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unexamined cofactors re folic acid antagonist research include methanol (made into formaldehyde and then formic acid in humans) from tobacco and wood smoke, alcohol beverages, aspartame, demethylation of caffeine: Rich Murray 2008.12.01

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  • rmforall@comcast.net
    unexamined cofactors re folic acid antagonist research include methanol (quickly turns into formaldehyde and then formic acid in humans) from tobacco and wood
    Message 1 of 1 , Dec 1, 2008
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      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
      http://rmforall.blogspot.com/2008_10_01_archive.htm
      Monday, December 1, 2008
      http://groups.yahoo.com/group/aspartameNM/message/1569


      http://www.eurekalert.org/pub_releases/2008-12/cmaj-met112408.php

      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 pregnancy.

      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.

      ABSTRACT

      Background
      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.

      Methods
      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.

      Results
      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.

      Conclusions
      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@... .
      ____________________________________________________



      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
      2008.02.24
      http://rmforall.blogspot.com/2008_02_01_archive.htm
      Sunday, February 24, 2008
      http://groups.yahoo.com/group/aspartameNM/message/1524


      http://www.blackwell-synergy.com/doi/abs/10.1111/j.1530-0277.2007.00541.x

      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.
      doi:10.1111/j.1530-0277.2007.00541.x

      Abstract

      Background:
      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.

      Objective:
      To determine if FA levels are higher in the alcohol-drinking population and
      to assess its neurotoxicity in organotypic hippocampal rat brain slice
      cultures.

      Methods:
      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.

      Results:
      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 ]

      Conclusions:
      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; E-mail: b.kapur@...;

      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.
      ____________________________________________________



      detailed critiques of JE Garst folic acid proposals by experts HJ Roberts
      and M Alemany: Murray 2008.03.20
      http://rmforall.blogspot.com/2008_02_01_archive.htm
      Thursday, March 20, 2008
      http://groups.yahoo.com/group/aspartameNM/message/1530


      RE: 5 mg folic acid helps methanol to not form toxic formaldehyde and formic
      acid -- no effect re formaldehyde from methanol in human breast and arterial
      epithelial tissue: Garth: Monte 2008.03.19
      http://rmforall.blogspot.com/2008_02_01_archive.htm
      Wednesday, March 19, 2008
      http://groups.yahoo.com/group/aspartameNM/message/1529


      Re: 5 mg folic acid helps methanol to not form toxic formaldehyde
      and formic acid, but most research has neglected folic acid deficiency
      re cancer, birth defects, and neurotoxicity -- flaws in many studies
      on aspartame -- breakthrough insights by John E Garst, PhD
      toxicologist: Murray 2008.03.19
      http://rmforall.blogspot.com/2008_02_01_archive.htm
      Wednesday, March 19, 2008
      http://groups.yahoo.com/group/aspartameNM/message/1528


      5 mg folic acid helps methanol to not form toxic formaldehyde and formic
      acid, but most research has neglected folic acid deficiency re cancer, birth
      defects, and neurotoxicity -- flaws in many studies on aspartame --
      breakthrough insights by John E Garst, PhD toxicologist: Murray 2008.03.19
      http://rmforall.blogspot.com/2008_02_01_archive.htm
      Wednesday, March 19, 2008
      http://groups.yahoo.com/group/aspartameNM/message/1528
      _____________________________________________________


      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 2007.11.18
      http://rmforall.blogspot.com/2007_11_01_archive.htm
      Wednesday, November 14, 2007
      http://groups.yahoo.com/group/aspartameNM/message/1490


      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
      http://rmforall.blogspot.com/2008_02_01_archive.htm
      Monday, February 11, 2008
      http://groups.yahoo.com/group/aspartameNM/message/1517

      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
      http://rmforall.blogspot.com/2007_12_01_archive.htm
      Wednesday, December 26 2007
      http://groups.yahoo.com/group/aspartameNM/message/1498

      Monte WC., Is your Diet Sweetener killing you? Fitness Life. 2007 Nov; 33:
      31-33.
      Monte WC., A Deadly Experiment. Fitness Life. 2007 Dec; 34: 38-42.
      Monte WC., Bittersweet: Aspartame Breast Cancer Link. Fitness Life. 2008
      Feb; 34: 21-22.

