just wanted to add

when i was 15-17 years old, i was the right hand guy for a local moneys
mushroom producer in langley,,,

i did every step in the growing of mushrooms,,,  most important to this
production, is  ''sterilization''

keeping OUT bad spores was pertinent to a healthy crop.

everytime we entered each barn,,  we would spray our footwear, with
Formyldehyde!!!!  told not to get it on our hands!!!!!  ya right lame a.s  2
gallon pump sprayer leaked all over our hands when spraying,,,,

 i am sure i breathed in this crap,,, it was used alot, to kill anything
and keep it out of the sterilized barns,,,  with their heated /moisture
sweating,  it was easy for foreign items to grow inside,,, the hot wet
conditions,,,

i always wondered if this had anything to do with anything  for me????
cheers
bobbyD

ps -ever seen a button,white mushroom 1 foot in diameter???

new details on how formaldehyde and formic acid from methanol are
neurotoxic:  Chun Lai Nie, Rong Giao He, et al, PLoS ONE 2(7): e629
2007.07.18 Chinese Academy of Sciences, Beijing: Murray 20097.09.01
http://groups.yahoo.com/group/aspartameNM/message/1470

" Recent studies have shown that neurodegeneration is closely related
to misfolding and aggregation of neuronal tau. "

" The significant protein tau aggregation induced by formaldehyde and
the severe toxicity of the aggregated tau to neural cells may suggest
that toxicity of methanol and formaldehyde ingestion is related to tau
misfolding and aggregation. "

" Neuronal tau is an important protein in promoting and stabilizing
the microtubule system involved in cellular transport and neuronal
morphogenesis. "

" Both formaldehyde and acetaldehyde can go through the blood-brain
barrier and cause some lesions to CNS, especially our visual system
[38].

Clinically, the lethal dose of formaldehyde for human beings is about
0.08% in the circulation [39].

We have shown in the present study that formaldehyde can significantly
induce tau aggregation and polymerization at concentrations even lower
than 0.08%, the clinical dose of toxicosis. "

" Formaldehyde exposure leads to formation of DNA/protein crosslinks,
a major mechanism of DNA damage.

The DNA/protein crosslinks have been used as a measure of dose in drug
delivery [20].

Formaldehyde, as a crosslinking agent, also reacts with thiol and
amino groups, leading to protein polymerization [21], [22].

Furthermore, methanol ingestion is an important public health concern
because of the selective actions of its toxic metabolites,
formaldehyde and formic acid, on the retina, the optic nerves and the
central nervous system (CNS) [23].

Illicit consumption of industrial methylated spirits can cause severe
and even fatal illness [24].

In the liver and retina, methanol is oxidized by alcohol
dehydrogenase, resulting in formaldehyde.

In semicarbazide-sensitive amine oxidase (SSAO)-mediated pathogenesis
of Alzheimer's disease, formaldehyde interacts with ?-amyloids and
produces irreversibly cross-linked neurotoxic amyloid-like complexes
[21], [22], [25].

We have examined the role of formaldehyde in misfolding of protein tau
[26].

In particular, we investigated the toxicity of formaldehyde-induced
tau aggregates on human neuroblastoma cells (SH-SY5Y cell line) and
rat hippocampal cells [27].

The results showed that low concentrations (0.01-0.1%) of formaldehyde
are sufficient to induce formation of amyloid-like tau aggregates,
which can induce apoptosis of both SH-SY5Y and hippocampal cells.

This may be significant to understand the mechanism of chronic damage
caused by methanol toxicity and formaldehyde stress [18], [28].

However, we have still not known the mechanism of protein tau
aggregation in the presence of formaldehyde at low concentrations.

The present study concerns the characteristic of misfolding and
polymerization of extracellular and intracellular neuronal tau induced
by formaldehyde at low concentrations. "

http://www.plosone.org/article/fetchArticle.action?articleURI=info:doi/10.1371/j
ournal.pone.0000629
free full text

Formaldehyde at Low Concentration Induces Protein Tau into Globular
Amyloid-Like Aggregates In Vitro and In Vivo
Chun Lai Nie 1,
Yan Wei 1,
Xinyong Chen 2,
Yan Ying Liu 1,
Wen Dui 1,
Ying Liu 1,
Martyn C. Davies 2, Martyn.Davies@nottingham.ac.uk,
Saul J.B. Tendler 2,   Saul.Tendler@nottingham.ac.uk,
Rong Giao He 1*  herq@sun5.ibp.ac.cn,
1 State Key Laboratory of Brain and Cognitive Science, Institute of
Biophysics, Graduate School, Chinese Academy of Sciences, Chaoyang
District, Beijing, China,
2 Laboratory of Biophysics and Surface Analysis, School of Pharmacy,
The University of Nottingham, Nottingham, United Kingdom

Abstract

Recent studies have shown that neurodegeneration is closely related to
misfolding and aggregation of neuronal tau.

