THIRD STUDY BY EXPERT GREEK TEAM OF NEUROTOXICITY IN INFANT RATS BY ASPARTAME (OR ITS PARTS, METHANOL, PHENYLALANINE, ASPARTIC ACID)

Compiled By Rich Murray, MA
Room For All
1943 Otowi Road
Santa Fe, New Mexico 87505 USA
Telephone: 505-501-2298
E-Mail: rmforall@comcast.net
Web Site: http://health.groups.yahoo.com/group/aspartameNM



Posted: 05 September 2007


Subject: Third study by expert Greek team of neurotoxicity in infant rats by aspartame (or its parts, methanol, phenylalanine, aspartic acid), KH Schulpis et al, Food Chem Toxicol 2007.06.16: Murray 2007.08.05


Third study by expert Greek team of neurotoxicity in infant rats by aspartame (or its parts, methanol, phenylalanine, aspartic acid), KH Schulpis et al, Food Chem Toxicol 2007.06.16: Murray 2007.08.05
http://groups.yahoo.com/group/aspartameNM/message/1459


Food Chem Toxicol. 2007 Jun 16;[Epub ahead of print]
The effect of aspartame metabolites on the suckling rat frontal cortex acetylcholinesterase. An in vitro study.
Simintzi I,
Schulpis KH,
Angelogianni P,
Liapi C,
Tsakiris S.
Department of Experimental Physiology, Medical School, University of Athens
P.O. Box 65257, GR 15401 Athens, Greece.

Aspartame (ASP) consumption is suggested to be implicated with muscarinic dysfunction.

The aim of this work was to evaluate the effect of ASP and its metabolites on acetylcholinesterase (AChE) activity in rat frontal cortex and pure enzyme.

Rat frontal cortex homogenate or pure enzyme AchE (eel E. Electricus) were incubated with ASP and each of ASP components, phenylalanine (Phe), aspartic acid (asp), and methanol (MeOH) for 1h at 37 degrees C.

AChE was measured spectrophotometrically.

The results showed that incubation of rat tissue or pure enzyme with the sum of ASP metabolites, as reported to be found in the CSF after 150 or 200mg/kg ASP consumption, inhibited frontal cortex and pure AChE about -11% to -29% (p<0.001).

Asp, Phe or MeOH concentrations related to their CSF levels after ingestion of abuse or toxic ASP doses, when separately incubated with frontal cortex or pure AChE, resulted in a significant decrease of the enzyme activities.

In conclusion:

ASP compounds may directly and/or indirectly act on the frontal cortex AChE.

High or toxic doses of the sweetener remarkably decreased the enzyme activity.

If this in vitro finding comes into human reality, it may be suggested that cholinergic symptoms are related to the consumption of the above ASP doses. PMID: 17673349

http://groups.yahoo.com/group/aspartameNMmessage/1447
Second study by expert Greek team of neurotoxicity in infant rats by aspartame (or its parts, methanol, phenylalanine, aspartic acid), KH Schulpis et al, Toxicology 2007.05.18: Murray 2007.07.04

Toxicology. 2007 May 18; [Epub ahead of print]
l-Cysteine and glutathione restore the reduction of rat hippocampal Na(+), K(+)-ATPase activity induced by aspartame metabolites.
Simintzi I,
Schulpis KH,
Angelogianni P,
Liapi C,
Tsakiris S.
Department of Experimental Physiology
Medical School, Athens University
P.O. Box 65257, GR-15401 Athens, Greece.

Studies have implicated aspartame (ASP) ingestion in neurological problems.

The aim of this study was to evaluate hippocampal Na(+),K(+)-ATPase and Mg(2+)-ATPase activities after incubation with ASP or each of ASP metabolites, phenylalanine (Phe), methanol (MeOH) and aspartic acid (asp) separately.

Suckling rat hippocampal homogenates or pure Na(+),K(+)-ATPase were incubated with ASP metabolites.

Na(+),K(+)-ATPase and Mg(2+)-ATPase activities were measured spectrophotometrically.

Incubation of hippocampal or pure Na(+),K(+)-ATPase with ASP concentrations (expected in the cerebrospinal fluid (CSF)) after ASP consumption of 34, 150 or 200 mg/kg resulted in hippocampal enzyme activity reduction of 26%, 50% or 59%, respectively, whereas pure enzyme was remarkably stimulated.

