aspartame, caffeine, MSG, alcohol may cause migraine headaches, C Sun-Edelstein, A Mauskop, The New York Headache Center, Clin J Pain 2009 June: Rich Murray 2009.05.25
- aspartame, caffeine, MSG, alcohol may cause migraine headaches, C
Sun-Edelstein, A Mauskop, The New York Headache Center, Clin J Pain 2009
June: Rich Murray 2009.05.25
Monday, May 25, 2009
Clin J Pain. 2009 Jun; 25(5): 446-52.
Foods and supplements in the management of migraine headaches.
Sun-Edelstein C, Mauskop A.
The New York Headache Center, New York, NY 10021, USA. drsun@...
[ Alexander Mauskop, MD, Director, 30 East 76th Street, New York, NY 10021
Westchester: 99 Maple Avenue, White Plains, NY 10605 Tel: 212-794-3550
http://www.nyheadache.com/blog/ Alexander Mauskop's blog
Although a wide range of acute and preventative medications are now
available for the treatment of migraine headaches, many patients will not
have a significant improvement in the frequency and severity of their
headaches unless lifestyle modifications are made.
Also, given the myriad side effects of traditional prescription medications,
there is an increasing demand for "natural" treatment like vitamins and
supplements for common ailments such as headaches.
Here, we discuss the role of food triggers in the management of migraines,
and review the evidence for supplements in migraine treatment.
A review of the English language literature on preclinical and clinical
studies of any type on food triggers, vitamins, supplements, and migraine
headaches was conducted.
A detailed nutritional history is helpful in identifying food triggers.
Although the data surrounding the role of certain foods and substances in
triggering headaches is controversial, certain subsets of patients may be
sensitive to phenylethylamine, tyramine, aspartame, monosodium glutamate,
nitrates, nitrites, alcohol, and caffeine.
The available evidence for the efficacy of certain vitamins and supplements
in preventing migraines supports the use of these agents in the migraine
The identification of food triggers, with the help of food diaries, is an
inexpensive way to reduce migraine headaches.
We also recommend the use of the following supplements in the preventative
treatment of migraines, in decreasing order of preference: magnesium,
Petasites hybridus, feverfew, coenzyme Q10, riboflavin, and alpha lipoic
acid. PMID: 19454881
Alexander Mauskop, MD FAAN, DIRECTOR,
Dr. Mauskop is the Director and founder of the New York Headache Center. He
is board-certified in Neurology with subspecialty certification in Headache
Dr. Mauskop has been conducting research in the field of headaches for over
20 years and has published numerous articles in scientific journals. He has
delivered over 400 scientific presentations and lectures and serves as a
reviewer for the New England Journal of Medicine, Neurology, Headache, and
several other medical journals.
Dr. Mauskop is a Fellow of the American Academy of Neurology, Fellow of the
New York Academy of Medicine and member of other professional organization.
He is an Associate Professor of Neurology at SUNY - Downstate Medical
Center, Past-President of the Eastern Pain Association, and, for the past 21
years, has been the Director of an annual educational symposium for
Over 200 doctors from around the world have visited the New York Headache
Center to learn advanced treatment techniques, such as Botox injections,
magnesium infusions, and other.
Dr. Mauskop is a licensed acupuncturist and author of The Headache
Alternative: A Neurologist's Guide to Drug-Free Relief, a book published by
Dell and What Your Doctor May Not Tell You About Migraines: The Breakthrough
Program That Can Help End Your Pain, published by Warner Books.
He has repeatedly been chosen as one of New York magazine's Best Doctors in
New York, as one of New York Times Magazine's, "Super Doctors" and as Castle
and Connolly's "Best Doctors". Dr. Mauskop has appeared on local and
national television shows, including Tom Brokaw's News Hour, Extra, and PBS
specials, and he has been featured in Vogue, O Magazine, and many other
publications. He has given lectures at institutions such as Cornell,
Harvard, Columbia, NYU and Dartmouth Medical Schools, Mayo and Cleveland
Christina Sun-Edelstein MD, Headache and Epilepsy Specilist
Dr. Christina Sun-Edelstein is a Board-Certified Neurologist with
subspecialty training and experience in both Headache and Epilepsy.
