methanol (11% of aspartame), made by body into formaldehyde in many vulnerable tissues, causes modern diseases of civilization, summary of a century of research, Woodrow C Monte PhD, Medical Hypotheses journal: Rich
Murray 2009.11.15
http://rmforall.blogspot.com/2009_11_01_archive.htm
Sunday, November 15, 2009
http://groups.yahoo.com/group/aspartameNM/message/1589
_____________________________________________________
Methanol: A Chemical Trojan Horse as the Root of the Inscrutable U
Prepublication Copy; Medical Hypotheses -- 06 November 2009
(10.1016/j.mehy.2009.09.059)
http://www.medical-hypotheses.com/article/S0306-9877(09)00693-8/abstract
Woodrow C. Monte PhD
Professor of Food Science (retired)
Arizona State University
corresponding author : Woodrow C. Monte PhD
470 South Rainbow Drive
Page, Arizona 86040
Key Words:
food epidemiology; diseases of civilization; methanol; formaldehyde;
aspartame; autism; multiple sclerosis; Alzheimer's; U-shaped curve.
Abstract:
Until 200 years ago, methanol was an extremely rare component of
the human diet and is still rarely consumed in contemporary hunter
and gatherer cultures.
With the invention of canning in the 1800s, canned and bottled
fruits and vegetables, whose methanol content greatly exceeds that
of' their fresh counterparts, became far more prevalent.
The recent dietary introduction of aspartame, an artificial sweetener,
11% methanol by weight, has also greatly increased methanol
consumption.
Moreover, methanol is a major component of cigarette smoke,
known to be a causative agent of many diseases of civilization
(DOC).
Conversion to formaldehyde in organs other than the liver is
the principal means by which methanol may cause disease.
The known sites of class I alcohol dehydrogenase (ADH I),
the only human enzyme capable of metabolizing methanol to
formaldehyde, correspond to the sites of origin for many DOC.
Variability in sensitivity to exogenous methanol consumption may be
accounted for in part by the presence of aldehyde dehydrogenase
sufficient to reduce the toxic effect of formaldehyde production
in tissue through its conversion to the much less toxic formic acid.
The consumption or endogenous production of small amounts of
ethanol, which acts as a competitive inhibitor of methanol's
conversion to formaldehyde by ADH I, may afford some individuals
protection from DOC.
[ ----- Original Message -----
From: Woodrow Monte
To: rmforall@comcast.net ; mgold@tiac.net
Sent: Saturday, November 14, 2009 9:22 AM
Subject: Hi Rich Murray and Mark Gold from Woodrow Monte
Richard and Mark:
I hope all is well with you both.
I finally had the chance to put exactly what I have been thinking
relative to methanol and its relationship to formaldehyde and
formate [formic acid] into an article. The paper was accepted by the
journal Medical Hypothesis and is now on Pub Med in prepublication
corrected proof form.
http://www.ncbi.nlm.nih.gov/pubmed/19896282?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1
I have attached the pre-publication copy of the article.
The quote that follows is what the journal says that I can do with
this copy.
"the right to post a pre-print version of the journal article on
Internet web sites including electronic pre-print servers, and
to retain indefinitely such version on such servers or sites."
Please email me with any questions.
As you will see I have no faith in Formate or Formic Acid as
being the toxic agent for methanol.
The devil is in the aldehyde. [ Formaldehyde ]
Thanks for all your support in the past.
Woodrow ]
Introduction:
The quest for a small molecule as an etiological cause of the diseases
of civilization has always ignored one of its smallest and most stealthy
agents: methanol -- a molecule capable of effortless perivascular
access.
A rare component of unprocessed food, methanol has increased
incrementally in the human diet since the advent of commercialized
canning in the 1800s and most recently due to the popularity of
products sweetened with aspartame.
Although the extreme sensitivity of humans to methanol is well
established, its conversion to formaldehyde in situ within the vessels
of the brain and elsewhere is undetectable, making methanol placed
formaldehyde a paradigm of toxicity that is as compelling in theory
as it is difficult in practice to study.
The methanol toxicity literature of the last forty years has been
overwhelmingly in favor of a benign role for environmental dosages
of methanol.
Drawing on scant evidence from arguably inadequate animal models,
this research denies any significant link to formaldehyde, pointing
instead to a considerably less toxic and considerably more detectable
secondary metabolite -- formate. [formic acid]
Not insignificantly, much of the funding for such studies comes from
sources with a vested interest in maintaining public confidence in the
dietary safety of methanol.
The fact remains, however, that environmental methanol in humans
allows formaldehyde greater access to regions of the body prone to
disease, exposing vulnerable protein and DNA to methylation and
other modifications capable of inducing carcinogenicity,
mutagenicity, teratogenicity, and direct macrophage phagocytosis.
Given its many harmful effects, the potentially critical role of dietary
methanol in the increasing incidence of diseases of civilization needs
to be reexamined.
The Hypothesis:
Formaldehyde produced from dietary and environmental methanol
metabolized in situ at the non-hepatic sites of class I alcohol
dehydrogenase (ADH I) may play a role in many diseases of
civilization (DOC).
Ethanol may in turn act as a competitive inhibitor of methanol's
conversion to formaldehyde by ADH I, as reflected in the
U-shaped curve of alcohol consumption.
Discussion:
July 24, 1981, should be a significant date for scientists investigating
worldwide epidemics of Alzheimer's disease (AD),[#540],[#533]
multiple sclerosis (MS),[#77],[#214] atherosclerotic cardiovascular
disease (ACD),[#532] lupus,[#536] skin[#95] and breast cancer,
[#250],[#193] autism,[#525] and other diseases of civilization
(DOC).
On this date the U.S. Food and Drug Administration approved the
use of aspartame,[#472] a new artificial sweetener.[#473]
As aspartame eventually became a major source of methanol in the
civilized human diet,[#1] the incidence of DOC gradually began to
rise.
Rarely found in nature and an insignificant component of the diets of
Pleistocene man and present-day foragers, methanol has been
increasing incrementally in the diet of civilized humanity since 1806
when Nicolas Appert commercialized canning, a process that traps
methanol derived from the heating and storage of plant materials
containing pectin.[#1]
In addition to aspartame, and canned vegetables, fruits, and their
juices,[#28],[#29] a major source of the methanol
entering the modern civilized human body is cigarette smoke,[#62]
causatively linked to atherosclerosis, multiple sclerosis,[#68]
lupus,[#73] Alzheimer's disease,[#535] rheumatoid arthritis,[#332]
and other DOC.[#345]
A poison to which humans are particularly sensitive,[#3] methanol
was responsible for the loss of hundreds of lives at the beginning of
the twentieth century[#17] when extensive animal testing determined
it was safer than ethanol, allowing its first use in foods and
drugs.[#165]
Because the toxicity of methanol in the human system cannot be
properly tested in animals, the results of this research were specious.
Searching for the cause of the metabolic anomaly that makes the
human relationship to methanol distinct from all laboratory animal
models, including primates,[#116] has always been muddied by
industrial agendas[#39] with a vested interest in proving that the
formaldehyde produced from methanol in the human body does no
harm.[#40],[#121]
The prevalence of compromised literature and the lack of an
applicable animal model may explain why methanol, which fits many
of the criteria of availability and stealth that one would expect of a
usual suspect, has not yet caught the attention of scientists searching
for the elusive etiologic agent of DOC.
The single article that posits methanol as the possible direct cause of
multiple sclerosis[#8] is never cited in the MS literature.
A recent series of comprehensive in-vitro studies has also
convincingly linked Alzheimer's disease to very low concentrations of
formaldehyde.
This research mentions methanol as a possible invivo source,[#234],
[#235] but significantly, it neglects to stress the fact that there is no
simpler way for formaldehyde to get past the blood brain barrier
than in the form of this smallest of alcohols.[#367]
Methanol is itself harmless but is a Trojan horse for formaldehyde,
a chemical that can pose a severe risk to humans,[#7] who appear
to be the only mammal exclusively endowed with a hepatic catalase
enzyme incapable of removing dietary methanol before it can enter
the general circulation.[#52]
Once methanol runs the gauntlet of first-pass metabolism, its
detoxification is no longer exclusive to the liver.
Formaldehyde, the first metabolite of methanol, can then be
produced within the arteries and veins,[#220] heart,[#503]
brain,[#218] lungs,[#221] breast,[#358] bone,[#503]
and skin.[#221]
These major organs harbor extra hepatic sites of the only remaining
human enzyme capable of metabolizing methanol,
class I alcohol dehydrogenase (ADH I).[#112]
Methanol transports its potential to become formaldehyde past
normal biological barriers in the brain and elsewhere that
environmental formaldehyde itself cannot usually penetrate.[#122]
That formaldehyde produced in these organs from methanol has
not been detected directly in humans should not be surprising since
formaldehyde vanishes within minutes, binding to
macromolecules[#114] even when a solution of it is injected directly
into tissue[#122] or spiked into cell-free human serum.[#236]
Although methylation caused by this toxic process could be
functionally destructive to the macromolecule so modified, the
addition of methyl groups to large molecules renders the modification
and its source invisible to any clinical or histological testing
procedure.[#122],[#236]
However, in a study by Trocho et al., a portion of the C14 labeled
methanol moiety of aspartame was shown to bind to such
macromolecules via formaldehyde and not pass directly into the
one-carbon cycle via formate as predicted by the generally accepted
model of methanol toxicity,[#40] a model developed from studying
the severe methanol poisoning of monkeys, not the chronic
environmental exposure of humans.
Formate derived from methanol metabolism is never measurable in
human blood when small environmentally reflective doses of methanol
are administered.[#42]
During acute methanol poisoning, where the methanol concentration
of the portal vein far exceeds that of ethanol, liver ADH I would be
saturated with methanol.
The liver's ample supply of aldehyde dehydrogenase would assure
production of formic acid, which is metabolized very slowly,
causing leakage of formate into the general circulation.
Formate is not, however, a significant poison to humans and has,
in fact, been used therapeutically and as a food additive.[#365]
It certainly would be more convenient to have a stable, measurable
entity such as formate to predict the danger of exposure to methanol,
but an iron-clad case for the toxicological significance of this much
less toxic, secondary metabolite has not yet been made.[#55]
Moreover, the results of Trocho's elegant study should give one
pause before accepting the widely held premise that formate and
not formaldehyde is the toxic component of methanol poisoning.
Laboratories that publish the most cited works are often financially
supported by industries with much to lose were the safety of methanol
disproved.
This research must be carefully reconsidered before we can dismiss
the potential threat posed by formaldehyde strategically placed by
dietary methanol.
Formaldehyde produced within the cell immediately reacts with water
to produce formal hydrate,[#27] a strong acid[#114] with twice the
number of available hydrogen ions as the next methanol metabolite,
formic acid.
Formal hydrate produced from methanol by the ADH I sites found in
the intima, media, and adventitia lining of the circulatory system of the
heart and brain[#220] would be expected to diffuse into the localized
tissue, quickly methylating basic molecules such as myelin basic
protein (MS)[#224] and tau protein (Alzheimer's).[#234]
Such changes have been shown in these disease states.
Formaldehyde, also known to uncouple oxidative phosphorylation
and inhibit phosphorylation within cells,[#113] could contribute to
these changes reported in MS[#224] and Alzheimer's.[#506]
The immune system reacts swiftly to methylation of protein by
formaldehyde -- a phenomenon put to good use by the vaccine
industry for the last hundred years.[#26]
Macrophages have activation sites specifically for formaldehyde
modified protein[#23] and are well known to have a ravenous
appetite for LDLs reacted with small aldehydes.[#507]
This induces the esterification of phagocytized LDL cholesterol and
the subsequent transformation of the macrophages to
foam cells,[#508] similar to the sequence of events leading to
atheroma production adjacent to the intima layer of the human aorta,
rich in ADH I.[#220]
The potential for antibody production against methylated self-protein
phagocytized by macrophages has never been investigated.
Ethanol in low concentrations acts as a powerful competitive
inhibitor[#439] with a 16:1 preference for ethanol to acetaldehyde
over the conversion of methanol of formaldehyde by ADH I.[#389]
For this reason, ethanol is used, without FDA approval, as the
preferred antidote for accidental methanol poisoning in emergency
rooms throughout the world.[#253]
Very low levels of ethanol in the bloodstream would substantively
prevent all formaldehyde production from dietary methanol
anywhere in the body.
Protection from formaldehyde production may account for the yet
unexplained dose region of apparent improvement in the
U-shaped curve of alcohol consumption.
Epidemiologic studies show moderate consumption of alcohol is
associated with a reduced risk of myocardial infarction,[#485]
dementia,[#534] lupus,[#73] and other DOC.
Low doses of ethanol appear to provide a preventative measure
against the causes of DOC.[#279]
Recent studies of individuals who consumed at least one alcoholic
drink per day show subjects had an additional 86 percent
reduction in risk of myocardial infarction if they were genetically
endowed with a genotype of ADH I that was 2.5 times slower to
metabolize ethanol than the control
These findings were "consistent with the hypothesis that a slower
rate of clearance of alcohol enhances the beneficial effect of
moderate alcohol consumption on the risk of cardiovascular
disease."[#483]
A compelling explanation of the dose region of adverse effects of
the U-shaped curve with high ethanol consumption, which shows
increased risk of these same diseases, could be the mechanism by
which humans habituate to high consumption of ethanol.
The induction of the P450 hepatic microsomal ethanol oxidizing
system[#175] results in a considerably higher clearance rate of
ethanol from the bloodstream for an extended period of time, thus
accounting for more consumption leading to statistically less time
of protection.
Small amounts of supplemental alcohol not sufficient to induce
P450 might be expected to prolong the residence time and avoid
gaps in the protection afforded by ethanol in preventing methanol
placed formaldehyde.
It appears that the average person, whether or not an imbiber,
may typically have endogenous ethanol in the blood[#174]
produced by gut fermentation.[#363]
This ethanol must pass through the liver via the hepatic portal vein
coincidently with dietary methanol absorbed from the gut contents.
The liver has the highest concentration of ADH I in the body.
Even traces of ethanol in the blood, however, would seem to
indicate the absence of available sites remaining for the oxidation
of the much less competitive methanol, allowing most dietary
methanol to pass freely into the general circulation.
What follows is a biochemical game of musical chairs as methanol
travels round and round the circulation, waiting for the ethanol levels
to reach zero and the music to stop.
The closest ADH I free to service the methanol will convert it to
formaldehyde. If this happens in the liver, where there are ample
supplies of aldehyde dehydrogenase, metabolism to carbon dioxide
will proceed safely.
In mammary epithelium, however,
where human class I alcohol dehydrogenase is highly expressed[#358]
but active aldehyde dehydrogenase[#216] is scarce, methanol placed
formaldehyde could become a problem.
Formaldehyde is a class I carcinogen[#11] and mutagen[#449]
with methanol providing its only easy avenue into this tissue.
In the vasculature of the brain[#218] and other ADH I positive
organs, the consequences may be similarly troublesome.
The obvious way to prevent formaldehyde from damaging this
sensitive tissue is to keep the music playing, a solution dependent
on our ability to answer the following questions:
Just how much ethanol is essential in this seemingly inscrutable
U-shaped curve?
What measures should we take to combat this chemical Trojan horse,
thereby reducing the methanol contamination in the diet of civilization
and making it more like the diet of our ancient ancestors?
Both research areas present intriguing inquiries, but as a food
scientist, I would stress the relative ease and greater benefits of
investigating the latter.
Proposed test of the hypothesis:
Under strict medical supervision this hypothesis would best be tested
on experimental subjects suffering from relapsing multiple sclerosis.
Without here getting into great detail, the preferred mode of
administration of small amounts of ethanol would be via gaseous
administration at sufficient, carefully controlled, atmospheric
concentration to maintain a constant 1-2 parts per million ethanol
concentrations in the test subjects bloodstream.
At such low levels, well below the ambient concentrations of ethanol
in the average pub environment, ethanol is quite safe and not
detectable in the air via the olfactory system of most people.
A water vaporization control would work well and be conducive to
a double blind study.
Vaporous administration of ethanol is well covered in the literature,
and is used frequently to induce alcohol intoxication of test animals
for toxicity testing purposes.
BIBLIOGRAPHY
1. Monte WC.
Aspartame; Methanol and the Public Health.
Journal of Applied Nutrition 1984;36(1):42-58.
3. Roe O.
Methanol Poisoning Its clinical course pathogenesis and treatment.
Acta Medica Scandinavica 1946;126:1-252.
7. Trocho C, Pardo R, Fafecas I, Virgili J, Remesar X,
Fernandez-Lopez JA, et al.
Formaldehyde derived from dietary aspartame
binds to tissue components in vivo.
Life Sci 1988;63(5):337-49.
[ http://groups.yahoo.com/group/aspartameNM/message/925
aspartame puts formaldehyde adducts into tissues, Part 1/2
full text, Trocho & Alemany 1998.06.26: Murray 2002.12.22 ]
8. Henzi H.
Chronic Methanol Poisoning with the Clinical and
Pathologic-Anatomical Features of Multiple Sclerosis
Medical Hypothesis.
Med Hypothesis 1984;13:63-75.
11. Rousseau M, Straif K, Siemiatycki J.
IARC Carcinogen Update (Formaldehyde now Class 1
carcinogen).
Environmental Health Perspectives 2005;113(9):A580.
17. Wimer W, Russell J, Kaplan H.
Alcohols Toxicology.
Southwest Research Institute
San Antonio TX: Noyes Data Corporation.; 1983.
18. Gaul H, Wallace C, Auer R.
MR findings in methanol intoxication.
Am J Neuroradiol 1995;16:1783-6.
26. Metz B, Jiskoot W, Hennink W, Crommelin D, Kersten G.
Physicochemical and immunochemical techniques predict the
quality of diphtheria toxoid vaccines.
Vaccine 2003;22:156-67.
27. Means G, Feeney R.
Chemical Modification of Proteins.
Francisco, CA.: Holden-Day, Inc; 1971.
28. Kirchner J, Miller J.
Volatile Water-Soluble and Oil Constituents of Valencia
Orange Juice.
Agricultural and Food Chemistry 1957;5(4):283.
29. Lund E, Kirkland C, Shaw P.
Methanol. Ethanol. and Acetaldehyde Contents of Citrus Products.
Agricultural and Food Chemistry 1981;29:361.
39. Gordon G.
NutraSweet Questions Swirl
(How Sweet It Isn't -- a UPI Investigative Report ).
Seattle Times. Seattle, Wash. Oct 13, 1987. p. F1:
United Press International; 1987.
[ http://www.dorway.com/upipart1.txt
http://groups.yahoo.com/group/aspartameNM/message/262
aspartame expose 96K Oct 1987 Part 1/3: Gregory Gordon,
UPI reporter: Murray 2000.07.10 ]
40. Tephly T.
Comments on the purported generation of formaldehyde from
the sweetener aspartame [letter: not peer-reviewed].
Life Sci 1999;65:157-60.
42. Heinzow B.
Formic acid in urine -- a significant parameter in environmental
diagnosis?