Moreover, incubation with hippocampal homogenate of each one of the corresponding in the CSF ASP metabolites related to the intake of common, high/abuse doses of the sweetener, inhibited Na(+),K(+)-ATPase, while pure enzyme was activated.

Hippocampal Mg(2+)-ATPase remained unaltered.

Addition of l-cysteine (cys) or reduced glutathione (GSH) in ASP mixtures, related with high/toxic doses of the sweetener, completely or partially restored the inactivated membrane Na(+),K(+)-ATPase, whereas the activated pure enzyme activity returned to normal.

CSF concentrations of ASP metabolites related to common, abuse/toxic doses of the additive significantly reduced rat hippocampal Na(+),K(+)-ATPase activity, whereas pure enzyme was activated. Cys or GSH completely or partially restored both enzyme activities. PMID: 17602817

Kleopatra H. Schulpis, MD, PhD.
Institute of Child Health
Aghia Sophia Children's Hospital
GR-11527 Athens (Greece)
Tel. +30 1 7708291, Fax +30 1 7700111
inchildh@otenet.gr


http://groups.yahoo.com/group/aspartameNMmessage/1444
Expert Greek group finds aspartame (or its parts, methanol, phenylalanine, aspartic acid) harm infant rat brain enzyme activity, KH Schulpis et al, Pharmacol. Res. 2007.05.13: Murray 2007.06.23

Pharmacol Res. 2007 May 13; [Epub ahead of print]
The effect of aspartame on acetylcholinesterase activity in hippocampal homogenates of suckling rats.
Simintzi I,
Schulpis KH,
Angelogianni P,
Liapi C,
Tsakiris S.
Department of Experimental Physiology
Medical School, University of Athens
P.O. Box 65257, GR-15401 Athens, Greece.

BACKGROUND:

Neurological disturbances have been implicated with aspartame (ASP) consumption, and the cholinergic system with acetylcholinesterase (AChE) seems actively involved.

AIM:

To evaluate the effect of ASP and its metabolites on rat hippocampal AChE activity.

METHODS:

Hippocampal homogenate or pure enzyme AChE (eel E. electricus) was incubated with the sum or each of ASP components, phenylalanine (Phe), aspartic acid (asp) and methanol (MeOH) for 1 h at 37 degrees C.

AChE activity was measured spectrophotometrically.

RESULTS:

Incubation of rat tissue or pure enzyme with the sum of ASP metabolites in concentrations in CSF (the concentrations were calculated according to the CSF/plasma concentration ratios) following 150 or 200 mgkg(-1) of ASP consumption, resulted in significant enzyme activity reductions of 25 and 31% for hippocampal AChE and 11% (p<0.01) and 19% for pure enzyme, respectively.

Aspartic acid concentrations of 0.42 or 0.56 mM significantly reduced the enzyme activities by 13 and 20% for hippocampal AChE and 15 and 18% for pure enzyme, respectively.

Phe concentrations of 0.042 or 0.083mM decreased the enzyme activity by 12% (p<0.01) and 20% (p<0.001) for hippocampal AchE and 15 and 18% (p<0.001) for pure enzyme, respectively.

Methanol concentrations of 0.60 or 0.80 mM remarkably inhibited hippocampal AChE by about 18 and 22% and pure enzyme by about 14 and 20%, respectively.

CONCLUSIONS:

Low concentrations of ASP components had no effect on hippocampal and pure AChE activity, whereas high or toxic concentrations remarkably decreased both enzyme activities.

Muscarinic symptoms may be related to the latter concentrations of ASP metabolites. PMID: 17580119

Kleopatra H. Schulpis, MD, PhD.
Institute of Child Health
Aghia Sophia Children's Hospital
GR-11527 Athens (Greece) Tel. +30 1 7708291, Fax +30 1 7700111
inchildh@otenet.gr


Metab Brain Dis. 2006 Mar; 21(1): 21-8. Epub 2006 May 6.
The effect of in vitro homocystinuria on the suckling rat hippocampal acetylcholinesterase.
Schulpis KH,
Kalimeris K,
Bakogiannis C,
Tsakiris T,
Tsakiris S.
Inborn Errors of Metabolism Department
Institute of Child Health Research Center
Aghia Sophia Children's Hospital, Athens, Greece.

