteers were randomly assigned to receive OFI (1600
IU) and identical placebo, given 5 hours before alcohol consumption.
During 4 hours, subjects consumed up to 1.75 g of alcohol per kilogram of
body weight.
Hangover severity (9 symptoms) and overall well-being were assessed on a
scale (0-6), and blood and urine samples were obtained the following
morning.
Two weeks later, the study protocol was repeated with OFI and placebo
reversed. RESULTS: Fifty-five subjects completed both the OFI and placebo
arms of the study.
Three of the 9 symptoms- nausea, dry mouth, and anorexia- were significantly
reduced by OFI (all P<.05).
Overall, the symptom index was reduced by 2.7 points on average (95%
confidence interval, -0.2 to 5.5; P ==.07), and
the risk of a severe hangover (>/= points) was reduced by half (odds
ratio, 0.38; 95% confidence interval, 0.16-0.88; P ==.02).
C-reactive protein levels were strongly associated with hangover severity;
the mean symptom index was 4.1 (95% confidence interval, 1.2-7.1; P ==.007)
higher in subjects with morning C-reactive protein levels greater than 1.0
mg/L.
In addition, C-reactive protein levels were 40% higher after subjects
consumed placebo compared with OFI.
CONCLUSIONS: The symptoms of the alcohol hangover are largely due to the
activation of inflammation.
An extract of the OFI plant has a moderate effect on reducing hangover
symptoms, apparently by inhibiting the production of inflammatory mediators.
Publication Types: Clinical Trial Randomized Controlled Trial PMID: 15226168
JAMA. 2001 Jul 11; 286(2): 165-6.
Alcohol use as a prognostic factor following myocardial infarction.
Wiese JG, Shlipak M.
Publication Types: Letter PMID: 11448272
Jeffrey G Wiese medsched@tulane.edu; medrugby@tulane.edu ;
medicine@tulane.edu ; jwiese@tulane.edu ;
title Assistant Professor description Med-General Internal
telephonenumber +1 504 988-1143
US Dept. of Veterans Affairs Medical Center -- San Francisco California
4150 Clement St. San Francisco Ca. 94121 - (415)-221-4810
Michael Shlipak shlip@itsa.ucsf.edu Fax 415-379-5573
Title ASSOC PROF IN RES-MEDCOMP-A Department General Internal Medicine
Campus Phone 415-750-2093 Campus Phone 2 415-221-4810x3381
Campus Address Box VAMC - 111, VAMC 111A1
University of California, San Francisco San Francisco, CA. 94143 - VAMC
Shlipak MG once had Hunninghake DB as a co-author, who once helped with a
well-known but misleading pro-aspartame research study. This probably is a
chance connection, but there are several immense corporate vested interests
that operate to confuse and defuse methanol toxicity research.
Jha AK, Varosy PD, Kanaya AM, Hunninghake DB, Hlatky MA, Waters DD,
Furberg CD, Shlipak MG.
Differences in medical care and disease outcomes among black and white women
with heart disease.
Circulation. 2003 Sep 2; 108(9): 1089-94. Epub 2003 Aug 25. PMID: 12939228
Leon AS, Hunninghake DB, Bell C, Rassin DK, Tephly TR.
Safety of long-term large doses of aspartame.
Arch Intern Med. 1989 Oct;149(10):2318-24. PMID: 2802896
criticized in detail in
http://groups.yahoo.com/group/aspartameNM/message/622
Gold: Koehler: Walton: Van Den Eeden: Leon:
aspartame toxicity: Murray 2001.06.04 rmforall four double-blind studies
http://www.baybio.org/wt/page/brd_browner
Warren S. Browner, M.D., M.P.H.
Vice President, Academic Affairs & Scientific Director
California Pacific Medical Care Research Institute
Warren S. Browner, M.D., M.P.H., is Vice President Academic Affairs and
Scientific Director of the Research Institute at California Pacific Medical
Center. His current research focuses on the causes and effects of vascular
calcification, as well as methods for classifying phenotypic expression of
longevity and frailty.
Dr. Browner is a graduate of Harvard College, and received an M.D. from the
University of California, San Francisco, and an M.P.H. from the University
of California, Berkeley. He completed his residency in internal medicine and
was a Mellon Scholar in Clinical Epidemiology at UCSF.
He was on the full-time faculty at UCSF for 15 years, most recently as Chief
of General Internal Medicine and Acting Chief of the Medical Service at the
San Francisco VA Medical Center, and is currently Adjunct Professor of
Medicine and Epidemiology & Biostatistics. He also serves as the Executive
Editor of the American Journal of Medicine, as a Research Associate for the
National Bureau of Economic Research (Program on Health Care), and as a
member of the VA' s national Cooperative Studies Evaluation Committee. He
has published more than 100 peer-reviewed original research articles, is the
author of Publishing and Presenting Clinical Research, and a co-author of
Designing Clinical Research: An Epidemiologic Approach.
http://www.fda.gov/cdrh/panel/cv/cv254.pdf
CURRICULUM VITA (REVISED MAY 28, 2003)
Warren S. Browner, MD, MPH
CURRENT POSITION Vice-President Academic Affairs
Scientific Director, Research Institute California Pacific Medical Center
2340 Clay Street, Room 114 San Francisco, CA 94115
Phone: (415) 600-1400 FAX: (415) 885-8686
Professor of Medicine, and Epidemiology & Biostatistics (adjunct)
School of Medicine university of California at San Francisco
Warren Browner Medicine-VAMC warren@cooper.cpmc.org
415-600-1400 VAMC - 111
Warren Browner warren@cooper.cpmc.org
Title Adjunct Professor Department Medicine-VAMC
Campus Phone 415-750-2093 Campus Phone 2 415-597-9193
Fax 415-885-8686
Private Practice Address Private Practice Phone 415-600-1400
VP, Acad Affairs, CPMC
2340 Clay Street, Room 114 San Francisco, CA. 94115
Campus Address Box VAMC - 111,
University of California, San Francisco San Francisco, CA. 94143 - VAMC
***************************************************************
http://groups.yahoo.com/group/aspartameNM/message/1047
Avoiding Hangover Hell 12.31.3 Mark Sherman, AP writer: Robert Swift, MD:
[formaldehyde from methanol in aspartame]: Murray 1.16.4 rmforall
[ Rich Murray: This information is highly relevant for toxicity from
formaldehyde formed from the methanol component, readily released in the GI
tract, of aspartame (NutraSweet, Equal, E951). Robert Swift MD of Brown
University states that methanol accumulates in the blood, is somewhat
countered by ethyl alcohol, and is more toxic for woman, who have less body
water than men to dilute it. This all agrees with the case reports on
aspartame reactors, the majority female, who report headache, GI symptoms,
malaise, fatigue, brain fog, dry mouths, and eye problems. ]
"...What are some of the symptoms of hangover?
I think the predominant symptom of hangover is headache. Most people
experience a headache, and many experience some gastrointestinal symptoms,
predominantly nausea and sometimes vomiting. There's a sense of general
malaise, of just not feeling well, feeling like you're fatigued, can't
concentrate. People's mouths feel very dry because they're dehydrated....
....The second theory is that the hangover is due not to the alcohol per se
but other things in the alcohol, the so-called congeners. A beverage alcohol
is usually not 100 percent pure. For example, whiskey may be distilled, but
then it's stored in charred-oak barrels for years and years, so you get all
of these compounds that leach out of the barrels and then get degraded over
time. There are hundreds of biological compounds in alcohol beverages. Of
course, with wine and beer, you actually add yeast to the grapes or the
malted barley or whatever, so there are lots of chemicals in it.
The other thing is that the yeast also makes other kinds of alcohols. When
yeast ferments sugar and alcohol, the vast majority of what it makes is
ethyl alcohol, which is the alcohol we drink. But the yeast can also produce
other alcohols, such as smaller alcohols like methanol (or wood alcohol),
and methanol's pretty toxic. It can cause blindness, in fact, if you drink
it pure.
