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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

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  • Rich Murray
    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
    Message 1 of 1 , May 12, 2009
      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, 1,572 posts in a public archive

      group with 1191 members, 23,458 posts in a public archive

      Bukowski R, Malone FD, Porter FT, Nyberg DA, Comstock CH, et al. (2009)
      Preconceptional Folate Supplementation and the Risk of Spontaneous Preterm
      Birth: A Cohort Study. PLoS Med 6(5): e1000061.
      doi:10.1371/journal.pmed.1000061 free full text, public access
      PLoS Medicine www.plosmedicine.org 11 May 2009

      "Hispanic ethnicity, black or Asian race, nulliparity, and prior preterm
      birth were associated with higher risk of spontaneous preterm birth (Table
      3). The effects of Hispanic ethnicity, black or Asian race, nulliparity, and
      prior preterm birth were stronger for early spontaneous preterm birth.
      Maternal age and smoking did not have significant effects after adjustment
      for remaining characteristics (Table 3)."
      [ Note by Rich Murray: Due to some genetic mutations that impair the role of
      folic acid in safely metabolizing methanol, often an over one part in
      ten-thousand impurity in alcohol drinks, non-whites are more vulnerable to
      alcohol intoxication, hangover, and toxicity -- and probaby harm to the
      fetus. The unexamined co-factors of alcohol and aspartame drink exposure may
      be potent enough to dominate the cohort data. ]

      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


      Brief Summary:

      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
      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, b.kapur@...;
      Arthur C. Vandenbroucke, PhD, FCACB
      Yana Adamchik,
      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
      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

      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.

      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; 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


      Public release date: 1-Dec-2008
      Contact: Kim Barnhardt kim.barnhardt@...
      613-731-8610 x2224
      Canadian Medical Association Journal

      Maternal exposure to folic acid antagonists increases risks

      Exposure to folic acid antagonists during pregnancy is associated with a
      higher risk of placenta-mediated adverse outcomes such as preeclampsia,
      placental abruption, fetal growth restriction or fetal death reports a
      retrospective cohort study published in CMAJ
      http://www.cmaj.ca/press/pg1263.pdf .

      Folic acid antagonists include a broad range of drugs used to treat
      epilepsy, mood disorders, hypertension and infections. As approximately 50%
      of pregnancies in industrialized countries like Canada are unplanned, there
      is a risk of unintended exposure to these medications.

      The study, conducted by researchers from Ottawa, Montreal, Saskatoon and
      Hunan, China looked at 14,982 women who had taken folic acid antagonists one
      year prior to delivery and 59,825 women who did not. Dr. Shi Wu Wen and
      co-researchers found that maternal exposure to folic acid antagonists was
      associated with a slightly higher risk of adverse pregnancy outcomes. They
      suggest re-classifying some folic acid antagonists and recommend increased
      folic acid supplements for women requiring folic acid antagonists during

      In a related commentary http://www.cmaj.ca/press/pg1243.pdf , Dr. Joel Ray
      suggests the research study presents some "thought-provoking findings, but
      the results may not be ready for adoption by clinical practitioners or drug
      policy makers." He cites some real concerns with the study design and the
      need for clinically relevant finding as cautions about translating findings
      into practice.

      http://content.nejm.org/cgi/content/abstract/343/22/1608 abstract
      http://content.nejm.org/cgi/content/full/343/22/1608 free full text
      The New England Jouranal of Medicine
      Volume 343: 1608-1614 November 30, 2000 Number 22
      Folic Acid Antagonists during Pregnancy and the Risk of Birth Defects
      Sonia Hernández-Díaz, M.D., Dr.P.H., Martha M. Werler, Sc.D., Alexander M.
      Walker, M.D., Dr.P.H., and Allen A. Mitchell, M.D.


      Multivitamin supplementation in pregnant women may reduce the risks of
      cardiovascular defects, oral clefts, and urinary tract defects in their
      infants. We evaluated whether the folic acid component of multivitamins is
      responsible for the reduction in risk by examining the associations between
      maternal use of folic acid antagonists and these congenital malformations.

      We assessed exposure to folic acid antagonists that act as dihydrofolate
      reductase inhibitors and to certain antiepileptic drugs in 3870 infants with
      cardiovascular defects, 1962 infants with oral clefts, and 1100 infants with
      urinary tract defects and also in 8387 control infants with malformations
      the risk of which is not reduced after vitamin supplementation. Mothers were
      interviewed within six months after delivery about their medication use
      during pregnancy.