Our previous results show that neuronal tau aggregates in formaldehyde
solution and that aggregated tau induces apoptosis of SH-SY5Y and
hippocampal cells.

In the present study, based on atomic force microscopy (AFM)
observation, we have found that formaldehyde at low concentrations
induces tau polymerization whilst acetaldehyde does not.

Neuronal tau misfolds and aggregates into globular-like polymers in
0.01-0.1% formaldehyde solutions.

Apart from globular-like aggregation, no fibril-like polymerization
was observed when the protein was incubated with formaldehyde for 15
days.

SDS-PAGE results also exhibit tau polymerizing in the presence of
formaldehyde.

Under the same experimental conditions, polymerization of bovine serum
albumin (BSA) or ?-synuclein was not markedly detected.

Kinetic study shows that tau significantly misfolds and polymerizes in
60 minutes in 0.1% formaldehyde solution.

However, presence of 10% methanol prevents protein tau from
polymerization.

This suggests that formaldehyde polymerization is involved in tau
aggregation.

Such aggregation process is probably linked to the tau's special "worm-
like" structure, which leaves the ?-amino groups of Lys and thiol
groups of Cys exposed to the exterior.

Such a structure can easily bond to formaldehyde molecules in vitro
and in vivo.

Polymerizing of formaldehyde itself results in aggregation of protein
tau.

Immunocytochemistry and thioflavin S staining of both endogenous and
exogenous tau in the presence of formaldehyde at low concentrations in
the cell culture have shown that formaldehyde can induce tau into
amyloid-like aggregates in vivo during apoptosis.

The significant protein tau aggregation induced by formaldehyde and
the severe toxicity of the aggregated tau to neural cells may suggest
that toxicity of methanol and formaldehyde ingestion is related to tau
misfolding and aggregation.

Funding: This project was supported by NSFB (06J11),
the NSFC (Nos. 90206041, 30570536 and 30621004)
and 973-Project (2006CB500703 and 2006CB911003).

Competing interests: The authors have declared that no competing
interests exist.

Academic Editor: Christophe Herman, Baylor College of Medicine, United
States of America

Citation: Nie CL, Wei Y, Chen X, Liu YY, Dui W, et al. (2007)
Formaldehyde at Low Concentration Induces Protein Tau into Globular
Amyloid-Like Aggregates In Vitro and In Vivo. PLoS ONE 2(7): e629. doi:
10.1371/journal.pone.0000629

Received: March 5, 2007; Accepted: June 13, 2007; Published: July 18,
2007

Copyright: © 2007 Nie et al. This is an open-access article
distributed under the terms of the Creative Commons Attribution
License, which permits unrestricted use, distribution, and
reproduction in any medium, provided the original author and source
are credited.

* To whom correspondence should be addressed. E-mail:
herq@sun5.ibp.ac.cn

Introduction

Neuronal tau is an important protein in promoting and stabilizing the
microtubule system involved in cellular transport and neuronal
morphogenesis.
The tau molecule can be subdivided into an amino-terminal domain that
projects from the microtubule surface and a carboxy-terminal
microtubule-binding domain.
The discovery that incubation of bacterially expressed human tau with
sulphated glycosaminoglycans leads to bulk assembly of tau filaments
[1], making it possible to obtain structural information [2].
By using circular dichroism measurement, Schweer et al. have found
that protein tau lacks secondary structures and is considered in a
"worm-like" conformation with a high flexibility [3].
Therefore, the side-chains of amino acids such as Lys, Cys, Thr and
Ser are mostly exposed and vulnerable to chemical modification.

Recently, many laboratories have found that misfolding and aggregation
of protein tau are involved in neurodegeneration [2], [4] -- [6].

Protein tau has been found as the major component of paired helical
filaments in neurofibrillary tangles in the brains of Alzheimer's
patients, where abnormal hyper-phosphorylation induces tau to misfold
and form the paired helical filaments, depositing in the cytoplasm of
neurons [7] -- [10].

