Both of the articles posted below, pro and con, were originally comments on these two articles:
Is Aspartame A Dangerous Man Made Poison – Part One?
Is Aspartame A Dangerous Man Made Poison – Part Two?
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John E. Garst, Ph.D. (Medicinal Chemistry, Pharmacology, Toxicology, and Nutrition)
Your comments about aspartame safety issues are outdated and thoroughly rejected by science. There are two poorly understood realities and both deal with the vitamin folic acid. The first reality is that all aspartame research prior to 2009 is seriously and fatally flawed (and hence so is all criticism of aspartame based on such science). It was all done in a scientifically unacceptable manner as was established in preliminary work presented at the Society of Toxicology (Seattle, USA) and the American Chemical Society (New Orleans, USA) national meetings in 2008. Full comments are currently being preparing for regular publication. At those locations it was demonstrated that inappropriate controls were used in all aspartame research starting with the original Searle work and extending through the oft-cited Soffritti et al work published over the past several years (and even other work thereafter). The standard control-versus-treated animal experiments are simply invalid for aspartame, because aspartame is hydrolyzed to methanol and methanol (actually through its oxidation products formaldehyde and formate) has long been known to deplete a vitamin, namely folic acid. No properly done experiment can deplete a vitamin, but all experiments to date claiming problems have done just that! Hence, both controlled and treated groups of animals must be provided either the appropriate microgram amounts of folic acid supplement to counter methanol-induced loss OR both controlled and treated groups of animals must be provided the same intake of methanol, one directly and the other from aspartame. (However, the latter is an experimentally more challenging option.) This blatant and continuous error in virtually all aspartame research invalidates all claims of harm from aspartame. That said various other studies found “no effect” from aspartame. Such animal studies were either of such short duration that folate depletion was not evidenced or equally likely were performed with corn/soybean or other diets rich in folate, such that they would not be expected to show any effect.
The second reality is that this same underlying folate issue explains human problems attributed by critics to aspartame. The folate enzyme system metabolizes the common dietary ingredient methanol and processes methanol’s oxidation products formaldehyde and formate, which are innate metabolites of many substances. Although required only in 400-600 microgram quantities, many people are folate deficient both because some people refuse to take vitamin supplements and avoid folate fortified grain products (donuts, etc), but also because some people (~20%) have genetic problems that increase their need for folate above that required by others. You should realize the adverse effects claimed by antiaspartame critics can be systematically linked far better to shortage of this vitamin (and possibly also the connected B12). This includes “migraines, dizziness, shaking and tremors, seizures, mental confusion, change in mood, Alzheimer’s and permanent blindness or other issues” linked to aspartame. A simple review of the primary literature at http://www.ncbi.nlm.nih.gov/pubmed/ will show these issues are far better connected to folate and specifically folate deficiency, folate genetics issues, and homocysteine accrual than to aspartame [for example, type “folate,headache” without the quotes into the search line and find 43 references compared with “aspartame,headache” without the quotes for which there are 33 references.] Folate deficiency also underlies birth defects, many cancers (including breast cancer), and other conditions, so people susceptible to headaches from aspartame might actually be susceptible to many other more threatening health-related issues associated with this folate deficiency. But it is these underlying folate issues and not aspartame that explain much of this mostly internet issue. The antiaspartame critics just don’t understand the issues involved, preferring instead to manufacture a controversy where none exists. And this continues even after I showed the fallacy of all rodent aspartame research.
For either animal or man the consequences of the folate deficiency that result are the incorporation of structurally weak uridylate (uracil, http://en.wikipedia.org/wiki/Uracil) bases in DNA in place of stronger thymidylate (methyluridylate called thymine, http://en.wikipedia.org/wiki/Thymine) and/or the accrual of toxic homocysteine (http://en.wikipedia.org/wiki/Homocysteine), most likely because of insufficient methylation of homocysteine to afford methionine (http://en.wikipedia.org/wiki/Methionine). Much has been written about the “excitotoxic” amino acids that form the aspartame framework (phenylalanine and aspartic acid) by aspartame critics. However, those excitotoxic amino acids occur at far greater concentrations in everyday food, so neither of these amino acids are issues for most people. However, what seems to be consistently missed by the antiaspartame critics (including Blaylock) is that homocysteine is a far stronger excitotoxin than any constituent of aspartame (or oral MSG). (For a better understanding of the relationships involved and how science knows about the connection between the DNA and homocysteine in this issue, download http://cebp.aacrjournals.org/cgi/reprint/14/12/2999 and study Figure 1 at the top of page 3000. Note too that the methanol from aspartame or from many other sources is oxidized to formaldehyde and that to formic acid and that is converted to the 10-formyltetrahydrofolate (10-formylTHF) at the bottom of the upper right circle.)
