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
- 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@...
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
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.
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.
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
Sunday, February 24, 2008
Alcoholism: Clinical and Experimental Research
Volume 31 Issue 12 Page 2114-2120, December 2007
Bhushan M. Kapur, b.kapur@...;
Arthur C. Vandenbroucke, PhD, FCACB
Denis C. Lehotay, dlehotay@...;
Peter L. Carlen carlen@...;
(2007) Formic Acid, a Novel Metabolite of Chronic Ethanol Abuse, Causes
Neurotoxicity, Which Is Prevented by Folic Acid
Alcoholism: Clinical and Experimental Research 31 (12), 2114-2120.
Methanol is endogenously formed in the brain and is present as a congener in
most alcoholic beverages.
Because ethanol is preferentially metabolized over methanol (MeOH) by
alcohol dehydrogenase, it is not surprising that MeOH accumulates in the
This suggests that the alcohol-drinking population will have higher levels
of MeOH's neurotoxic metabolite, formic acid (FA).
FA elimination is mediated by folic acid.
Neurotoxicity is a common result of chronic alcoholism.
This study shows for the first time that FA, found in chronic alcoholics, is
neurotoxic and this toxicity can be mitigated by folic acid administration.
To determine if FA levels are higher in the alcohol-drinking population and
to assess its neurotoxicity in organotypic hippocampal rat brain slice
Serum and CSF FA was measured in samples from both ethanol abusing and
control patients, who presented to a hospital emergency department. [ CSF =
Cerebral Spinal Fluid ]
FA's neurotoxicity and its reversibility by folic acid were assessed using
organotypic rat brain hippocampal slice cultures using clinically relevant
Serum FA levels in the alcoholics (mean ± SE: 0.416 +- 0.093 mmol/l, n = 23)
were significantly higher than in controls (mean ± SE: 0.154 +- 0.009
mmol/l, n = 82) (p < 0.0002).
FA was not detected in the controls' CSF (n = 20), whereas it was >0.15
mmol/l in CSF of 3 of the 4 alcoholic cases.
Low doses of FA from 1 to 5 mmol/l added for 24, 48 or 72 hours to the rat
brain slice cultures caused neuronal death as measured by propidium iodide
When folic acid (1 umol/l) was added with the FA, neuronal death was
prevented. [ umol = micromole ]
Formic acid may be a significant factor in the neurotoxicity of ethanol
This neurotoxicity can be mitigated by folic acid administration at a
clinically relevant dose.
Formic Acid, Folic Acid, Methanol, Neurotoxicity, Alcoholism.
From the Department of Clinical Pathology (BMK), Sunnybrook Health Science
Centre, Division of Clinical Pharmacology and Toxicology, The Hospital for
Sick Children, Toronto, Ontario, Canada;
St. Michael's Hospital (ACV), Toronto, Canada;
Department of Laboratory Medicine and Pathobiology, (BMK, ACV), Faculty of
Medicine, University of Toronto, Toronto, Ontario, Canada;
Departments of Medicine (Neurology) and Physiology (YA, PLC), Toronto
Western Research Institute, University of Toronto, Toronto, Ontario, Canada;
and University of Saskatchewan (DLC), Saskatchewan, Canada.
Received for publication May 1, 2007; accepted September 24, 2007.
Reprint requests: Dr. Bhushan M. Kapur, Department of Clinical Pathology,
Sunnybrook Health Science Centre, 2075 Bayview Ave, Toronto, Ontario, M4N
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.
detailed critiques of JE Garst folic acid proposals by experts HJ Roberts
and M Alemany: Murray 2008.03.20
Thursday, March 20, 2008
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
Wednesday, March 19, 2008
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
Wednesday, March 19, 2008
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
Wednesday, March 19, 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 2007.11.18
Wednesday, November 14, 2007
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
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
Monte WC., Is your Diet Sweetener killing you? Fitness Life. 2007 Nov; 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
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.
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.
* Occupational Medicine
* Ergonomics Consultation
* Industrial Hygiene
* Hearing Conservation
* Respiratory Surveillance
* On-Site Medical Monitoring
-Audiometric Testing - Exclusive TTC -Test, Train Counsel approach
-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
Revised June 25, 1998 ]
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
Bernadene A. Magnuson,
George A. Burdock,
Robert M. Kroes, [deceased]
Gary M. Marsh,
Michael W. Pariza,
Peter S. Spencer,
William J. Waddell,
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]
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
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
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