Zentralbl Hyg Umweltmed 1992;192(5):455-61.
52. Roe O.
Species Differences in Methanol Poisoning.
I. Minimal Lethal Doses. Symptoms. and
Toxic Sequelae of Methanol Poisoning in Humans
and Experimental Animals.
CRC Critical Reviews in Toxicology 1982;18:376-90.
55. Smith E, Taylor R.
Acute Toxicity of Methanol in the Folate-Deficient Acatalasemic
Mouse.
Toxicology 1982;25:271.
62. Neuberg C, Kobel M.
Uber die encymatische Abspaltung von Methylalkohol aus Pektin
durch ein Ferment dis Tabaks.
Zeitschrift Für Lebensmitteluntersuchung Und -Forschung A
1939;77(3):272.
68. Hernan M, Jick S, Logroscino G, Olek M, Ascherio A,
Jick H.
Cigarette smoking and the progression of multiple sclerosis.
Brain 2005;128(6):1461-65.
73. Hardy C, Palmer B, Muir K, Sutton A, Powell R.
Smoking history. alcohol consumption. and systemic lupus
erythematosus: a case-control study.
Ann Rheum Dis 1998;57:451-5.
77. Hirtz D, Thurman D, Gwinn-Hardy K, Mohamed M,
Chaudhuri A, Zalutsky R.
How common are the "common" neurologic disorders?
Neurology 2007;68:326-37.
95. Christenson L, Borrowman T, Vachon C, Tollefson M,
Otley C, Weaver A, et al.
Incidence of Basal Cell and Squamous Cell Carcinomas
in a Population Younger Than 40 Years.
JAMA 2005;294(6):681-90.
112. Kini M, Cooper J.
Biochemistry of Methanol Poisoning-III;
The Enzymic Pathway for the Conversion of Methanol to
Formaldehyde.
Biochemical Pharmacology 1961;8:207.
113. Kini M, Cooper J.
Biochemistry of Methanol Poisoning;
The Effect of Methanol and its Metabolites on Retinal Metabolism.
Biochemical Journal 1962;82:164.
114. French D, Edsall J.
The Reactions of Formaldehyde with Amino Acids and Proteins.
Adv.Protein Chem 1945;2:277.
116. Cooper J, Kini M.
Biochemical Aspects of methanol Poisoning.
Biochemical Pharmacology 1962;11:405
.
121. Tephly T, McMartin K.
Methanol metabolism and toxicity.
In: Stegink L, Filer L, editors.
Aspartame: Physiology and Biochemistry.
New York: Marcel Dekker Inc.; 1984. p. 111-40.
122. von Oettingen W.
The Aliphatic Alcohols Their Toxicity and Potential Dangers in
Relation to Their Chemical Constitution and Their Fate in
Metabolism.
Public Health Bulletin 1943;281:8.
165. Wood C.
Death and Blindness as a Result of Poisoning by Methyl Alcohol
or Wood Alcohol and Its Various Preparations.
International Clinics; A Quarterly of Clinical Lectures 1906;16:68.
174. Lester D.
The Concentration of Apparent Endogenous Ethanol.
Q J StudAlcohol 1962;23:17.
175. Lieber C, DeCarli L.
Hepatic Microsomal Ethanol-Oxidizing System. In vitro
characteristics and adaptive properties in vivo.
The Journal of Biological Chemistry 1970;245(10):2505-12.
193. Kingsbury K.
The Changing Face Of Breast Cancer.
TIME Magazine 2007;107(16):36.
214. Redelings M, McCoy L, Sorvillo V.
Multiple Sclerosis Mortality and Patterns of Comorbidity in the
United States from 1990 to 2000.
Neuroepidemiology 2006;26:102-07.
216. Crabb D, Matsumoto M, Chang D, You M.
Overview of the role of alcohol dehydrogenase and aldehyde
dehydrogenase and their variants in the genesis of
alcohol-related pathology.
Proceedings of the Nutrition Society 2004;63:49-63.
218. Mori O, Haseba T, Kameyama K, Shimizu H.
Histological distribution of class III alcohol dehydrogenase in
human brain.
Brain Research 2000;852:186-90.
220. Allili-Hassani A, Martinez S, Peralba J.
Alcohol dehydrogenase of human and rat blood vessels.
FEBS Letters 1997;405:26-30.
221. Buehler R, Hess M, Wartburg J.
Immunohistochemical Localization of Human Liver Alcohol
Dehydrogenase in Liver Tissue. Cultured Fibroblasts and
HeLa Cells.
American Association of Pathologists 1982;108(1):89-99.
224. Kim J, Mastronardi F, Wood D, Lubman D, Zand R,
Moscarello M.
Multiple Sclerosis: An important role for post-translational
modifications of myelin basic protein in pathogenesis.
Molecular & Cellular Proteomics 2003;2(7):453-62.
234. Nie C, Wei Y, Chen X, Liu Y, Dui W, Liu Y, et al.
Formaldehyde at Low Concentration Induces Protein Tau
into Globular Amyloid-Like Aggregates In Vitro and In Vivo.
PLoS ONE 2007;2(7:e629):1-13.
235. Nie C, Wang X, Liu Y, Perrett S, He R.
Amyloid-like aggregates of neuronal tau induced by formaldehyde
promote apoptosis of neuronal cells.
BMC Neuroscience 2007;8(9):1-16.
236. Köppel C, Baudisch H, Schneider V, Ibe K.
Suicidal ingestion of formalin with fatal complications.
Intensive Care Med 1990;16(3):212-4.
250. Krieger N.
Is breast cancer a disease of affluence. poverty. or both?
The case of African American women.
Am J Public Health 2002;92(4):611-13.
253. McCoy H, Cipolle R, Ehlers S, Sawchuk R, Zaske D.
Severe Methanol Poisoning: Application of a Pharmacokinetic
Model for Ethanol Therapy and Hemodialysis.
Amer J Med 1979;67:604-7.
279. Kloner R, Rezkalla S. Kloner RA. Rezkalla SH.
To drink or not to drink? That is the question.
Circulation 2007;116(11):306-17.
332. Costenbader K, Karlson E.
Cigarette smoking and autoimmune disease: what can we learn
from epidemiology?
Lupus 2006;15(11):737-45.
345. Wald N, Hackshaw A.
Cigarette smoking: an epidemiological overview.
Brit. Med. Bull 1996;52(1):3-11.
358. Triano E, Slusher L, Atkins T, Beneski J, Gestl S.
Class I Alcohol Dehydrogenase Is Highly Expressed in Normal
Human Mammary Epithelium but not in Invasive Breast Cancer:
Implications for Breast Carcinogenesis.
Cancer Research Arch 2003;63:3092-100.
363. Turner C, Spanel P, Smith D.
A longitudinal study of ethanol and acetaldehyde in the exhaled
breath of healthy volunteers using selected-ion flow-tube mass
spectrometry.
Rapid Commun Mass Spectrom 2006;20:61-8.
365. Irving GW.
Evaluation of the Health Aspects of Formic Acid, Sodium Formate,
and Ethyl Formate as Food Ingredients.
Bethesda Md: Federation of American Societies for Experimental
Biology; 1974 No.: NTIS Doc PB-266 282, 1976.
(NTIS Doc PB-266 282, 1976).
367. Yant W, Schrenk H.
Distribution of methanol in dogs after inhalation and administration
by stomach tube and subcutaneously.
J Ind Hyg Toxicol 1937;19:337-45.
389. Jones A.
Elimination Half-life of Methanol During Hangover.
Pharmacology & Toxicology 1987;60:217-20.
439. Zatman L.
The Effect of Ethanol on the Metabolism of Methanol in Man.
Biochem J 1946;40:67.
449. Grafstrom R, Fornace A, Autrup H, Lechner J, Harris C.
Formaldehyde Damage to DNA and Inhibition of DNA Repair
in Human Bronchial Cells.
Science 1983;220:216-18.
472. Smith R.
Aspartame Approved Despite Risks.
Science 1981;213(28):986-87.
473. Dickson D.
Aspartame sugar substitute. New court overruled.
Nature 292:283 1981;292(July 23):283.
483. Hines LM., Meir S, Stampfer J, Jingma H, Gaziano M.
Genetic Variation in Alcohol Dehydrogenase and the Beneficial
Effect of Moderate Alcohol Consumption on Myocardial
Infarction.
N Engl J Med 2001;344(8):549-55.
485. Klatsky A.
Alcohol, wine, and vascular diseases -- an abundance of paradoxes.
Am J Physiol Heart Circ Physiol 2008;294:582-83.
503. Estonius M, Svensson S, Höög J.
Alcohol dehydrogenase in human tissues: localisation of transcripts
coding for five classes of the enzyme.
FEBS Lett. 1996;397:338-42.
506. Luo Y, Ingram V.
Uncoupling of mitochondria activates protein phosphatases and
inactivates MBP protein kinases.
J Alzheimers Dis 2001;3(6):593-98.
507. Kawamura M, Heinecke J, Chait A.
Increased uptake of alpha-hydroxy aldehyde-modified
low density lipoprotein by macrophage scavenger receptors.
J Lipid Res. 41(7):1054 2000;41(7):1054-59.
508. Fogelman A, Shechter I, Seager J, Hokom M, Child J,
Edwards P.
Malondialdehyde alteration of low density lipoproteins leads to
cholesteryl ester accumulation in human monocyte-macrophages.
Proc Natl Acad Sci. 1980;77(4):2214-8.
525. Blaxill M.
What's going on? The question of time trends in autism.
Public Health 2004;119(6):536-51.
532. Yusuf S, Ounpuu S, Anand S.
The global epidemic of atherosclerotic cardiovascular disease.
Med Princ Pract 2002;11(Suppl 2):3-8.
533. Waldman M.
Are We Experiencing an Alzheimer's Epidemic?
Presentation (Abstract 90)
[AD/PD 2009: 9th International Conference on Alzheimer's
and Parkinson's Diseases:] ; 2009.
http://www.medscape.com/viewarticle/590106
534. Sink K.
Moderate Alcohol Consumption May Lower Dementia Risk in
Cognitively Normal Elderly.
Presentation. Alzheimer's Association
2009 International Conference on Alzheimer's Disease (ICAD),
Vienna. www.medscape.com
535. Mehlig K, Skoog I, Guo X, Schütze M, Gustafson D,
Waern M, et al.
Alcoholic Beverages and Incidence of Dementia: 34-Year Follow-up
of the Prospective Population Study of Women in Göteborg.
Am J Epidemiol 2008;167(6):684-91.
536. Uramoto K, Michet C, Thumboo J, Sunku J, O'Fallon W,
Gabriel S.
Trends in the incidence and mortality of systemic lupus
erythematosus, 1950-1992.
Arthritis Rheum 1999;42(1):46-50.
540. Casserly I, Topol E.
Convergence of atherosclerosis and Alzheimer's disease:
inflammation, cholesterol, and misfolded proteins.
Lancet 2004;363(9415):1139-46.
_____________________________________________________
old tiger roars -- Woodrow C Monte, PhD -- aspartame causes
many breast cancers, as ADH enzyme in breasts makes methanol
from diet soda into carcinogenic formaldehyde -- same in dark
wines and liquors, Fitness Life 2008 Jan.: Murray 2008.02.11
http://rmforall.blogspot.com/2008_02_01_archive.htm
Monday, February 11, 2008
http://groups.yahoo.com/group/aspartameNM/message/1517
role of formaldehyde, made by body from methanol from foods
and aspartame, in steep increases in fetal alcohol syndrome,
autism, multiple sclerosis, lupus, teen suicide, breast cancer,
Nutrition Prof. Woodrow C. Monte, retired, Arizona State U.,
two reviews, 190 references supplied, Fitness Life,
New Zealand 2007 Nov, Dec: Murray 2007.12.26
http://rmforall.blogspot.com/2007_12_01_archive.htm
Wednesday, December 26 2007
http://groups.yahoo.com/group/aspartameNM/message/1498
Monte WC., Is your Diet Sweetener killing you?
Fitness Life. 2007 Nov; 33: 31-33.
Monte WC., A Deadly Experiment.
Fitness Life. 2007 Dec; 34: 38-42.
Monte WC., Bittersweet: Aspartame Breast Cancer Link.
Fitness Life. 2008 Feb; 34: 21-22.
Article 1 http://www.thetruthaboutstuff.com/review1.shtml
Article 2 http://www.thetruthaboutstuff.com/review2.shtml
Article 3 http://www.thetruthaboutstuff.com/review3.shtml
http://www.thetruthaboutstuff.com/articles.shtml
223 references with abstracts or full and partial texts
http://groups.yahoo.com/group/aspartameNM/message/870
Aspartame: Methanol and the Public Interest 1984: Monte:
Murray 2002.09.23 rmforall
Dr. Woodrow C. Monte Aspartame: methanol, and the public health.
Journal of Applied Nutrition 1984; 36 (1): 42-54.
(62 references) Professsor of Food Science [retired 1992]
Arizona State University, Tempe, Arizona 85287
woodymonte@xtra.co.nz; woodymonte@canyoncountry.net;
The methanol from 2 L of diet soda, 5.6 12-oz cans, 20 mg/can, is
112 mg, 10% of the aspartame.
The EPA limit for water is 7.8 mg daily for methanol (wood alcohol),
a deadly cumulative poison.
Many users drink 1-2 L daily.
The reported symptoms are entirely consistent with chronic methanol
toxicity. (Fresh orange juice has 34 mg/L, but, like all juices, has 16
times more ethanol, which strongly protects against methanol.)
"The greater toxicity of methanol to man is deeply rooted in the
limited biochemical pathways available to humans for detoxification.
The loss of uricase (EC 1.7.3.3.),
formyl-tetrahydrofolate synthetase (EC 6.3.4.3.) (42)
and other enzymes (18) during evolution sets man apart from all
laboratory animals including the monkey (42).
There is no generally accepted animal model
for methanol toxicity (42, 59).
Humans suffer "toxic syndrome" (54) at a minimum lethal dose
of <1 gm/kg, much less than that of monkeys, 3-6 g/kg (42, 59).
The minimum lethal dose of methanol
in the rat, rabbit, and dog is 9.5, 7.0 , and 8.0 g/kg, respectively (43);
ethyl alcohol is more toxic than methanol to these test animals (43)."
Recent research [see links at end of post] supports his focus on the
methanol to formaldehyde toxic process:
"The United States Environmental Protection Agency in their
Multimedia Environmental Goals for Environmental Assessment
recommends a minimum acute toxicity concentration
of methanol in drinking water at 3.9 parts per million,
with a recommended limit of consumption below 7.8 mg/day (8).
This report clearly indicates that methanol:
"...is considered a cumulative poison due to the low rate of excretion
once it is absorbed. In the body, methanol is oxidized to
formaldehyde and formic acid; both of these metabolites are
toxic." (8)...
Recently the toxic role of formaldehyde (in methanol toxicity) has
been questioned (34).
No skeptic can overlook the fact that, metabolically, formaldehyde
must be formed as an intermediate to formic acid production (54).
Formaldehyde has a high reactivity which may be why it has not been
found in humans or other primates during methanol poisoning (59)....
If formaldehyde is produced from methanol and does have a
reasonable half life within certain cells in the poisoned organism
he chronic toxicological ramifications could be grave.
Formaldehyde is a known carcinogen (57) producing squanous-cell
carcinomas by inhalation exposure in experimental animals (22).
The available epidemiological studies do not provide adequate data
for assessing the carcinogenicity of formaldehyde in man (22, 24, 57).
However, reaction of formaldehyde with deoxyribonucleic acid
(DNA) has resulted in irreversible denaturation that could interfere
with DNA replication and result in mutation (37)..."
It is certain that high levels of aspartame use,
above 2 liters daily for months and years,
must lead to chronic formaldehyde-formic acid toxicity.
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.
J. Nutrition 1973 Oct; 103(10): 1454-1459.
Metabolism of aspartame in monkeys.
Oppermann JA, Muldoon E, Ranney RE.
Dept. of Biochemistry, Searle Laboratories,
Division of G.D. Searle and Co. Box 5110, Chicago, IL 60680
They found that about 70 % of the radioactive methanol in aspartame
put into the stomachs of 3 to 7 kg monkeys
was eliminated within 8 hours, with little additional elimination,
as carbon dioxide in exhaled air and as water in the urine.
They did not mention that this meant that about 30 % of the methanol
must transform into formaldehyde and then into formic acid,
both of which must remain as toxic products in all parts of the body.
They did not report any studies on the distribution of radioactivity
in body tissues, except that blood plasma proteins after 4 days
held 4 % of the initial methanol.
This study did not monitor long-term use of aspartame.
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/1463
Direct and indirect cellular effects of aspartame on the brain,
Humphries P, Pretorius E, Naude H, U. Pretoria, South Africa,
Eur J Clin Nutr. 2007 Aug 8: Murray 2007.08.12
http://groups.yahoo.com/group/aspartameNM/message/1340
aspartame groups and books: updated research review
of 2004.07.16: Murray 2006.05.11
details on 6 epidemiological studies since 2004 on diet soda
(mainly aspartame) correlations, as well as 14 other mainstream
studies on aspartame toxicity since summer 2005:
Murray 2007.11.18
http://rmforall.blogspot.com/2007_11_01_archive.htm
Wednesday, November 14, 2007
http://groups.yahoo.com/group/aspartameNM/message/1490
older women drinking over 2 aspartame beverages daily had 30%
decline kidney function in 11 years, Nurses Health Study, Julie Lin,
Gary C Curhan, Brigham and Women's Hospital, Boston:
Rich Murray 2009.11.02
http://rmforall.blogspot.com/2009_11_01_archive.htm
Monday, November 2, 2009
http://groups.yahoo.com/group/aspartameNM/message/1588
consider co-factors (methanol, formaldehyde, and protective folic
acid), re UK FSA test of aspartame in candy bars on 50 reactors,
Stephen L Atkin, Hull York Medical School:
Rich Murray 2009.09.29
http://rmforall.blogspot.com/2009_09_01_archive.htm
Tuesday, September 29, 2009
http://groups.yahoo.com/group/aspartameNM/message/1587
Included herein is substantial mainstream evidence that the natural
conversion in humans of orally ingested methanol into formaldehyde
and then formic acid results in substantial, durable, cumulative
retention of toxic reaction products.
Adequate folic acid levels expedite the safe metabolism of methanol
in most people.
Ethyl alcohol and folic acid in vegetables and fruits are sufficient
to protect most people from conversion of their methanol into
formaldehyde.
Many common agents interfere with folic acid (folic acid antagonists).
Additionally, genetic variations are potent.
About 3/4 of reactors are female.
Those who rarely have alcohol hangovers may be substantially immune
to methanol and formaldehyde.
Recent exposure to alcohol beverages, tobacco and wood smoke,
and a large variety of formaldehyde sources may compromise the
clarity of aspartame reaction tests.
Aspartame reactors often report allergies to many agents, with similar
symptoms: mercury (amalgams and fish), MSG and free glutamate in
foods (for instance, hydrolyzed vegetable or yeast protein), carbon
monoxide, molds, many foods, etc. -- up to Multiple Chemical
Sensitivity.