She graduated from SUNY Brooklyn College of Medicine with honors, and then
completed her neurology residency at Mount Sinai Medical Center in New York.
Dr. Sun-Edelstein subsequently spent a year in Melbourne, Australia as an
Epilepsy Fellow at St. Vincent's Hospital, then returned to New York for her
fellowship training in Headache Medicine at Roosevelt Hospital's Headache
During her Headache Fellowship, and in clinical practice since then, Dr. Sun
Edelstein has accumulated a great deal of experience in diagnosing and
managing headache patients. She has also participated in research trials,
and has skills in developing and implementing research protocols.
Dr. Sun-Edelstein's awards and honors include the American Academy of
Neurology's Resident Scholarship Award, the David Coddon Memorial Award
(given by the Headache Cooperative of New England), the American Headache
Society's Clinical Fellowship Award, and the American Headache Society's
Travel Award. She has also been published in academic journals such as
Archives of Neurology and Headache, and has written multiple headache topics
for the online medical reference UptoDate.
Anne Remmes, MD, Headache and Sleep Medicine Specialist.
Assistant Professor of Clinical Neurology, Columbia University.
Dr. Remmes is a noted specialist in the treatment of headaches and sleep
disorders. Dr. Remmes is an Associate Professor of Clinical Neurology at
New York's Columbia-Presbyterian Medical Center. Dr. Remmes previously
served as Director of Headache and Sleep Medicine at Columbia University's
College of Physicians and Surgeons.
Dr. Remmes received her medical degree from the State university of New York
at Stony brook, and a B.A. from Marquette University. She is a Fellow of the
American Sleep Disorders Association. Dr. Remmes has received training in
internal medicine, neurology and sleep medicine, and teaches and lectures
extensively on the management of headaches, face and neck pain, and sleep
disorders. She recently contributed the chapter "Sleep Disorders" to Current
Medical Diagnosis & Treatment in Neurology (McGraw-Hill Medical, 2006), a
key reference book for primary care physicians managing patients with
Lynda J. Krasenbaum, MSN, APRN, BC, Headache Specialist, Assistant Director
Lynda Krasenbaum is a nationally board-certified Advanced Nurse Practitioner
with extensive experience in headache diagnosis, treatment and management.
Ms. Krasenbaum works independently in our Center as a headache provider and
is on faculty as an Adjunct Assistant Professor at Columbia University.
After receiving her undergraduate degree from Syracuse University, Ms.
Krasenbaum worked at Johns Hopkins Hospital in Neurology, Neurosurgery and
Psychiatry. She then obtained her graduate degree from the University of
Pennsylvania and practiced thereafter at the Hospital of the University of
Pennsylvania, Dartmouth Hitchcock Medical Center and Columbia University
Medical Center, eventually specializing in Headaches. She has been in
practice for over 13 years.
In addition to clinical practice, Ms. Krasenbaum has participated in many
research trials. She has been an invited speaker at professional educational
events. She has worked with the NHF (National Headache Foundation) on
educational headache monographs, Columbia University College of Physicians
and Surgeons with their nationally-taught Headache Mini-Fellowships, the
HCNE (Headache Consortium of New England) Annual Headache Conference, the
DHMC (Dartmouth Hitchcock Medical Center) Headache Symposium, NPACE (Nurse
Practitioner Associates for Continuing Education) Regional Conferences,
Cephalalgia. 2009 Apr; 29(4): 445-52.
Chronic migraine and medication overuse headache: clarifying the current
International Headache Society classification criteria.
Sun-Edelstein C, Bigal ME, Rapoport AM.
The New York Headache Center, New York, NY 10021, USA. drsun@...