      The relative risks of cardiovascular defects and oral clefts in infants
      whose mothers were exposed to dihydrofolate reductase inhibitors during the
      second or third month after the last menstrual period, as compared with
      infants whose mothers had no such exposure, were 3.4 (95 percent confidence
      interval, 1.8 to 6.4) and 2.6 (95 percent confidence interval, 1.1 to 6.1),
      respectively. The relative risks of cardiovascular defects, oral clefts, and
      urinary tract defects after maternal exposure to antiepileptic drugs were
      2.2 (95 percent confidence interval, 1.4 to 3.5), 2.5 (95 percent confidence
      interval, 1.5 to 4.2), and 2.5 (95 percent confidence interval, 1.2 to 5.0),
      respectively. Use of multivitamin supplements containing folic acid
      diminished the adverse effects of dihydrofolate reductase inhibitors, but
      not that of antiepileptic drugs.

      Folic acid antagonists, which include such common drugs as trimethoprim,
      triamterene, carbamazepine, phenytoin, phenobarbital, and primidone, may
      increase the risk not only of neural-tube defects, but also of
      cardiovascular defects, oral clefts, and urinary tract defects. The folic
      acid component of multivitamins may reduce the risks of these defects.

      Source Information
      From the Slone Epidemiology Unit, Boston University School of Public Health,
      Brookline, Mass. (S.H.-D., M.M.W., A.A.M.); and the Department of
      Epidemiology, Harvard School of Public Health, Boston (S.H.-D., A.M.W.).

      Address reprint requests to Dr. Hernández-Díaz at the Slone Epidemiology
      Unit, Boston University School of Public Health, 1371 Beacon St., Brookline,
      MA 02446, or at shernan@... .

      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:
      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.
      http://www.cuk.ac.kr/eng/ sysop@...
      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."
      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, 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

      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


      Public release date: 11-May-2009

      Contact: Andrew Hyde <press@...> 44-122-346-3330
      Public Library of Science
      Preconceptional folic acid supplements are associated with reduced risk of
      premature birth

      Taking folic acid supplements for at least a year before conception is
      associated with reduction in the risk of premature birth, according to a
      study by Radek Bukowski (from the University of Texas Medical Branch, United
      States of America) and colleagues, published in this week's PLoS Medicine.

      Although most pregnancies last about 40 weeks, many babies (for example
      around 12% in the United States) are born before 37 completed weeks of
      pregnancy. Babies born prematurely are less likely to survive than full-term
      babies and are more likely to have breathing difficulties and learning or
      developmental disabilities. Currently, there are no effective methods of
      prevention or treatment of premature (preterm) birth, but previous studies
      have suggested that lower concentrations of folate (folic acid) are
      associated with shorter duration of pregnancy. Bukowski and colleagues
      therefore tested this idea, by analyzing data collected from a cohort of
      nearly 35,000 pregnant women.

      The results of this study showed that taking folate supplements for at least
      one year before conception was associated with a 70% reduction in
      spontaneous premature birth between 20 and 28 weeks (a reduction from 0.27%
      to 0.04%), and a 50% reduction between 28 and 32 weeks (reduction from 0.38%
      to 0.18%), as compared to the rate of preterm birth when mothers did not
      take additional folate supplementation. Folate supplementation for less than
      a year before conception was not linked to a reduction in the risk of
      premature birth in this study, and folate supplementation was not associated
      with any other complications of pregnancy.

      In a related commentary also published in this week's PLoS Medicine,
      Nicholas Fisk from the University of Brisbane, Australia, and colleagues
      (who were not involved in the original study) say "Methodologically, the
      study has several strengths... It is based on a huge dataset, with
      prospective recording of dietary supplements and potential confounders, and
      gestational age determined accurately on first trimester ultrasound. Those
      born preterm because of intervention were appropriately censored."
      Nevertheless, Nicholas Fisk and colleagues also point out limitations to the
      study -- for example, this was a secondary analysis of a Down syndrome
      screening study, so information on folic acid dose, formulation (with or
      without other supplements), and daily compliance is incomplete. The study
      design was observational, so the presence of other factors, such as
      healthier behaviors on the part of women who take folate supplements, may
      explain the findings. Further evidence as to whether folic acid prevents
      spontaneous preterm birth will require a randomized controlled trial.
      Callaway L, Colditz PB, Fisk NM (2009) Folic Acid Supplementation and
      Spontaneous Preterm Birth: Adding Grist to the Mill? PLoS Med 6(5):
      e1000077. doi:10.1371/journal.pmed.1000077



      Radek Bukowski
      University of Texas Medical Branch
      Department of Obstetrics and Gynecology
      301 University Blvd, Galveston, TX 77555
      409-747-4923 rkbukows@...