Recently, a great deal of evidence has demonstrated that oxidation and
glycation stresses are key causal factors of neuronal degenerative
diseases [11] -- [13].
Both of them inevitably produce a variety of unsaturated carbonyls as
intermediates, like malondialdehyde and 4-hydroxynonenal, which
usually cause carbonyl-amino crosslinking and lead to accumulation of
irreversible changes (like lipofuscin) related to various
neurodegenerative diseases in particular [14] -- [16].
Such carbonyl stress-related reactions (carbonylation) can form
unstable and reversible 1:1 amino-carbonyl (Shiff's base) compounds at
an early stage of protein modification [16], [17].
Carbonylation binds and blocks ?-/?- amino groups, and results in
changes in charge and conformation of a protein.

In order to investigate the relationship between carbonylation and
protein tau misfolding, the basic and simplest carbonyl compound
formaldehyde [18] has come into our attentions.

Formaldehyde is a common environmental agent found in paint, cloth,
exhaust gas and many other medicinal and industrial products [19].

Formaldehyde exposure leads to formation of DNA/protein crosslinks, a
major mechanism of DNA damage.

The DNA/protein crosslinks have been used as a measure of dose in drug
delivery [20].

Formaldehyde, as a crosslinking agent, also reacts with thiol and
amino groups, leading to protein polymerization [21], [22].

Furthermore, methanol ingestion is an important public health concern
because of the selective actions of its toxic metabolites,
formaldehyde and formic acid, on the retina, the optic nerves and the
central nervous system (CNS) [23].

Illicit consumption of industrial methylated spirits can cause severe
and even fatal illness [24].

In the liver and retina, methanol is oxidized by alcohol
dehydrogenase, resulting in formaldehyde.

In semicarbazide-sensitive amine oxidase (SSAO)-mediated pathogenesis
of Alzheimer's disease, formaldehyde interacts with ?-amyloids and
produces irreversibly cross-linked neurotoxic amyloid-like complexes
[21], [22], [25].

We have examined the role of formaldehyde in misfolding of protein tau
[26].

In particular, we investigated the toxicity of formaldehyde-induced
tau aggregates on human neuroblastoma cells (SH-SY5Y cell line) and
rat hippocampal cells [27].

The results showed that low concentrations (0.01-0.1%) of formaldehyde
are sufficient to induce formation of amyloid-like tau aggregates,
which can induce apoptosis of both SH-SY5Y and hippocampal cells.

This may be significant to understand the mechanism of chronic damage
caused by methanol toxicity and formaldehyde stress [18], [28].

However, we have still not known the mechanism of protein tau
aggregation in the presence of formaldehyde at low concentrations.

The present study concerns the characteristic of misfolding and
polymerization of extracellular and intracellular neuronal tau induced
by formaldehyde at low concentrations.....

Discussion

Clinical lethal dose of formaldehyde

Why did we investigate tau misfolding in the presence of formaldehyde
at low concentrations (0.01-0.1%)?

Methanol and ethanol are metabolized to formaldehyde and acetaldehyde
respectively in our hepatocytes and some neural cells [36], [37].

Both formaldehyde and acetaldehyde can go through the blood-brain
barrier and cause some lesions to CNS, especially our visual system
[38].

Clinically, the lethal dose of formaldehyde for human beings is about
0.08% in the circulation [39].

We have shown in the present study that formaldehyde can significantly
induce tau aggregation and polymerization at concentrations even lower
than 0.08%, the clinical dose of toxicosis.

The same low concentration of formaldehyde did not induce
polymerization of BSA though theoretically it will cause any protein
to polymerize if the concentration is high enough.

On the other hand, although it is known that acetaldehyde is acutely
toxic and would covalently bind to proteins and other macromolecules
[40], in our AFM and SDS-PAGE studies we did not observe tau
polymerization caused by acetaldehyde at the concentration range that
we studied (0.1-1%)......

Tau aggregation relating to methanol and formaldehyde toxicity

Methanol is an ocular toxicant, which causes visual dysfunction and
often leads to blindness after acute exposure.

However, physiological and biochemical changes responsible for the
toxicity have not yet been well understood [28].

According to a recent report, humans are uniquely sensitive to the
toxicity of methanol, as they have limited capacity to oxidize and
detoxify formic acid.