Despite the recent advances in the understanding and classification of the
chronic daily headaches, considerable controversy still exists regarding the
classification of individual headaches, including chronic migraine (CM) and
medication overuse headache (MOH).
The original criteria, published in 2004, were difficult to apply to most
patients with these disorders and were subsequently revised, resulting in
broader clinical applicability.
Nonetheless, they remain a topic of debate, and the revisions to the
criteria have further added to the confusion.
Even some prominent headache specialists are unsure which criteria to use.
We aimed to explain the nature of the controversies surrounding the entities
of CM and MOH.
A clinical case will be used to illustrate some of the problems faced by
clinicians in diagnosing patients with chronic daily headache.
Expert Rev Neurother. 2009 Mar; 9(3): 369-79.
Role of magnesium in the pathogenesis and treatment of migraine.
Sun-Edelstein C, Mauskop A.
The New York Headache Center, New York, NY 10021, USA. drsun@...
Magnesium is an important intracellular element that is involved in numerous
Deficiencies in magnesium may play an important role in the pathogenesis of
migraine headaches by promoting cortical spreading depression, alteration of
neurotransmitter release and the hyperaggregation of platelets.
Given this multifaceted role of magnesium in migraine, the use of magnesium
in both acute and preventive headache treatment has been researched as a
potentially simple, inexpensive, safe and well-tolerated option.
Studies have shown that preventive treatment with oral magnesium and acute
headache treatment with intravenous magnesium may be effective, particularly
in certain subsets of patients.
In this review, the pathogenesis of migraine will be discussed, with an
emphasis on the role of magnesium.
Studies on the use of intravenous and oral magnesium in migraine treatment
will be discussed and recommendations will be made regarding the use of
magnesium in treating migraine headaches. PMID: 19271946
Curr Pain Headache Rep. 2008 Dec; 12(6): 447-50.
Complementary and alternative approaches to the treatment of tension-type
Sun-Edelstein C, Mauskop A.
The New York Headache Center, New York, NY 10021, USA. drsun@...
Although pharmacotherapy with NSAIDs and tricyclic antidepressants comprises
the traditional treatment of tension-type headaches (TTHs), the use of other
therapeutic approaches in combination with medications can increase the
success of treatment.
Patients with comorbid mood disorders and unremitting headaches may
particularly benefit from some nonpharmacologic approaches.
This review focuses on complementary and alternative approaches to TTH
treatment, including psychological therapies, acupuncture, and physical
treatments. PMID: 18973739
formaldehyde, aspartame, and migraines, the first case series, Sharon E
Jacob-Soo, Sarah A Stechschulte, UCSD, Dermatitis 2008 May: Rich Murray
Friday, July 18, 2008
Dermatitis. 2008 May-Jun; 19(3): E10-1.
Formaldehyde, aspartame, and migraines: a possible connection.
Jacob SE, Stechschulte S.
Department of Dermatology and Cutaneous Surgery, University of Miami,
Miami, FL, USA.
Aspartame is a widely used artificial sweetener that has been linked
to pediatric and adolescent migraines.
Upon ingestion, aspartame is broken, converted, and oxidized into
formaldehyde in various tissues.
We present the first case series of aspartame-associated migraines
related to clinically relevant positive reactions to formaldehyde on
patch testing. PMID: 18627677
re huge reduction in preterm births: folic acid prevents harm from
formaldehyde and formic acid made by body from methanol in alcohol drinks
and aspartame, BM Kapur, DC Lehotay, PL Carlen at U. Toronto, Alc Clin Exp
Res 2007 Dec: Rich Murray 2009.05.12
Tuesday, May 12, 2009
"Of course, everyone chooses, as a natural priority, to enjoy
peace, joy, and love by helping to find, quickly share, and positively
act upon evidence about healthy and safe food, drink, and
Rich Murray, MA Room For All rmforall@...