When methanol is metabolized in the liver, it's converted to formaldehyde,
which is embalming fluid. So when you drink alcohol that contains some
methanol, your body first gets rid of the ethyl alcohol but the methanol
stays in your blood. It doesn't get degraded, and it actually builds up over
time. Then when you've burned up all the ethanol, you start to metabolize
the methanol and produce formaldehyde as a byproduct of that, and some
people feel that produces the symptoms.
Why do some people argue that a drink in the morning cures hangover?
The "hair of the dog that bit you"-a drink in the morning-might make you
feel better because you stop the metabolism of methanol and the formation of
formaldehyde because you've got alcohol in your system again. That could
help the withdrawal theory, too. If you are withdrawing from alcohol, so to
speak, you give yourself a little bit of alcohol to "detox" yourself.
Do certain types of alcohol beverages have more methanol than others?
Yes. There appears to be a relationship between the likelihood of getting a
hangover and how dark the alcohol is. The color means that the alcohol has
more junk in it. The darker color is somehow reflecting the level of
congeners. So more clear-colored alcohols, like vodka and gin, are less
likely to give you a hangover than a darker-colored alcohol, like a whiskey
or a scotch, bourbon or brandy. Likewise, among wines, people often find
they're more likely to get a headache from red wine rather than white wine.
Sulfites in red wine may contribute to hangover in people who are sensitive
to them....
....Does body weight play a role?
Body weight will play a role in that it affects the concentration of alcohol
and other substances that ultimately get into your body. The concentration
is actually affected by the amount of water in your body, which is partially
dependent upon your weight but not entirely. When people do calculations of
alcohol-how much alcohol will it take to achieve to a certain blood alcohol
level-they look at what's called "lean body weight" because the alcohol
doesn't go into the fat. So a fat person isn't necessarily more resistant to
the effect of alcohol because they may have the same amount of body water as
somebody who's very skinny.
Men have more body water than women do, so if a man and a woman who weigh
the same drink the same quantity, the man will have a lower blood alcohol
than the woman will, because the woman has less body water to dissolve the
alcohol...."
http://handi-stop.com/forums/postboard/posts/886.html
by Mark Sherman Dec 31, 2003
[ Associated Press writer, Washington DC 202-776-9400 ]
" When methanol is metabolized in the liver, it's converted to formaldehyde,
which is embalming fluid. So when you drink alcohol that contains some
methanol, your body first gets rid of the ethyl alcohol but the methanol
stays in your blood. It doesn't get degraded, and it actually builds up over
time. Then when you've burned up all the ethanol, you start to metabolize
the methanol and produce formaldehyde as a byproduct of that, and some
people feel that produces the symptoms.
Do certain types of alcohol beverages have more methanol than others?
Yes. There appears to be a relationship between the likelihood of getting a
hangover and how dark the alcohol is. The color means that the alcohol has
more junk in it. The darker color is somehow reflecting the level of
congeners. So more clear-colored alcohols, like vodka and gin, are less
likely to give you a hangover than a darker-colored alcohol, like a whiskey
or a scotch, bourbon or brandy. Likewise, among wines, people often find
they're more likely to get a headache from red wine rather than white wine.
Sulfites in red wine may contribute to hangover in people who are sensitive
to them. "
http://www.kansascity.com/mld/kansa...lth/7725474.htm
Posted on Fri, Dec. 12, 2003
[ Robert M. Swift M.D. Title: Associate Director
Department: Bio Med Alcohol & Addiction
Email: Robert_Swift_MD@Brown.EDU
Mailing Address: Box G-BH, Brown University, Providence, RI 02912-G
Telephone: (401) 457-3066 Other Telephone: (401) 444-1836 ]
Avoiding Hangover Hell by Christine Haran
[ weekly@healthology.com Managing Editor ]
"I'll never drink again." It's a claim many of us have made the morning
after a debauched night while struggling to face the daylight with a
pounding headache, a parched tongue and a distinctly queasy feeling in the
pit of the stomach.
For many, this promise is short-lived and is particularly hard to maintain
during the holiday season. As Robert Swift, MD, a professor of psychiatry at
Brown university Medical School and associate chief of research at the
Providence VA Medical Center in Rhode Island, points out, people tend to
increase their alcohol consumption during the holidays when there are more
parties and people have more leisure time.
So if you've overindulged at the office holiday party, you might find
yourself not only deeply embarrassed but also seeking a quick hangover cure.
Hangover remedies abound and include such treats as anchovies, tea made from
rabbit droppings and, of course, another stiff drink. But do any of them
work? Below, Dr. Swift talks about what exactly causes a hangover, how best
to cope-and how to avoid such misery in the first place.
What is hangover?
Hangover is a "collection" of symptoms that occur after a bout of alcohol
drinking. It's that simple.
What predisposes some people to hangover?
There are some studies that suggest that there may be some genetic
predispositions to hangover, although that's not clear. Obviously, larger
quantities of alcohol are more likely to produce more severe hangovers. And
there are a lot of other factors that may go into it as well. There is some
evidence that the type of alcohol consumed may relate to hangover, the time
of day that the alcohol's consumed, whether one is drinking instead of
sleeping, whether you eat while you're drinking, and how well hydrated you
are.
Can you give a sense of how many drinks are needed over what period of time
for an average person to end up with a hangover?
That's hard to know because it depends on a lot of factors, and it's an
individual sort of thing. There are people who are drink very, very
heavily-who are alcoholics-and never get a hangover and there are some who
drink very heavily and they do get hangovers.
What the worse time of day to drink in terms of hangover?
It's interesting. On the one hand, alcohol consumed in the morning tends to
be more intoxicating, believe it or not. But by and large, most people drink
in the evening and late at night, and that means that they may be drinking
instead of sleeping and alcohol influences the quality of sleep as well. As
a result, one ends up sleep deprived, and that can certainly exacerbate
hangover symptoms.
Does body weight play a role?
Body weight will play a role in that it affects the concentration of alcohol
and other substances that ultimately get into your body. The concentration
is actually affected by the amount of water in your body, which is partially
dependent upon your weight but not entirely. When people do calculations of
alcohol-how much alcohol will it take to achieve to a certain blood alcohol
level-they look at what's called "lean body weight" because the alcohol
doesn't go into the fat. So a fat person isn't necessarily more resistant to
the effect of alcohol because they may have the same amount of body water as
somebody who's very skinny.
Men have more body water than women do, so if a man and a woman who weigh
the same drink the same quantity, the man will have a lower blood alcohol
than the woman will, because the woman has less body water to dissolve the
alcohol.
What are some of the symptoms of hangover?
I think the predominant symptom of hangover is headache. Most people
experience a headache, and many experience some gastrointestinal symptoms,
predominantly nausea and sometimes vomiting. There's a sense of general
malaise, of just not feeling well, feeling like you're fatigued, can't
concentrate. People's mouths feel very dry because they're dehydrated.
What is happening in the body to cause these symptoms?
That's still not entirely known. There are two major theories about the
causes of hangover. The first theory is the withdrawal theory, which
suggests that hangover is really a type of mild alcohol withdrawal. If you
look at people's brains in a brain wave machine, even though people may be
feeling fatigued and tired, their brain is actually stimulated.
And that's what alcohol withdrawal is: It's a hyperstimulatory state.
Chronic alcoholics, if they stop drinking, get anxious, they get excited,
they can't sleep, they get the shakes. They may even hallucinate. It's
thought that even one bout of heavy drinking may induce a state of kind of
mild central nervous system excitation and people perceive that as a
hangover.
The second theory is that the hangover is due not to the alcohol per se but
other things in the alcohol, the so-called congeners. A beverage alcohol is
usually not 100 percent pure. For example, whiskey may be distilled, but
then it's stored in charred-oak barrels for years and years, so you get all
of these compounds that leach out of the barrels and then get degraded over
time. There are hundreds of biological compounds in alcohol beverages. Of
course, with wine and beer, you actually add yeast to the grapes or the
malted barley or whatever, so there are lots of chemicals in it.