Aspartame reactors often take many steps to exercise, reduce stress,
lower salt, emphasize organic plant foods, reduce drug and chemical
exposures, limit protein and fat intake, use vitamin and mineral
supplements, limit processed foods -- thus complicating attempts to
create a matching control group, and introducing uncertainty about
whether the reactors are as vulnerable now as in the past, when they
may have had more negative factors for years.
So, genetic background, age, sex, obesity, existing illnesses, diet,
exercise, environmental toxins, medicines and drugs, parental
exposure to all these factors, and more may corrode the "gold
standard" of a single exposure double-blind experimental test,
especially for a rather modest test group of 50.
Perhaps, a more productive research strategy would be to test 10
reactors, one at a time, for 24 hours each, using a wide range of
tests, recording the enormous individual variations that are usually
swamped by taking group data averages.
Computerized tests facilitate fast, affordable measures of cognitive
and memory effects.
Full audio and video recording is now available.
Dimethyl dicarbonate, an approved additive for reducing fungi in
wines, perhaps with a neutral taste, quickly releases about the same
level of methanol upon ingestion as aspartame drinks, making
possible studies free of any possible "excitotoxic" effects of
aspartic acid and phenylalanine, while allowing a third beverage
to be a control substance.
This approach would also contribute to the meager research literature
about the role of methanol in alcohol hangovers.
aspartame reactors may send detailed feedback to Andrew Wadge,
UK Food Standards Agency to guide new pilot study re bad
reactions: Rich Murray 2009.06.22
http://rmforall.blogspot.com/2009_06_01_archive.htm
Monday, June 22, 2009
http://groups.yahoo.com/group/aspartameNM/message/1577
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.dorway.com/products.txt
[ rearranged, 11% methanol added ]
From the Nutrasweet Web Site: (amounts in various "foods")
Product Category -- Serving Size -- aspartame -- 11% methanol
Gelatin Dessert ----------- 8 ounces -----190 mg ---- 21 mg
Carbonated Beverage --- 12 ounces ----- 180 ------- 20
" ------------------------ 48 ounces ----- 720 ------- 79
Powdered Drink -------- 12 ounces ----- 180 -------- 20
Fruit Drink (10% juice) -- 12 ounces ----- 140 -------15.4
Hot Chocolate ----------- 12 ounces ----- 100 -------11
Yogurt ------------------- 8 ounces ----- 124 --------13.6
Ice Cream ---------------- 8 ounces ----- 100 ------- 11
Pudding Dessert ---------- 8 ounces ------ 50 --------- 5.5
Frozen Novelty ----------- 2-3 ounces ---- 50 --------- 5.5
Gum ----------------------- 1 stick -------- 6-8 -------- 0.7-0.9
Vitamins ------------------ 1 vitamin ------ 4 ---------- 0.44
Breath mint ---------------- 1 mint --------- 1.5 -------- 0.17
http://groups.yahoo.com/group/aspartameNM/message/846
aspartame in Merck Maxalt-MLT worsens migraine,
AstraZeneca Zomig, Eli Lilly Zyprexa,
J&J Merck Pepcid AC (Famotidine 10mg) Chewable Tab,
Pfizer Cool Mint Listerine Pocketpaks: Murray 2002.07.16
Migraine MLT-Down: an unusual presentation of migraine
in patients with aspartame-triggered headaches.
Newman LC, Lipton RB Headache 2001 Oct; 41(9): 899-901.
[ Merck 10-mg Maxalt-MLT, for migraine, has 3.75 mg aspartame,
while 12 oz diet soda has 200 mg. ]
Headache Institute, St. Lukes-Roosevelt Hospital Center,
New York, NY
Department of Neurology newmanache@aol.com
Albert Einstein College of Medicine, Bronx, NY
Innovative Medical Research RLipton@aecom.yu.edu
http://groups.yahoo.com/group/aspartameNM/message/855
Blumenthall & Vance: aspartame chewing gum headaches
Nov 1997: Murray 2002.07.28
Harvey J. Blumenthal, MD, Dwight A Vance, RPh
Chewing Gum Headaches. Headache 1997 Nov; 37(10): 665-6.
Department of Neurology, University of Oklahoma College of
Medicine, Tulsa, USA. neurotulsa@aol.com
Aspartame, a popular dietetic sweetener, may provoke headache in
some susceptible individuals. Herein, we describe three cases of
young women with migraine who reported their headaches could be
provoked by chewing gum sweetened with aspartame.
[ 6-8 mg aspartame per stick chewing gum ]
http://groups.yahoo.com/group/aspartameNM/message/1143
antiseptic? antifungal? antiviral? methanol (formaldehyde, formic
acid) disposition: Bouchard M et al, full plain text, 2001:
substantial
sources are degradation of fruit pectins, liquors, aspartame, smoke:
Murray 2005.01.05 rmforall
http://www.toxsci.oupjournals.org/cgi/content/full/64/2/169
free full text
A Biologically Based Dynamic Model for Predicting the Disposition
of Methanol and Its Metabolites in Animals and Humans.
Michèle Bouchard,
Robert C. Brunet,
Pierre-Olivier Droz,
and Gaétan Carrier.
Toxicological Sciences 64, 169-184 (2001)
Copyright © 2001 by the Society of Toxicology
[ extracts ]
"Exposure to methanol also results from the consumption of certain
foodstuffs (fruits, fruit juices, certain vegetables, aspartame
sweetener, roasted coffee, honey) and alcoholic beverages (Health
Effects Institute, 1987; Jacobsen et al., 1988).
[ It's unusual for a mainstream journal article to mention "fruits,
fruit juices, certain vegetables, aspartame sweetener" and "alcoholic
beverages" to be methanol sources.]
... little is known about the chronic effects of low exposure doses...
Systemic methanol is extensively metabolized by liver alcohol
dehydrogenase [ ADH ] and catalase-peroxidase enzymes to
formaldehyde, which is in turn rapidly oxidized to formic acid by
formaldehyde dehydrogenase enzymes...
Formaldehyde, as it is highly reactive, forms relatively stable
adducts with cellular constituents...
Primates and humans appear to be more susceptible to the acute
toxicity of methanol than rodents...
Although methanol has been reported to be metabolized mainly in
the liver, pulmonary metabolism is also likely to occur. Indeed,
the catalase-peroxidase system responsible for a major fraction of
methanol metabolism in rats is widely distributed in mammalian
tissues...
The model included a constant background whole body methanol
burden of 2.133 mmol, which corresponds to the mean blood
concentration of 0.5 mg/L of methanol measured by Osterloh et al.
(1996) in control subjects at the end of an 8-h frequent blood
sampling period...
... once formed, a substantial fraction of formaldehyde is converted
to unobserved forms. This pathway contributes to a long-term
unobserved compartment. The latter, most plausibly, represents
either the formaldehyde that ( directly or after oxidation to
formate )
binds to various endogenous molecules (Heck et al., 1983; Roe,
1982)...
That substantial amounts of methanol metabolites or by-products
are retained for a long time is verified by Horton et al. (1992)
who estimated that 18 h following an iv injection of 100 mg/kg
of 14C-methanol in male Fischer-344 rats, only 57% of the
dose was eliminated from the body. From the data of Dorman
et al. (1994) and Medinsky et al. (1997), it can further be
calculated that 48 h following the start of a 2-h inhalation
exposure to 900 ppm of 14C-methanol vapors in female
cynomolgus monkeys, only 23% of the absorbed 14C-methanol
was eliminated from the body. These findings are corroborated by
the data of Heck et al. (1983) showing that 40% of a
14C-formaldehyde inhalation dose remained in the body 70 h
postexposure...
Experimental studies on the detailed time profiles following
controlled repeated exposures to methanol are lacking...
Thus, in monkeys and plausibly humans, a much larger fraction of
body formaldehyde is rapidly converted to unobserved forms
rather than passed on to formate and eventually CO2."
If we assume 30% retention of durable cumulative toxic products of
formaldehyde and formic acid, then a 12-oz can diet drink gives 200
mg aspartame, 22 mg methanol, and 7 mg formaldehyde and formic
acid at 30% cumulative retention. We may add that well known
sources of formaldehyde include both wood and tobacco smoke,
and, notoriously, mobile homes. Two teams give evidence that
formaldehyde and formic acid from methanol in ethanol drinks
(often far above the 100 mg/L methanol in red wines, two times the
level in aspartame drinks) are the main cause of the many symptoms
of "morning after" hangovers.
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
Furthermore, BM Kapur et al, 2007 give evidence that formic acid
from methanol in ethanol drinks is a major cause of Fetal Alcohol
Syndrome, readily preventable by adequate levels of folic acid,
which expedites the safe metabolism of formaldehyde, in most
people.
"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." ...
"MeOH concentrations between 4 and 4500 mg/l can be present
in various alcoholic beverages (Sprung et al., 1988)."
A variety of mutations, as well as aspirin and many painkillers,
impede folic acid. However, fruits and vegetables give enough folic
acid to mitigate harm from their methanol. Then again, formaldehyde
may in many people treat infections by fungi, bacteria, and virusus.
All these unexamined co-factors have confused attempts to study
aspartame toxicity for three decades.
http://groups.yahoo.com/group/aspartameNM/message/1141
Nurses Health Study can quickly reveal the extent of aspartame
(methanol, formaldehyde, formic acid) toxicity: Murray 2004.11.21
The Nurses Health Study is a bonanza of information about the health
of probably hundreds of nurses who use 6 or more cans daily of diet
soft drinks -- they have also stored blood and tissue samples from
their immense pool of subjects, over 100,000 for decades.
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
A widely proclaimed NIH-AARP mass survey by U Lim et al. 2006,
while failing to show specific cancers with feeble diet drink
consumption data for a year for seniors, did find that 4% of a
half-million seniors drank 3 and more cans daily diet soda
[ 12-oz can gives 200 mg aspartame, 22 mg methanol,
7 mg formaldehyde and formic acid at 30% cumulative retention ]
aspartame mg/d
0 ---- under 100 - 100-200 - 200-400 - 400-600 - 600-1200 -
cohort %
46 ------- 25 ------ 13 ------- 7 --------- 5 ------ about 3 ----
over 1200 mg/d
under 1%
This is the first good data about the percentage of aspartame users
who use over 3 cans daily, averaging 5 cans daily at 200 mg per 12
oz can diet soda.
About 4% of 473,984 is 19,000 people, with a peak intake of 17
cans daily, and average 5 cans daily.
It would be worthwhile to investigate a wide variety of symptoms for
the 0.1 % of highest level users, about 500 people.
For about 200 million USA aspartame users, this would be 200,000
people.
The highest level 3400 mg aspartame [ 17 12-oz cans ] gives
11% = 374 mg methanol, 48 times the recommended daily limit of
consumption of 7.8 mg as recommended by the
Environmental Protection Agency (EPA).3
At 30% retention of cumulative toxic products of formaldehyde and
formic acid, these would be 125 mg, 60 times higher than the 1999
EPA alarm level for formaldehyde in daily drinking water of
1 ppm = 2 mg for average daily drinking water of 2 L daily.
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
40 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@catholic.ac.kr
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@RMV.se;
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
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
[ extracts ]
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
[ Extract ]
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.
Case Series
Six patients (ages 16 to 75 years) were referred for evaluation of
recalcitrant dermatitis. By history, five of the patients were noted
to have developed migraines following aspartame consumption; the
sixth reported dermatitis flares associated with diet cola
consumption of >2 liters/day.
All six patients had current environmental exposures to formaldehyde
or formaldehyde-releasing preservatives in their personal hygiene
products and/or regular consumption of "sugar-free food" artificially
sweetened with aspartame.
Based on their histories and clinical presentations, these patients
were patch-tested with the North American Contact Dermatitis
Group 65-allergen Standard Screening Series and selected
chemicals from the University of Miami vehicle, fragrance, bakery,
and textile trays.
All six patients had positive reactions to formaldehyde, and four had
additional positive reactions to formaldehyde-releasing preservatives
(FRPs). Expert counseling on allergen avoidance (including
avoidance of formaldehyde, FRPs, and aspartame) and alternative
product recommendations were provided to the patients.
At their follow-up appointments (between 8 and 12 weeks), all the
patients showed clearance of their dermatitis. Four patients (two
inadvertently) resumed their consumption of aspartame and
subsequently returned for an additional follow-up visit. Three of the
first five patients had recurrences of both their migraines and their
dermatitis; the sixth patient (who had no migraines) had a positive
rechallenge dermatitis. These four patients were again counseled on
avoidance regimen.
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
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@contactderm.net;
Sarah A. Stechschulte, BA sstechschulte@gmail.com
_____________________________________________________
Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298 rmforall@comcast.net
http://groups.yahoo.com/group/AstroDeep/messages
http://RMForAll.blogspot.com new primary archive
http://groups.yahoo.com/group/aspartameNM/messages
group with 142 members, 1,589 posts in a public archive
http://groups.yahoo.com/group/aspartame/messages
group with 1204 members, 23,955 posts in a public archive
http://groups.yahoo.com/group/rmforall/messages
participant, Santa Fe Complex www.sfcomplex.org
_____________________________________________________
Sunday, November 15, 2009
methanol (11% of aspartame), made by body into formaldehyde in many vulnerable tissues, causes modern diseases, Woodrow C Monte PhD
Re: [meteorite-list] Observations on Age of Carolina Bays: Paul H: Rich Murray 2009.11.15
Re: [meteorite-list] Observations on Age of Carolina Bays: Paul H: Rich Murray 2009.11.15
http://rmforall.blogspot.com/2009_11_01_archive.htm
Sunday, November 15, 2009
http://groups.yahoo.com/group/astrodeep/message/32
Hello all,
I am very appreciative of Paul's conscientious, careful
contributions, based on civility, reason, and public evidence.
Will there be many confirmations of ET markers in classic
Carolina Bays? And in similar clusters in many parts of the
world?
Will a single place and time be found for a single or multiple
sources, or multiple sources with multiple places and times?
Are data already available for mineral elements and isotopes
at classic and possible Carolina Bay type craters?
I find cracked, broken, overturned, and tossed bedrocks
up to 2 m size at many craters near Santa Fe, New Mexico.
Many of these rocks have white, grey, greenish, red-brown,
and black glazes or coatings, from 0.1 to 10 cm thick, even
curled around the edge of bedrock layers for 10 cm,
often with rough surface textures with little wind or water
erosion.
Also ordinary white quartz rocks up to 20 cm, glazed on one
side with what appears as 0.2 to 3 cm melted quartz,
sometimes with a yellow tinge.
And 3 m thick level sandstone layers, exposed roadcuts
about 30 m above the landscape, that have up to 10 cm white
and gray mineral layers that appear to have been plastered on
the vertical surfaces.
I will glad to show visitors my samples, and to give tours of
accessible sites -- many right beside public roads.
I will be happy to search for sites with Google Earth for free
within 80 km of any location, so they can be studied by those
who live near the center coordinates.
Best, Rich Murray
exact Carolina Bay crater locations, RB Firestone, A West, et al,
two YD reviews, 2008 June, 2009 Nov, also 3
upcoming abstracts: Rich Murray 2009.11.14
http://rmforall.blogspot.com/2009_11_01_archive.htm
Saturday, November 14, 2009
http://groups.yahoo.com/group/astrodeep/message/31
nanodiamond evidence for 12,900 BP Clovis extinction impact,
Santa Rosa Island, discussion on Scientific American website,
Carolina Bay type craters east of Las Vegas, NM:
Rich Murray 2009.09.15
http://rmforall.blogspot.com/2009_06_01_archive.htm
Friday, July 24, 2009
http://groups.yahoo.com/group/AstroDeep/28
widespread Carolina Bay type craters from Clovis comet
12,900 Ya BP? -- 0.7 M long NS crater with fractured
red sandstone on SW rim, CR C 53A, 20 miles E of
Las Vegas, NM: Rich Murray 2009.06.08
http://rmforall.blogspot.com/2009_06_01_archive.htm
Monday, June 8, 2009
http://groups.yahoo.com/group/AstroDeep/27
_____________________________________________________
----- Original Message -----
From:
To:
Sent: Sunday, November 15, 2009 12:46 PM
Subject: [meteorite-list] Observations on Age of Carolina Bays
______________________________________________
http://www.meteoritecentral.com
Meteorite-list mailing listis
Meteorite-list@meteoritecentral.com
http://six.pairlist.net/mailman/listinfo/meteorite-list
As I will discuss in a paper that I am preparing, Carolina Bays
are not at all difficult to date in terms of their age relative to the
Younger Dryas as documented in a number of published, peer-
reviewed papers and specific Cultural Resource Management
reports. There is a huge amount of information available about
either the age or relative age of the Carolina Bays to be found
by carefully and persistently digging through the large number
of publications about them and the geomorphology of the
Atlantic coastal plain.
1. Radiocarbon dates are all minimum dates indicating
when ground water conditions allowed the preservation of
organic material within them. All the basal dates tells a person
is the last time that a bay was permanently filled with water
because of a rising groundwater table, which is greatly influenced
by rises and falls in eustatic sea level. Despite the fact that the
radiocarbon dates are only minimum dates, they clearly
demonstrate that the Carolina Bays predate the Younger Dryas
event.
2. Optically Stimulated Luminescence (OSL) dating is now
a well established and proven dating method, which gives
credible dates for the age of these landforms. A person might
argued for mxing of older and younger sand, except that
Dr. Ivester, whom I personally discussed this matter with
on the GSA 2008 Meeting sand mantle, biomantle, mima
mound field trip told me that he did not find the anomalies
in the raw data for his dates that such mixing would create.
Also, a person can always use single-grain OSL dating to
unequivocally test for such mixing. Given that Dr. Ivester is
a very experienced Quaternary geologist, the claim he dated
the wrong material, in my opinion is the type of lame excuse
that I hear from Young Earth creationists when the data
refutes what they want to believe is the truth. If a person is
going to make this claim, they need to back it up with hard
and well-documented facts for it to be credible in any
manner at all.
3. The pollen records from several Carolina Bays clearly
go back to the last Glacial Maximum and in one bay,
back to Oxygen Isotope Stage 5a. In many more Carolina
Bays, the paleoenvironmental records start during full
glacial conditions, several thousands of years before the
hypothesized Younger Dryas event. Common sense and
basic stratigraphic principles dictate that the Carolina Bays
containing these records existed before any hypothesized
Younger Dryas events, as it is physically impossible for
any sort of exterrestrial event / impact to create craters
thousands of years before it occurs. It is impossible for
mixing of sediment to have produced these records, as
the paleoenvironmental records recovered from Carolina
Bays correlate precisely in time and nature to palynological
records from non-Carolina Bay lakes and swamps in the
same area as a Carolina Bay.
4. Cross-cutting relationships between well dated fluvial
terraces (lacking Carolina Bays) cut and inset into older
terraces and the Carolina Bays they exhibit establish the
minimum age of Carolina Bays. Similarly the superposition
dunes fields, which formed during the Late Glacial
Maximum and lacking Carolina Bays, upon Carolina
Bays that they partial bury, establish the pre-Younger
Dryas age of the Carolina Bays. Both cross-cutting
relationships and superposition are documented in great
detail by LIDAR DEMs available for large parts of the
Atlantic Coast.