      Article 1 http://www.thetruthaboutstuff.com/review1.shtml
      Article 2 http://www.thetruthaboutstuff.com/review2.shtml
      Article 3 http://www.thetruthaboutstuff.com/review3.shtml

      http://www.thetruthaboutstuff.com/articles.shtml 223 references with
      abstracts or full and partial texts
      _____________________________________________________



      ASE 3.3.1. "Exposure to Formaldehyde From Methanol in Aspartame

      As is described later, methanol is metabolized to formaldehyde, which is rapidly further metabolized."

      "For example, the demethylation of the caffeine found in one cup of coffee produces 30 mg of formaldehyde (Imbus, 1988)."

      ASE 151. Imbus, H. R. (1988) A review of regulatory risk assessment with formaldehyde as an example. Regulatory Toxicology and Pharmacology 8 , pp. 356-366. [ crossref ]

      [ http://lib.bioinfo.pl/pmid:3905920 [ not in PubMed ]

      J Allergy Clin Immunol. 1985 Dec; 76(6):831-40 3905920 (P,S,G,E,B)
      Clinical evaluation of patients with complaints related to formaldehyde exposure.
      H R Imbus

      Formaldehyde is a very widely used chemical in our present society and one with which every physician has had a first-hand experience in his early days of training in the anatomy laboratory. The National Institute of Occupational Safety and Health lists 52 occupations that expose people to formaldehyde. In recent years, however, the increasing use of formaldehyde resins in the production of building materials such as particleboard and urea-formaldehyde foam insulation has resulted in exposures of large numbers of people in nonoccupational settings. Consumer products such as cosmetics, cigarettes, textiles, furniture, draperies, and preservatives release formaldehyde. It is present in the outdoor atmosphere from products of combustion and automobile exhaust and likewise in the home from such things as gas cooking. These more widespread and increased exposures have resulted in concern regarding potential health effects. Therefore, it is likely that physicians have or will encounter patients who wish evaluations of a present or potential health effect from formaldehyde. This article is for the purpose of providing assistance in such evaluation.
      Mesh-terms: Acute Disease; Animals; Asthma :: chemically induced; Chronic Disease; Dermatitis, Contact :: etiology; Drug Hypersensitivity :: diagnosis; Drug Hypersensitivity :: etiology; Environmental Exposure; Formaldehyde :: toxicity; Human; Mice; Occupational Diseases :: chemically induced; Radioimmunoassay; Rats; Respiratory Function Tests; Respiratory Hypersensitivity :: diagnosis; Skin Tests; Time Factors;

      http://www.nclabor.com/osha/etta/indguide/ig31.pdf 38 page
      A Guide to Formaldehyde 1988 July H. R. Imbus
      Health & Hygiene, Inc.
      420 Gallimore Dairy Road, Greensboro, NC 27409
      910-655-1818
      www.Health-Hygiene.com/

      http://web.archive.org/web/19981205114939/health-hygiene.com/

      Merger Information

      Impact Health Services, Inc. Merged with Health & Hygiene/ELB

      In June, 1998, Impact Health Services, Inc., was merged with U.S. HealthWorks, parent company of Health & Hygiene/ELB. Impact Health Services is the largest mobile testing company providing hearing and respiratory surveillance services throughout the country. Founded in 1972, and operating out of Kansas City, Missouri, Impact has grown to serve over 5,000 client sites in all the 48 continental United States.