The other thing is that the yeast also makes other kinds of alcohols. When
yeast ferments sugar and alcohol, the vast majority of what it makes is
ethyl alcohol, which is the alcohol we drink. But the yeast can also produce
other alcohols, such as smaller alcohols like methanol (or wood alcohol),
and methanol's pretty toxic. It can cause blindness, in fact, if you drink
it pure.
When methanol is metabolized in the liver, it's converted to formaldehyde,
which is embalming fluid. So when you drink alcohol that contains some
methanol, your body first gets rid of the ethyl alcohol but the methanol
stays in your blood. It doesn't get degraded, and it actually builds up over
time. Then when you've burned up all the ethanol, you start to metabolize
the methanol and produce formaldehyde as a byproduct of that, and some
people feel that produces the symptoms.
Do certain types of alcohol beverages have more methanol than others?
Yes. There appears to be a relationship between the likelihood of getting a
hangover and how dark the alcohol is. The color means that the alcohol has
more junk in it. The darker color is somehow reflecting the level of
congeners. So more clear-colored alcohols, like vodka and gin, are less
likely to give you a hangover than a darker-colored alcohol, like a whiskey
or a scotch, bourbon or brandy. Likewise, among wines, people often find
they're more likely to get a headache from red wine rather than white wine.
Sulfites in red wine may contribute to hangover in people who are sensitive
to them.
How can people treat a hangover?
Prevention is best. Avoid alcohol and you won't get a hangover. Drinking in
moderation will also help. Mixing alcohol with other beverages, drinking
slowly. Drinking alcohol with food will reduce the concentration of alcohol
in your stomach. It will dilute it and be less irritating to the stomach.
Also when people drink and eat at the same time, less alcohol is absorbed
into their blood because the alcohol's absorbed more slowly and therefore
more of it gets metabolized by the liver and the stomach before it gets into
the blood stream.
If you have overindulged, are there any options?
If you have overindulged, remedies abound. I think for thousands of years
probably there have been reported remedies for hangover. But there really is
very little that has been scientifically proven to improve a hangover. In
fact, I don't know of anything.
So people should just treat their symptoms?
People should treat their symptoms, but even treating the symptoms can have
side effects. For example, if you have a headache, you can take an
antiinflammatory medication like aspirin or ibuprofen. But, those can be
irritating to the stomach, which has already been irritated from the night
before. And after you've been drinking a lot of alcohol, you should not take
acetaminophen (Tylenol) because it has some toxicity to the liver, which is
actually magnified by drinking alcohol. In fact, there have been questions
about whether there ought to be a warning on the label.
Rehydrating will help, though people aren't as dehydrated as much as they
feel dry. But actually drinking fluids, having some carbohydrate in case
your blood sugar's down, having something mild in the stomach if there's
some stomach irritation, is a good idea.
Is there anything good about a hangover?
The question that one could argue philosophically is that a hangover might
be good for you because it deters you from drinking too much the next time.
***************************************************************
hangovers from formaldehyde from methanol (aspartame?): Schwarcz: Murray
1.18.3
----- Original Message -----
From: "Rich Murray" <rmforall@att.net>
To: <weekly@healthology.com>
Cc: <Robert_Swift_MD@Brown.EDU>; "joe.schwarcz" <joe.schwarcz@mcgill.ca>;
"Woodrow Monte" <woodymonte@xtra.co.nz>; "Mark D. Gold"
<mgold@holisticmed.com>; <jonmargo@sover.net>
Sent: Friday, January 16, 2004 10:21 PM
Subject: Avoiding Hangover Hell 12.31.3 Mark Sherman, AP writer: Robert
Swift, MD: [formaldehyde from methanol in aspartame]: Murray 1.16.4 rmforall
[ http://groups.yahoo.com/group/aspartameNM/message/1045
aspartame and formaldehyde toxicity discussion:
Schwarcz: Murray 12.13.3 rmforall ]
Jan 18 2003 Hey, Joe Schwarcz, It's easy to toss off a "shoot the
messenger" crack like "anti-aspartame fanatics are nuts". Would you please
buttress your credibility as a scientist by citing specific faults in the
following mainstream scientific selections:
Rich Murray, MA Room For All rmforall@comcast.net
1943 Otowi Road, Santa Fe, New Mexico 87505 USA 505-986-9103
http://groups.yahoo.com/group/aspartameNM/message/910
formaldehyde & formic acid from methanol in aspartame:
Murray: 12.9.2 rmforall
It is certain that high levels of aspartame use, above 2 liters daily
for months and years, must lead to chronic formaldehyde-formic acid
toxicity, since 11% of aspartame (1,120 mg in 2L diet soda, 5.6 12-oz
cans) is 123 mg methanol (wood alcohol), immediately released into the
body after drinking (unlike the large levels of methanol locked up in
molecules inside many fruits), then quickly transformed into
formaldehyde, which in turn becomes formic acid, both of which in
time 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. [Metabolism of aspartame in monkeys.
Oppermann JA, Muldoon E, Ranney RE.
J. Nutrition 1973 Oct; 103(10): 1454-1459.]
If 10% of the methanol is retained as formaldehyde, that would give 12
mg daily formaldehyde accumulation, about 60 times more than the 0.2 mg
from 10% retention of the 2 mg EPA daily limit for formaldehyde in water.
Bear in mind that the EPA limit for formaldehyde in drinking water is
1 ppm, or 2 mg daily for a typical daily consumption of 2 L of water.
http://groups.yahoo.com/group/aspartameNM/message/835
RTM: ATSDR: EPA limit 1 ppm formaldehyde in drinking water July 1999
5.30.2 rmforall
This long-term low-level chronic toxic exposure leads to typical
patterns of increasingly severe complex symptoms, starting with
headache, fatigue, joint pain, irritability, memory loss, and
leading to vision and eye problems, and even seizures. In many cases
there is addiction. Probably there are immune system disorders, with a
hypersensitivity to these toxins and other chemicals.
http://groups.yahoo.com/group/aspartameNM/message/872
immune system reactions due to formaldehyde from the 11% methanol in
aspartame: Thrasher: Tephly: Monte: Murray 9.27.2 rmforall
J. Nutrition 1973 Oct; 103(10): 1454-1459.
Metabolism of aspartame in monkeys.
Oppermann JA, Muldoon E, Ranney RE.
Dept. of Biochemistry, Searle Laboratories,
Division of G.D. Searle and Co. Box 5110, Chicago, IL 60680
They found that about 70% of the radioactive methanol in aspartame put
into the stomachs of 3 to 7 kg monkeys was eliminated within 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
at 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.]
Their followup report in 1976 included only three human subjects, who were
tested with aspartame made with C-14 phenylalanine and then C-14 aspartate--
but never the methanol component! Instead of mentioning the dreaded word
"formaldehyde" anywhere in the text and citations, they only showed, on
Figure 1, Metabolic pathways followed by aspartame, using arrows to show
reaction paths,
Asp-Phe-Me --> intestinal esterases ---> Asp-Phe + MeOH -->
one-carbon metabolic pool --> CO2 + formyl metabolites
J Toxicol Environ Health. 1976 Nov; 2(2): 441-51.
Comparative metabolism of aspartame in experimental animals and humans.
Ranney RE, Oppermann JA, Muldoon E, McMahon FG.
Aspartame [SC-18862; 3-amino-N-(alpha-carboxyphenethyl) succinamic acid,
methyl ester, the methyl ester of aspartylphenylalanine] is a sweetening
agent that organoleptically has about 180 times the sweetness of sugar.
The metabolism of aspartame has been studied in mice, rats, rabbits, dogs,
monkeys, and humans.
The compound was digested in all species in the same way as are natural
constituents of the diet.
Hydrolysis of the methyl group by intestinal esterases yielded methanol,
which was oxidized in the one-carbon metabolic pool to CO2.
The resultant dipeptide was split at the mucosal surface by dipeptidases and
the free amino acids were absorbed.
The aspartic acid moiety was transformed in large part to CO2 through its
entry into the tricarboxylic acid cycle.