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505
http://RMForAll.blogspot.com new primary archive
group with 140 members, 1,573 posts in a public archive
group with 1197 members, 23,476 posts in a public archive
methanol impurity in alcohol drinks [ and aspartame ] is turned into
neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol Syndrome,
BM Kapur, DC Lehotay, PL Carlen at U. Toronto, Alc Clin Exp Res 2007 Dec.
plain text: detailed biochemistry, CL Nie et al. 2007.07.18: Murray
Sunday, February 24, 2008
Methanol in small amounts is present along with ethanol in beverage
[Murray: and about the same amounts from aspartame diet sodas]
The body's natural enzymes preferentially metabolize ethanol while
methanol breaks down into highly neurotoxic Formic Acid.
Use of high levels of Folic Acid was found to inhibit brain damage
caused by the methanol.
The use of Folic Acid during pregnancy has been recommended
for several years to prevent neural tube defects.
However, this study indicates that even higher levels of Folic Acid
can be very beneficial to the developing baby, particularly where
alcohol exposure is a factor.
Folic Acid is mandated as an additive to all flour sold in Canada.
The debate has begun on its required addition to all beverage
alcohol to help mitigate damage caused to both infants and adults.
Formic Acid in the Drinking patient and the expectant mother
Dr. Bhushan M. Kapur
Departments of Laboratory Medicine,
St. Michael's Hospital , Toronto, Ontario, Canada
Methanol is produced endogenously in the pituitary glands of humans
and is present as a congener in almost all alcoholic beverages.
Ethanol and methanol are both bio-transformed by alcohol
dehydrogenase; however, ethanol has greater affinity for the enzyme.
Since ethanol is preferentially metabolized by the enzyme, it is not
surprising that trace amounts of methanol, most likely originating from
both sources, have been reported in the blood of people
who drink alcohol.
Toxicity resulting from methanol is very well documented
in both humans and animals and is attributed to its toxic metabolite
To understand ethanol toxicity
and Fetal Alcohol Spectrum Disorders, it is important to consider
methanol and its metabolite, formic acid, as
potential contributors to the toxic effects of alcohol.
Accumulation of methanol suggests that alcohol-drinking
population should have higher than baseline levels of formic acid.
Our preliminary studies do indeed show this.
Chronic low-level exposure to methanol has been suggested to
impair human visual functions.
Formic acid is known to be toxic to the optic nerve.
Ophthalmological abnormalities are a common finding in children
whose mothers used alcohol during pregnancy.
Formic acid, a low molecular weight substance, either crosses the
placenta or may be formed in-situ from the water soluble methanol
that crosses the placenta.
Embryo toxicity from formic acid has been reported
in an animal model.
To assess neurotoxicity we applied low doses of formic acid
to rat brain hippocampal slice cultures.
We observed neuronal death with a time and dose response.
Formic acid requires folic acid as a cofactor for its elimination.
Animal studies have shown that when folate levels are low, the
elimination of formic acid is slower and formate levels are elevated.
When folic acid was added along with the formic acid
to the brain slice cultures, neuronal death was prevented.
Therefore, folate deficient chronic drinkers may be at higher risk of
Women who are folic acid deficient and consume alcohol may have
higher levels of formic acid and should they become pregnant,
their fetus may be at risk.
To our knowledge low level chronic exposure to formic acid and its
relationship to folic acid in men or women who drink alcohol has
never been studied.
Our hypothesis is that the continuous exposure to low levels of
formic acid is toxic to the fetus and may be part of the etiology of
Fetal Alcohol Spectrum Disorders.
Alcoholism: Clinical and Experimental Research
Volume 31 Issue 12 Page 2114-2120, December 2007
Bhushan M. Kapur, b.kapur@...;
Arthur C. Vandenbroucke, PhD, FCACB
Denis C. Lehotay, dlehotay@...;
Peter L. Carlen carlen@...;
(2007) Formic Acid, a Novel Metabolite of Chronic Ethanol Abuse, Causes
Neurotoxicity, Which Is Prevented by Folic Acid
Alcoholism: Clinical and Experimental Research 31 (12), 2114-2120.