In summary, there is no valid science questioning aspartame’s safety, but there is substantial direct and indirect evidence that any personal issues with aspartame reflect not aspartame per se, but a personal folate deficiency (see http://en.wikipedia.org/wiki/Folate_deficiency), folate polymorphism genetic issues, http://en.wikipedia.org/wiki/Methylenetetrahydrofolate_reductase), and/or issues with related biochemistry linked to vitamin B12 (http://en.wikipedia.org/wiki/Vitamin_B12). There is no data supporting any adverse effect for aspartame that cannot simply and completely be explained by the folate deficiency, folate genetics, and the homocysteine paradigm. This new information only suggests aspartame is even safer, now that what I have reported above is known to all the regulatory authorities. Given these new, stronger indications of safety, science no longer has any reason to doubt the safety of aspartame. And the European equivalent of the US FDA on April 20 just again validated the safety of aspartame, http://www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_1211902454309.htm.
John E. Garst, Ph.D. (Medicinal Chemistry, Pharmacology, Toxicology, and Nutrition)
(FYI, the author has absolutely no financial or biasing connection with the aspartame, the soft drink or their related industries and have made not one penny from my opposition, unlike many antiaspartame critics who sell books and offer irrelevant treatment. Their clearly stated goals are lawsuits, where none are justified. The author has an undergraduate degree in chemistry (with emphasis in organic and biological chemistry) from the University of Kansas, a Ph.D. in Medicinal Chemistry (Pharmacy) from the University of Iowa, postdoctoral experience at Yale University (Molecular Biophysics & Biochemistry) and two postdoctoral fellowships at Vanderbilt University (physiology-pharmacology (mentor moved), then nutritional toxicology) and taught nutritional toxicology at the University of Illinois (Champaign-Urbana, UIUC) besides having conducted federally funded research at Vanderbilt, UIUC, and at several other universities before recently entering into semi-retirement.)
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An Opposing View…
by Rich Murray
groups.yahoo.com/group/aspartameNM/messages
I hope JE Garst’s pointed, detailed, referenced claims are investigated quickly and thoroughly.
An important issue is how many people have genetic mutations that make them unable to benefit from the protection that adequate folic acid offers against methanol and its natural toxic products in the human body, formaldehyde and formic acid.
severe brain harm in obese — aspartame a co-factor? — body turns its methanol into formaldehyde and formic acid:
Rich Murray 2009.08.27
http://rmforall.blogspot.com/2009_08_01_archive.htm
Thursday, August 27, 2009
http://groups.yahoo.com/group/aspartameNM/message/1585
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four Murray AspartameNM reviews in SE Jacob & SA Stechschulte debate with EG Abegaz & RG Bursey of Ajinomoto re migraines from formaldehyde from aspartame, Dermatitis 2009 May: TE Hugli — folic acid with V-C protects:
Rich Murray 2009.08.12
http://rmforall.blogspot.com/2009_08_01_archive.htm
Wednesday, August 12, 2009
http://groups.yahoo.com/group/aspartameNM/message/1582
Formaldehyde, aspartame, migraines: a possible connection.
Abegaz EG, Bursey RG.
Dermatitis. 2009 May-Jun;20(3):176-7; author reply 177-9.