Phenylalanine was primarily incorporated into body protein either unchanged
or as its major metabolite, tyrosine. PMID: 827618
[At the end of this post are more lengthly details on industry bias in
aspartame, methanol, formaldehyde, formic acid research]
http://groups.yahoo.com/group/aspartameNM/message/915
formaldehyde toxicity: Thrasher & Kilburn: Shaham: EPA: Gold: Murray:
Wilson: CIIN: 12.12.2 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.
Sam-1 Trust, Alto, New Mexico, USA.
http://www.drthrasher.org/formaldeh...o_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
Med Hypotheses. 1984 Jan; 13(1): 63-75.
Chronic methanol poisoning with the clinical and pathologic-anatomical
features of multiple sclerosis.
Henzi H.
The details of two cases of chronic methanol poisoning are presented. Both
patients initially developed clinical symptoms of multiple sclerosis: visual
disturbances, intention tremor, reduced abdominal reflexes, impaired
coordination and difficulties with walking. After the exposure to methanol
had ceased the multiple sclerosis symptoms persisted in patient 1 but
disappeared gradually in patient 2 (patient 2 had a history of excessive
alcohol consumption, which is a critical fact in this discussion).
Ultimately autopsies confirmed this picture: histological examination of
patient 1 revealed plaques in the spinal cord, in the stem and in the
proximity of the lower horn of one lateral ventricle, whereas no localized
demyelination could be found in patient 2. The results are discussed in
connection with the theory ("Methanol Hypothesis") that under certain
circumstances multiple sclerosis itself is induced by formaldehyde stemming
from the metabolism of methanol. Publication Types: Case Reports PMID:
6708848
"This article outlines the case of a biology teacher whose chronic
formaldehyde exposure resulted in heightened sensitivity to formaldehyde,
three tonic-clonic seizures, and dramatic amnesia as well as other cognitive
dysfunction."
Robert B. Perna, Ernest J. Bordini, Maria Deinzer-Lifrak
A Case of Claimed Persistent Neuropsychological Sequelae of Chronic
Formaldehyde Exposure. Clinical, Psychometric, and Functional Findings
Archives of Clinical Neuropsychology 16 (1) (2001) pp. 33-44.
Arch Clin Neuropsychol. 2001 Jan; 16(1): 33-44. [27 citations]
A case of claimed persistent neuropsychological sequelae of chronic
formaldehyde exposure. Clinical, psychometric, and functional findings.
Perna RB, Bordini EJ, Deinzer-Lifrak M.
Comprehensive Neuropsychological Services of the Southern Tier, Vestal, NY
Many anecdotal cases and some clinical studies have demonstrated that
formaldehyde exposure can cause multiple health-related problems and
cerebral dysfunction.
The U.S. Consumer Product Safety Commission has documented multiple hazards
related to formaldehyde exposure.
Some of this research has suggested that low levels of exposure can be very
hazardous to one's health and can potentially result in heightened chemical
sensitivities, seizures, and cognitive decline.
Some research suggests that exposure results in long-term immunological
changes, cell neurofilament protein changes, and demyelination.
Symptomatically, exposure has been associated with respiratory problems,
excessive fatigue, headaches, mood changes, and impaired attention,
concentration, and memory functioning.
This article outlines the case of a biology teacher whose chronic
formaldehyde exposure resulted in heightened sensitivity to formaldehyde,
three tonic-clonic seizures, and dramatic amnesia as well as other cognitive
dysfunction. PMID: 14590191
http://www.cpancf.com/
Clinical Psychology Asssociates of North Central Florida
Gainesville Office 2121 NW 40th Terr. Ste B. Gainesville, FL 32605
Ph: (352) 336-2888 Fax: (352) 371-1730
Ocala Office 3002 SE 1st Ave., Bldg. 300 Ocala, FL 32 Ph: (352) 629-1100
http://www.cpancf.com/NRE00151.pdf
NeuroRehabilitation 17 (2002) 93-104 IOS Press
Advances and issues in the diagnostic differential of malingering versus
brain injury
Robert B Perna, Ph.D. Neuropsychologist Dr.Perna@juno.com
Department: pain management
Facility: Southern Tier Pain Management Ctr.
Vestal, New York, 13850
Work Phone: 607-754-2313 Fax: 607-754-6926
http://www.usm.maine.edu/lac/ot/faculty%20&%20staff.htm
Robert B. Perna, Ph.D.; Part Time Instructor, OTH 610
Educational and Experiential Background
Robert is a part-time adjunct faculty who teaches Neuroscience in the
Occupational Therapy program. He is a clinical neuro-psychologist, the
director of a CARF accredited post-acute brain injury program, and is board
certified in psychopharmacology. He has completed many residencies at
University of Michigan Medical School and the Miami Heart Institute. He has
authored and co-authored more than fifty journal articles related to
neuro-psychology and rehabilitation.
http://www.forensicneuropsychology.com/_wsn/page2.html
http://www.psyfin.com/directory/det...?ListingsID=p41
Ernest J. Bordini Ph.D. http://www.cpancf.com cpancf@aol.com
2121 NW 40th Terrace Ste B Gainesville/Ocala, FL 32605
Phone: (352) 336-2888 Fax: (352) 371-1730
Licenses: Psychologist
Services: Clinical Psychology Associates of N. Central Florida, P.A.
provides services to children, adolescents, adultis, and seniors.
Psychological, Forensic and Neuropsychological Assessment. Employee
Assistance Programs.
Maria Deinzer-Lifrak, PhD deinlif@aol.com
Comprehensive Neuropsychological Services
490 Western Avenue Albany, NY 12203 518-458-2314
http://groups.yahoo.com/group/aspartameNM/message/925
aspartame puts formaldehyde adducts into tissues, Part 1/2
full text, Trocho & Alemany 6.26.98: Murray 12.22.2 rmforall
http://groups.yahoo.com/group/aspartameNM/message/926
aspartame puts formaldehyde adducts into tissues, Part 2/2
full text, Trocho & Alemany 6.26.98: Murray 12.22.2 rmforall
http://ww.presidiotex.com/barcelona/index.html
Trocho C, Pardo R, Rafecas I, Virgili J, Remesar X,
Fernandez-Lopez JA, Alemany M ["Trok-ho"]
Formaldehyde derived from dietary aspartame binds to tissue
components in vivo. Life Sci 1998 Jun 26; 63(5): 337-49.
Departament de Bioquimica i Biologia Molecular, Facultat de Biologia,
Universitat de Barcelona, Spain.
http://www.presidiotex.com/barcelona/index.html
Maria Alemany, PhD (male) alemany@porthos.bio.ub.es
http://groups.yahoo.com/group/aspartameNM/message/864
Murray: Butchko, Tephly, McMartin: Alemany: aspartame formaldehyde
adducts in rats 9.8.2 rmforall
Prof. Alemany vigorously affirms the validity of the Trocho study
against criticism:
Butchko, HH et al [24 authors], Aspartame: review of safety.
Regul. Toxicol. Pharmacol. 2002 April 1; 35 (2 Pt 2): S1-93, review
available for $35, [an industry paid organ]. Butchko:
"When all the research on aspartame, including evaluations in both the
premarketing and postmarketing periods, is examined as a whole, it is
clear that aspartame is safe, and there are no unresolved questions
regarding its safety under conditions of intended use."
[ They repeatedly pass on the ageless industry deceit that the methanol
in fruits and vegetables is as as biochemically available as that in
aspartame-- see the 1984 rebuttal by Monte, below.
In the same report, Schiffman concludes on page S49, not citing any
research after 1997, "Thus, the weight of the scientific evidence
indicates that aspartame does not cause headache."
Dr. Susan S. Schiffman, Dept. of Psychiatry, Duke University
sss@acpub.duke.edu 919-684-3303, 660-5657
http://groups.yahoo.com/group/aspartameNM/message/864
Murray: Butchko, Tephly, McMartin: Alemany: aspartame formaldehyde
adducts in rats 9.8.2 rmforall ]
http://groups.yahoo.com/group/aspartameNM/message/911
RTP ties to industry criticized by CSPI: Murray: 12.9.2 rmforall
Confirming evidence and a general theory are given by Pall (2002):
http://groups.yahoo.com/group/aspartameNM/message/909
testable theory of MCS type diseases, vicious cycle of nitric oxide &
peroxynitrite: MSG: formaldehyde-methanol-aspartame:
Martin L. Pall: Murray: 12.9.2 rmforall
http://groups.yahoo.com/group/aspartameNM/message/855
RTM: Blumenthall & Vance:
aspartame chewing gum headaches Nov 1997 7.28.2 rmforall
Harvey J. Blumenthal, MD, Dwight A Vance, RPh
Chewing Gum Headaches.