Methanol is endogenously formed in the brain and is present as a congener in
most alcoholic beverages.
Because ethanol is preferentially metabolized over methanol (MeOH) by
alcohol dehydrogenase, it is not surprising that MeOH accumulates in the
This suggests that the alcohol-drinking population will have higher levels
of MeOH's neurotoxic metabolite, formic acid (FA).
FA elimination is mediated by folic acid.
Neurotoxicity is a common result of chronic alcoholism.
This study shows for the first time that FA, found in chronic alcoholics, is
neurotoxic and this toxicity can be mitigated by folic acid administration.
To determine if FA levels are higher in the alcohol-drinking population and
to assess its neurotoxicity in organotypic hippocampal rat brain slice
Serum and CSF FA was measured in samples from both ethanol abusing and
control patients, who presented to a hospital emergency department. [ CSF =
Cerebral Spinal Fluid ]
FA's neurotoxicity and its reversibility by folic acid were assessed using
organotypic rat brain hippocampal slice cultures using clinically relevant
Serum FA levels in the alcoholics (mean ± SE: 0.416 +- 0.093 mmol/l, n = 23)
were significantly higher than in controls (mean ± SE: 0.154 +- 0.009
mmol/l, n = 82) (p < 0.0002).
FA was not detected in the controls' CSF (n = 20), whereas it was >0.15
mmol/l in CSF of 3 of the 4 alcoholic cases.
Low doses of FA from 1 to 5 mmol/l added for 24, 48 or 72 hours to the rat
brain slice cultures caused neuronal death as measured by propidium iodide
When folic acid (1 umol/l) was added with the FA, neuronal death was
prevented. [ umol = micromole ]
Formic acid may be a significant factor in the neurotoxicity of ethanol
This neurotoxicity can be mitigated by folic acid administration at a
clinically relevant dose.
Formic Acid, Folic Acid, Methanol, Neurotoxicity, Alcoholism.
From the Department of Clinical Pathology (BMK), Sunnybrook Health Science
Centre, Division of Clinical Pharmacology and Toxicology, The Hospital for
Sick Children, Toronto, Ontario, Canada;
St. Michael's Hospital (ACV), Toronto, Canada;
Department of Laboratory Medicine and Pathobiology, (BMK, ACV), Faculty of
Medicine, University of Toronto, Toronto, Ontario, Canada;
Departments of Medicine (Neurology) and Physiology (YA, PLC), Toronto
Western Research Institute, University of Toronto, Toronto, Ontario, Canada;
and University of Saskatchewan (DLC), Saskatchewan, Canada.
Received for publication May 1, 2007; accepted September 24, 2007.
Reprint requests: Dr. Bhushan M. Kapur, Department of Clinical Pathology,
Sunnybrook Health Science Centre, 2075 Bayview Ave, Toronto, Ontario, M4N
3M5, Canada; Fax: 416-813-7562; E-mail: b.kapur@...;
Copyright 2007 by the Research Society on Alcoholism. DOI:
Alcoholism: Clinical and Experimental Research 2007 Dec.
Alcohol Clin Exp Res, Vol. 31, No 12, 2007: pp 2114-2120
NEUROTOXICITY AND BRAIN damage are common concomitants findings of chronic
alcoholism (Carlen and Wilkinson, 1987; Carlen et al., 1981; Harper, 2007).
The cause of ethanol-induced neurotoxicity is still unclear.
We present here a novel hypothesis for neurotoxicity: increased formic acid
(FA) levels produced from methanol (MeOH), whose catabolism is blocked by
Axelrod and Daly (1965) demonstrated the endogenous formation of MeOH from
S-adenosylmethionine (SAM) in the pituitary glands of humans and various
other mammalian species.
Presence of MeOH in the breath of human subjects was reported by Ericksen
and Kulkarni (1963).