5. Stratified archaeological sites demonstrate how
Carolina Bays have been modified after the Younger
Dryas. Carolina Bays on restricted government
reservations indicate how historic argriculture and
urban development have modified Carolina Bays
during the last few decades by comparison.
6. All the presence of hypothesized impactites filling
the Carolina Bays indicates is that preexisting Carolina
Bays was filled by material from this hypothesized impact.
The presence of hypothetical impactites within the loose
soils of coastal plain sands forming the rim of Carolina
Bays indicates that bioturbation mixed material fell
on the surface into the loose sand forming the rims.
The churning of surface materials deep into thick sandy
epipedons is a well documented and well known process.
7. In the northern extent of the distribution of Carolina
Bays, their orientation varies by over 120 degrees, and based
upon cross-cutting relationships and great differences in
the degree of degradation of their rims, there are strong
indications of multiple generations of Carolina Bays having
formed at greatly different times. The claim by Firestone that
both the Carolina Bays and playa and other lakes point at a
central point is based on him having overlooked a significant
amount of orientation data that both subtly and grossly
contradicts and ultimately refutes his claim.
8. Although it is still in the realm of speculation, there
appears to be evidence that indicates that the Carolina Bays
in the Midlothian area are much older than the typical
Carolina Bays that are found on Pleistocene coast-wise
terraces.
In my opinion, as far as the Carolina Bays are concerned,
they are a nothing more than a time-consuming red herring
of gigantic proportions. Even if the Carolina Bays are impact
features of some sort, they clearly are much too old be
connected in anyway with a Younger Dryas event.
I am not going into references and figures because I am
pulling this all together into a paper that I am working on
and will submit to a journal that I know will both welcome
it and have it rigerously peer-reviewed. Before submitting
it, I will also have two or three select people review it.
Yours, Paul H.
_____________________________________________________
Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298 rmforall@comcast.net
http://groups.yahoo.com/group/AstroDeep/messages
http://RMForAll.blogspot.com new primary archive
http://groups.yahoo.com/group/aspartameNM/messages
group with 142 members, 1,588 posts in a public archive
http://groups.yahoo.com/group/aspartame/messages
group with 1204 members, 23,955 posts in a public archive
http://groups.yahoo.com/group/rmforall/messages
participant, Santa Fe Complex www.sfcomplex.org
_____________________________________________________
http://rmforall.blogspot.com/2009_11_01_archive.htm
Sunday, November 15, 2009
http://groups.yahoo.com/group/astrodeep/message/32
Hello all,
I am very appreciative of Paul's conscientious, careful
contributions, based on civility, reason, and public evidence.
Will there be many confirmations of ET markers in classic
Carolina Bays? And in similar clusters in many parts of the
world?
Will a single place and time be found for a single or multiple
sources, or multiple sources with multiple places and times?
Are data already available for mineral elements and isotopes
at classic and possible Carolina Bay type craters?
I find cracked, broken, overturned, and tossed bedrocks
up to 2 m size at many craters near Santa Fe, New Mexico.
Many of these rocks have white, grey, greenish, red-brown,
and black glazes or coatings, from 0.1 to 10 cm thick, even
curled around the edge of bedrock layers for 10 cm,
often with rough surface textures with little wind or water
erosion.
Also ordinary white quartz rocks up to 20 cm, glazed on one
side with what appears as 0.2 to 3 cm melted quartz,
sometimes with a yellow tinge.
And 3 m thick level sandstone layers, exposed roadcuts
about 30 m above the landscape, that have up to 10 cm white
and gray mineral layers that appear to have been plastered on
the vertical surfaces.
I will glad to show visitors my samples, and to give tours of
accessible sites -- many right beside public roads.
I will be happy to search for sites with Google Earth for free
within 80 km of any location, so they can be studied by those
who live near the center coordinates.
Best, Rich Murray
exact Carolina Bay crater locations, RB Firestone, A West, et al,
two YD reviews, 2008 June, 2009 Nov, also 3
upcoming abstracts: Rich Murray 2009.11.14
http://rmforall.blogspot.com/2009_11_01_archive.htm
Saturday, November 14, 2009
http://groups.yahoo.com/group/astrodeep/message/31
nanodiamond evidence for 12,900 BP Clovis extinction impact,
Santa Rosa Island, discussion on Scientific American website,
Carolina Bay type craters east of Las Vegas, NM:
Rich Murray 2009.09.15
http://rmforall.blogspot.com/2009_06_01_archive.htm
Friday, July 24, 2009
http://groups.yahoo.com/group/AstroDeep/28
widespread Carolina Bay type craters from Clovis comet
12,900 Ya BP? -- 0.7 M long NS crater with fractured
red sandstone on SW rim, CR C 53A, 20 miles E of
Las Vegas, NM: Rich Murray 2009.06.08
http://rmforall.blogspot.com/2009_06_01_archive.htm
Monday, June 8, 2009
http://groups.yahoo.com/group/AstroDeep/27
_____________________________________________________
----- Original Message -----
From:
To:
Sent: Sunday, November 15, 2009 12:46 PM
Subject: [meteorite-list] Observations on Age of Carolina Bays
______________________________________________
http://www.meteoritecentral.com
Meteorite-list mailing listis
Meteorite-list@meteoritecentral.com
http://six.pairlist.net/mailman/listinfo/meteorite-list
As I will discuss in a paper that I am preparing, Carolina Bays
are not at all difficult to date in terms of their age relative to the
Younger Dryas as documented in a number of published, peer-
reviewed papers and specific Cultural Resource Management
reports. There is a huge amount of information available about
either the age or relative age of the Carolina Bays to be found
by carefully and persistently digging through the large number
of publications about them and the geomorphology of the
Atlantic coastal plain.
1. Radiocarbon dates are all minimum dates indicating
when ground water conditions allowed the preservation of
organic material within them. All the basal dates tells a person
is the last time that a bay was permanently filled with water
because of a rising groundwater table, which is greatly influenced
by rises and falls in eustatic sea level. Despite the fact that the
radiocarbon dates are only minimum dates, they clearly
demonstrate that the Carolina Bays predate the Younger Dryas
event.
2. Optically Stimulated Luminescence (OSL) dating is now
a well established and proven dating method, which gives
credible dates for the age of these landforms. A person might
argued for mxing of older and younger sand, except that
Dr. Ivester, whom I personally discussed this matter with
on the GSA 2008 Meeting sand mantle, biomantle, mima
mound field trip told me that he did not find the anomalies
in the raw data for his dates that such mixing would create.
Also, a person can always use single-grain OSL dating to
unequivocally test for such mixing. Given that Dr. Ivester is
a very experienced Quaternary geologist, the claim he dated
the wrong material, in my opinion is the type of lame excuse
that I hear from Young Earth creationists when the data
refutes what they want to believe is the truth. If a person is
going to make this claim, they need to back it up with hard
and well-documented facts for it to be credible in any
manner at all.
3. The pollen records from several Carolina Bays clearly
go back to the last Glacial Maximum and in one bay,
back to Oxygen Isotope Stage 5a. In many more Carolina
Bays, the paleoenvironmental records start during full
glacial conditions, several thousands of years before the
hypothesized Younger Dryas event. Common sense and
basic stratigraphic principles dictate that the Carolina Bays
containing these records existed before any hypothesized
Younger Dryas events, as it is physically impossible for
any sort of exterrestrial event / impact to create craters
thousands of years before it occurs. It is impossible for
mixing of sediment to have produced these records, as
the paleoenvironmental records recovered from Carolina
Bays correlate precisely in time and nature to palynological
records from non-Carolina Bay lakes and swamps in the
same area as a Carolina Bay.
4. Cross-cutting relationships between well dated fluvial
terraces (lacking Carolina Bays) cut and inset into older
terraces and the Carolina Bays they exhibit establish the
minimum age of Carolina Bays. Similarly the superposition
dunes fields, which formed during the Late Glacial
Maximum and lacking Carolina Bays, upon Carolina
Bays that they partial bury, establish the pre-Younger
Dryas age of the Carolina Bays. Both cross-cutting
relationships and superposition are documented in great
detail by LIDAR DEMs available for large parts of the
Atlantic Coast.
5. Stratified archaeological sites demonstrate how
Carolina Bays have been modified after the Younger
Dryas. Carolina Bays on restricted government
reservations indicate how historic argriculture and
urban development have modified Carolina Bays
during the last few decades by comparison.
6. All the presence of hypothesized impactites filling
the Carolina Bays indicates is that preexisting Carolina
Bays was filled by material from this hypothesized impact.
The presence of hypothetical impactites within the loose
soils of coastal plain sands forming the rim of Carolina
Bays indicates that bioturbation mixed material fell
on the surface into the loose sand forming the rims.
The churning of surface materials deep into thick sandy
epipedons is a well documented and well known process.
7. In the northern extent of the distribution of Carolina
Bays, their orientation varies by over 120 degrees, and based
upon cross-cutting relationships and great differences in
the degree of degradation of their rims, there are strong
indications of multiple generations of Carolina Bays having
formed at greatly different times. The claim by Firestone that
both the Carolina Bays and playa and other lakes point at a
central point is based on him having overlooked a significant
amount of orientation data that both subtly and grossly
contradicts and ultimately refutes his claim.
8. Although it is still in the realm of speculation, there
appears to be evidence that indicates that the Carolina Bays
in the Midlothian area are much older than the typical
Carolina Bays that are found on Pleistocene coast-wise
terraces.
In my opinion, as far as the Carolina Bays are concerned,
they are a nothing more than a time-consuming red herring
of gigantic proportions. Even if the Carolina Bays are impact
features of some sort, they clearly are much too old be
connected in anyway with a Younger Dryas event.
I am not going into references and figures because I am
pulling this all together into a paper that I am working on
and will submit to a journal that I know will both welcome
it and have it rigerously peer-reviewed. Before submitting
it, I will also have two or three select people review it.
Yours, Paul H.
_____________________________________________________
Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298 rmforall@comcast.net
http://groups.yahoo.com/group/AstroDeep/messages
http://RMForAll.blogspot.com new primary archive
http://groups.yahoo.com/group/aspartameNM/messages
group with 142 members, 1,588 posts in a public archive
http://groups.yahoo.com/group/aspartame/messages
group with 1204 members, 23,955 posts in a public archive
http://groups.yahoo.com/group/rmforall/messages
participant, Santa Fe Complex www.sfcomplex.org
_____________________________________________________
Saturday, November 14, 2009
exact Carolina Bay crater locations, RB Firestone, A West, et al, two YD reviews, 2008 June, 2009 Nov, also 3 new abstracts: Rich Murray 2009.11.14
exact Carolina Bay crater locations, RB Firestone, A West, et al, two YD reviews, 2008 June, 2009 Nov, also 3 upcoming abstracts: Rich Murray 2009.11.14
http://rmforall.blogspot.com/2009_11_01_archive.htm
Saturday, November 14, 2009
http://groups.yahoo.com/group/astrodeep/message/31
___________________________________________________
http://ie.lbl.gov/mammoth/mammoth.html Firestone paper links
http://ie.lbl.gov/mammoth/TunguskaConferenceA4_Firestone.pdf
37 pages
Firestone, R.B.; West, A.; Revay Zs.; Hagstrum J.T.; Belgya T.;
Que Hee S.S.; and Smith, A.R. (2008)
Analysis of the Younger Dryas Impact Layer,
100 years since Tunguska phenomenon: past, present, and future,
June 26-28, Moscow, in press. 54 references
R.B. Firestone 1,
A. West 2,
Zs. Revay 3,
J. T. Hagstrum 4,
T. Belgya 3,
S.S. Que Hee 5,
and A.R. Smith 1
1 Lawrence Berkeley National Laboratory, Berkeley, Ca 94720,
[ #43 Henderson, G.M.; Hall, B.L.; Smith, A.; & Robinson, L.F.
(2006) Chem. Geol. 226, 298-308 ]
2 GeoScience Consulting, Box 1636, Dewey, Arizona 86327,
3 Institute for Isotope and Surface Chemistry,
P.O. Box 77, H-1525 Budapest, Hungary,
4 U.S. Geological Survey, 345 Middlefield Road MS 937,
Menlo Park, CA 94025,
5 University of California, Los Angeles, ICP-MS Facility,
Los Angeles, CA 90095
Abstract
We have uncovered a thin layer of magnetic grains and
microspherules, carbon spherules, and glass-like carbon at
nine sites across North America, a site in Belgium, and
throughout the rims of 16 Carolina Bays.
It is consistent with the ejecta layer from an impact event and
has been dated to 12.9 ka BP coinciding with the onset of
Younger Dryas (YD) cooling and widespread megafaunal
extinctions in North America.
At many locations the impact layer is directly below a black mat
marking the sudden disappearance of the megafauna and Clovis
people.
The distribution pattern of the Younger Dryas boundary (YDB)
ejecta layer is consistent with an impact near the Great Lakes
that deposited terrestrial-like ejecta near the impact site and
unusual, titanium-rich projectile-like ejecta further away.
High water content associated with the ejecta, up to 28 at.%
hydrogen (H), suggests the impact occurred over the Laurentide
Ice Sheet.
YDB microspherules and magnetic grains are highly enriched in
TiO2.
Magnetic grains from several sites are enriched in iridium (Ir), up
to 117 ppb.
The TiO2/FeO, K/Th, TiO2/Zr, Al2O3/FeO+MgO, CaO/Al2O3,
REE/chondrite, FeO/MnO ratios and SiO2, Na2O, K2O, Cr2O3,
Ni, Co, U, Th and other trace element abundances are inconsistent
with all terrestrial and extraterrestrial (ET) sources except for
KREEP, a lunar igneous rock rich in potassium (K), rare-earth
elements (REE), phosphorus (P), and other incompatible elements
including U and Th.
Normal Fe, Ti, and 238U/235U isotopic abundances were found
in the magnetic grains, but 234U was enriched over equilibrium
values by 50% in Murray Springs and by 130% in Belgium.
40K abundance is enriched by up to 100% in YDB sediments and
Clovis chert artifacts.
Highly vesicular carbon spherules containing nanodiamonds,
glass-like carbon, charcoal and soot found in large quantities in
the YDB layer are consistent with an impact followed by intense
burning.
Four holes in the Great Lakes, some deeper than Death Valley,
are proposed as possible craters produced by the airburst
breakup of a loosely aggregated projectile.
from Table 2:
CLOVIS SITES:
Blackwater Draw, NM----- 34.27564N 103.32633W
Chobot, AB, CAN--------- 52.99521N 114.71773W
Gainey, MI----------------- 42.93978N,, 83.72111W
Murray Springs, AZ --------31.57103N 110.17814W
Wally's Beach, AB--------- 49.34183N 113.15440W
Topper, SC -- T-1--------- 33.00554N,, 81.49001W
Topper, SC -- T-2--------- 33.00545N,, 81.49056W
CLOVIS-AGE SITES:
Daisy Cave, CA----------- 34.04207N 120.32009W
Lake Hind, MB, CAN----- 49.43970N 100.69783W
Lommel, BELGIUM------- 51.23580N,,,,, 5.26403E
Morley drumlin, AB-------- 51.14853N, 114.93546W
CAROLINA BAYS: (with paleosol beneath)
Blackville, SC -- T13------- 33.36120N 81.30440W
Myrtle Beach, SC -- M31-- 33.83776N 78.69565W
Lk Mattamuskeet -- LM---- 35.51865N 76.267917W
Howard Bay, NC -- HB---- 34.81417N 78.84753W
[ http://ie.lbl.gov/mammoth/PP43A_10.pdf ] poster 1.07 MB
CAROLINA BAYS: (no paleosol reached)
Myrtle Beach, SC -- M33-- 33.81883N 78.74181W
Myrtle Beach, SC -- M24-- 33.83118N 78.72379W
Myrtle Beach, SC -- M32-- 33.84034N 78.70906W
Salters Lake, NC -- B14--- 34.70992N 78.62043W
Lumberton, NC -- L33----- 34.75566N 79.10870W
Lumberton, NC -- L28----- 34.77766N 79.05008W
Lumberton, NC -- L31----- 34.78117N 79.04774W
Lumberton, NC -- L32----- 34.79324N 79.01871W
Moore Cty, NC -- MC1--- 35.30104N 78. 84753W
Sewell, NC -- FS3--------- 34.95800N 78.70280W
Lake Phelps -- LP---------- 35.78412N 76.434383W
I looked all these up with Google Earth and Maps.
In many cases, many craters overlap complexly, so it
is not clear which is the one studied.
It is always easy to find many more in each cluster.
http://journalofcosmology.com/Extinction105.html 20 pages
Firestone, R. B., 2009,
The Case for the Younger Dryas Extraterrestrial Impact Event:
Mammoth, Megafauna, and Clovis Extinction, 12,900 Years Ago.
Journal of Cosmology. vol. 2, pp. 256-285. 67 references
Abstract
The onset of >1000 years of Younger Dryas cooling, broad-scale
extinctions, and the disappearance of the Clovis culture in North
America simultaneously occurred 12,900 years ago followed
immediately by the appearance of a carbon-rich black layer at
many locations.
In situ bones of extinct megafauna and Clovis tools occur only
beneath this black layer and not within or above it.
At the base of the black mat at 9 Clovis-age sites in North
America and a site in Belgium numerous extraterrestrial impact
markers were found including magnetic grains highly enriched in
iridium, magnetic microspherules, vesicular carbon spherules
enriched in cubic, hexagonal, and n-type nanodiamonds,
glass-like carbon containing Fullerenes and nanodiamonds,
charcoal, soot, and polycyclic aromatic hydrocarbons.
The same impact markers were found mixed throughout the
sediments of 15 Carolina Bays, elliptical depressions along the
Atlantic coast, whose parallel major axes point towards either
the Great Lakes or Hudson Bay. The magnetic grains and
spherules have an unusual Fe/Ti composition similar to lunar
Procellarum KREEP Terrane and the organic constituents are
enriched in 14C leading to radiocarbon dates often well into
the future.
These characteristics are inconsistent with known meteorites
and suggest that the impact was by a previous unobserved,
possibly extrasolar body.
The concentration of impact markers peaks near the Great Lakes
and their unusually high water content suggests that a 4.6 km-wide
comet fragmented and exploded over the Laurentide Ice Sheet
creating numerous craters that now persist at the bottom of the
Great Lakes.
The coincidence of this impact, the onset of Younger Dryas
cooling, extinction of the megafauna, and the appearance of a
black mat strongly suggests that all these events are directly
related.
These results have unleashed an avalanche of controversy
which I will address in this paper.
Keywords: Younger Dryas, Extinctions, Extraterrestrial Impacts,
Black Mat, Clovis, Mammoth, Megafauna
"West also investigated sediment from 15 Carolina Bays,
elliptical depressions found along the Atlantic coast from
New England to Florida (Eyton and Parkhurst, 1975),
whose parallel major axes point towards either the
Great Lakes or Hudson Bay as seen in Fig. 3.