Headache 1997 Nov-Dec; 37(10): 665-6.
Department of Neurology, university of Oklahoma college of Medicine,
Tulsa, USA. neurotulsa@aol.com
Aspartame, a popular dietetic sweetener, may provoke headache in some
susceptible individuals. Herein, we describe three cases of young women
with migraine who reported their headaches could be provoked by chewing
gum sweetened with aspartame. [6-8 mg aspartame per stick chewing gum]
Here is a detailed personal case report. The jumbled, run-together syntax
and multiple typos are also common in aspartame reactors who are just
starting to detox. Note that this all unfolded within the last year, and
that symptoms are triggered by aspartame chewing gum, 6-8 mg aspartame per
stick. Ms Linsley has exercised unusual initiative in searching out and
testing possible dietary triggers. There are hundreds of similar reports in
the archives of http://health.groups.yahoo.com/group/aspartame/messages ,
759 members and 16,419 posts in just over 5 years.
From: "Linda Linsley" <lindalinsley@yahoo.com>
To: <aspartame@yahoogroups.com>
Subject: [Aspartame Support] Aspartame Poisoned
Date: Saturday, January 17, 2004 9:01 PM
Here's where I am at this point in time.
I'm 50, a former athlete (my dad became an olympic
coach), a self-learner and I always ask "why", "what
happens if",etc. I learned a long time ago that just
because someone "says so" isn't always enough.
So when things began to go wrong a year ago I recovered
quickly from the shock and set out to find out what
else it could be. Long story abbreviated:
symptoms;(each time I re-tell this I remember more
clearly what happened. my notes are tucked away
somewhere). White flashes in eyes, re-curring
dejavu's, dizziness, confusion, disorientation,
nausea, vomiting, undescribable/unidentifiable tase
and smell, thrown off feet/chair, head-bobbing, one
time only--loss of consciousness while driving, foot
bouncing off ground for no reason, incredible
sleepiness that I HAD to stop for and pass out
for(always had warning), inability to
focus/concentrate, memory loss, decline in grammar
and math skills, decline in reading and figuring out
written/oral directions, disproportionate loss of
muscle tone, stiffness, joint pain, asthma-like
symptoms, hearing loss, vision changes, pains in
chest and liver, poor coordination and balance, mood
swings, depression, fatigue, when under physical
stress/exertion my body would swell like arthritis(I
could have sworn it was attacking itself!),
reactions of doctors over the years; many tests, all normal.
The first list of symptoms that involved the head were
the ones I went for help with in 2002. Prior to that I
was actually kicked out of my physicians office because
I complained about all the tests and the money I spent
on them. With a new doctor that I'd hardly been to,
I was a bit hesitant. I didn't want to scare him, too,
and get the reputation of being a hypochondriac, so
I was real pleasant with him. He said I needed a
psychiatrist. Second opinion, and third doctor, did
mri, saw spots, referred me to neurologist, said to
call him if I needed any help, tossed out phrase
"m.s." POSSIBILITY, said needed more tests. When I
had another episode while waiting for neurologist
appointment that was 4 months away, he was merely
polite. no help. Then I thought I'd mention a few
more symptoms to him and he replied "You'd be surprised
what we can imagine when we think there's something
wrong with us". Finally saw neurologist, had second
mri, spots the same. She said "Yes, you have the
symptoms of m.s., but until you lose the use of an
arm or leg for three days due to numbness and tingling,
I won't even consider the possibility of it! Check the
internet (but be careful--there's a lot of
mis-information out there). Check with the M.S.
Society!" I did. They said "Get a different doctor!"!
I had noticed, on my own, that these "dejavu
incidents" seemed connected to foods. I got a
different doctor after a while. After the run I'd
had with doctors, I was tired of the whole thing and was
planning on only using the E.R. from then on. While
in limbo between the old/new doctor, I practiced the
diet a proffessor had told me about. His wife was
diagnosed with m.s. and had recovered quite a bit on it.
Things were going quite well as I was able to stick to it
better (with new motivation). One day I had another
"dejavu episode" and was worried that I didn't have
a doctor I could rely on, as well as confused at what
caused it. If my theory about food was right, then
what happened? I was driving down the road at the
time ( I'm a good compensator for the dizziness), and it
was passed, so I popped a piece of gum in my mouth
and THAT WAS IT! I had just bought another pack of Extra.
I hadn't had any for a month now...same time when I
was doing well! O.K.! If my theory was correct, then
I could eat anything (within reason--I still wasn't
sure yet) that I'd been avoiding and IF IT WAS the gum, I
should have no other symptoms. (they would go in
clusters for a period of 12-42 hours)... So I dropped
the gum, pigged out on forbidden items and HAD NO
TROUBLE AT ALL! The doctors refused to respond to
and acknowledge that. When I got my new doctor, I said
not much about it.
I began to search the Internet. Found
Dr. Betty Martini on the aspartame group, then Connie
at the Kicksugar group, while also changing my
experiments on myself which lead to discovering a
variety of additives that were responsible for the
symptoms. As I found out more additives I would
check it out on the sites for confirmation.
foods I avoid now are aspartame, msg, hydrolyzed
animal protien, aspartic acid, natural flavorings
sucrose, dextrose, maltodextrin, corn syrup, high
fructose corn syrup, disodium guanylate, monosodium
glutamate, disodium phosphate( and any other "ate"),
diglycerides and artificial flavorings.
For now, that's the way things are. Have I totally
ruled out m.s. or something else? Not really because
of the mri that showed spots on the brain. Only
time and consistency will prove anything. There seems to
be a period of de-toxification when tolerance levels
are better (saturation point?) during which I can
indulge in damaging substances for a while with no reactions.
However, saturation point is reached again and I
notice tiny occurances of some of the earlier
symptoms. Sticking with the "pure diet" is
difficult, especially when there are those around who don't
follow it....and that's just about everyone I come
in contact with!
BUT THE RESPONSIBILITY LIES WITH ME
to do what is best for me regardless of what is
considered "normal".
********************************************************************
Sent: Jan 17 2003 3:35 PM joe.schwarcz@mcgill.ca
Ohhhhh ...how a little learning is a dangerous thing...
The stuff about hangover is all correct, in fact I have written on it
myself (attached) but it has nothing to do with aspartame toxicity. In
fact if you take the trouble to check with Dr. Swift you will learn that
he thinks the anti-aspartame fanatics are nuts.
Dr. Joe Schwarcz, Director McGill Office for Science and Society
514-398-6238 McGill university 801 Sherbrooke St. West Montreal, QC.
Canada H3A 2K6
"... But in all likelihood, the greatest contributor to the hangover is
methanol. This alcohol is found in small concentrations in many beverages,
a byproduct of fermentation. It is metabolized by the same enzymes as
ethanol, but the products this time are formaldehyde and formic acid which
produce the hangover symptoms. Why does this happen only the morning after?
Because the enzymes prefer to work on ethanol instead of methanol. Only
when all the ethanol has been metabolized, do they switch to methanol.... "
The Scoop On Booze
The police officers could hardly believe their eyes. The eighteen year-old
driver they had just pulled over sat there speechless, a wad of white fabric
sticking out of his mouth. He had ripped the crotch out of his underwear
and stuffed it into his mouth in an apparent attempt to fool the
breathalyzer. Some scientific memory about the absorbency of cotton must
have stirred in his confused mind to prompt the bizarre act. But the
breathalyzer was not fooled. Neither was it fooled by the teenager who was
caught ferociously sucking on pennies after being stopped. He must have
remembered a bit of the chemistry he had learned about alcohol. The bit
about alcohol being oxidized to acetaldehyde by the action of copper. He
figured he'd be in the clear since the breathalyzer tests for alcohol in the
breath, and not acetaldehyde. Unfortunately the genius didn't remember the
reaction quite right. Ethanol, the alcohol of beverages, can indeed be
converted to acetaldehyde by copper, but only when the copper is red hot!
