Compiled By Rich Murray, MA
Room For All
1943 Otowi Road
Santa Fe, New Mexico 87505 USA
Telephone: 505-501-2298
Web Site:

Posted: 28 May 2009

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.
[ Alexander Mauskop, MD, Director, 30 East 76th Street, New York, NY 10021
Telephone: 877-669-4323
Westchester: 99 Maple Avenue, White Plains, NY 10605 Tel: 212-794-3550 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 treatment.

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 Medicine.

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 physicians.

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 Clinics.

Christina Sun-Edelstein MD, Headache and Epilepsy Specialist

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 Institute.

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 neurological disorders.

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, among others.

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.

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. PMID: 19291245

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.

Magnesium is an important intracellular element that is involved in numerous cellular functions.

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 hyper-aggregation 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 headache.
Sun-Edelstein C, Mauskop A.
The New York Headache Center, New York, NY 10021, USA.

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 2008.07.18
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


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 environment."

Rich Murray, MA Room For All
1943 Otowi Road, Santa Fe, New Mexico 87505


Methanol impurity in alcohol drinks [ and aspartame ] is turned intoneurotoxic 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 2008.02.24
Sunday, February 24, 2008

Brief Summary:

Methanol in small amounts is present along with ethanol in beverage alcohol.
[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 formic acid.

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 organ damage.

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,;
Arthur C. Vandenbroucke, PhD, FCACB
Yana Adamchik,
Denis C. Lehotay,;
Peter L. Carlen; Alcoholism: Clinical and Experimental Research 31 (12), 2114-2120.



Methanol is endogenously formed in the brain and is present as a congener in most alcoholic beverages.

Because ethanol is preferentially metabolized over methanol (MeOH) by alcohol dehydrogenase, it is not surprising that MeOH accumulates in the alcohol-abusing population.

This suggests that the alcohol-drinking population will have higher levels of MeOH's neurotoxic metabolite, formic acid (FA).

FA elimination is mediated by folic acid.

Neurotoxicity is a common result of chronic alcoholism.

This study shows for the first time that FA, found in chronic alcoholics, is neurotoxic and this toxicity can be mitigated by folic acid administration. To determine if FA levels are higher in the alcohol-drinking population and to assess its neurotoxicity in organotypic hippocampal rat brain slice cultures.

Serum and CSF FA was measured in samples from both ethanol abusing and control patients, who presented to a hospital emergency department. [ CSF = Cerebral Spinal Fluid ]

FA's neurotoxicity and its reversibility by folic acid were assessed using organotypic rat brain hippocampal slice cultures using clinically relevant concentrations.

Serum FA levels in the alcoholics (mean SE: 0.416 +- 0.093 mmol/l, n = 23) were significantly higher than in controls (mean SE: 0.154 +- 0.009 mmol/l, n = 82) (p < 0.0002).

FA was not detected in the controls' CSF (n = 20), whereas it was >0.15 mmol/l in CSF of 3 of the 4 alcoholic cases.

Low doses of FA from 1 to 5 mmol/l added for 24, 48 or 72 hours to the rat brain slice cultures caused neuronal death as measured by propidium iodide staining.

When folic acid (1 umol/l) was added with the FA, neuronal death was prevented. [ umol = micromole ]

Formic acid may be a significant factor in the neurotoxicity of ethanol abuse.

This neurotoxicity can be mitigated by folic acid administration at a clinically relevant dose.

Key Words:
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

Copyright 2007 by the Research Society on Alcoholism. DOI:10.1111/j.1530-0277.2007.00541.x
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 ethanol.

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, 1971).

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 neurotoxic.

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

Pld 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: Murray 2007.08.31
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: Murray 2006.01.20

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 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.
Department of Forensic Toxicology,
University Hospital, SE-581 85 Linkoping, Sweden.

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

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. Full text 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

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. 22"

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

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