Most alcoholic beverages also have a small amount of MeOH as a congener
(Sprung et al., 1988).
As ethanol (EtOH) has a higher affinity for alcohol dehydrogenase (ADH) than
MeOH, EtOH is preferentially metabolized (Mani et al., 1970).
As a result, MeOH accumulation from endogenously produced MeOH, and/or, that
consumed as part of an alcoholic beverage, has been reported in
concentrations up to 2 mmol/l in heavy drinkers (Majchrowicz and Mendelson,
Toxicity resulting from MeOH consumption is extensively documented in both
humans and animals and has been attributed to its metabolite, FA (Benton and
Calhoun, 1952; Roe, 1946, 1955; Wood, 1912; Wood and Buller, 1904).
The rate of formate oxidation and elimination is dependent on adequate
levels of hepatic folic acid, particularly hepatic tetrahydrofolate (THF)
(Johlin et al., 1987; Tephly and McMartin, 1974).
Significantly higher formate levels were obtained when folate-deficient
animals were exposed to MeOH as compared with folate-sufficient animals (Lee
et al., 1994; McMartin et al., 1975; Noker et al., 1980).
To understand ethanol's toxicity, one must consider FA produced from MeOH,
and its elimination mediated by folic acid.
We postulate that in the chronically drinking patient, we will find higher
levels of FA than in the nondrinking population, and that formate is
We also hypothesize that treatment with folic acid, which is a critical
factor in the catabolism of FA, can prevent or diminish FA neurotoxicity.
unexamined cofactors re folic acid antagonist research include methanol
(quickly turns into formaldehyde and then formic acid in humans) from
tobacco and wood smoke, alcohol beverages, aspartame, demethylation of
caffeine: Rich Murray 2008.12.01
Monday, December 1, 2008
details on 6 epidemiological studies since 2004 on diet soda (mainly
aspartame) correlations, as well as 14 other mainstream studies
on aspartame toxicity since summer 2005: Murray 2007.11.27
aspartame groups and books:
updated research review of 2004.07.16: Murray 2006.05.11
old tiger roars -- Woodrow C Monte, PhD -- aspartame causes
many breast cancers, as ADH enzyme in breasts makes methanol
from diet soda into carcinogenic formaldehyde -- same in dark
wines and liquors, Fitness Life 2008 Jan.: Murray 2008.02.11
Monday, February 11, 2008
"Alcohol dehydrogenase ADH is required for the conversion of
methanol to formaldehyde (112).
ADH is not a common enzyme in the human body -- not many cells
in the human body contain this enzyme.
The human breast is one of the few organs in the body with a high
concentration of ADH (190b), and it is found there exclusively in the
mammary epithelial cells, the very cells known to transform into
adenocarcinoma (190c) (breast cancer).
The most recent breast cancer scientific literature implicates ADH
as perhaps having a pivotal role in the formation of breast cancer,
indicating a greater incidence of the disease in those
with higher levels of ADH activity in their breasts (190a)."
role of formaldehyde, made by body from methanol from foods
and aspartame, in steep increases in fetal alcohol syndrome, autism,
multiple sclerosis, lupus, teen suicide, breast cancer, Nutrition
Prof. Woodrow C. Monte, retired, Arizona State U., two reviews,
190 references supplied, Fitness Life, New Zealand
2007 Nov, Dec: Murray 2007.12.26
Wednesday, December 26 2007
Since no adequate data has ever been published on the
exact disposition of toxic metabolites in specific tissues in humans
of the 11 % methanol component of aspartame,
the many studies on morning-after hangover from the methanol
impurity in alcohol drinks are the main available resource to date.
highly toxic formaldehyde, the cause of alcohol hangovers, is
made by the body from 100 mg doses of methanol from
dark wines and liquors, dimethyl dicarbonate, and aspartame:
DMDC: Dimethyl dicarbonate 200mg/L in drinks
adds methanol 98 mg/L ( becomes formaldehyde in body ):
EU Scientific Committee on Foods 2001.07.12: Murray 2004.01.22
"...DMDC was evaluated by the SCF in 1990
and considered acceptable for
the cold sterilization of soft drinks and fruit juices at levels of
addition up to 250 mg/L (1)
...DMDC decomposes primarily to CO2 and methanol ...