Thus, the toxicity of methanol in humans is characterized by formic
acidaemia, metabolic acidosis, blindness or serious visual impairment,
mild central nervous system depression and even death [23], [27],
[28].

However, methanol toxicosis induces progressive complications to CNS.

It is hard to explain the progressively chronic damage by local
accumulation of formic acid alone.

Therefore, the potential effect of formaldehyde on protein misfolding
may be significant, although formaldehyde remains in the human body
for only a short time.

In semicarbazide-sensitive amine oxidase (SSAO)-mediate pathogenesis
of Alzheimer's disease, formaldehyde interacts with ?-amyloids and
produces irreversibly cross-linked neurotoxic amyloid-like complexes
[21], [22], [25].

Our studies showed that formaldehyde induced neuronal tau to
aggregate.

The amyloid-like tau induces apoptosis of SY5Y and hippocampal cells
[27].

In fact, chemically, formaldehyde reacts with thiol and amino groups
instantly, resulting in subsequent misfolding of neuronal tau (Figure
11).

This suggests that amyloid-like tau is involved in methanol toxicosis,
especially the damage of neurons and the resulted complications after
exposure to formaldehyde.

Although there have been many studies on methanol and formaldehyde
intoxication [23], [24], none of them has addressed the contribution
of protein misfolding to the pathological mechanism, in particular the
effect of formaldehyde on protein conformation and polymerization.

Interestingly, neurofibrillary tangles have been found in brains of
chronic alcoholics possessing neuropathological signs of thiamine-
deficiency [40], [47].

This suggests that tau misfolding may be involved in the alcohol-
induced pathological pathway.

Khlistunova and his colleagues found that neuronal tau repeat domain
could aggregate in vivo and was toxic to neuronal cells.

The degree of tau aggregation and toxicity depends on the propensity
of the ?-structure [2], [48].

In the present study, we have demonstrated that amyloid-like
intracellular tau aggregates could induce cell apoptosis, a similar
result as that obtained for extracellular amyloid or ?-synuclein [49]
-- [51].

This suggests that an enriched ?-sheet structure is important to
amyloid-like protein aggregation and neurotoxicity.

In our experiments, a low concentration of formaldehyde induced both
extracellular and intracellular tau proteins to aggregate into cell-
toxic amyloid-like granular aggregates [27].

It appears to provide a new mechanism for triggers of tauopathies in
the formaldehyde toxicosis.....

Acknowledgments

We thank Ms. Ya-Qun Zhang for technical assistance and Dr. Ya-Jie Xu
for providing the clone of HA-tau40.
Author Contributions
Conceived and designed the experiments: RH. Performed the experiments:
CN YW YL WD. Analyzed the data: CN. Wrote the paper: CN RH YL XC MD
ST.

References.....

#19 Quievryn G, Zhitkovich A. (2000) Loss of DNA-protein crosslinks
from formaldehyde-exposed cells occurs through spontaneous hydrolysis
and an active repair process linked to proteosome function.
Carcinogenesis 21: 1573 -- 1580. Find this article online

#20 Heck H, Casanova M. (1999) Pharmacodynamics of formaldehyde:
applications of a model for the arrest of DNA replication by DNA-
protein cross-links. Toxicol Appl Pharmacol 160: 86 -- 100. Find this
article online

#21 Yu PH, Lu LX, Fan H, Kazachkov M, Jiang ZJ, et al. (2006)
Involvement of semicarbazide-sensitive amine oxidase-mediated
deamination in lipopolysaccharide-induced pulmonary inflammation. Am J
Pathol 168: 718 -- 726. Find this article online

#22 Yu PH. (2001) Involvement of cerebrovascular semicarbazide-
sensitive amine oxidase in the pathogenesis of Alzheimer's disease and
vascular dementia. Med Hypotheses 57: 175 -- 179. Find this article
online

#23 Eells JT, Henry MM, Lewandowski MF, Seme MT, Murray TG. (2000)
Development and characterization of a rodent model of methanol-induced
retinal and optic nerve toxicity. Neurotoxicology 21: 321 -- 330. Find
this article online

#24 Dayan AD, Paine AJ. (2001) Mechanisms of chromium toxicity,
carcinogenicity and allergenicity: review of the literature from 1985
to 2000. Hum Exp Toxicol 20: 439 -- 451. Find this article online