Homocystinuria is due to enzymatic deficiencies resulting in elevated blood levels of homocysteine (Hcy), homocystine (Hci), and/or methionine (Met) and the clinical presentation of mental retardation, seizures, and cardiovascular disease.

Since these symptoms may be closely implicated with acetylcholinesterase (AChE) activity, we aimed to investigate whether this metabolic disorder affects the hippocampal AChE activity in 21 days suckling Wistar rat hippocampus.

Various concentrations of Hcy, Hci (0.05-0.5 mM), or Met (0.05-2 mM)

as well as Mixture A (Mix A) (0.3 mM (Hcy)+0.2 mM (Hci)+1.0 mM (Met) = in vitro cystathionine beta-synthase deficiency homocystinuria)

Mix B1 (Hcy 0.3 mM + Hci 0.2 mM = in vitro severe methylenetetrahydrofolate reductase deficiency homocystinuria)

or Mix B2 (Hcy 0.1 mM+Hci 0.05 mM = in vitro mild methylenetetrahydrofolate reductase deficiency homocystinuria)

were preincubated with homogenized hippocampii or with eel Electrophorus electricus pure AChE.

AChE was evaluated spectrophotometrically.

Hcy or Met stimulated hippocampal AChE by 50% (p < 0.001) at low concentrations of the amino acids (up to 0.3-0.5 mM), whereas Hci inhibited the enzyme by 40% (p < 0.001).

Mix A, Mix B1, or Mix B2 activated hippocampal AchE by 40, 30, (p < 0.001), and 12% (p < 0.01), respectively.

In contrast, the S-containing amino acids, Mix A, Mix B1, Mix B2 failed to affect the pure AChE activity.

CONCLUSIONS:

a) The presence of -SH group in Hcy and Met may result in hippocampal AChE stimulation and the redox isomer Hci in the inhibition of the enzyme, probably by producing free radicals,

and b) The SH-amino acids seem to affect the hippocampal enzyme indirectly, possibly by lipid(s)-protein modifications(s) and Hci by inducing oxidative stress, since no effect was observed on pure AChE activity. PMID: 16773467


http://groups.yahoo.com/group/aspartameNM/message/1279
All three aspartame metabolites harm human erythrocyte [red blood cell] membrane enzyme activity, KH Schulpis et al, two studies in 2005, Athens, Greece, 2005.12.14: 2004 research review, RL Blaylock: Murray 2006.01.14

"High or abuse concentrations of ASP hydrolysis products significantly decreased the membrane enzyme activity, which was completely or partially prevented by L-cysteine or reduced GSH."

[ Definition of Erythrocyte
Erythrocyte:
A cell that contains hemoglobin and can carry oxygen to the body. Also called a red blood cell (RBC). The reddish color is due to the hemoglobin. Erythrocytes are biconcave in shape, which increases the cell's surface area and facilitates the diffusion of oxygen and carbon dioxide. This shape is maintained by a cytoskeleton composed of several proteins. Erythrocytes are very flexible and change shape when flowing through capillaries. Immature erythrocytes, called reticulocytes, normally account for 1-2 percent of red cells in the blood. ]

Eur J Clin Nutr. 2005 Dec 14; [Epub ahead of print]
The effect of L-cysteine and glutathione on inhibition of Na(+), K(+)-ATPase activity by aspartame metabolites in human erythrocyte [red blood cell] membrane.
Schulpis KH, Kleopatra H. Schulpis, MD, PhD.
Institute of Child Health, Aghia Sophia Children's Hospital
GR-11527 Athens (Greece) +30 1 7708291, Fax +30 1 7700111
inchildh@otenet.gr
Papassotiriou I, biochem@paidon-agiasofia.gr
Tsakiris T,
Tsakiris S. Stylianos Tsakiris. stsakir@cc.uoa.gr
1 Institute of Child Health, Research Center
'Aghia Sophia' Children's Hospital, Athens, Greece.
ggbriass@med.uoc.gr ersi_voskaridou@yahoo.com mmoschov@med.uoa.gr siahanidou@hotmail.com


Background:

Reports have implicated Aspartame
(N-L-a-aspartyl-L-phenylalanine methyl ester, ASP) in neurological problems.