[ Note: Sterilization of bacteria and fungi is a toxic process,
probably due to the inevitable conversion in the body of methanol
into highly toxic formaldehyde and then formic acid. ]
The use of 200 mg DMDC per liter would add 98 mg/L of methanol
to wine which already contains an average of about 140 mg/L
from natural sources.
methanol products (formaldehyde and formic acid) are main cause
of alcohol hangover symptoms [same as from similar amounts of
methanol, the 11% part of aspartame]: YS Woo et al, 2005 Dec:
Addict Biol. 2005 Dec;10(4): 351-5.
Concentration changes of methanol in blood samples during
an experimentally induced alcohol hangover state.
Woo YS, Yoon SJ, Lee HK, Lee CU, Chae JH, Lee CT, Kim DJ.
Chuncheon National Hospital, Department of Psychiatry,
The Catholic University of Korea, Seoul, Korea.
Songsin Campus: 02-740-9714 Songsim Campus: 02-2164-4116
Songeui Campus: 02-2164-4114
http://www.cuk.ac.kr/eng/sub055.htm eight hospitals
[ Han-Kyu Lee ]
A hangover is characterized by the unpleasant physical and mental
symptoms that occur between 8 and 16 hours after drinking alcohol.
After inducing experimental hangover in normal individuals,
we measured the methanol concentration prior to
and after alcohol consumption
and we assessed the association between the hangover condition
and the blood methanol level.
A total of 18 normal adult males participated in this study.
They did not have any previous histories of psychiatric
or medical disorders.
The blood ethanol concentration prior to the alcohol intake
(2.26+/-2.08) was not significantly different from that
13 hours after the alcohol consumption (3.12+/-2.38).
However, the difference of methanol concentration
between the day of experiment (prior to the alcohol intake)
and the next day (13 hours after the alcohol intake)
was significant (2.62+/-1.33/l vs. 3.88+/-2.10/l, respectively).
A significant positive correlation was observed
between the changes of blood methanol concentration
and hangover subjective scale score increment when covarying
for the changes of blood ethanol level (r=0.498, p<0.05).
This result suggests the possible correlation of methanol
as well as its toxic metabolite to hangover. PMID: 16318957
[ The toxic metabolite of methanol is formaldehyde, which in turn
partially becomes formic acid -- both potent cumulative toxins
that are the actual cause of the toxicity of methanol.]
This study by Jones AW (1987) found next-morning hangover
from red wine with 100 to 150 mg methanol
(9.5 % w/v ethanol, 100 mg/l methanol, 0.01 %).
Fully 11% of aspartame is methanol --
1,120 mg aspartame in 2 L diet soda,
almost six 12-oz cans, gives 123 mg methanol (wood alcohol).
Pharmacol Toxicol. 1987 Mar; 60(3): 217-20.
Elimination half-life of methanol during hangover.
Jones AW. wayne.jones@...;
Department of Forensic Toxicology,
University Hospital, SE-581 85 Linkoping, Sweden.
This paper reports the elimination half-life of methanol in human
Experiments were made during the morning after the subjects had
consumed 1000-1500 ml red wine
(9.5 % w/v ethanol, 100 mg/l methanol)
the previous evening. [ 100 to 150 mg methanol ]
The washout of methanol from the body
coincided with the onset of hangover.
The concentrations of ethanol and methanol in blood were
determined indirectly by analysis of end-expired alveolar air.
In the morning when blood-ethanol dropped
below the Km of liver alcohol dehydrogenase (ADH)
of about 100 mg/l (2.2 mM),
the disappearance half-life of ethanol was 21, 22, 18 and 15 min.
in 4 test subjects respectively.