No abstract available. PMID: 19470307
Eyassu G. Abegaz *
Robert G. Bursey
Ajinomoto Corporate Services LLC, Scientific & Regulatory Affairs,
1120 Connecticut Ave., N.W., Suite 1010, Washington, DC 20036
* Corresponding author. Tel.: +1 202 457 0284;
fax: +1 202 457 0107.
abegazee@ajiusa.com (E.G. Abegaz),
burseyb@ajiusa.com (R.G. Bursey)
“For example, fruit juices, coffee, and alcoholic beverages produce significantly greater quantities of formaldehyde than aspartame- containing products. [6]”
“[6] Magnuson BA, Burdock GA, Doull J, et al. Aspartame: a safety evaluation based on current use levels, regulations, and toxicological and epidemiological studies.
Crit Rev Toxicol 2007;37:629-727″
[ two detailed critiques of industry affiliations and biased science in 99 page review with 415 references by BA Magnuson, GA Burdock and 8 more, Critical Reviews in Toxicology,
2007 Sept.: Mark D Gold 13 page:
also Rich Murray 2007.09.15: 2008.03.24
http://rmforall.blogspot.com/2008_03_01_archive.htm
Monday, March 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1531
"Nearly every section of the Magnuson (2007) review has research that is misrepresented and/or crucial pieces of information are left out.
In addition to the misrepresentation of the research, readers (including medical professionals) are often not told that
this review was funded by the aspartame manufacturer, Ajinomoto, and the reviewers had enormous conflicts of interest." ]
http://www.medscape.com/viewarticle/579335
Dermatitis. 2008; 19(3): E10-E11.
© 2008 American Contact Dermatitis Society
Formaldehyde, Aspartame, and Migraines: A Possible Connection
Sharon E. Jacob; Sarah Stechschulte
Published: 09/17/2008
Abstract
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.
[ much more..... ]
http://groups.yahoo.com/group/aspartameNM/message/1495
folic acid prevents neurotoxicity from formic acid, made by body from methanol impurity in alcohol drinks [ also 11 % of aspartame ], BM Kapur, PL Carlen, DC Lehotay, AC Vandenbroucke,
Y Adamchik, U. of Toronto, 2007 Dec., Alcoholism Cl. Exp. Res.:
Murray 2007.11.27
http://news.yahoo.com/s/livescience/20090825/sc_livescience/obesepeoplehavesever
ebraindegeneration
Obese People Have ‘Severe Brain Degeneration’
livescience.com – Tue Aug 25, 10:35 am ET
A new study finds obese people have 8 percent less brain tissue than normal-weight individuals. Their brains look 16 years older than the brains of lean individuals, researchers said today.
Those classified as overweight have 4 percent less brain tissue and their brains appear to have aged prematurely
by 8 years.
The results, based on brain scans of 94 people in their 70s, represent “severe brain degeneration,” said Paul Thompson, senior author of the study and a UCLA professor of neurology.
“That’s a big loss of tissue and it depletes your cognitive reserves, putting you at much greater risk of Alzheimer’s and other diseases that attack the brain,” said Thompson. “But you can greatly reduce your risk for Alzheimer’s,
if you can eat healthily and keep your weight under control.”
The findings are detailed in the online edition of the journal Human Brain Mapping.
Obesity packs many negative health effects, including increased risk of heart disease, Type 2 diabetes, hypertension and some cancers. It’s also been shown to reduce sexual activity.
More than 300 million worldwide are now classified as obese, according to the World Health Organization. Another billion are overweight. The main cause, experts say: bad diet, including an increased reliance on highly processed foods.
Obese people had lost brain tissue in the frontal and temporal lobes, areas of the brain critical for planning and memory, and in the anterior cingulate gyrus (attention and executive functions), hippocampus (long-term memory) and basal ganglia (movement), the researchers said in a statement today.
Overweight people showed brain loss in the basal ganglia, the corona radiata, white matter comprised of axons, and the parietal lobe (sensory lobe).
“The brains of obese people looked 16 years older than the brains of those who were lean, and in overweight people looked 8 years older,” Thompson said.
Obesity is measured by body mass index (BMI), defined as the weight in kilograms divided by the square of the height in meters. A BMI over 25 is defined as overweight, and a BMI of over 30 as obese.