Then there are those whose alibi is that they had just rinsed their mouth
with mouthwash. But this doesn't wash either. Sure, mouthwashes contain
alcohol, and a false breathalyzer reading is possible, but only if the
mouthwash was used immediately before giving a breath sample. Alcohol from
a mouthwash dissipates within a couple of minutes and guidelines state that
a suspect has to be observed for several minutes before a breathalyzer test
is undertaken.
Is it surprising that people resort to such curious acts when they've
overindulged? Not really. After all, alcohol certainly affects the brain.
And the rest of the body as well. The chemistry involved is absolutely
fascinating. Of course, before alcohol can affect the brain, it has to get
there. Most of the alcohol we consume is absorbed into the bloodstream from
the stomach and the small intestine. But not all of the alcohol makes it
through. Some is metabolized in the mucosa that lines the stomach and
intestine. Here, enzymes convert ethanol first to acetaldehyde and then to
acetic acid, neither of which is inebriating. In men, about 30% of a dose
of alcohol meets its metabolic end in this fashion, but there is a definite
gender bias here. The female stomach and intestinal lining is only about
half as efficient at breaking down ethanol, so more makes it into the
circulation. This explains why women may become tipsy more easily.
Once the alcohol is in the bloodstream, it passes through the liver. The
liver is the body's main detoxicating organ and it detects alcohol as a
potential troublemaker. First, an enzyme called alcohol dehydrogenase snips
a couple of hydrogen atoms out of the ethanol molecule, converting it to
acetaldehyde. Then aldehyde dehydrogenase transforms this intermediate into
acetic acid which is either excreted or used by the body as a source of
energy as it is broken down into carbon dioxide and water. A gram of
ethanol can provide about seven calories in this fashion. If the intake of
alcohol is sufficiently high, the liver's detoxicating system becomes
overburdened and some of the alcohol slips through unmetabolized. It can
then wreak havoc in the brain.
Ethanol does this by interfering with "neurotransmitters," the chemicals
brain cells use to communicate among themselves. At low alcohol levels,
receptors for glutamate are activated leading to stimulation and a loss of
inhibition. This is the "social lubricant" effect of alcohol. But as the
concentration of alcohol rises, glutamate receptors actually become less
responsive and words begin to slu randcocktailpartyamnesiabegins.
Other neu rotransmittersystemsarealsoaffected.Gammaaminobutanoicacid
(GABA) is known as an inhibitory neurotransmitter because it prevents nerve
cells from firing excessively. Alcohol stimulates GABA activity which
eventually causes sedation and relaxation. And that is only part of a very
complex picture.
Eventually the effects wear off as the alcohol is excreted or is metabolized
as it passes through the liver again. But as this is happening, there is
often a matter of nausea, headaches and a flushed face to deal with. The
culprit here is acetaldehyde, some of which escapes from the liver before
being converted to acetic acid. As we well know, not everyone suffers these
symptoms to the same degree. Many people of Asiatic origin are severely
affected by facial flushing because nature has dealt them a very slow acting
version of aldehyde dehydrogenase, the enzyme that normally degrades
acetaldehyde. Indeed, the same concept lies behind a prescription drug
known as disulfiram (Antabuse) which is given to alcoholics. The idea is
that the drug inactivates aldehyde dehydrogenase, forcing acetaldehyde into
the circulation. This should make the drinker so sick that he gives up the
booze. Unfortunately, he usually gives up the drug instead.
Some of the effects of acetaldehyde can linger till the morning after and
contribute to hangover. Interestingly, the hangover business hasn't been as
extensively researched as one would think. That's because solving the
problem would come with quite a bit of social baggage. The concern is that
elimination of the hangover could cause people to drink more. Still, we do
know that there is more to the hangover than just the remnants of
acetaldehyde. The metabolism of alcohol in the liver produces some free
radical debris which is usually taken care of by glutathione, one of the
body's most important antioxidants. When the system is overwhelmed, these
free radicals can contribute to the hangover. That is why there has been
some success in treating hangovers with supplements of N-acetylcysteine
(NAC) which serves as a source of cysteine, the critical compound the body
needs to generate more glutathione. Eggs also contain cysteine which may
explain their folkloric use to treat hangovers.
The hangover is actually multifactorial. Dehydration plays an important
role as does hypoglycemia caused by the alcohol mediated loss of sugar in
the urine. But in all likelihood, the greatest contributor to the hangover
is methanol. This alcohol is found in small concentrations in many
beverages, a byproduct of fermentation. It is metabolized by the same
enzymes as ethanol, but the products this time are formaldehyde and formic
acid which produce the hangover symptoms. Why does this happen only the
morning after? Because the enzymes prefer to work on ethanol instead of
methanol. Only when all the ethanol has been metabolized, do they switch to
methanol. This then explains the "hair of the dog" remedy for hangovers. A
drink in the morning supplies ethanol for the enzymes to act on so they'll
leave methanol alone. As the enzymes busily metabolize the ethanol,
methanol is excreted in the urine without being converted to formic acid. A
Bloody Mary may be the best choice here, because vodka contains very little
methanol. Confirmation about the critical role of methanol in hangovers
comes from a study showing that treatment with 4-methylpyrazole, a drug that
blocks the breakdown of methanol, can eliminate the symptoms.
I must admit to feeling a little queasy talking about hangover cures.
Alcohol can be an extremely destructive beverage. It is probably more
damaging to society than all illicit drugs combined. Cirrhosis of the
liver, strokes, breast cancer, oral cancers, domestic violence and sexual
assault have all been linked to alcohol abuse. In North America there is an
alcohol related car accident every 30 seconds. And if that isn't
frightening enough, excessive alcohol can shrink the genitals and have
feminizing effects on men. Less testosterone is produced, so the sex drive
suffers. But for those who want to look on the bright side, less
testosterone means less likelihood of baldness.
Henny Youngman, whom some would call a comedian, once remarked that when he
read about the evils of drinking he gave up reading. I hope you won't do
the same. There is nothing funny about being drunk. Drunks destroy their
own lives and kill others. What can we do? Well, university of Georgia
researchers have found that blood alcohol can be reduced significantly by
inserting a tube into the rectum and piping in alcohol dehydrogenase and
oxygen. Sounds good to me.
*******************************************************************
[more details on industry bias in aspartame, methanol, formaldehyde, formic
acid research]
In spring 1999, an eminent pro-aspartame scientist Christian Tschanz had
NutraSweet Co. give me their $ 130 review text of their research, "The
Clinical Evaluation of a Food Additive: Assessment of Aspartame" (1996), by
Christian Tschanz, Harriett H. Butchko, W. Wayne Stargel, and Frank N.
Kotsonis, all apartame stalwarts.
Chapter 5: "Metabolism and Pharmacokinetics of Radiolabeled Aspartame in
Normal Subjects", by Aziz Karim and Thomas Burns, has 10 pages and 10
citations. Page 63, Figure 4, Metabolic products derived from aspartame,
beta-aspartame, and DKP, does not list formaldehyde or formic acid.
The tangle of black arrows includes two paths from Aspartame to Methanol to
"CO2 + Body Constituents". Now, that's pretty good public relations spin,
eh? "Body Constituents", indeed? This is systematic and persistent deceit,
as pernicious as it is profitable. Aziz Karim, PhD is a "Distinguished
Research Fellow and Sr. Director, Clinical Research, G.D. Searle and
Company, Skokie, Illinois", where Thomas Burns, M.S. is a "Clinical Research
Manager". Hey, with a MA in psychology, I'm qualified to call a foul play
on these guys.