The corresponding elimination half-lives of methanol
were 213, 110, 133 and 142 min. in these same individuals.
The experimental design outlined in this paper can be used
to obtain useful data on elimination kinetics of methanol
in human volunteers without undue ethical limitations.
Circumstantial evidence is presented to link methanol
or its toxic metabolic products, formaldehyde and formic acid,
with the pathogenesis of hangover. PMID: 3588516
Thrasher (2001): "The major difference is that the Japanese
demonstrated the incorporation of FA and its metabolites
into the placenta and fetus.
The quantity of radioactivity remaining in maternal and fetal tissues
at 48 hours was 26.9 % of the administered dose." [ Ref. 14-16 ]
Arch Environ Health 2001 Jul-Aug; 56(4): 300-11.
Embryo toxicity and teratogenicity of formaldehyde. [100 references]
Thrasher JD, Kilburn KH. toxicology@...
Sam-1 Trust, Alto, New Mexico, USA.
www.drthrasher.org/formaldehyde_embryo_toxicity.html full text
http://www.drthrasher.org/formaldehyde_1990.html full text
Jack Dwayne Thrasher, Alan Broughton, Roberta Madison.
Immune activation and autoantibodies in humans
with long-term inhalation exposure to formaldehyde.
Archives of Environmental Health. 1990; 45: 217-223.
"Immune activation, autoantibodies, and anti-HCHO-HSA antibodies
are associated with long-term formaldehyde inhalation."
formaldehyde in FEMA trailers and other sources (aspartame,
dark wines and liquors, tobacco smoke): Murray 2008.01.30
Wednesday, January 30, 2008
The FEMA trailers give about the same amount of formaldehyde
daily as from a quart of dark wine or liquor, or two quarts
(6 12-oz cans) of aspartame diet soda, from their over 1 tenth gram
methanol impurity (one part in 10,000),
which the body quickly makes into formaldehyde -- enough
to be the major cause of "morning after" alcohol hangovers.
Methanol and formaldehyde also result from many fruits and
vegetables, tobacco and wood smoke, heater and vehicle exhaust,
household chemicals and cleaners, cosmetics, and new cars, drapes,
carpets, furniture, particleboard, mobile homes, buildings, leather ...
so all these sources add up and interact
with many other toxic chemicals.
formaldehyde from many sources, including aspartame, is major cause of
Allergic Contact Dermatitis, SE Jacob, T Steele, G Rodriguez, Skin and
Aging 2005 Dec.: Murray 2008.03.27
Thursday, March 27, 2008
"For example, diet soda and yogurt containing aspartame (Nutrasweet),
release formaldehyde in their natural biological degradation.
One of aspartame's metabolites, aspartic acid methyl ester, is
converted to methanol in the body, which is oxidized to formaldehyde
in all organs, including the liver and eyes. 22
Patients with a contact dermatitis to formaldehyde have been seen to
improve once aspartame is avoided. 22
Notably, the case that Hill and Belsito reported had a 6-month history
of eyelid dermatitis that subsided after 1 week of avoiding diet soda.
Avoiding formaldehyde allergic reactions in children, aspartame,
vitamins, shampoo, conditioners, hair gel, baby wipes, Sharon E Jacob,
MD, Tace Steele, U. Miami, Pediatric Annals 2007 Jan.: eyelid contact
dermatitis, AM Hill, DV Belsito, 2003 Nov.: Murray 2008.03.27
Thursday, March 27, 2008
Sharon E. Jacob, MD, Assistant Professor of Medicine (Dermatology)
University of California, San Diego 200 W. Arbor Drive #8420, San
Diego, CA 92103-8420
Tel: 858-552-8585 ×3504 Fax: 305-675-8317 sjacob@...;
opportunities re BA Magnuson, GA Burdock et al., Aspartame Safety
Evaluation 2007 Sept., Critical Reviews in Toxicology:
Rich Murray 2008.07.11
Friday, July 11, 2008