#25 Gubisne-Haberle D, Hill W, Kazachkov M, Richardson JS, Yu PH.
(2004) Protein cross-linkage induced by formaldehyde derived from
semicarbazide-sensitive amine oxidase-mediated deamination of
methylamine. J Pharmacol Exp Ther 310: 1125 -- 1132. Find this article
online

#26 Nie CL, Zhang W, Zhang D, He RQ. (2005) Changes in conformation of
human neuronal tau during denaturation in formaldehyde solution.
Protein Pept Lett 12: 75 -- 78. Find this article online

#27 Nie CL, Wang XS, Liu Y, Perrett S, He RQ. (2007) Amyloid-like
aggregates of neuronal tau induced by formaldehyde promote apoptosis
of neuronal cells. BMC Neurosci 8: 9. Find this article online

#28 Garner CD, Lee EW, Louis-Ferdinand RT. (1995) Muller cell
involvement in methanol-induced retinal toxicity. Toxicol Appl
Pharmacol 130: 101 -- 107. Find this article online

#32 Pomerantz M, Bittner S, Khader SB.  (1982) "Formaldehyde
semicarbazone." J Org Chem 47: 2217 -- 2218. Find this article online

#36 Barceloux DG, Bond GR, Krenzelok EP, Cooper H, Vale JA. (2002)
American Academy of Clinical Toxicology practice guidelines on the
treatment of methanol poisoning. J Toxicol Clin Toxicol 40: 415 --
446. Find this article online

#37 Valentine WM. (1990) Toxicology of selected pesticides, drugs, and
chemicals. Short-chain alcohols. Vet. Clin. North Am. Small Anim.
Pract 20: 515 -- 523. Find this article online

#38 Shcherbakova LN, Tel'pukhov VI, Trenin SO, Bashilov IA, Lapkina
TI.  (1986) [Permeability of the blood-brain barrier to intra-arterial
formaldehyde]. Biull Eksp Biol Med 102: 573 -- 575.

#39 Erkrath KD, Adebahr G, Kloppel A.  (1981) [Lethal intoxication by
formalin during dialysis (author's transl)]. Z Rechtsmed 87: 233 --
236. Find this article online

#40 Niemela O. (1999) Aldehyde-protein adducts in the liver as a
result of ethanol-induced oxidative stress. Front Biosci 4: D506  --
D513. Find this article online

#45 Jiang W, Schwendeman SP. (2000) Formaldehyde-mediated aggregation
of protein antigens: comparison of untreated and formalinized model
antigens. Biotechnol Bioeng 70: 507 -- 517. Find this article online

#46 Rait VK, O'Leary TJ, Mason JT. (2004) Modeling formalin fixation
and antigen retrieval with bovine pancreatic ribonuclease A: I-
structural and functional alterations. Lab Invest 84: 292 -- 299. Find
this article online

#47 Cullen KM, Halliday GM.  (1995) Neurofibrillary tangles in chronic
alcoholics. Neuropathol Appl Neurobiol 21: 312 -- 318. Find this
article online.....
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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/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@catholic.ac.kr

http://groups.yahoo.com/group/aspartameNM/message/1143
methanol (formaldehyde, formic acid) disposition: Bouchard M et al,
full
plain text, 2001: substantial sources are degradation of fruit
pectins,
liquors, aspartame, smoke: Murray 2005.04.02
http://www.toxsci.oupjournals.org/cgi/content/full/64/2/169

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). The methanol is immediately released
into the body after drinking .
Within hours, the liver turns much of the methanol into formaldehyde,
and then much of that into formic acid, both of which in time
are partially eliminated as carbon dioxide and water.

However, about 30 % of the methanol remains in the body
as cumulative durable toxic metabolites of formaldehyde
and formic acid -- 37 mg daily,
a gram every month, accumulating in and affecting every tissue.

If only 10 % of the methanol is retained daily as formaldehyde,
that would give 12 mg daily formaldehyde accumulation -- about
60 times more than the 0.2 mg from 10 % retention
of the 2 mg EPA daily limit for formaldehyde in drinking water.