      Headquartered in Greensboro, North Carolina, Health & Hygiene/ELB, which was merged with U.S. HealthWorks in 1996, is one of the country's largest safety and health consulting companies offering consulting, training, products and services in the areas of industrial hygiene, occupational safety and ergonomics, training, occupational health, hearing conservation, respiratory surveillance, and OSHA compliance.

      As a result of the recent merger, Health & Hygiene/ELB and Impact Health Services have been merged to form U.S. HealthWorks-Preventive Services Division. U.S. HealthWorks has appointed Jeffrey C. Morrill, formerly CEO of Impact, as President of the new Preventive Services Division, Susan Megerson, formerly President of Impact, will be managing on-site testing operations, and Hank Barnum, formerly Sr. V.P.-Operations of Health & Hygiene/ELB, will be managing consulting operations.

      Company Overview

      U.S. HealthWorks-Preventive Services is the nation's largest training and consulting firm assisting employers and employer associations with the safety and health concerns of their workforce. We are now also the nation's largest provider of on-site medical surveillance and training services. Our mission is to reduce absenteeism and its inherent costs by helping to provide a workplace free of injuries and illnesses.

      This is accomplished by assisting with regulatory compliance programs (OSHA, DOT, JCAHO, EPA, etc.) and other preventative measures such as training, loss control, and elimination of substance abuse.

      Workplace absenteeism due to injuries and illnesses represents an enormous cost to employers in wages for the absent employee and replacement employee, medical costs, workers compensation premiums, regulatory fines, legal expenses, retraining and rehabilitation. U.S. HealthWorks-Preventive Services strives to significantly reduce these costs by emphasizing preventative services and products.
      Services Include:

      * Occupational Medicine
      * Ergonomics Consultation
      * Industrial Hygiene
      * Hearing Conservation
      * Respiratory Surveillance
      * On-Site Medical Monitoring
      -Audiometric Testing - Exclusive TTC -Test, Train Counsel approach
      -Pulmonary Testing
      -Medical Clearance for Respirator Use
      -Respirator Fit Testing
      * Health Management Software & Equipment
      * Safety Services
      * TIOSH -- Training Institute for Occupational Safety & Health
      * Data Management
      * On-Site Employee Training
      * Customized Hearing Protection and Communication Devices
      * Network of Occupational Health Clinics

      420 Gallimore Dairy Road
      Greensboro, NC 27409
      Phone 336-665-1818
      Fax 336-665-0847
      Revised June 25, 1998 ]


      From:

      opportunities re BA Magnuson, GA Burdock et al., Aspartame Safety Evaluation
      2007 Sept., Critical Reviews in Toxicology: Rich Murray 2008.07.11
      http://rmforall.blogspot.com/2008_07_01_archive.htm
      Friday, July 11, 2008
      http://groups.yahoo.com/group/aspartameNM/message/1550

      Bernadene A. Magnuson,
      George A. Burdock,
      John Doull,
      Robert M. Kroes, [deceased]
      Gary M. Marsh,
      Michael W. Pariza,
      Peter S. Spencer,
      William J. Waddell,
      Ronald Walker,
      Gary Murray Williams.
      "Aspartame: A Safety Evaluation Based on Current Use Levels, Regulations,
      and Toxicological and Epidemiological Studies,"
      Critical Reviews in Toxicology, 37(8), 629-727, 2007 Sept [415 references]

      http://www.utoronto.ca/nutrisci/faculty/Magnuson/
      Bernadene A. Magnuson, Ph.D.
      Adjunct Associate Professor, Department of Nutritional Sciences
      Senior Scientific and Regulatory Consultant, Cantox Health Science
      International, 2233 Argentia Road, Suite 308, Mississauga, ON L5N 2X7
      Tel: (905) 542 2900 Fax: (905) 542 1011 BMagnuson@...;
      _____________________________________________________



      "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 rmforall@...
      505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

      http://RMForAll.blogspot.com new primary archive

      http://groups.yahoo.com/group/aspartameNM/messages
      group with 133 members, 1,569 posts in a public archive

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