Similar bays have tentatively been identified in Texas,
New Mexico, Kansas, and Nebraska (Kuzilla, 1988)
although they are far less common in this region.
Their major axes also point towards the Great Lakes.
The formation of the Carolina Bays was originally ascribed
to meteor impacts (Melton and Schriever, 1933) but when
no meteorites were found they were variously ascribed
to marine, eolian, or other terrestrial processes.
West found abundant microspherules, carbon spherules,
glass-like carbon, charcoal, Fullerenes, and soot throughout
the Carolina Bays but not beneath them as shown in Fig. 4.
Outside of the Bays these markers were only found only
in the YDB layer as in other Clovis-age sites."
"Figure 3. The Carolina Bays are >>500,000 elliptical,
shallow lakes, wetlands, and depressions, up to >>10 km long,
with parallel major axes (see inset) pointing toward the
Great Lakes or Hudson Bay.
Similar features found in fewer numbers in the plains states
also point towards the Great Lakes.
These bays were not apparent topographical features
until the advent of aerial photography."
This figure shows nice color LIDAR typographic images
of 8 craters, 0.5 to 4 km wide.
I used Ctr + in Windows Vista to expand the NA map, counting
18 elliiptical craters in the Great Plains:
Texas 4
New Mexico 3
Colorado 2
Kansas 4
Nebraska 5.
It's not easy to locate the LIDAR craters on the photo images
of Google Maps and Earth, but I've had a lot of practice with
these states and all over Earth this year, including brief visits to
many craters in New Mexico and Kauai.
I managed to find Salt Lake, NM, and Coyote Lake, TX.
The features are often complex enough to make assigning a
size fairly arbitrary.
Nice maps and typo maps and tourist info are available free on:
www.trails.com
www.goingoutside.com
Salt Lake, New Mexico 34.079932 -103.089600,
1.177 km lowest crater elevation, NEE axis, EES rim el 1.215,
N edge el 1.183, ~10x3.7, E from center 7 km to Texas and
18 km to Coyote Lake (another LIDAR image), much white
deposits, N of Rd 235ew, just S of Rd 88 S Roosevelt Road 10,
24 km E of 206ns, 26 km EES of Portales, striking "comb" of
many parallel ditches running into lake from E side
Little Salt Lake is 7 km W of center, el 1.183, 3.6 wide, E comb,
very similar and obviously connected
Coyote Lake, Texas 34.102105 -102.872902 1.162 site N 1.200
15 km SW of Muleshoe, size 5.7x4.3, E comb, W of Rd 214 ns
Baileyboro Lake 34.0045 -102.8206 1.155 site SW 1.186
no comb, size 2
Upper White Lake 33.9426 -102.7678 1.129 site W 1.171
S,E comb, size 1.8, 2 km W of Rd 214ns
just 1 km NE is a double crater, 1.129 site W 1.169,
S,E comb, 1.6x1.3, just W of Rd 214ns
then just N is Muleshoe National Wildlife Refuge, same size,
with a .24 wide flat round dark crater 1.667 site W 1.170
just E across Rt 214ns is Upper Pauls Lake, complex 2 km size,
1.129 site W 1.147
33.860831 -101.449100 1.038 site W 1.125
NNE 15x8, 29 km SSE of craters by Rd 214ns,
10 km W of Rd 385ns, 15 km SW of Littlefield on Rd 84nwse,
comb on whole E side
Returning to New Mexico, Lane Salt Lake, similar to Salt Lake
33.465718 -103.608318 1.265 site 1.300 size 10x4 NE
90 km SW of Salt Lake, E comb
34.038716 -103.350290, el 1.266, site about 1.269, .16 wide,
W of 206ns, just S of S Roosevelt Rd 15, dark
34.026073 -103.399379 1.278 site 1.283 size .76,
extends to SW
34.026338 -103.437950 1.279 site 1.287,
cut by Rd 235ew size 1.5
WSNM 32.755610 -106.413363 1.186 site S 1.210 68x33 km
White Sands National Monument, gypsum sand
Howard Bay, NC -- HB---- 34.81417 -78.84753
[ Wet center marked in blue on Google Maps Terrain,
named Pages Lake .7x.2, with Mines Creek NW to SE
at both ends, but built over on Google Earth,
34.815274 -783014 .030 is lowest point,
just SW of Rd 87, is 13.7 km W of Marshy Bay,
which is NW of Bladen Lakes State Forest.
site W .044 N .044 E creek .010 S .043 all at 1.3 radius,
Rd 87 cuts NW across NE half, farms completely hide crater,
steep bare brown red rise to NWSE ridge from .030 to .044
from .090 to 1.17 radius must be NE rim.
Many local farm roads provide convenient access
across crater interior. ]
[ http://ie.lbl.gov/mammoth/PP43A_10.pdf ] poster 1.07 MB
R. Kobres 1,
G. A. Howard 2 ( george@restorationsystems.com ),
A.West 3 ,
R. B. Firestone 4,
J. P. Kennett 5,
D. Kimbel 2,
W. Newell 2
1 U. of Georgia, Athens, GA, 30602,
2 Restoration Systems, L.L.C., Raleigh, NC 27604,
3 GeoScience Consulting, Dewey, Arizona 86327,
4 Lawrence Berkeley National Lab Berkeley, CA 94720,
5 Dept. of Earth Sciences, U. of California, Santa Barbara, CA 93106.
B23A-0948
Surface Vertical Exaggeration = 7x
Scale: 250 meters
Bay is 2.6 km long
The Carolina Bays are a group of up to 500,000 lakes and
wetlands stretching from Florida to New Jersey
along the Atlantic Ocean.
They are up to11 km in length and about 15 meters in depth.
The elliptical shapes, overlapping rims (Fig.1, left), and common
orientation towards the Great Lakes region have generated many
hypotheses about how the Bays formed.
Extraterrestrial Impact.
This hypothesis was developed by Melton and Schriever (1933)
and expanded by Prouty, (1934) and Eyton and Parkhurst(1970),
who proposed that a meteorite or comet exploded above the
Great Lakes, producing no primary crater.
The secondary fragments and/orshock wave from that blast
formed rough, shallow craters on the Atlantic Coast, and,
over time, wind and water altered those craters to form the
Carolina Bays.
The Impact Hypothesis accounts fo rthe orientation of Bays,
overlapping raised rims, and the fact that they do not appear
to be forming today.
However, there are problems:
(a) reported Bay ages vary by tens of thousands of years; and
(b) no one has found impact material in the Bays, such as
shocked quartz or other ET markers.
Wind-and-Water.
This hypothesis was offered in various versions
first by Raisz (1934) and others, whosuggested that wind
created deflation basins or parabolic dunes, which later
filled to become lakes that evolved into Carolina Bays.
Johnson (1942) proposed that springs or groundwater
dissolution of soluble minerals caused subsidence, which formed
water-filled depressions that became the Bays.
Kaczorowski (1976) formulated what has become one of the
prevailing views, suggesting that strong ice-age winds blew
across irregular lakes, generating powerful eddy-currents.
Those currents gradually reshaped the lakes into oriented,
elliptical Carolina Bays, whose long axes were perpendicular
to the prevailing wind direction.
The rims were built from wind-transported sand that
accumulated from the dry lake beds during droughts.
While this overall hypothesis clarifies many Bay features,
it has several key weaknesses.
The theory can not explain:
(a)how wind and water could create up to four layers of
stacked Bays with overlapping Bay rims, as seen in Fig.1; and
(b) why modern severe wind and water action, such as occurs
during hurricanes, does not produce or reshape Bays
on the Coastal Plain today.
Objective:
Because of the above questions, the Bay controversy has
remained unresolved for more than 80 years.
In this investigation, we tested these various hypotheses by
examining Howard Bay, which is located about 2km north of
the town of Duartin, Bladen County, North Carolina.
RESULTS
Nine suites of samples were extracted along the 2.6-km long axis
of Howard Bay using a combination of trenching and coring with
an AMS Soil Core Sampler.
Maximum depths varied from about 2 to10 meters.
ET Markers.
Analysis of the samples reveals an assemblage of abundant
carbon spherules (Fig.2), magneticgrains, microspherules,
glass-like carbon, and iridium, typical of the12.9-ka YDB
impact layer found at many other non-bay sites
across North America.
The impact layer conforms to the bottom of the basin
(dark blue on the core symbols), suggesting that the markers
began to be deposited immediately or soon after the Bay formed.
Fig.3 shows the results from Core #11 near the center of
Howard Bay, where carbon spherules are found from
nearly the surface down to about 7.5 meters deep.
Glass-like carbon abundances (not shown) followed
a similar pattern.
Iridium (15 ppb) was found at the lowest level of the basin.
Silt and Clay.
Trenching shows that theBay is filled with >6m of cross-bedded
eolian sand (Fig.4) with no evidence of lacustrine sedimentation.
As a further test, sediment from Core #11 was analyzed with
Standard ASTM sieves, and the results are shown in Fig.3.
The top1 meter averaged about 14% silt and clay, and from
about 1 to 9 meters, there is 0.3% to 6% silt and clay,
values consistent with eolian deposition.
There is typically less than a few percent of any particles
larger than medium sand.
DISCUSSION
Analysis reveals that, unlike typical, peat-rich Carolina Bays,
Howard Bay essentially lacks peat, diatoms, pollen, and other
organic materials, and it also lacks substantial silt and clay.
That suggests this Bay never held water for a sustained
length of time.
Furthermore, the presence of extensive eolian sand calls
into question prevailing hypotheses
(a) that all Bays were lakes and ponds in the past and that
their shapes were formed by wave action, and
(b) that ground water movement led to subsidence that
formed the Bay.
In addition, the presence of impact markers, including high
concentrations of iridium in a layer just above the basal
sediments of this Bay, supports the impact hypothesis
for Bay formation.
The age of Howard Bay appears consistent with and
not older than the YD impact event;
however, our research did not address the reported anomalous
ages of other Bays, a question which remains unresolved.
REFERENCES
1. Melton, F.A. & Scriever, W. (1933) J. Geol. 41, 52-56.
2. Prouty, W.F. (1952) Bulletin of the GSA, Vol. 63, 167-224..
3. Eyton, J.R. & J.I. Parkhurst (1975)
Dept. of Geography Paper No. 9, U. of Illinois.
4. Raisz, (1934) J. Geol., Vol. 42:839-848
5. Johnson, D.W. (1942) The Origin of the Carolina Bays.
Columbia University Press, New York.
6. Kaczorowski, R.T. (1976) The Carolina Bays:
a comparison with modern oriented lakes,
PhD thesis, University of South Carolina, Columbia.
Base image courtesy of James M. Salmons,
President, GeoDataCorp.,
104 E Horton St., Zebulon, NC 27597,
919-269-5744 www.GeoDataMapping.com ]
[ Fig. 1 is a LIDAR elevation image of Marshy Bay,
Google Maps and Earth give fine natural color view,
resolution .001 km, size 3.3x1.8 km, el .033 km,
4 km E of Cedar Creek Road ns, Rd 53ns,
30 km E of Hwy 95ns, 40 km SE of Fayetteville,
NW of or part of Bladen Lakes State Forest,
90 km NW of the coast at Wilmington ]
with Little Singletary Lake [ North Carolina 28399 ]
and Horseshoe Lake
to the lower L and lower R, all oriented NW. ]
One side in the debate has conceded a major point to their critics,
while presenting more evidence for many other major points.
AGU Fall Meeting 2009
ID# PP31D-1389
Location: Poster Hall (Moscone South)
Time of Presentation: Dec 16 8:00 AM - 12:20 PM
The platinum group metals in Younger Dryas Horizons
are terrestrial
Y. Wu 1; E. Wikes 1; J. Kennett 2; A. West 3; M. Sharma 1
1. Dept of Earth Sciences, Dartmouth College, Hanover, NH
2. Department of Earth Sciences,
University of California, Santa Barbara, CA, USA.
3. GeoScience Consulting, Dewey, AZ, USA.
The Younger Dryas (YD) event, which began 12,900 years ago,
was a period of abrupt and rapid cooling in the
Northern Hemisphere whose primary cause remains unclear.
The prevalent postulated mechanism is a temporary shutdown
of the thermohaline circulation following the breakup of an ice
dam in North America.
Firestone et al. (2007) proposed that the cooling was triggered
by multiple cometary airbursts and/or impacts that engendered
enormous environmental changes and disrupted the thermohaline
circulation.
The evidence in support for this hypothesis is a black layer in
North America and in Europe marking the YD boundary
containing charcoal, soot, carbon spherules and glass-like carbon
suggesting extensive and intense forest fires.
This layer is also enriched in magnetic grains high in iridium,
magnetic microspherules, fullerenes containing extraterrestrial
He-3, and nanodiamonds.
Whereas the nanodiamonds could be produced in an impact or
arrive with the impactor, the cometary burst/impact hypothesis
remains highly controversial as the YD horizon lacks important
impact markers such as craters, breccias, tektites and
shocked minerals.
Firestone et al. (2007) contend that bulk of Ir found at the YD
boundary is associated with magnetic grains.
The key issue is whether this Ir is meteorite derived.
We used Ir and Os concentrations and Os isotopes to
investigate the provenance of the platinum group metals in the
YD horizon.
The bulk sediment samples from a number of North American
YD sites (Blackwater Draw, Murray Springs, Gainey,
Sheriden Cave, and Myrtle Beach) and a site in Europe (Lommel)
do not show any traces of meteorite derived Os and Ir.
The [Os] = 2 to 45 pg/g in these sediments and the 187Os/188Os
ratios are similar to the upper continental crustal values (~1.3),
much higher than those in meteorites (0.13).
Higher [Os] is observed in Blackwater Draw (= 194 pg/g).
However, the Os/Ir ratio in Blackwater Draw is 5
(not 1 as expected for a meteorite) and
187Os/188Os ratio = 1.35, which remains constant above and
below the YD horizon.
Kennett et al. (2009) report 200 ppb of nanodiamonds and
about 4 ppb of Ir in bulk sediments from Murray Springs.
Since chondritic meteorites contain approximately 400 ppm
of presolar nanodiamonds and about 500 ppb of osmium,
simple mixing requires that the YD horizon at Murray Springs
should contain about 250 pg/g of Os.
However, the observed Os concentration of YD horizon at
Murray Springs is only 45 pg/g and the 187Os/188Os ratio is 1.66.
These observations suggest that if there was an impact that
produced the nanodiamonds and dispersed them,
it did not provide Os (and Ir) to the Murray Springs and other
North American sites.
We have so far separated and analyzed magnetic grains from
Gainey and Lommel and find their [Os] and 187Os/188Os
ratios consistent with a terrestrial origin.
The [Os] of microspherules analyzed so far are too low to be
derived from meteorites.
Our analyses therefore do not support an extraterrestrial origin of
the platinum metals in YD horizons from North America and Europe.
Contact Information: Yingzhe Wu, Hanover, New Hampshire, USA 03755
AGU Fall Meeting 2009
ID# PP31D-1392
Location: Poster Hall (Moscone South)
Time of Presentation: Dec 16 8:00 AM - 12:20 PM
Nanodiamonds and Carbon Spherules from Tunguska, the K/T
Boundary, and the Younger Dryas Boundary Layer
J. H. Wittke 1; T. E. Bunch 1; A. West 2; J. Kennett 3;
D. J. Kennett 4; G. A. Howard 5
1. Dept. of Geology, Northern Arizona Univ., Flagstaff, AZ, USA.
2. GeoScience Consulting, Dewey, AZ, USA.
3. Dept. of Earth Science and Marine Science Institute,
Univ. of California, Santa Barbara, CA, USA.
4. Dept. of Anthropology, Univ. of Oregon, Eugene, OR, USA.
5. Restoration Systems, LLC, Raleigh, NC, USA.
More than a dozen markers, including nanodiamonds (NDs) and
carbon spherules (CS), occur in a sedimentary layer marking the
onset of the Younger Dryas (YD) cooling episode at ~12.9 ka.
This boundary layer, called the YDB, has been found at nearly
forty locations across North America, Europe, and Asia,
although not all markers are present at any given site.
Firestone et al. (2007) and Kennett et al. (2008, 2009)
proposed that these markers resulted from a cosmic
impact/airburst and impact-related biomass burning.
Here we report features common to the YDB event, the
Cretaceous-Tertiary (K/T) impact, and the Tunguska airburst
of 1908.
In sediments attributed to each event, we and other
researchers have recovered NDs either inside or closely
associated with CS, which appear to be the high-temperature
by-products of biomass burning.
CS range in diameter from about 500 nanometers to
4 millimeters with a mean of ~100 microns,
and they typically contain NDs, including lonsdaleite
(hexagonal diamonds), in the interior matrix and in the crust.
To date, CS and NDs have been found in the K/T layer
in the United States, Spain, and New Zealand.
Similarly, CS and NDs have been found in the YDB layer
in the United States, Canada, United Kingdom, Belgium,
the Netherlands, Germany, and France.
Thus far, every site examined contains NDs and/or CS in the
K/T and YDB layers; conversely, we have yet to detect CS
associated with NDs in any non-YDB sediments tested.
Five allotropes of NDs have been identified in association with
CS: cubic diamonds, lonsdaleite, n-diamonds, p-diamonds,
and i-carbon, which are differentiated by slight variations
in their crystalline structure.
All allotropes have been identified using scanning electron
microscopy (SEM), high-resolution electron microscopy (HREM),
and transmission electron microscopy (TEM) with confirmation
by selected area diffraction (SAED).
Lonsdaleite is found on Earth only in three instances:
(1) in the laboratory, where it is produced by shock synthesis
under a high-temperature-high-pressure regime
(~1000°C to 1700°C at 15 GPa) or by carbon vapor deposition
(CVD) under a very-high-temperature-low-pressure regime
(~13,000°C at 300 Torr) (Maruyama et al., 1993);
(2) after arrival on Earth inside extraterrestrial material; and
(3) as a result of high-temperature cosmic impact/airbursts.
Lonsdaleite associated with CS has been found in sediments
only at the K/T, the YDB, and Tunguska, consistent with the
hypothesis that all three events have cosmic origins,
although the nature of the impactors may have been different.
Contact Information: James H. Wittke,
Flagstaff, Arizona, USA, 86011-4099
AGU Fall Meeting 2009
ID# PP33B-08
Location: 2006 (Moscone West)
Time of Presentation: Dec 16 3:04 PM - 3:16 PM
Testing Younger Dryas ET Impact (YDB) Evidence
at Hall's Cave, Texas
T. W. Stafford 1; E. Lundelius 2; J. Kennett 3; D. J. Kennett 4;
A. West 5; W. S. Wolbach 6
1. Stafford Research, Inc., Lafayette, CO, USA.
2. Dept. of Geological Sciences, Univ. of Texas, Austin, TX, USA.
3. Dept. of Earth Science & Marine Science Institute,
Univ. of California, Santa Barbara, CA, USA.