      Related PLoS Medicine Perspective:



      Nicholas M Fisk
      University of Queensland Centre for Clinical Research
      Centre for Clinical Research, Herston, Brisbane, Queensland 4029, Australia
      (61) 07 3346 5500 (61) 07 3346 5599 (fax) n.fisk@...


      Editors' Summary

      Background. Most pregnancies last about 40 weeks, but sometimes the new
      family member arrives early. Every year, half a million babies in the United
      States (12.5% of all babies) are born prematurely (before 37 completed weeks
      of pregnancy). Sadly, premature babies are more likely to die
      than full-term babies and many have short- and/or long-term health problems.
      Premature babies often have breathing problems, they are susceptible to
      life-threatening infections, and they are more likely to have learning and
      developmental disabilities than those born on time. The severity of these
      health problems depends on the degree of prematurity -- pre-term babies born
      between 34 and 36 weeks of pregnancy rarely develop severe disabilities, but
      a quarter of babies born before 28 weeks of pregnancy develop serious
      lasting disabilities and half have learning and behavioral problems.
      Although doctors have identified some risk factors for early delivery (for
      example, smoking), it is impossible to predict who will have an early birth
      and there is no effective way to prevent preterm births.

      Why Was This Study Done? Some researchers think that folate supplements may
      prevent preterm births. Folate (folic acid), a vitamin found in leafy green
      vegetables, fruits, and dried beans, helps to prevent neural tube birth
      defects. Consequently, women are encouraged to take folic acid
      supplements throughout (and preferably before) pregnancy and many
      governments now mandate that bread, pasta, and other grain products be
      fortified with folic acid to help women get sufficient folate. There is some
      evidence that women who deliver early have less folate in their blood than
      women who deliver at term. Furthermore, folate supplementation during
      pregnancy has increased the length of pregnancy in some but not all clinical
      trials. A possible explanation for these mixed results is that the duration
      of pregnancy reflects conditions in the earliest stages of pregnancy or
      before conception and that folate supplementation needs to start before
      conception to reduce the risk of preterm birth. In this study, the
      researchers test
      this idea by analyzing data collected from nearly 35,000 pregnant women
      enrolled in a study that was originally designed to investigate screening
      for Down's syndrome.

      What Did the Researchers Do and Find? During the first three months of their
      pregnancy, the women were asked whether they had taken folate supplements
      before conception. The duration of each pregnancy was estimated from
      ultrasound measurements taken early in the pregnancy and from the time of
      delivery. During the study, 1,658 women had spontaneous preterm deliveries
      before 37 weeks and 160 delivered before 32 weeks. After allowing for other
      maternal characteristics that might have affected the likelihood of preterm
      delivery, the risk of spontaneous preterm delivery between 20 and 28 weeks
      was 70% lower in women who took folate supplements for more than a year
      before becoming pregnant than in women who didn't take a supplement.
      Long-term folate supplementation also reduced the risk of preterm delivery
      between 28 and 32 weeks by 50% but did not affect the risk of preterm birth
      beyond 32 weeks. Folate supplementation for less than a year before
      conception did not reduce the risk of preterm birth, and folate
      supplementation was not associated with any other complications of

      What Do These Findings Mean? These findings show that folate supplementation
      for a year or more before conception is associated with a 50%-70% decrease
      in early (but not late) spontaneous preterm births and that the longer a
      woman takes folate supplements before becoming pregnant, the lower her risk
      of a preterm birth.

      Although the researchers allowed for maternal
      characteristics that might have affected the duration of pregnancy, it is
      possible that folate supplementation may not be responsible for the
      reduction in preterm birth risk seen in this study. For example, taking
      folate supplements may be a marker of healthy behavior and the women taking
      the supplements might have been doing something else that was reducing
      their risk of preterm birth. However, despite this and other limitations of
      this study, these findings suggest that long term folate supplementation
      before conception is worth investigating further as a potential way to
      prevent preterm births.

      Radek Bukowski <rkbukows@...>;
      CH Comstock <ccomstock@...>;
      FD Malone <fmalone@...>;
      DA Nyberg <Nyberg@...>;
      Nicholas Fisk <n.fisk@... >;
      Andrew Hyde <press@...>;
      PB Colditz <p.colditz@...>;
      LK Callaway <l.callaway@...>;
      Mary E D'Alton <md511@...>;
      RL Berkowitz <rb2212@...>;
      GD Hankins ghankins@...;
      KA Eddleman <keith.eddleman@...>;
      SJ Gross <susan.gross@...>;
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