Aim:

To evaluate Na(+), K(+)-ATPase activities in human erythrocyte [red blood cell] membranes after incubation with the ASP metabolites, phenylalanine (Phe), methanol (MeOH) and aspartic acid (Asp).

Methods:

Erythrocyte [red blood cell] membranes were obtained from 12 healthy individuals and were incubated at 37 degrees C for 1 h with the sum or each of the ASP metabolites separately, which are commonly measured in blood after ASP ingestion.

Na(+), K(+)-ATPase and Mg(2+)-ATPase activities were measured spectrophotometrically.

Results:

Membrane Mg(2+)-ATPase activity was not altered.

The sum of ASP metabolite concentrations corresponding to 34, 150 or 200 mg/kg of the sweetener ingestion resulted in an inhibition of the membrane Na(+), K(+)-ATPase by -30, -40, -48%, respectively.

MeOH concentrations of 0.14, 0.60 or 0.80 mM decreased the enzyme activity by -25, -38, -43%, respectively.

Asp concentrations of 2.80, 7.60 or 10.0 mM inhibited membrane Na(+), K(+)-ATPase by -26, -40, -46%, respectively.

Phe concentrations of 0.14, 0.35 or 0.50 mM reduced the enzyme activity by -24, -44, -48%, respectively.

Preincubation with L-cysteine or reduced glutathione (GSH) completely or partially restored the inhibited membrane Na(+), K(+)-ATPase activity by high or toxic ASP metabolite concentrations.

Conclusions:

Low concentrations of ASP metabolites had no effect on Na(+), K(+)-ATPase activity.

High or abuse concentrations of ASP hydrolysis products significantly decreased the membrane enzyme activity, which was completely or partially prevented by L-cysteine or reduced GSH. [reduced glutathione]

European Journal of Clinical Nutrition advance online publication, 14 December 2005; doi:10.1038/sj.ejcn.1602355. PMID: 16391576


http://groups.yahoo.com/group/aspartameNM/message/1213
Aspartame (methanol, phenylalanine, aspartic acid) effects, detailed expert studies in 2005 Aug and 1998 July, Tsakiris S, Schulpis KH, Karikas GA, Kokotos G, Reclos RJ, et al, Aghia Sophia Children's Hospital, Athens, Greece: Murray 2005.09.09

[ The lowest dose level tested, 34 mg aspartame per kg body weight, well below the FDA daily human limit of 50 mg/kg, 16 12-oz cans, caused enzyme activity reduction by -33% in human red blood cell membranes. ]

However, a missed opportunity in both studies is that the inevitable, extremely and cumulatively toxic products of methanol in the human body, formaldehyde and formic acid, which are responsible for the toxicity of methanol, were not independently tested.

"It is concluded that low concentrations of ASP metabolites had no effect on the [human red blood cell] membrane enzyme activity, whereas high or toxic concentrations partially or remarkably decreased the [human red blood cell] membrane AChE activity, respectively. Additionally, neurological symptoms, including learning and memory processes, may be related to the high or toxic concentrations of the sweetener metabolites." ] Pharmacol Res. 2005 Aug 26; [Epub ahead of print]
The effect of aspartame metabolites on human [red blood cell] erythrocyte membrane acetylcholinesterase activity.
Tsakiris S,
Giannoulia-Karantana A,
Simintzi I,
Schulpis KH.
Department of Experimental Physiology, Medical School
University of Athens,
P.O. Box 65257, GR-154 01 Athens, Greece.

Stylianos Tsakiris. stsakir@cc.uoa.gr

Giannoulia-Karantana A. First Department of Pediatrics, Aghia Sophia Children's Hospital, University of Athens, Greece.

Kleopatra H. Schulpis, MD, PhD.
Institute of Child Health
Aghia Sophia Children's Hospital
GR-11527 Athens (Greece) Tel. +30 1 7708291, Fax +30 1 7700111 inchildh@otenet.gr
[ Papoutsakis T. tina.papoutsakis@hua.gr
Papadopoulos G.
Department of Biochemistry and Biotechnology
University of Thessaly, Ploutonos 26, 41221 Larisa, Greece
papg@chem.auth.gr ]

Abstract:

Studies have implicated aspartame (ASP) with neurological problems. The aim of this study was to evaluate acetylcholinesterase (AChE) activity in human erythrocyte [red blood cell] membranes after incubation with the sum of ASP metabolites, phenylalanine (Phe), methanol (met) and aspartic acid (aspt), or with each one separately.