4. Dept. of Anthropology, Univ. of Oregon, Eugene, OR, USA.
5. GeoScience Consulting, Dewey, AZ, USA.
6. Dept. of Chemistry, DePaul Univ., Chicago, IL, USA.
Hall's Cave, Kerrville County Texas, 167 km WSW of Austin,
provides a unique opportunity for testing the presence of a
chronostratigraphic datum (YDB layer) containing rare and
exotic proxies, including nanodiamonds, aciniform soot, and
magnetic spherules, the origins of which remain controversial,
but possibly derive from a cosmic impact ~12,900 CAL BP.
The karst-collapse cave in Cretaceous limestone on the
Edwards Plateau contains ? 3.7 m of stratified clays grading to
clayey silts recording continuous deposition from 16 ka RC yr
to present.
The cave's small catchment area and mode of deposition were
constant, and the stratigraphy is well dated based on 162
AMS 14C dates from individual vertebrate fossils, snails,
charcoal, and sediment chemical fractions.
The cave sequence contains an abundant small animal vertebrate
fossil record, exhibiting biostratigraphic changes, and the timing
of the late Pleistocene megafaunal extinction is consistent with
that elsewhere in North America.
At 151 cm below datum is the extremely sharp, smooth contact
separating lower, dusky red (2.5YR3/2) clays below from
overlying dark reddish brown (5YR3/3) clays (forming a
20-cm-thick dark layer) and dating to 13,000 CAL BP,
at or close to the age of the YDB datum elsewhere.
This appears to be the most distinctive lithologic change of the
deglacial sequence.
Sediments at or within 10 cm of this contact contain the local
extinction of 4 species of bats, the local extinction of the prairie dog
(Cynomys sp.) and perhaps other burrowing mammals in response
to decrease in soil thickness, and the uppermost occurrence of 6
late Pleistocene megafaunal taxa that, although rare in the cave,
do not extend younger than 12.9 ka.
We collected and analyzed sediments at high resolution above
and below the distinct lithologic contact at 151 cm.
The red clays from 151 to 153 cm and immediately preceding the
lithologic contact contain an abundance of nanodiamonds
(5 different allotropes), aciniform soot at 2400 ppm, magnetic
spherules, and carbon spherules, all of which we interpret as
evidence for a unique chronostratigraphic marker (YDB)
in the Western Hemisphere.
Because the age of this horizon is ~ 13,000 CAL BP, we
interpret the age of the event as the beginning of the
Younger Dryas cooling.
Regional soil erosion began ~15,000 CAL BP and continued
until 7000 CAL BP, but dating suggests that there is no
discontinuity or hiatus in deposition, and thus, the exotic materials
in that layer are not considered to be erosional accumulations.
Future analyses include sub-centimeter sampling over the
YD boundary, quantification of nanodiamonds and other
event-proxies within 1000 yr of the boundary and in sediments
several 1000 years older and younger, continued refinement of
the AMS 14C record to determine within 50 yr the location of
12,900 CAL BP datum and high resolution analysis
of small animal biostratigraphy.
Contact Information: Thomas W. Stafford,
Lafayette, Colorado 80026
[ 30.135347 -99.537902 M. Jennifer Cooke et al, 2003 Oct,
study of Hall's Cave, 4 p ]
www.geo.utexas.edu/faculty/banner/Publications/Halls_Cave_Geology_03.pdf
For most of these craters, white minerals are striking.
Analysis of elements and isotopes should prove any evidence
of ET origin, and indicate temperatures and pressures
of deposition onto target rocks from steam explosions
of ice comet fragments.
The shared level of minimal erosion indicates
a shared early Holocene origin.
Amateurs should be encouraged to contribute observations
and samples.
Scientists can organize a center for analyzing samples at a
modest profit, while freely sharing data and research.
Websites, online journals, videos, magazines, books, and
movies can generate reasonable profits in the service of science.
The emerging insights into a past universal truama will lead
to a increased shared sense of community in our human family.
It is necessary to assess any future risks.
nanodiamond evidence for 12,900 BP Clovis extinction impact,
Santa Rosa Island, discussion on Scientific American website,
Carolina Bay type craters east of Las Vegas, NM:
Rich Murray 2009.09.15
http://rmforall.blogspot.com/2009_06_01_archive.htm
Friday, July 24, 2009
http://groups.yahoo.com/group/AstroDeep/28
widespread Carolina Bay type craters from Clovis comet
12,900 Ya BP? -- 0.7 M long NS crater with fractured
red sandstone on SW rim, CR C 53A, 20 miles E of
Las Vegas, NM: Rich Murray 2009.06.08
http://rmforall.blogspot.com/2009_06_01_archive.htm
Monday, June 8, 2009
http://groups.yahoo.com/group/AstroDeep/27
For Google Earth, here are the Windows/Linux keyboard
commands that make it easy to "fly" easily,
creating an intuitive 3D grasp of the landscape -- my laptop
runs at 1 GHZ with a graphics card, Windows Vista, Chrome,
and 3 GB RAM:
Full screen mode: F11
Lat/Long grid: Ctrl L
Slow movement down: add Alt before other keys
Zoom in, out: PgUp, PgDn keys
Move left, right, forward, back: arrow keys
Tilt view up, down: Shift down arrow, up arrow
Rotate view in circle clockwise, counterclockwise:
Shift right arrow, left arrow
Tilt up towards horizon, down towards directly below:
Shift down arrow, up arrow
Stop, start movement: space bar
Look in any direction: Ctrl, left mouse button and drag
New placemark: Ctrl Shift P
To delete or rewrite a placemark title,
right click it and select Properties.
Reset view to north as forward: n
Reset tilt to top-down view: u
Select Tools to select Web to return to your other screens.
It's easy to look down about 45 degrees while moving straight
ahead in any direction at an eye elevation of 1-200 km,
scanning a straight strip half-way around the world,
stopping to placemark, examine, and measure any features.
http://worldwind.arc.nasa.gov/java/
Requirements: a 3D video card with updated drivers is necessary.
World Wind has been tested on Nvidia, ATI/AMD, and Intel
platforms using Windows, MacOS 10.4, and Fedora Core 6.
WW gives exact altitudes and ocean depths.
WW images omit human features and give good resolution
from above 30 km.
http://worldwind.arc.nasa.gov/graphics/keychart.jpg
Keyboard controls:
Pan: arrow keys
Rotate LR: A,D keys
Tilt forward down, back up: W,S keys
Zoom down, up: 7 or Home, 1 or End
Stop: space bar or 5.
Position info: F10
Crosshairs: F9
Boundaries: F5
Placenames: F6
Lat/Long Lines: F7
Planet Axis: F8
Dynamic Layers: F1
_____________________________________________________
Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298 rmforall@comcast.net
http://groups.yahoo.com/group/AstroDeep/messages
http://RMForAll.blogspot.com new primary archive
http://groups.yahoo.com/group/aspartameNM/messages
group with 142 members, 1,588 posts in a public archive
http://groups.yahoo.com/group/aspartame/messages
group with 1204 members, 23,955 posts in a public archive
http://groups.yahoo.com/group/rmforall/messages
participant, Santa Fe Complex www.sfcomplex.org
_____________________________________________________
http://rmforall.blogspot.com/2009_11_01_archive.htm
Saturday, November 14, 2009
http://groups.yahoo.com/group/astrodeep/message/31
___________________________________________________
http://ie.lbl.gov/mammoth/mammoth.html Firestone paper links
http://ie.lbl.gov/mammoth/TunguskaConferenceA4_Firestone.pdf
37 pages
Firestone, R.B.; West, A.; Revay Zs.; Hagstrum J.T.; Belgya T.;
Que Hee S.S.; and Smith, A.R. (2008)
Analysis of the Younger Dryas Impact Layer,
100 years since Tunguska phenomenon: past, present, and future,
June 26-28, Moscow, in press. 54 references
R.B. Firestone 1,
A. West 2,
Zs. Revay 3,
J. T. Hagstrum 4,
T. Belgya 3,
S.S. Que Hee 5,
and A.R. Smith 1
1 Lawrence Berkeley National Laboratory, Berkeley, Ca 94720,
[ #43 Henderson, G.M.; Hall, B.L.; Smith, A.; & Robinson, L.F.
(2006) Chem. Geol. 226, 298-308 ]
2 GeoScience Consulting, Box 1636, Dewey, Arizona 86327,
3 Institute for Isotope and Surface Chemistry,
P.O. Box 77, H-1525 Budapest, Hungary,
4 U.S. Geological Survey, 345 Middlefield Road MS 937,
Menlo Park, CA 94025,
5 University of California, Los Angeles, ICP-MS Facility,
Los Angeles, CA 90095
Abstract
We have uncovered a thin layer of magnetic grains and
microspherules, carbon spherules, and glass-like carbon at
nine sites across North America, a site in Belgium, and
throughout the rims of 16 Carolina Bays.
It is consistent with the ejecta layer from an impact event and
has been dated to 12.9 ka BP coinciding with the onset of
Younger Dryas (YD) cooling and widespread megafaunal
extinctions in North America.
At many locations the impact layer is directly below a black mat
marking the sudden disappearance of the megafauna and Clovis
people.
The distribution pattern of the Younger Dryas boundary (YDB)
ejecta layer is consistent with an impact near the Great Lakes
that deposited terrestrial-like ejecta near the impact site and
unusual, titanium-rich projectile-like ejecta further away.
High water content associated with the ejecta, up to 28 at.%
hydrogen (H), suggests the impact occurred over the Laurentide
Ice Sheet.
YDB microspherules and magnetic grains are highly enriched in
TiO2.
Magnetic grains from several sites are enriched in iridium (Ir), up
to 117 ppb.
The TiO2/FeO, K/Th, TiO2/Zr, Al2O3/FeO+MgO, CaO/Al2O3,
REE/chondrite, FeO/MnO ratios and SiO2, Na2O, K2O, Cr2O3,
Ni, Co, U, Th and other trace element abundances are inconsistent
with all terrestrial and extraterrestrial (ET) sources except for
KREEP, a lunar igneous rock rich in potassium (K), rare-earth
elements (REE), phosphorus (P), and other incompatible elements
including U and Th.
Normal Fe, Ti, and 238U/235U isotopic abundances were found
in the magnetic grains, but 234U was enriched over equilibrium
values by 50% in Murray Springs and by 130% in Belgium.
40K abundance is enriched by up to 100% in YDB sediments and
Clovis chert artifacts.
Highly vesicular carbon spherules containing nanodiamonds,
glass-like carbon, charcoal and soot found in large quantities in
the YDB layer are consistent with an impact followed by intense
burning.
Four holes in the Great Lakes, some deeper than Death Valley,
are proposed as possible craters produced by the airburst
breakup of a loosely aggregated projectile.
from Table 2:
CLOVIS SITES:
Blackwater Draw, NM----- 34.27564N 103.32633W
Chobot, AB, CAN--------- 52.99521N 114.71773W
Gainey, MI----------------- 42.93978N,, 83.72111W
Murray Springs, AZ --------31.57103N 110.17814W
Wally's Beach, AB--------- 49.34183N 113.15440W
Topper, SC -- T-1--------- 33.00554N,, 81.49001W
Topper, SC -- T-2--------- 33.00545N,, 81.49056W
CLOVIS-AGE SITES:
Daisy Cave, CA----------- 34.04207N 120.32009W
Lake Hind, MB, CAN----- 49.43970N 100.69783W
Lommel, BELGIUM------- 51.23580N,,,,, 5.26403E
Morley drumlin, AB-------- 51.14853N, 114.93546W
CAROLINA BAYS: (with paleosol beneath)
Blackville, SC -- T13------- 33.36120N 81.30440W
Myrtle Beach, SC -- M31-- 33.83776N 78.69565W
Lk Mattamuskeet -- LM---- 35.51865N 76.267917W
Howard Bay, NC -- HB---- 34.81417N 78.84753W
[ http://ie.lbl.gov/mammoth/PP43A_10.pdf ] poster 1.07 MB
CAROLINA BAYS: (no paleosol reached)
Myrtle Beach, SC -- M33-- 33.81883N 78.74181W
Myrtle Beach, SC -- M24-- 33.83118N 78.72379W
Myrtle Beach, SC -- M32-- 33.84034N 78.70906W
Salters Lake, NC -- B14--- 34.70992N 78.62043W
Lumberton, NC -- L33----- 34.75566N 79.10870W
Lumberton, NC -- L28----- 34.77766N 79.05008W
Lumberton, NC -- L31----- 34.78117N 79.04774W
Lumberton, NC -- L32----- 34.79324N 79.01871W
Moore Cty, NC -- MC1--- 35.30104N 78. 84753W
Sewell, NC -- FS3--------- 34.95800N 78.70280W
Lake Phelps -- LP---------- 35.78412N 76.434383W
I looked all these up with Google Earth and Maps.
In many cases, many craters overlap complexly, so it
is not clear which is the one studied.
It is always easy to find many more in each cluster.
http://journalofcosmology.com/Extinction105.html 20 pages
Firestone, R. B., 2009,
The Case for the Younger Dryas Extraterrestrial Impact Event:
Mammoth, Megafauna, and Clovis Extinction, 12,900 Years Ago.
Journal of Cosmology. vol. 2, pp. 256-285. 67 references
Abstract
The onset of >1000 years of Younger Dryas cooling, broad-scale
extinctions, and the disappearance of the Clovis culture in North
America simultaneously occurred 12,900 years ago followed
immediately by the appearance of a carbon-rich black layer at
many locations.
In situ bones of extinct megafauna and Clovis tools occur only
beneath this black layer and not within or above it.
At the base of the black mat at 9 Clovis-age sites in North
America and a site in Belgium numerous extraterrestrial impact
markers were found including magnetic grains highly enriched in
iridium, magnetic microspherules, vesicular carbon spherules
enriched in cubic, hexagonal, and n-type nanodiamonds,
glass-like carbon containing Fullerenes and nanodiamonds,
charcoal, soot, and polycyclic aromatic hydrocarbons.
The same impact markers were found mixed throughout the
sediments of 15 Carolina Bays, elliptical depressions along the
Atlantic coast, whose parallel major axes point towards either
the Great Lakes or Hudson Bay. The magnetic grains and
spherules have an unusual Fe/Ti composition similar to lunar
Procellarum KREEP Terrane and the organic constituents are
enriched in 14C leading to radiocarbon dates often well into
the future.
These characteristics are inconsistent with known meteorites
and suggest that the impact was by a previous unobserved,
possibly extrasolar body.
The concentration of impact markers peaks near the Great Lakes
and their unusually high water content suggests that a 4.6 km-wide
comet fragmented and exploded over the Laurentide Ice Sheet
creating numerous craters that now persist at the bottom of the
Great Lakes.
The coincidence of this impact, the onset of Younger Dryas
cooling, extinction of the megafauna, and the appearance of a
black mat strongly suggests that all these events are directly
related.
These results have unleashed an avalanche of controversy
which I will address in this paper.
Keywords: Younger Dryas, Extinctions, Extraterrestrial Impacts,
Black Mat, Clovis, Mammoth, Megafauna
"West also investigated sediment from 15 Carolina Bays,
elliptical depressions found along the Atlantic coast from
New England to Florida (Eyton and Parkhurst, 1975),
whose parallel major axes point towards either the
Great Lakes or Hudson Bay as seen in Fig. 3.
Similar bays have tentatively been identified in Texas,
New Mexico, Kansas, and Nebraska (Kuzilla, 1988)
although they are far less common in this region.
Their major axes also point towards the Great Lakes.
The formation of the Carolina Bays was originally ascribed
to meteor impacts (Melton and Schriever, 1933) but when
no meteorites were found they were variously ascribed
to marine, eolian, or other terrestrial processes.
West found abundant microspherules, carbon spherules,
glass-like carbon, charcoal, Fullerenes, and soot throughout
the Carolina Bays but not beneath them as shown in Fig. 4.
Outside of the Bays these markers were only found only
in the YDB layer as in other Clovis-age sites."
"Figure 3. The Carolina Bays are >>500,000 elliptical,
shallow lakes, wetlands, and depressions, up to >>10 km long,
with parallel major axes (see inset) pointing toward the
Great Lakes or Hudson Bay.
Similar features found in fewer numbers in the plains states
also point towards the Great Lakes.
These bays were not apparent topographical features
until the advent of aerial photography."
This figure shows nice color LIDAR typographic images
of 8 craters, 0.5 to 4 km wide.
I used Ctr + in Windows Vista to expand the NA map, counting
18 elliiptical craters in the Great Plains:
Texas 4
New Mexico 3
Colorado 2
Kansas 4
Nebraska 5.
It's not easy to locate the LIDAR craters on the photo images
of Google Maps and Earth, but I've had a lot of practice with
these states and all over Earth this year, including brief visits to
many craters in New Mexico and Kauai.
I managed to find Salt Lake, NM, and Coyote Lake, TX.
The features are often complex enough to make assigning a
size fairly arbitrary.
Nice maps and typo maps and tourist info are available free on:
www.trails.com
www.goingoutside.com
Salt Lake, New Mexico 34.079932 -103.089600,
1.177 km lowest crater elevation, NEE axis, EES rim el 1.215,
N edge el 1.183, ~10x3.7, E from center 7 km to Texas and
18 km to Coyote Lake (another LIDAR image), much white
deposits, N of Rd 235ew, just S of Rd 88 S Roosevelt Road 10,
24 km E of 206ns, 26 km EES of Portales, striking "comb" of
many parallel ditches running into lake from E side
Little Salt Lake is 7 km W of center, el 1.183, 3.6 wide, E comb,
very similar and obviously connected
Coyote Lake, Texas 34.102105 -102.872902 1.162 site N 1.200
15 km SW of Muleshoe, size 5.7x4.3, E comb, W of Rd 214 ns
Baileyboro Lake 34.0045 -102.8206 1.155 site SW 1.186
no comb, size 2
Upper White Lake 33.9426 -102.7678 1.129 site W 1.171
S,E comb, size 1.8, 2 km W of Rd 214ns
just 1 km NE is a double crater, 1.129 site W 1.169,
S,E comb, 1.6x1.3, just W of Rd 214ns
then just N is Muleshoe National Wildlife Refuge, same size,
with a .24 wide flat round dark crater 1.667 site W 1.170
just E across Rt 214ns is Upper Pauls Lake, complex 2 km size,
1.129 site W 1.147
33.860831 -101.449100 1.038 site W 1.125
NNE 15x8, 29 km SSE of craters by Rd 214ns,
10 km W of Rd 385ns, 15 km SW of Littlefield on Rd 84nwse,
comb on whole E side
Returning to New Mexico, Lane Salt Lake, similar to Salt Lake
33.465718 -103.608318 1.265 site 1.300 size 10x4 NE
90 km SW of Salt Lake, E comb
34.038716 -103.350290, el 1.266, site about 1.269, .16 wide,
W of 206ns, just S of S Roosevelt Rd 15, dark
34.026073 -103.399379 1.278 site 1.283 size .76,
extends to SW
34.026338 -103.437950 1.279 site 1.287,
cut by Rd 235ew size 1.5
WSNM 32.755610 -106.413363 1.186 site S 1.210 68x33 km
White Sands National Monument, gypsum sand
Howard Bay, NC -- HB---- 34.81417 -78.84753
[ Wet center marked in blue on Google Maps Terrain,
named Pages Lake .7x.2, with Mines Creek NW to SE
at both ends, but built over on Google Earth,
34.815274 -783014 .030 is lowest point,
just SW of Rd 87, is 13.7 km W of Marshy Bay,
which is NW of Bladen Lakes State Forest.
site W .044 N .044 E creek .010 S .043 all at 1.3 radius,
Rd 87 cuts NW across NE half, farms completely hide crater,
steep bare brown red rise to NWSE ridge from .030 to .044
from .090 to 1.17 radius must be NE rim.
