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
http://rmforall.blogspot.com/2009_05_01_archive.htm
Tuesday, May 12, 2009
http://groups.yahoo.com/group/aspartameNM/message/1572


"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 140 members, 1,572 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1191 members, 23,458 posts in a public archive
_____________________________________________________


http://medicine.plosjournals.org/perlserv/?request=get-document&doi=10.1371/jour\
nal.pmed.1000077
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
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.faslink.org/Formic%20Acid%20Kapur.htm

Brief Summary:

Methanol in small amounts is present along with ethanol in beverage
alcohol.
[Murray: and about the same amounts from aspartame diet sodas]

The body's natural enzymes preferentially metabolize ethanol while
methanol breaks down into highly neurotoxic Formic Acid.

Use of high levels of Folic Acid was found to inhibit brain damage
caused by the methanol.

The use of Folic Acid during pregnancy has been recommended
for several years to prevent neural tube defects.

However, this study indicates that even higher levels of Folic Acid
can be very beneficial to the developing baby, particularly where
alcohol exposure is a factor.

Folic Acid is mandated as an additive to all flour sold in Canada.

The debate has begun on its required addition to all beverage
alcohol to help mitigate damage caused to both infants and adults.


Formic Acid in the Drinking patient and the expectant mother
Dr. Bhushan M. Kapur
Departments of Laboratory Medicine,
St. Michael's Hospital , Toronto, Ontario, Canada

Abstract

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.

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.


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@... .


http://groups.yahoo.com/group/aspartameNM/message/1490
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

http://groups.yahoo.com/group/aspartameNM/message/1340
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
http://rmforall.blogspot.com/2008_02_01_archive.htm
Monday, February 11, 2008
http://groups.yahoo.com/group/aspartameNM/message/1517

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


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.

http://groups.yahoo.com/group/aspartameNM/message/1469
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

http://groups.yahoo.com/group/aspartameNM/message/1052
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

http://europa.eu.int/comm/food/fs/sc/scf/out96_en.pdf

"...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.

http://groups.yahoo.com/group/aspartameNM/message/1286
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
volunteers.
Experiments were made during the morning after the subjects had
consumed 1000-1500 ml red wine
(9.5 % w/v ethanol, 100 mg/l methanol)
the previous evening. [ 100 to 150 mg methanol ]
The washout of methanol from the body
coincided with the onset of hangover.
The concentrations of ethanol and methanol in blood were
determined indirectly by analysis of end-expired alveolar air.
In the morning when blood-ethanol dropped
below the Km of liver alcohol dehydrogenase (ADH)
of about 100 mg/l (2.2 mM),
the disappearance half-life of ethanol was 21, 22, 18 and 15 min.
in 4 test subjects respectively.
The corresponding elimination half-lives of methanol
were 213, 110, 133 and 142 min. in these same individuals.
The experimental design outlined in this paper can be used
to obtain useful data on elimination kinetics of methanol
in human volunteers without undue ethical limitations.
Circumstantial evidence is presented to link methanol
or its toxic metabolic products, formaldehyde and formic acid,
with the pathogenesis of hangover. PMID: 3588516


Thrasher (2001): "The major difference is that the Japanese
demonstrated the incorporation of FA and its metabolites
into the placenta and fetus.
The quantity of radioactivity remaining in maternal and fetal tissues
at 48 hours was 26.9 % of the administered dose." [ Ref. 14-16 ]

Arch Environ Health 2001 Jul-Aug; 56(4): 300-11.
Embryo toxicity and teratogenicity of formaldehyde. [100 references]
Thrasher JD, Kilburn KH. 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
http://rmforall.blogspot.com/2008_01_01_archive.htm
Wednesday, January 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1508

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
2008.07.18
http://rmforall.blogspot.com/2008_07_01_archive.htm
Friday, July 18, 2008
http://groups.yahoo.com/group/aspartameNM/message/1553
___________________________________________________


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
http://rmforall.blogspot.com/2008_03_01_archive.htm
Thursday, March 27, 2008
http://groups.yahoo.com/group/aspartameNM/message/1533

"For example, diet soda and yogurt containing aspartame (Nutrasweet),
release formaldehyde in their natural biological degradation.

One of aspartame's metabolites, aspartic acid methyl ester, is
converted to methanol in the body, which is oxidized to formaldehyde
in all organs, including the liver and eyes. 22

Patients with a contact dermatitis to formaldehyde have been seen to
improve once aspartame is avoided. 22

Notably, the case that Hill and Belsito reported had a 6-month history
of eyelid dermatitis that subsided after 1 week of avoiding diet soda.
22"


Avoiding formaldehyde allergic reactions in children, aspartame,
vitamins, shampoo, conditioners, hair gel, baby wipes, Sharon E Jacob,
MD, Tace Steele, U. Miami, Pediatric Annals 2007 Jan.: eyelid contact
dermatitis, AM Hill, DV Belsito, 2003 Nov.: Murray 2008.03.27
http://rmforall.blogspot.com/2008_03_01_archive.htm
Thursday, March 27, 2008
http://groups.yahoo.com/group/aspartameNM/message/1532

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
http://rmforall.blogspot.com/2008_07_01_archive.htm
Friday, July 11, 2008
http://groups.yahoo.com/group/aspartameNM/message/1550
____________________________________________________


http://www.eurekalert.org/pub_releases/2009-05/plos-pfa050609.php

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

PRESS-ONLY PREVIEW OF THE ARTICLE:
http://www.plos.org/press/plme-06-05-bukowski.pdf

READ THE EDITORS' SUMMARY OF THE PAPER:
http://www.plos.org/press/plme-06-05-bukowski-summary.pdf

CONTACT:
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:

IN YOUR COVERAGE PLEASE USE THIS URL TO PROVIDE ACCESS TO THE FREELY
AVAILABLE PAPER:
http://medicine.plosjournals.org/perlserv/?request=get-document&doi=10.1371/jour\
nal.pmed.1000077

PRESS-ONLY PREVIEW OF THE ARTICLE:
http://www.plos.org/press/plme-06-05-fisk.pdf

CONTACT:
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@...

http://www.plos.org/press/plme-06-05-bukowski-summary.pdf

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
pregnancy.

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@...>;
Lorraine.Dugoff@...;
Ilan.Timor@...;
Stephen_Carr@...;
honor_wolfe@...;
____________________________________________________