Erythrocyte [human red blood cell] membranes were obtained from 12 healthy individuals and were incubated with ASP hydrolysis products for 1h at 37 degrees C. AChE was measured spectrophotometrically.

Incubation of membranes with ASP metabolites corresponding with 34 mg/kg, 150 mg/kg or 200 mg/kg of ASP consumption resulted in an enzyme activity reduction by -33%, -41%, and -57%, respectively.

Met concentrations 0.14 mM, 0.60 mM, and 0.80 mM decreased the enzyme activity by -20%, -32% or -40%, respectively.

Aspt concentrations 2.80 mM, 7.60 mM or 10.0 mM inhibited membrane AChE acitivity by -20%, -35%, and -47%, respectively.

Phe concentrations 0.14 mM, 0.35 mM or 0.50 mM reduced the enzyme activity by -11%, -33%, and -35%, respectively.

Aspt or Phe concentrations 0.82 mM or 0.07 mM, respectively, did not alter the membrane AChE activity.

It is concluded that low concentrations of ASP metabolites had no effect on the membrane enzyme activity, whereas high or toxic concentrations partially or remarkably decreased the membrane AChE activity, respectively. Additionally, neurological symptoms, including learning and memory processes, may be related to the high or toxic concentrations of the sweetener metabolites. PMID: 16129618


http://groups.yahoo.com/group/aspartameNM/message/939
Aspartame (aspartic acid, phenylalanine) binding to DNA:
Karikas July 1998: Murray 2003.01.05 rmforall
Karikas GA, Schulpis KH, Reclos GJ, Kokotos G
Measurement of molecular interaction of aspartame and its metabolites with DNA. Clin Biochem 1998 Jul; 31(5): 405-7.
Dept. of Chemistry, University of Athens, Greece
http://www.chem.uoa.gr
gkokotos@atlas.uoa.gr
G.J. Reclos reklos@otenet.gr

http://groups.yahoo.com/group/aspartameNM/message/1088
Murray, full plain text & critique:
Chronic aspartame in rats affects memory, brain cholinergic receptors, and brain chemistry, Christian B, McConnaughey M et al, 2004 May: 2004.06.05

Pharmacol Biochem Behav. 2004 May; 78(1): 121-7.
Chronic aspartame affects T-maze performance, brain cholinergic receptors and Na(+),K(+)-ATPase in rats.
Christian B, McConnaughey K, Bethea E, Brantley S, Coffey A, Hammond L, Harrell S, Metcalf K, Muehlenbein D, Spruill W, Brinson L, McConnaughey M.
Department of Pharmacology, Brody School of Medicine
East Carolina University, Greenville, NC 27858, USA;
North Carolina School of Science and Mathematics
Durham, NC 27811.
http://www.ecu.edu/pharmacology/faculty/mcconnaughey.html
Mona M. McConnaughey, Ph.D. Research Assistant Professor
Department: PHARMACOLOGY & TOXICOLOGY
Office: Brody Medical Science 6E-120A 252-744-2756
MCCONNAUGHEYM@mail.ecu.edu

This study demonstrated that chronic aspartame consumption in rats can lead to altered T-maze performance and increased muscarinic cholinergic receptor densities in certain brain regions. Control and treated rats were trained in a T-maze to a particular side and then periodically tested to see how well they retained the learned response. Rats that had received aspartame (250 mg/kg/day) in the drinking water for 3 or 4 months showed a significant increase in time to reach the reward in the T-maze, suggesting a possible effect on memory due to the artificial sweetener. Using [(3)H]quinuclidinyl benzilate (QNB) (1 nM) to label muscarinic cholinergic receptors and atropine (10(-6) M) to determine nonspecific binding in whole-brain preparations, aspartame-treated rats showed a 31 % increase in receptor numbers when compared to controls. In aspartame-treated rats, there was a significant increase in muscarinic receptor densities in the frontal cortex, midcortex, posterior cortex, hippocampus, hypothalamus and cerebellum of 80 %, 60 %, 61 %, 65 %, 66 % and 60 %, respectively. The midbrain was the only area where preparations from aspartame-treated rats showed a significant increase in Na(+),K(+)-ATPase activity. It can be concluded from these data that long-term consumption of aspartame can affect T-maze performance in rats and alter receptor densities or enzymes in brain. PMID: 15159141