Many local farm roads provide convenient access
across crater interior. ]
[ http://ie.lbl.gov/mammoth/PP43A_10.pdf ] poster 1.07 MB
R. Kobres 1,
G. A. Howard 2 ( george@restorationsystems.com ),
A.West 3 ,
R. B. Firestone 4,
J. P. Kennett 5,
D. Kimbel 2,
W. Newell 2
1 U. of Georgia, Athens, GA, 30602,
2 Restoration Systems, L.L.C., Raleigh, NC 27604,
3 GeoScience Consulting, Dewey, Arizona 86327,
4 Lawrence Berkeley National Lab Berkeley, CA 94720,
5 Dept. of Earth Sciences, U. of California, Santa Barbara, CA 93106.
B23A-0948
Surface Vertical Exaggeration = 7x
Scale: 250 meters
Bay is 2.6 km long
The Carolina Bays are a group of up to 500,000 lakes and
wetlands stretching from Florida to New Jersey
along the Atlantic Ocean.
They are up to11 km in length and about 15 meters in depth.
The elliptical shapes, overlapping rims (Fig.1, left), and common
orientation towards the Great Lakes region have generated many
hypotheses about how the Bays formed.
Extraterrestrial Impact.
This hypothesis was developed by Melton and Schriever (1933)
and expanded by Prouty, (1934) and Eyton and Parkhurst(1970),
who proposed that a meteorite or comet exploded above the
Great Lakes, producing no primary crater.
The secondary fragments and/orshock wave from that blast
formed rough, shallow craters on the Atlantic Coast, and,
over time, wind and water altered those craters to form the
Carolina Bays.
The Impact Hypothesis accounts fo rthe orientation of Bays,
overlapping raised rims, and the fact that they do not appear
to be forming today.
However, there are problems:
(a) reported Bay ages vary by tens of thousands of years; and
(b) no one has found impact material in the Bays, such as
shocked quartz or other ET markers.
Wind-and-Water.
This hypothesis was offered in various versions
first by Raisz (1934) and others, whosuggested that wind
created deflation basins or parabolic dunes, which later
filled to become lakes that evolved into Carolina Bays.
Johnson (1942) proposed that springs or groundwater
dissolution of soluble minerals caused subsidence, which formed
water-filled depressions that became the Bays.
Kaczorowski (1976) formulated what has become one of the
prevailing views, suggesting that strong ice-age winds blew
across irregular lakes, generating powerful eddy-currents.
Those currents gradually reshaped the lakes into oriented,
elliptical Carolina Bays, whose long axes were perpendicular
to the prevailing wind direction.
The rims were built from wind-transported sand that
accumulated from the dry lake beds during droughts.
While this overall hypothesis clarifies many Bay features,
it has several key weaknesses.
The theory can not explain:
(a)how wind and water could create up to four layers of
stacked Bays with overlapping Bay rims, as seen in Fig.1; and
(b) why modern severe wind and water action, such as occurs
during hurricanes, does not produce or reshape Bays
on the Coastal Plain today.
Objective:
Because of the above questions, the Bay controversy has
remained unresolved for more than 80 years.
In this investigation, we tested these various hypotheses by
examining Howard Bay, which is located about 2km north of
the town of Duartin, Bladen County, North Carolina.
RESULTS
Nine suites of samples were extracted along the 2.6-km long axis
of Howard Bay using a combination of trenching and coring with
an AMS Soil Core Sampler.
Maximum depths varied from about 2 to10 meters.
ET Markers.
Analysis of the samples reveals an assemblage of abundant
carbon spherules (Fig.2), magneticgrains, microspherules,
glass-like carbon, and iridium, typical of the12.9-ka YDB
impact layer found at many other non-bay sites
across North America.
The impact layer conforms to the bottom of the basin
(dark blue on the core symbols), suggesting that the markers
began to be deposited immediately or soon after the Bay formed.
Fig.3 shows the results from Core #11 near the center of
Howard Bay, where carbon spherules are found from
nearly the surface down to about 7.5 meters deep.
Glass-like carbon abundances (not shown) followed
a similar pattern.
Iridium (15 ppb) was found at the lowest level of the basin.
Silt and Clay.
Trenching shows that theBay is filled with >6m of cross-bedded
eolian sand (Fig.4) with no evidence of lacustrine sedimentation.
As a further test, sediment from Core #11 was analyzed with
Standard ASTM sieves, and the results are shown in Fig.3.
The top1 meter averaged about 14% silt and clay, and from
about 1 to 9 meters, there is 0.3% to 6% silt and clay,
values consistent with eolian deposition.
There is typically less than a few percent of any particles
larger than medium sand.
DISCUSSION
Analysis reveals that, unlike typical, peat-rich Carolina Bays,
Howard Bay essentially lacks peat, diatoms, pollen, and other
organic materials, and it also lacks substantial silt and clay.
That suggests this Bay never held water for a sustained
length of time.
Furthermore, the presence of extensive eolian sand calls
into question prevailing hypotheses
(a) that all Bays were lakes and ponds in the past and that
their shapes were formed by wave action, and
(b) that ground water movement led to subsidence that
formed the Bay.
In addition, the presence of impact markers, including high
concentrations of iridium in a layer just above the basal
sediments of this Bay, supports the impact hypothesis
for Bay formation.
The age of Howard Bay appears consistent with and
not older than the YD impact event;
however, our research did not address the reported anomalous
ages of other Bays, a question which remains unresolved.
REFERENCES
1. Melton, F.A. & Scriever, W. (1933) J. Geol. 41, 52-56.
2. Prouty, W.F. (1952) Bulletin of the GSA, Vol. 63, 167-224..
3. Eyton, J.R. & J.I. Parkhurst (1975)
Dept. of Geography Paper No. 9, U. of Illinois.
4. Raisz, (1934) J. Geol., Vol. 42:839-848
5. Johnson, D.W. (1942) The Origin of the Carolina Bays.
Columbia University Press, New York.
6. Kaczorowski, R.T. (1976) The Carolina Bays:
a comparison with modern oriented lakes,
PhD thesis, University of South Carolina, Columbia.
Base image courtesy of James M. Salmons,
President, GeoDataCorp.,
104 E Horton St., Zebulon, NC 27597,
919-269-5744 www.GeoDataMapping.com ]
[ Fig. 1 is a LIDAR elevation image of Marshy Bay,
Google Maps and Earth give fine natural color view,
resolution .001 km, size 3.3x1.8 km, el .033 km,
4 km E of Cedar Creek Road ns, Rd 53ns,
30 km E of Hwy 95ns, 40 km SE of Fayetteville,
NW of or part of Bladen Lakes State Forest,
90 km NW of the coast at Wilmington ]
with Little Singletary Lake [ North Carolina 28399 ]
and Horseshoe Lake
to the lower L and lower R, all oriented NW. ]
One side in the debate has conceded a major point to their critics,
while presenting more evidence for many other major points.
AGU Fall Meeting 2009
ID# PP31D-1389
Location: Poster Hall (Moscone South)
Time of Presentation: Dec 16 8:00 AM - 12:20 PM
The platinum group metals in Younger Dryas Horizons
are terrestrial
Y. Wu 1; E. Wikes 1; J. Kennett 2; A. West 3; M. Sharma 1
1. Dept of Earth Sciences, Dartmouth College, Hanover, NH
2. Department of Earth Sciences,
University of California, Santa Barbara, CA, USA.
3. GeoScience Consulting, Dewey, AZ, USA.
The Younger Dryas (YD) event, which began 12,900 years ago,
was a period of abrupt and rapid cooling in the
Northern Hemisphere whose primary cause remains unclear.
The prevalent postulated mechanism is a temporary shutdown
of the thermohaline circulation following the breakup of an ice
dam in North America.
Firestone et al. (2007) proposed that the cooling was triggered
by multiple cometary airbursts and/or impacts that engendered
enormous environmental changes and disrupted the thermohaline
circulation.
The evidence in support for this hypothesis is a black layer in
North America and in Europe marking the YD boundary
containing charcoal, soot, carbon spherules and glass-like carbon
suggesting extensive and intense forest fires.
This layer is also enriched in magnetic grains high in iridium,
magnetic microspherules, fullerenes containing extraterrestrial
He-3, and nanodiamonds.
Whereas the nanodiamonds could be produced in an impact or
arrive with the impactor, the cometary burst/impact hypothesis
remains highly controversial as the YD horizon lacks important
impact markers such as craters, breccias, tektites and
shocked minerals.
Firestone et al. (2007) contend that bulk of Ir found at the YD
boundary is associated with magnetic grains.
The key issue is whether this Ir is meteorite derived.
We used Ir and Os concentrations and Os isotopes to
investigate the provenance of the platinum group metals in the
YD horizon.
The bulk sediment samples from a number of North American
YD sites (Blackwater Draw, Murray Springs, Gainey,
Sheriden Cave, and Myrtle Beach) and a site in Europe (Lommel)
do not show any traces of meteorite derived Os and Ir.
The [Os] = 2 to 45 pg/g in these sediments and the 187Os/188Os
ratios are similar to the upper continental crustal values (~1.3),
much higher than those in meteorites (0.13).
Higher [Os] is observed in Blackwater Draw (= 194 pg/g).
However, the Os/Ir ratio in Blackwater Draw is 5
(not 1 as expected for a meteorite) and
187Os/188Os ratio = 1.35, which remains constant above and
below the YD horizon.
Kennett et al. (2009) report 200 ppb of nanodiamonds and
about 4 ppb of Ir in bulk sediments from Murray Springs.
Since chondritic meteorites contain approximately 400 ppm
of presolar nanodiamonds and about 500 ppb of osmium,
simple mixing requires that the YD horizon at Murray Springs
should contain about 250 pg/g of Os.
However, the observed Os concentration of YD horizon at
Murray Springs is only 45 pg/g and the 187Os/188Os ratio is 1.66.
These observations suggest that if there was an impact that
produced the nanodiamonds and dispersed them,
it did not provide Os (and Ir) to the Murray Springs and other
North American sites.
We have so far separated and analyzed magnetic grains from
Gainey and Lommel and find their [Os] and 187Os/188Os
ratios consistent with a terrestrial origin.
The [Os] of microspherules analyzed so far are too low to be
derived from meteorites.
Our analyses therefore do not support an extraterrestrial origin of
the platinum metals in YD horizons from North America and Europe.
Contact Information: Yingzhe Wu, Hanover, New Hampshire, USA 03755
AGU Fall Meeting 2009
ID# PP31D-1392
Location: Poster Hall (Moscone South)
Time of Presentation: Dec 16 8:00 AM - 12:20 PM
Nanodiamonds and Carbon Spherules from Tunguska, the K/T
Boundary, and the Younger Dryas Boundary Layer
J. H. Wittke 1; T. E. Bunch 1; A. West 2; J. Kennett 3;
D. J. Kennett 4; G. A. Howard 5
1. Dept. of Geology, Northern Arizona Univ., Flagstaff, AZ, USA.
2. GeoScience Consulting, Dewey, AZ, USA.
3. Dept. of Earth Science and Marine Science Institute,
Univ. of California, Santa Barbara, CA, USA.
4. Dept. of Anthropology, Univ. of Oregon, Eugene, OR, USA.
5. Restoration Systems, LLC, Raleigh, NC, USA.
More than a dozen markers, including nanodiamonds (NDs) and
carbon spherules (CS), occur in a sedimentary layer marking the
onset of the Younger Dryas (YD) cooling episode at ~12.9 ka.
This boundary layer, called the YDB, has been found at nearly
forty locations across North America, Europe, and Asia,
although not all markers are present at any given site.
Firestone et al. (2007) and Kennett et al. (2008, 2009)
proposed that these markers resulted from a cosmic
impact/airburst and impact-related biomass burning.
Here we report features common to the YDB event, the
Cretaceous-Tertiary (K/T) impact, and the Tunguska airburst
of 1908.
In sediments attributed to each event, we and other
researchers have recovered NDs either inside or closely
associated with CS, which appear to be the high-temperature
by-products of biomass burning.
CS range in diameter from about 500 nanometers to
4 millimeters with a mean of ~100 microns,
and they typically contain NDs, including lonsdaleite
(hexagonal diamonds), in the interior matrix and in the crust.
To date, CS and NDs have been found in the K/T layer
in the United States, Spain, and New Zealand.
Similarly, CS and NDs have been found in the YDB layer
in the United States, Canada, United Kingdom, Belgium,
the Netherlands, Germany, and France.
Thus far, every site examined contains NDs and/or CS in the
K/T and YDB layers; conversely, we have yet to detect CS
associated with NDs in any non-YDB sediments tested.
Five allotropes of NDs have been identified in association with
CS: cubic diamonds, lonsdaleite, n-diamonds, p-diamonds,
and i-carbon, which are differentiated by slight variations
in their crystalline structure.
All allotropes have been identified using scanning electron
microscopy (SEM), high-resolution electron microscopy (HREM),
and transmission electron microscopy (TEM) with confirmation
by selected area diffraction (SAED).
Lonsdaleite is found on Earth only in three instances:
(1) in the laboratory, where it is produced by shock synthesis
under a high-temperature-high-pressure regime
(~1000°C to 1700°C at 15 GPa) or by carbon vapor deposition
(CVD) under a very-high-temperature-low-pressure regime
(~13,000°C at 300 Torr) (Maruyama et al., 1993);
(2) after arrival on Earth inside extraterrestrial material; and
(3) as a result of high-temperature cosmic impact/airbursts.
Lonsdaleite associated with CS has been found in sediments
only at the K/T, the YDB, and Tunguska, consistent with the
hypothesis that all three events have cosmic origins,
although the nature of the impactors may have been different.
Contact Information: James H. Wittke,
Flagstaff, Arizona, USA, 86011-4099
AGU Fall Meeting 2009
ID# PP33B-08
Location: 2006 (Moscone West)
Time of Presentation: Dec 16 3:04 PM - 3:16 PM
Testing Younger Dryas ET Impact (YDB) Evidence
at Hall's Cave, Texas
T. W. Stafford 1; E. Lundelius 2; J. Kennett 3; D. J. Kennett 4;
A. West 5; W. S. Wolbach 6
1. Stafford Research, Inc., Lafayette, CO, USA.
2. Dept. of Geological Sciences, Univ. of Texas, Austin, TX, USA.
3. Dept. of Earth Science & Marine Science Institute,
Univ. of California, Santa Barbara, CA, USA.
4. Dept. of Anthropology, Univ. of Oregon, Eugene, OR, USA.
5. GeoScience Consulting, Dewey, AZ, USA.
6. Dept. of Chemistry, DePaul Univ., Chicago, IL, USA.
Hall's Cave, Kerrville County Texas, 167 km WSW of Austin,
provides a unique opportunity for testing the presence of a
chronostratigraphic datum (YDB layer) containing rare and
exotic proxies, including nanodiamonds, aciniform soot, and
magnetic spherules, the origins of which remain controversial,
but possibly derive from a cosmic impact ~12,900 CAL BP.
The karst-collapse cave in Cretaceous limestone on the
Edwards Plateau contains ? 3.7 m of stratified clays grading to
clayey silts recording continuous deposition from 16 ka RC yr
to present.
The cave's small catchment area and mode of deposition were
constant, and the stratigraphy is well dated based on 162
AMS 14C dates from individual vertebrate fossils, snails,
charcoal, and sediment chemical fractions.
The cave sequence contains an abundant small animal vertebrate
fossil record, exhibiting biostratigraphic changes, and the timing
of the late Pleistocene megafaunal extinction is consistent with
that elsewhere in North America.
At 151 cm below datum is the extremely sharp, smooth contact
separating lower, dusky red (2.5YR3/2) clays below from
overlying dark reddish brown (5YR3/3) clays (forming a
20-cm-thick dark layer) and dating to 13,000 CAL BP,
at or close to the age of the YDB datum elsewhere.
This appears to be the most distinctive lithologic change of the
deglacial sequence.
Sediments at or within 10 cm of this contact contain the local
extinction of 4 species of bats, the local extinction of the prairie dog
(Cynomys sp.) and perhaps other burrowing mammals in response
to decrease in soil thickness, and the uppermost occurrence of 6
late Pleistocene megafaunal taxa that, although rare in the cave,
do not extend younger than 12.9 ka.
We collected and analyzed sediments at high resolution above
and below the distinct lithologic contact at 151 cm.
The red clays from 151 to 153 cm and immediately preceding the
lithologic contact contain an abundance of nanodiamonds
(5 different allotropes), aciniform soot at 2400 ppm, magnetic
spherules, and carbon spherules, all of which we interpret as
evidence for a unique chronostratigraphic marker (YDB)
in the Western Hemisphere.
Because the age of this horizon is ~ 13,000 CAL BP, we
interpret the age of the event as the beginning of the
Younger Dryas cooling.
Regional soil erosion began ~15,000 CAL BP and continued
until 7000 CAL BP, but dating suggests that there is no
discontinuity or hiatus in deposition, and thus, the exotic materials
in that layer are not considered to be erosional accumulations.
Future analyses include sub-centimeter sampling over the
YD boundary, quantification of nanodiamonds and other
event-proxies within 1000 yr of the boundary and in sediments
several 1000 years older and younger, continued refinement of
the AMS 14C record to determine within 50 yr the location of
12,900 CAL BP datum and high resolution analysis
of small animal biostratigraphy.
Contact Information: Thomas W. Stafford,
Lafayette, Colorado 80026
[ 30.135347 -99.537902 M. Jennifer Cooke et al, 2003 Oct,
study of Hall's Cave, 4 p ]
www.geo.utexas.edu/faculty/banner/Publications/Halls_Cave_Geology_03.pdf
For most of these craters, white minerals are striking.
Analysis of elements and isotopes should prove any evidence
of ET origin, and indicate temperatures and pressures
of deposition onto target rocks from steam explosions
of ice comet fragments.
The shared level of minimal erosion indicates
a shared early Holocene origin.
Amateurs should be encouraged to contribute observations
and samples.
Scientists can organize a center for analyzing samples at a
modest profit, while freely sharing data and research.
Websites, online journals, videos, magazines, books, and
movies can generate reasonable profits in the service of science.
The emerging insights into a past universal truama will lead
to a increased shared sense of community in our human family.
