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

http://groups.yahoo.com/group/aspartame/messages
group with 1144 members, 23,083 posts in a public archive
_____________________________________________________