The research was funded by the National Institute on Aging, National Institute of Biomedical Imaging and Bioengineering, National Center for Research Resources, and the American Heart Association.
Hum Brain Mapp. 2009 Aug 6. [Epub ahead of print]
Brain structure and obesity.
Raji CA,
Ho AJ,
Parikshak NN,
Becker JT,
Lopez OL,
Kuller LH,
Hua X,
Leow AD,
Toga AW,
Thompson PM.
Department of Pathology, University of Pittsburgh, School of Medicine, Pittsburgh, Pennsylvania.
Obesity is associated with increased risk for cardiovascular health problems including diabetes, hypertension, and stroke.
These cardiovascular afflictions increase risk for cognitive decline and dementia, but it is unknown whether these factors, specifically obesity and Type II diabetes, are associated with specific patterns of brain atrophy.
We used tensor-based morphometry (TBM) to examine gray matter (GM) and white matter (WM) volume differences in 94 elderly subjects who remained cognitively normal for at least 5 years after their scan.
Bivariate analyses with corrections for multiple comparisons strongly linked body mass index (BMI), fasting plasma insulin (FPI) levels, and Type II Diabetes Mellitus (DM2) with atrophy in frontal, temporal, and subcortical brain regions.
A multiple regression model, also correcting for multiple comparisons, revealed that BMI was still negatively correlated with brain atrophy (FDR 30) showed atrophy in the frontal lobes, anterior cingulate gyrus, hippocampus, and thalamus compared with individuals with a normal BMI (18.5-25).
Overweight subjects (BMI: 25-30) had atrophy in the basal ganglia and corona radiata of the WM.
Overall brain volume did not differ between overweight and obese persons.
Higher BMI was associated with lower brain volumes in overweight and obese elderly subjects.
Obesity is therefore associated with detectable brain volume deficits in cognitively normal elderly subjects.
Hum Brain Mapp, 2009. (c) 2009 Wiley-Liss, Inc.
PMID: 19662657
http://www3.interscience.wiley.com/journal/122539667/abstract?CRETRY=1&SRETRY=0
Cyrus A. Raji 1 2,
April J. Ho 3,
Neelroop N. Parikshak 3,
James T. Becker 4 5 6, beckerjt@upmc.edu
Oscar L. Lopez 6, lopezol@upmc.edu
Lewis H. Kuller 7,
Xue Hua 3,
Alex D. Leow 3, feuillet@ucla.edu
Arthur W. Toga 3,
Paul M. Thompson 3 *
1 Department of Pathology, University of Pittsburgh, School of Medicine, Pittsburgh, Pennsylvania
2 Department of Radiology, University of Pittsburgh, School of Medicine, Pittsburgh, Pennsylvania
3 Laboratory of Neuro Imaging, Department of Neurology, University of California Los Angeles, School of Medicine, Los Angeles, California
4 Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, Pennsylvania
5 Department of Psychology, University of Pittsburgh, School of Medicine, Pittsburgh, Pennsylvania
6 Department of Neurology, University of Pittsburgh, School of Medicine, Pittsburgh, Pennsylvania
7 Department of Epidemiology, University of Pittsburgh, School of Medicine, Pittsburgh, Pennsylvania email: Paul M. Thompson ( thompson@loni.ucla.edu )
*Correspondence to Paul M. Thompson, Professor of Neurology,
Laboratory of Neuro Imaging, Department of Neurology,
UCLA School of Medicine, 635 Charles E. Young Drive South,
Suite 225E, Los Angeles, CA 90095-7332
Cyrus A. Raji and April J. Ho contributed equally to this work.
Funded by:
NIA
NIBIB
NCRR; Grant Number: AG016570, EB01651, RR019771
National Institute of Aging; Grant Number: AG 20098, AG05133, AG15928
American Heart Association; Grant Number: 0815465D
Keywords
brain atrophy . obesity . tensor-based morphometry
Received: 23 April 2009; Revised: 3 June 2009;
Accepted: 3 July 2009
Digital Object Identifier (DOI) 10.1002/hbm.20870
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positively act upon evidence about healthy and safe food, drink, and environment.”
Rich Murray, MA Room For All rmforall@comcast.net
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