Bear in mind that the EPA limit for formaldehyde in drinking water is
1 ppm, or 2 mg daily for a typical daily consumption of 2 L of water.

http://groups.yahoo.com/group/aspartameNM/message/835
ATSDR: EPA limit 1 ppm formaldehyde in drinking water July 1999:
Murray 2002.05.30

This long-term low-level chronic toxic exposure leads to typical
patterns of increasingly severe complex symptoms,
starting with headache, fatigue, joint pain, irritability, memory
loss,
rashes, and leading to vision and eye problems, and even seizures.
In many cases there is addiction. Probably there are immune system
disorders, with a hypersensitivity to these toxins and other
chemicals.

http://groups.yahoo.com/group/aspartameNM/message/1464
13 mainstream research studies in 24 months showing aspartame
toxicity, also 3 relevant studies on methanol and formaldehyde: Murray
2007.08.17

http://groups.yahoo.com/group/aspartameNM/message/1468
Formaldehyde induced urticarial vasculitis in male medical student,
age 40, Michael Pellizzari, Gillian Marshman, Flinders U.,
Australasian J. Dermatol. 2007 Aug: Murray 2007.08.29

http://groups.yahoo.com/group/aspartameNM/message/1453
Souring on fake sugar (aspartame), Jennifer Couzin,
Science 2007.07.06: 4 page letter to FDA from 12 eminent
USA toxicologists re two Ramazzini Foundation
cancer studies 2007.06.25: Murray 2007.07.18

http://groups.yahoo.com/group/aspartameNM/message/1457
aspartame bans, tis more an avalanche than a trend...: Rich Murray
2007.08.17

So far, USA print and broadcast media are deaf, blind, and dumb,
regarding recent major bans of aspartame and MSG in the UK and EU.

The EU Parliament voted July 12 to ban artificial sweeteners
in newly born and infant foods.

On May 15 four huge UK supermarket chains announced bans
of aspartame and MSG, food dyes, and many additives
to protect kids from ADHD --
Sainsbury, Tesco, Marks & Spencer, and ASDA, a unit of WalMart.

May 31: Coca-Cola and the much larger Cargill Inc.,
after years of secret development, with 24 patents,
will soon sell rebiana (stevia) in drinks and food
in the many nations where it is approved as a sweetener --
for decades a major sweetener in Japan, China, Korea, Taiwan,
Thailand, Malasia, Saint Kitts, Nevis,
Brazil, Peru, Paraguay, Uruguay, and Israel,
and an approved supplement in USA, Australia, and Canada,
according to Wikipedia.

http://groups.yahoo.com/group/aspartameNM/message/1454
recent research and news re aspartame and stevia: Murray 2007.08.16

"Of course, everyone chooses, as a natural priority,
to actively find, quickly share, and positively act
upon the facts about healthy and safe food, drink,
and environment."

Rich Murray, MA Room For All rmforall@comcast.net
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://groups.yahoo.com/group/aspartameNM/messages
group with 82 members, 1,470 posts in a public,
searchable archive http://RMForAll.blogspot.com

http://groups.yahoo.com/group/aspartameNM/message/1395
Aspartame Controversy, in Wikipedia democratic
encyclopedia, 72 references (including AspartameNM # 864
and 1173 by Murray, brief fair summary of much more research:
Murray 2007.01.01

http://groups.yahoo.com/group/aspartameNMmessage/1451
Artificial sweeteners (aspartame, sucralose) and coloring
agents will be banned from use in newly-born and baby foods,
the European Parliament decided: Latvia ban in schools 2006:
Murray 2007.07.12

http://groups.yahoo.com/group/aspartameNMmessage/1437
stevia to be approved and cyclamates limited by
Food Standards Australia New Zealand:
JMC Geuns critiques of two recent stevia studies by Nunes:
Murray 2007.05.29

http://groups.yahoo.com/group/aspartameNM/message/1427
more from The Independent, UK, Martin Hickman, re ASDA
(unit of Wal-Mart Stores) and Marks & Spencer ban of
aspartame, MSG, artificial chemical additives and dyes
to prevent ADHD in kids: urray 2007.05.16
http://news.independent.co.uk/uk/health_medical/article2548747.ece

http://groups.yahoo.com/group/aspartameNM/message/1426
ASDA (unit of Wal-Mart Stores WMT.N) and Marks & Spencer
will join Tesco and also Sainsbury to ban and limit
aspartame, MSG, artificial flavors dyes preservatives additives,
trans fats, salt "nasties" to protect kids from ADHD:
leading UK media: Murray 2007.05.15

http://groups.yahoo.com/group/aspartameNM/message/1438
Coca-Cola and Cargill Inc., after years of development,
with 24 patents, will soon sell rebiana (stevia)
in drinks and foods: Murray 2007.05.31

www.ncbi.nlm.nih.gov/sites/entrez search PubMed
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