They state that "in monkeys" with methanol or aspartame labelled in the
methyl ester, both with 14C, "...excretion of 14CO2 in the expired air
occured to the same extent (about 70% of the 14C dose) with both compounds,
indicating complete hydrolysis of the methyl ester moiety of aspartame
(Figure 6)." They said nothing about resulting levels in blood plasma,
urine, feces, or any body tissues. This is the typical commission by
omission strategy of industry research on aspartame.
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 afterwards, as carbon dioxide in exhaled
air and 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, nor give the
absolute levels for declining blood plasma proteins. This study did not
monitor long-term use of aspartame, which might reveal cumulative effects.
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
at 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 precision 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. "Dietary
methanol is derived in large part from fresh fruits and vetetables."
Nowhere in this report, or in the book chapter are mentioned the dread
words, "formaldehyde" and "formic acid".
Woodrow C. Monte, a Professor of Food Science at Arizona State university in
Tempe, drew completely opposite conclusions in his seminal review in 1984.
The same three reserchers, plus F.G. McMahon of Tulane university Medical
School, published a follow-up study, "Comparative metabolism of aspartame in
experimental animals and humans", J. Toxicology and Environmental Health 2:
441-451, 1976.
The abstract says, "Hydrolysis of the methyl group by intestinal esterases
yielded methanol, which was oxidized in the one-carbon metabolic pool to
CO2."
"The hypothetical pathways of metabolism, which aspartame was expected to
follow, are diagrammed in Fig. 1....The principle used to test the validity
of this hypothetical description of the metabolism of aspartame..."
Figure 1. shows in an nice orderly sequence that:
(a) MeOH ---> one-carbon metabolic pool ---> CO2 + formyl metabolites .
Meanwhile, this sentence jumps from p. 441 to 442 under Figure 1., "The
absorbed methanol would be incorporated into the one-carbon pool and would
be converted [jump] primarily to CO2 (Makar et.al., 1968; Tephly et al,
1964), although a small fraction might be incorporated into body
constituents."
The graphs present the same methanol in monkey data as in 1973, but the
nowhere is the specific percentage of exhaled CO2 mentioned. Methanol and
aspartame were also given to a few [unspecified] number of rats: "The major
fraction of the 14C was excreted in the expired air (Fig. 2)...Plasma levels
of 14C reached a peak [absolute data not given] at about 3 hr..."
In this follow-up report, for methanol and the methyl group in aspartame,
excretion in urine and feces were not mentioned in either the former monkey
or the new rat studies, the absolute plasma levels were not given, and, of
course, no measures were taken of 14C in body tissues. The only hint of the
possible role of formaldehyde and formic acid was the rather diffident term
"formyl metabolites" in Figure 1. Overall, we see consistent patterns of
avoiding any focus on the actual disposition of extremely toxic
formaldehyde and formic acid, both persistent and cumulative, in body
tissues. Subtle equivocation and qualification was expressed by such words
as "hypothetical", "was expected to follow", "would be", "primarily",
"although a small fraction might be incorporated into body constituents",
"major fraction". Methanol from aspartame was not studied in the other
species: rabbits, dogs, and humans.
It pays to investigate early studies, because then the coverup was less well
organized, more patchy. The loosely organized world-wide exponential
growth of science ensures that the line of inquiry of methanol to
formaldehyde and formic acid will pop up here and there, but no one is
encouraged to make the connection with aspartame, widely proclaimed as "the
most thoroughly tested food additive in history"-- until the momentous,
unheralded Trocho study established explosive results in June 1998.
http://groups.yahoo.com/group/aspartameNM/message/872
immune system reactions due to formaldehyde from the 11% methanol in
aspartame: Trasher: Tephly: Monte: Murray 9.27.2 rmforall
[selections]
Life Sci 1991; 48(11): 1031-41. The toxicity of methanol. Tephly TR.
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
ocular toxicity. 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 animals.
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
p. 1035 "In the past, formaldehyde has often been suggested as the
methanol metabolite which produces toxicity (34,35). Today, a great
deal of information is available concerning its lack of such a role.
The presence of elevated formaldehyde levels in body fluids or tissues
following methanol administration has not been observed.
No formaldehyde has been detected in blood, urine or tissues obtained
from methanol-treated animals (36,37) and, in methanol-poisoned humans,
formaldehyde increases have not been observed....
About 85% of a low dose of 14C-formaldehyde [radioactive label] is
excreted as pulmonary 14CO2 (49,50)....."
[This suggests that 15% of the formaldehyde is indeed retained in the
body, a very significant result, considering its extreme and complex
toxicity.]
49. W.B. Neely, Biochem. Pharmacol. 13: 1137-1142 (1964).
50. Xenobiotica 1982 Feb; 12(2): 119-24.
Formaldehyde metabolism by the rat: a re-appraisal.
Mashford PM, Jones AR.
1. The metabolism of [14C]formaldehyde
has been investigated in the male Sprague-Dawley rat.
It is extensively oxidized to CO2
and formate, which is excreted in the urine. 2. Two radioactive
compounds isolated from the urine of rats dosed with
[14C]formaldehyde have been identified as N-hydroxymethylurea and
N,N'-bis-(hydroxymethyl)urea, and shown to be urinary
artefacts. 3. Previous studies of the metabolism
of formaldehyde by rats have been re-appraised.
Differences in the rate of oxidation
of formaldehyde in various strains of rats result in the excretion of
different urinary metabolites and, in some cases, formaldehyde.
Excretion of formaldehyde leads to the formation of several artefacts
depending on the components present in the urine. PMID: 6806997
http://groups.yahoo.com/group/aspartameNM/message/1025
aspartame & formaldehyde toxicity: Murray 9.9.3 rmforall
[selection]
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
K.E. McMartin and T.R. Tephly, authors of many pro-aspartame studies, in
Biochemical Pharmacology (1979) remarked, "It is now generally accepted
that the toxicity of methanol is due to the formation of toxic metabolites,
either formaldehyde or formic acid." They put damage doses of methanol
into the stomachs of three monkeys, and, using insensitive tests, found no
formaldehyde in many tissues-- except for a single datum in the midbrain,
1.5 times the detection limit. The use of inadequate tests is common in
industry research that is funded to claim the safety of profitable toxins.
Since then, industry scientists have been very wary of doing studies on
primates, which all too easily show the dangers to humans.
[end of selection]
http://groups.yahoo.com/group/aspartameNM/message/910
formaldehyde & formic acid from 11% methanol in aspartame:
Murray: 12.9.2 rmforall
[selections]
This study admitted one datum that showed accumulation of formaldehye
in the midbrain from an acute toxicity dose of 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 time
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 and
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.
[ So, this is an acute toxicity study, with little relevance for chronic
long-term, low-level exposure.
"It is now generally accepted that the toxicity of methanol is due to
the formation of toxic metabolites (1,2), either formaldehyde or formic
acid."
Monkeys, like people, are susceptible to methanol toxicity.
This team cites their six previous methanol in monkey studies, from
1975 to 1977.
The report is difficult to understand, since the three monkeys were
treated differently, and different assays were used.
The assay used was the chromatropic acid method, with a detection limit
of .025 mmol/L. None of the five tissues showed any formaldehyde with
this assay, except the midbrain, 0.14 mmol/kg wet weight tissue [units
converted from their 0.14 micromole/gm]-- just 1.5 times the detection
limit of .09 mmol/kg wet tissue weight (given on p. 648).
[Since 1 kg of water is 1 L, 1 mmol/kg is equivalent to 1 mmol/L.]
Meanwhile, the blood formate level rose by 12 hours from .180 to
10.02 mEq/L. [I assume that a mEq is equivalent to a mmol-- let
me know if I'm wrong.] The formate detection limits for the assays
were not given in this report. The formate level in the vitreous humor
of the eye was 7.90 mEq/L. It is well known that formate is
extremely damaging to the eye. For unexplained reasons, formate levels
in the five tissues were not measured.
After 12 hours, the urine formaldehyde level was below detection level,
while urine formate was 115.80 mEq/L-- so much of the
formaldehyde had been converted into formic acid, another cumulative,
potent toxin.
"In the presence of high formate values and definitive evidence of
toxicity in methanol-poisoned monkeys, no measurable formaldehyde was
found in the body tissues that were tested."