Aspartame bans, tis more an avalanche than a trend...:
Rich Murray 2007.08.05
http://groups.yahoo.com/group/aspartameNM/message/1457

[ See also:
http://groups.yahoo.com/group/aspartameNM/message/1458
ASDA, Wal-Mart's UK supermarket chain, bans artificial colors, trans fats, MSG and aspartame, Marguerite Kelly, The Washington Post: Murray 2007.08.03 ]

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 2007.08.05

"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 80 members, 1,459 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/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/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

http://groups.yahoo.com/group/aspartameNM/message/1277
50% UK baby food is now organic - aspartame or MSG with food dyes harm nerve cells, CV Howard 3 year study funded by Lizzy Vann, CEO, Organix Brands, Children's Food Advisory Service: Murray 2006.01.13

http://groups.yahoo.com/group/aspartameNM/message/1271
Combining aspartame and quinoline yellow, or MSG and brilliant blue, harms nerve cells, eminent C. Vyvyan Howard et al, 2005 education.guardian.co.uk, Felicity Lawrence: Murray 2005.12.21

http://groups.yahoo.com/group/aspartameNM/message/1417
Formaldehyde as a potent unexamined cofactor in cancer research -- sources include methanol, dark wines and liquors, aspartame, wood and tobacco smoke: IARC Monographs on the Evaluation of Carcinogenic Risks to Humans implicate formaldehyde in #88 and alcohol drinks in #96: some related abstracts: Murray 2007.05.15

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

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://groups.yahoo.com/group/aspartameNM/message/1455
FEMA slow to safety test Katrina toxic trailers, Charles Babington, Associated Press -- 1 ppm formaldehyde in air is about half the daily dose from 3 cans aspartame diet soda and ten times the 1999 EPA alarm level for drinking water: Murray 2007.07.23

http://groups.yahoo.com/group/aspartameNMmessage/1447
Second study by expert Greek team of neurotoxicity in infant rats by aspartame (or its parts, methanol, phenylalanine, aspartic acid), KH Schulpis et al, Toxicology 2007.05.18: Murray 2007.07.04

http://groups.yahoo.com/group/aspartameNMmessage/1444
Expert Greek group finds aspartame (or its parts, methanol, phenylalanine, aspartic acid) harm infant rat brain enzyme activity, KH Schulpis et al, Pharmacol. Res. 2007.05.13: Murray 2007.06.23

http://groups.yahoo.com/group/aspartameNM/message/1414
Effect of aspartame on oncogene and suppressor gene expressions in mice, Katalin Gambos, Istvan Ember, et al, University of Pecs, Hungary, In Vivo 2007 Jan; scores of their relevant past studies since 1977: Murray 2007.04.14

http://groups.yahoo.com/group/aspartameNM/message/1373
Aspartame rat brain toxicity re cytochrome P450 enzymes, especially CYP2E1, Vences-Mejia A, Espinosa-Aguirre JJ et al, 2006 Aug, Hum Exp Toxicol: relevant abstracts re formaldehyde from methanol in alcohol drinks: Murray 2006.09.29

http://groups.yahoo.com/group/aspartameNM/message/1340
Aspartame groups and books: updated research review of 2004.07.16: Murray 2006.05.11

Dark wines and liquors, as well as aspartame, provide similar levels of methanol, above 120 mg daily, for long-term heavy users, 2 L daily, about 6 cans.

Within hours, methanol is inevitably largely turned into formaldehyde, and thence largely into formic acid -- the major causes of the dreaded symptoms of "next morning" hangover.

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). If 30% of the methanol is turned into formaldehyde, the amount of formaldehyde, 37 mg, is 18.5 times the USA EPA limit for daily formaldehyde in drinking water, 2.0 mg in 2 L average daily drinking water.