It is reasonable to surmise that more sensitive assays would have
found formaldehyde and formate bound to and reacted with a variety of
cellular substances in all tissues-- just as the 1998 Trocho study
confirmed.
Monkeys B and C were normal, not extra vulnerable to methanol, and were
given 3,000 mg/kg methanol, and samples taken at 18 hr. Formaldehyde
was detected only in the blood of Monkey B, while formate was found in
8 and 10, respectively, of the 10 fluid and tissue samples in Monkeys B
and C. For instance, the lowest value of formate, except for zero-time
blood, for each monkey was in the midbrain, 2.16 mmol/kg for
Monkey B (24 times the detection limit for the chromatropic acid
method) and 1.02 mmol/kg (1.3 times the detection for the dimedon
method) for Monkey C. This shows accumulation of formate in liver,
kidney, optic nerve, cerebrum, and midbrain. ]
"Thus, whereas one can associate formate intimately with ocular
toxicity in the monkey, no association of formaldehyde with ocular
toxicity can be made at this time. It is not possible to completely
eliminate formaldehyde as a toxic intermediate because formaldehyde
could be formed slowly within cells and interfere with normal cellular
function without ever obtaining levels that were detectable in body
fluids..."
"Acknowledgements-- This research was supported by NIH grant GM 19420
and GM 12675." [not funded by the industry]
[end of selections]
Often, pro-aspartame studies have titles and summaries that are not
supported by a close study of the details:
http://groups.yahoo.com/group/aspartameNM/message/891
flawed test for aspartame DNA damage: Jeffrey & Williams 2000: Murray:
11.20.2 rmforall
http://groups.yahoo.com/group/aspartameNM/message/925
aspartame puts formaldehyde adducts into tissues, Part 1/2
full text, Trocho & Alemany 6.26.98: Murray 12.22.2 rmforall
[selection]
"These are indeed extremely high levels for adducts of formaldehyde, a
substance responsible of chronic deleterious effects (33), that has also
been considered carcinogenic (34,47). The repeated occurrence of claims
that aspartame produces headache and other neurological and
psychological secondary effects-- more often than not challenged by
careful analysis-- (5,9,10,15,48) may eventually find at least a partial
explanation in the permanence of the formaldehyde label, since
formaldehyde intoxication can induce similar effects (49).
The cumulative effects derived from the incorporation of label in the
chronic administration model suggests that regular intake of aspartame
may result in the progressive accumulation of formaldehyde adducts.
It may be further speculated that the formation of adducts can help to
explain the chronic effects aspartame consumption may induce on
sensitive tissues such as brain (6,9,19,50). In any case, the possible
negative effects that the accumulation of formaldehyde adducts can
induce is, obviously, long-term. The alteration of protein integrity
and function may needs some time to induce substantial effects.
The damage to nucleic acids, mainly to DNA, may eventually induce cell
death and/or mutations.
The results presented suggest that the conversion of aspartame methanol
into formaldehyde adducts in significant amounts in vivo should 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."
http://groups.yahoo.com/group/aspartameNM/message/926
aspartame puts formaldehyde adducts into tissues, Part 2/2
full text, Trocho & Alemany 6.26.98: Murray 12.22.2 rmforall
http://ww.presidiotex.com/barcelona/index.html
Trocho C, Pardo R, Rafecas I, Virgili J, Remesar X,
Fernandez-Lopez JA, Alemany M ["Trok-ho"]
Formaldehyde derived from dietary aspartame binds to tissue
components in vivo. Life Sci 1998 Jun 26; 63(5): 337-49.
Departament de Bioquimica i Biologia Molecular, Facultat de Biologia,
Universitat de Barcelona, Spain.
http://www.presidiotex.com/barcelona/index.html
Maria Alemany, PhD (male) alemany@porthos.bio.ub.es
http://groups.yahoo.com/group/aspartameNM/message/864
Murray: Butchko, Tephly, McMartin: Alemany: aspartame formaldehyde
adducts in rats 9.8.2 rmforall
Prof. Alemany vigorously affirms the validity of the Trocho study
against criticism:
Butchko, HH et al [24 authors], Aspartame: review of safety.
Regul. Toxicol. Pharmacol. 2002 April 1; 35 (2 Pt 2): S1-93, review
available for $35, [an industry paid organ]. Butchko:
"When all the research on aspartame, including evaluations in both the
premarketing and postmarketing periods, is examined as a whole, it is
clear that aspartame is safe, and there are no unresolved questions
regarding its safety under conditions of intended use."
[ They repeatedly pass on the ageless industry deceit that the methanol
in fruits and vegetables is as as biochemically available as that in
aspartame-- see the 1984 rebuttal by Monte, below.
In the same report, Schiffman concludes on page S49, not citing any
research after 1997, "Thus, the weight of the scientific evidence
indicates that aspartame does not cause headache."
Dr. Susan S. Schiffman, Dept. of Psychiatry, Duke University
sss@acpub.duke.edu 919-684-3303, 660-5657
http://groups.yahoo.com/group/aspartameNM/message/864
Murray: Butchko, Tephly, McMartin: Alemany: aspartame formaldehyde
adducts in rats 9.8.2 rmforall ]
http://groups.yahoo.com/group/aspartameNM/message/911
RTP ties to industry criticized by CSPI: Murray: 12.9.2 rmforall
******************************************************************
http://www.dorway.com/wmonte.txt
Dr. Woodrow C. Monte Aspartame: methanol, and the public health.
Journal of Applied Nutrition 1984; 36 (1): 42-54.
(62 references) Professsor of Food Science [retired 1992]
Arizona State University, Tempe, Arizona 85287 woodymonte@xtra.co.nz
The methanol from 2 L of diet soda, 5.6 12-oz cans, 20 mg/can, is
112 mg, 10% of the aspartame. The EPA limit for water is 7.8 mg daily
for methanol (wood alcohol), a deadly cumulative poison. Many users
drink 1-2 L daily. The reported symptoms are entirely consistent with
chronic methanol toxicity. (Fresh orange juice has 34 mg/L, but, like all
juices, has 16 times more ethanol, which strongly protects against
methanol.)
http://groups.yahoo.com/group/aspartameNM/message/870
Aspartame: Methanol and the Public Interest 1984:
Monte: Murray 9.23.2 rmforall
Rereading this prescient classic review from 1984, I find its findings
are supported in much recent research, so I am again making the full
text widely available.
[ I have put my comments or corrections in square brackets, and spaced
the text to ease the reader's task. ]
For instance, I had forgotten this, which answers the industry PR "science"
that fruits and vegetables supply much more methanol than does aspartame:
Fruit and vegetables contain pectin with variable methyl ester content.
However, the human has no digestive enzymes for pectin (6, 25) particularly
the pectin esterase required for its hydrolysis to methanol (26).
Fermentation in the gut may cause disappearance of pectin (6) but the
production of free methanol is not guaranteed by fermentation (3). In fact,
bacteria in the colon probably reduce methanol directly to formic acid or
carbon dioxide (6) (aspartame is completely absorbed before reaching the
colon). Heating of pectins has been shown to cause virtually no
demethoxylation; even temperatures of 120 deg C produced only traces of
methanol (3). Methanol evolved during cooking of high pectin foods (7)
has been accounted for in the volatile fraction during boiling and
is quickly lost to the atmosphere (49). Entrapment of these volatiles
probably accounts for the elevation in methanol levels of certain
fruit and vegetable products during canning (31, 33).
Recent research [see links at end of post] supports his focus on the
methanol to formaldehyde toxic process:
The United States Environmental Protection Agency in their Multimedia
Environmental Goals for Environmental Assessment recommends a minimum
acute toxicity concentration of methanol in drinking water at 3.9 parts per
million, with a recommended limit of consumption below 7.8 mg/day (8). This
report clearly indicates that methanol:
"is considered a cumulative poison due to the low rate of excretion once it
is absorbed. In the body, methanol is oxidized to formaldehyde and
formic acid; both of these metabolites are toxic." (8)....
Recently the toxic role of formaldehyde (in |