It is necessary to assess any future risks.
nanodiamond evidence for 12,900 BP Clovis extinction impact,
Santa Rosa Island, discussion on Scientific American website,
Carolina Bay type craters east of Las Vegas, NM:
Rich Murray 2009.09.15
http://rmforall.blogspot.com/2009_06_01_archive.htm
Friday, July 24, 2009
http://groups.yahoo.com/group/AstroDeep/28
widespread Carolina Bay type craters from Clovis comet
12,900 Ya BP? -- 0.7 M long NS crater with fractured
red sandstone on SW rim, CR C 53A, 20 miles E of
Las Vegas, NM: Rich Murray 2009.06.08
http://rmforall.blogspot.com/2009_06_01_archive.htm
Monday, June 8, 2009
http://groups.yahoo.com/group/AstroDeep/27
For Google Earth, here are the Windows/Linux keyboard
commands that make it easy to "fly" easily,
creating an intuitive 3D grasp of the landscape -- my laptop
runs at 1 GHZ with a graphics card, Windows Vista, Chrome,
and 3 GB RAM:
Full screen mode: F11
Lat/Long grid: Ctrl L
Slow movement down: add Alt before other keys
Zoom in, out: PgUp, PgDn keys
Move left, right, forward, back: arrow keys
Tilt view up, down: Shift down arrow, up arrow
Rotate view in circle clockwise, counterclockwise:
Shift right arrow, left arrow
Tilt up towards horizon, down towards directly below:
Shift down arrow, up arrow
Stop, start movement: space bar
Look in any direction: Ctrl, left mouse button and drag
New placemark: Ctrl Shift P
To delete or rewrite a placemark title,
right click it and select Properties.
Reset view to north as forward: n
Reset tilt to top-down view: u
Select Tools to select Web to return to your other screens.
It's easy to look down about 45 degrees while moving straight
ahead in any direction at an eye elevation of 1-200 km,
scanning a straight strip half-way around the world,
stopping to placemark, examine, and measure any features.
http://worldwind.arc.nasa.gov/java/
Requirements: a 3D video card with updated drivers is necessary.
World Wind has been tested on Nvidia, ATI/AMD, and Intel
platforms using Windows, MacOS 10.4, and Fedora Core 6.
WW gives exact altitudes and ocean depths.
WW images omit human features and give good resolution
from above 30 km.
http://worldwind.arc.nasa.gov/graphics/keychart.jpg
Keyboard controls:
Pan: arrow keys
Rotate LR: A,D keys
Tilt forward down, back up: W,S keys
Zoom down, up: 7 or Home, 1 or End
Stop: space bar or 5.
Position info: F10
Crosshairs: F9
Boundaries: F5
Placenames: F6
Lat/Long Lines: F7
Planet Axis: F8
Dynamic Layers: F1
_____________________________________________________
Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298 rmforall@comcast.net
http://groups.yahoo.com/group/AstroDeep/messages
http://RMForAll.blogspot.com new primary archive
http://groups.yahoo.com/group/aspartameNM/messages
group with 142 members, 1,588 posts in a public archive
http://groups.yahoo.com/group/aspartame/messages
group with 1204 members, 23,955 posts in a public archive
http://groups.yahoo.com/group/rmforall/messages
participant, Santa Fe Complex www.sfcomplex.org
_____________________________________________________
Monday, November 02, 2009
older women drinking over 2 aspartame beverages weekly had 30% decline kidney function in 11 years, Nurses Health Study, Julie Lin, Gary C Curhan
older women drinking over 2 aspartame beverages daily had 30% decline kidney function in 11 years, Nurses Health Study, Julie Lin, Gary C Curhan, Brigham and Women's Hospital, Boston: Rich Murray 2009.11.02
http://rmforall.blogspot.com/2009_11_01_archive.htm
Monday, November 2, 2009
http://groups.yahoo.com/group/aspartameNM/message/1588
_____________________________________________________
"Lin's team looked at the cumulative average beverage intake,
derived from food questionnaires completed in 1984, 1986,
and 1990.
The women replied whether they drank the beverages less than
once a month, one to four times a month, two to six times weekly,
once daily but less than twice, or twice a day or more often."
[ Aspartame, approved in the USA for beverages in July, 1983,
was by far the dominant artificial sweetener in beverages
in 1984 to 1990. ]
3,267 women, median age 67 in 2000, in Nurses Health Study:
"When the researchers compared kidney function of the women
in 1989 and 2000, they found that 11.4% or 372 women
had a kidney function decline of 30% or more.
When they looked at the diet information, they found that the 30%
decline in kidney function was associated with drinking two or more
artificially sweetened sodas a day.
This was true even after taking into account factors such as age,
high blood pressure, diabetes, and physical activity."
http://www.modernmedicine.com/modernmedicine/Modern+Medicine+Now/ASN-Sodium-Sweeteners-and-Fructose-Raise-Health-Ri/ArticleNewsFeed/Article/detail/638324?contextCategoryId=40137
study presented at the American Society of Nephrology's
42nd Annual Meeting and Scientific Exposition,
held from Oct. 27 to Nov. 1 in San Diego
In separate studies, Julie Lin, M.D., and Gary Curhan, M.D.,
of Brigham and Women's Hospital in Boston, and colleagues
examined the effects of sodium and artificial sweeteners
on kidney function among more than 3,000 women
in the Nurses Health Study.
Higher dietary sodium intake was found to be associated
with a greater kidney function decline in women
with well-preserved kidneys, while the odds for kidney decline
doubled for women consuming two or more daily servings
of artificially sweetened soda.
"While more study is needed, our research suggests that higher
sodium and artificially sweetened soda intake are associated
with greater rate of decline in kidney function,"
Lin said in a statement.
http://www.webmd.com/news/20091102/diet-sodas-hard-on-the-kidneys
Diet Sodas May Be Hard on the Kidneys
Women Who Drink 2 or More Diet Sodas Daily Double
Their Risk of Kidney Function Decline, Study Shows
By Kathleen Doheny
WebMD Health News Reviewed by Louise Chang, MD
Nov. 2, 2009 -- Diet soda may help keep your calories in check,
but drinking two or more diet sodas a day may
double your risk of declining kidney function, a new study shows.
Women who drank two or more diet sodas a day had a 30% drop
in a measure of kidney function during the lengthy study follow-up,
according to research presented Saturday at the annual meeting
of the American Society of Nephrology in San Diego.
"Thirty percent is considered significant,'' says researcher
Julie Lin, MD, MPH, assistant professor of medicine
at Harvard Medical School and a staff physician at
Brigham and Women's Hospital in Boston.
That's especially true, she says, because most study participants
had well-preserved kidney function at the start of the study.
Diet Soda and Kidneys: Study Details
The researchers evaluated 3,256 women already participating in
the Nurses' Health Study who had submitted dietary information,
including their intake of sugary beverages -- sugar-sweetened
drinks, sugar-sweetened soda, and artificially sweetened soda.
Sugar-sweetened drinks included soda, fruit juices, punch,
and iced tea.
Information was also available on measures of kidney function.
Their median age was 67.
Lin's team looked at the cumulative average beverage intake,
derived from food questionnaires completed in 1984, 1986,
and 1990.
The women replied whether they drank the beverages less than
once a month, one to four times a month, two to six times weekly,
once daily but less than twice, or twice a day or more often.
Diet Soda and Kidneys: Study Results
When the researchers compared kidney function of the women
in 1989 and 2000, they found that 11.4% or 372 women had
a kidney function decline of 30% or more.
When they looked at the diet information, they found that the 30%
decline in kidney function was associated with drinking two or more
artificially sweetened sodas a day.
This was true even after taking into account factors such as age,
high blood pressure, diabetes, and physical activity.
Put another way: the women who drank two or more diet sodas
a day had a decline in their glomerular filtration rate, a measure of
kidney function, of 3 milliliters per minute per year.
''With natural aging, kidney function declines
about 1 mL per minute per year after age 40," Lin says.
No link was found with the other beverages.
And less than two sodas a day didn't seem to hurt.
"We didn't see any association up to two artificially sweetened
beverages a day," Lin says.
''A serving was reported as either a glass, a can, or a bottle
of a beverage," Lin tells WebMD.
''It was not more specific than that."
''The mechanisms aren't clear," Lin says of the association
she found.
In another study she presented at the meeting, she found higher
salt intake is also associated with faster kidney function decline.
All of the participants were women, so Lin can't say for sure
that the association holds for men, although she says there is
''no biological reason to think it wouldn't."
About 20 million Americans have some evidence of chronic
kidney disease, according to the society.
Kidney disease diagnoses have doubled
each of the last two decades. [4X more in 20 years ]
Diet Soda and Kidney Function: Industry Input
Asked to review the study findings, Maureen Storey,
senior vice president of science policy for the
American Beverage Association, says in a prepared statement:
"It's important to remember that this is an abstract presented
at an annual meeting."
She notes that the research needs further scrutiny by researchers.
She acknowledges that kidney disease is serious
but that diabetes and high blood pressure account for the majority
of kidney disease cases, ''not consumption of diet soda."
Diet Soda and Kidney Function: Dietitian's View
In reviewing the study, Connie Diekman, RD,
director of university nutrition for Washington University, St. Louis,
wonders if the link might have come about because of long-term
consumption, as many of the participants were older adults.
The link found, she says, "calls for more studies where
actual intake can be assessed, rather than taking the information
from food frequency questionnaires, which could be subject
to mistakes."
Diet drinks, she says, are ''generally low in important
health-promoting nutrients, so keeping them as a small part
of your eating plan would be a smart step."
Abstract - FC342 (login required)
Abstract - PO2751 (login required)
Abstract - FC037 (login required)
SOURCES:
Julie Lin, MD, MPH, assistant professor of medicine,
Harvard Medical School, staff physician,
Brigham and Women's Hospital, Boston.
American Society of Nephrology annual meeting,
San Diego, Oct 27-Nov. 1, 2009.
Connie Diekman, RD, director of university nutrition,
Washington University, St. Louis.
News release, American Beverage Association.
© 2009 WebMD, LLC. All rights reserved.
Kathleen Doheny
Kathleen Doheny is a Los Angeles-based journalist
specializing in health, fitness, and behavior topics.
In addition to writing for WebMD, her articles have appeared
in the Los Angeles Times, Shape, Natural Health,
and many other magazines and web sites.
Louise Chang, MD
Louise Chang, MD, is part of the WebMD medical editing team
and is responsible for reviewing WebMD news and feature
stories to ensure their medical accuracy.
She has always considered herself a patient advocate and
educator at heart.
She has had broad experience of both inpatient and outpatient
practice in urban and suburban settings.
Dr. Chang shares the WebMD mission to provide the most
accurate and useful medical information for people.
Dr. Chang completed her undergraduate degree at
Stanford University and attended medical school at
New York Medical College.
She completed her internal medicine residency at
Saint Vincent's Hospital in New York City,
where she also served as a chief resident from 2001-2002.
Immediately prior to joining WebMD, Dr. Chang worked as
an attending physician and clinical instructor at
Grady Memorial Hospital as part of the
Emory School of Medicine in downtown Atlanta,
seeing patients and working with and
teaching medical residents and students.
Dr. Chang is board-certified in internal medicine.
She is a member of both the American College of Physicians
and the Society of General Internal Medicine.
Her prior research work has been published and presented
at regional and national conferences.
http://www.scienceblog.com/cms/help-your-kidneys-pass-salt-and-diet-soda-26792.html
Help your kidneys: Pass on salt and diet soda
Individuals who consume a diet high in sodium or artificially
sweetened drinks are more likely to experience a decline in
kidney function, according to two papers being presented
at the American Society of Nephrology's annual meeting in
San Diego, California.
Julie Lin MD, MPH, FASN and Gary Curhan, MD, ScD, FASN
of Brigham and Women's Hospital studied more than 3,000
women participating in the Nurses Health Study to identify the
impact of sodium and sweetened drinks on kidney function.
"There are currently limited data on the role of diet in
kidney disease," said Dr. Lin. "While more study is needed,
our research suggests that higher sodium and artificially sweetened
soda intake are associated with greater rate of decline
in kidney function."
The first study,
"Associations of Diet with Kidney Function Decline," examined
the influence of individual dietary nutrients on kidney function
decline over 11 years in more than 3,000 women participants
of the Nurses Health Study. The authors found that
"in women with well-preserved kidney function,
higher dietary sodium intake was associated with greater kidney
function decline, which is consistent with experimental animal data
that high sodium intake promotes progressive kidney decline."
The second study, also conducted by Dr. Lin and Dr. Curhan,
"Associations of Sweetened Beverages with Kidney Function Decline,"
examined the influence of sugar-sweetened and artificially sweetened
beverages on kidney function decline in the same group
of Nurses Health Study participants.
An analysis of the nationally representative NHANES III participants
had previously reported an association between sugar-sweetened soda
and urinary protein, but data on kidney function change
was not available.
This investigation reported "a significant two-fold increased odds,
between two or more servings per day of artificially sweetened soda
and faster kidney function decline;
no relation between sugar-sweetened beverages and kidney
function decline was noted" said Dr. Lin.
This association persisted even after the study authors accounted
for age, caloric intake, obesity, high blood pressure, diabetes,
cigarette smoking, physical activity, and cardiovascular disease.
The mechanisms for kidney decline in the setting of high intake of
artificial sweetenters have not been previously studied
and deserve further investigation.
The study participants were older Caucasian women and the authors
note that the findings may not be directly applicable to men or people
of other ethnicities.
The authors report no financial disclosures.
EDITOR:
"Associations of Diet with Kidney Function Decline," (SA-FC342)
will be presented as part of a Free Communication Session at the
American Society of Nephrology's 42nd Annual Meeting and
Scientific Exposition on Oct. 31 at 4:24 pm in Room 25 of the
San Diego Convention Center in San Diego, CA.
"Associations of Sweetened Beverages with Kidney Function Decline,"
(SA-PO2751) will be presented as part of a Poster Session
from 10:00 am -- 12:00 pm in the Scientific Exposition Hall of the
San Diego Convention Center also on Oct. 31.
Both abstracts will be presented as part of a Press Briefing
on Oct. 30 at 12:15 pm in Room 12.
ASN Renal Week 2009, the largest nephrology meeting of its kind,
will provide a forum for 13,000 professionals to discuss the latest
findings in renal research and engage in educational sessions related
to advances in the care of patients with kidney and related disorders.
Renal Week 2009 will take place October 27 -- November 1
at the San Diego Convention Center in San Diego.
Founded in 1966, the American Society of Nephrology (ASN)
is the world's largest professional society devoted to the study
of kidney disease.
Comprised of 11,000 physicians and scientists, ASN continues
to promote expert patient care, to advance medical research,
and to educate the renal community.
ASN also informs policymakers about issues of importance to
kidney doctors and their patients.
ASN funds research, and through its world-renowned meetings
and first-class publications, disseminates information
and educational tools that empower physicians.
http://www.eurekalert.org/multimedia/pub/17613.php?from=147059
[ large photo ]
Contact: Shari Leventhal sleventhal@asn-online.org 202-558-8423
American Society of Nephrology
http://www.brighamandwomens.org/renal/Research/JLinClinProt.aspx
Dr. Lin’s research interests focuses on proteinuric renal diseases
and glomerulopathies.
Her current research examines associations between diet, lipids,
and inflammatory biomarkers and the development of nephropathy
in adult-onset diabetes mellitus using subjects participating in the
Nurses Health Study and Health Professionals Follow-Up Study.
10 studies listed 2001-2004
Julie Lin, M.D.,M.P.H.. Associate Physician.
Phone, (617) 732-6383. Fax, (617) 975-0840.
Office Address, Brigham and Women's Hospital, Renal Division
BWH, 75 Francis Street Boston, MA 02115 617-732-5500
http://www.brighamandwomens.org/renal/Research/clinical_research_faculty.aspx#jlin
Assistant Professor
Diabetic nephropathy, CKD and cardiovascular disease
Dr. Lin is a renal epidemiologist whose research interests focus
on proteinuric renal diseases, glomerulopathies, and chronic kidney
disease progression.
Research includes analyses of diet, lipids, genetics and
inflammatory biomarkers and nephropathy
in type 2 diabetes mellitus in participants of the Nurses Health Study
and Health Professionals Follow-Up Study.
Another area of interest is associations of chronic kidney disease
with quality of life measures in cognitive and physical functioning.
As the lead living kidney donor advocate
for Brigham and Women’s Hospital, Dr. Lin is also studying
outcomes and quality of life in living kidney donors in
collaboration with the Division of Transplantation Surgery.
She also has on-going collaborations with other investigators
within and outside of Harvard Medical School in projects that
examine cardiovascular disease risk in the setting
of chronic kidney disease.
3 previous studies published with GC Curhan
Channing Laboratory, Department of Medicine,
Brigham and Women's Hospital, Harvard Medical School,
Boston, MA, USA. jlin11@partners.org
http://www.brighamandwomens.org/renal/Research/clinical_research_faculty.aspx#gcurhan
Gary C. Curhan, MD, ScD Associate Professor
Epidemiology of CKD, nephrolithiasis, gout, hypertension
Dr. Curhan’s research focuses on the prevention of common
diseases by investigating scientifically and clinically important
questions and exploring the role of modifiable factors, chiefly
in the areas of nephrology and urology.
The synergy between his clinical training in nephrology and
doctoral work in epidemiology has produced a strong interest
in ‘metabolic epidemiology.’
In an effort to clarify and refine our insight into several prevalent
conditions, much of his work has examined and challenged
existing beliefs and commonly accepted practices,
often motivating important changes in clinical practice and
understanding.
Major ongoing areas or research include:
1) epidemiology of nephrolithiasis -- we are studying dietary
and lifestyle factors as well as the genetics of stone disease;
2) epidemiology of hypertension;
3) risk factors for renal function decline and change in albuminuria;
4) epidemiology of gout;
5) epidemiology of hearing loss;
6) mineral metabolism and risk of cardiovascular disease;
7) risk factors for community acquired pneumonia;
8) epidemiology of incontinence;
9) epidemiology of hyponatremia.
Dr. Curhan works closely with several faculty members
in the Renal Division and their efforts will hopefully lead to new
approaches to prevention and treatment of these common conditions.
Publications
Taylor EN, Fung TT, Curhan GC.
DASH-style diet and the risk of incident kidney stones.
J Am Soc Nephrol. 2009; (in press). (PMC Journal – In Process)
Forman JP, Stampfer MJ, Curhan GC.
Diet and lifestyle risk factors associated with incident hypertension
in women.
JAMA. 2009 Jul 22; 302(4):401-11
Choi HK, Curhan GC.
Soft drinks, fructose consumption, and the risk of gout in men –
A Prospective Cohort Study.
BMJ. 2008 Feb 9; 336(7639):309-12. PMCID: PMC2234536
Waikar SS, Mount DB, Curhan GC.
Mortality after hospitalization with mild, moderate,
and severe hyponatremia.
Am J Med. 2009; (in press).
Curhan SG, Eavey R, Shargorodsky J, Curhan GC.
Analgesic use and the risk of hearing loss in men.
Am J Med. 2009; (in press).
Department of Medicine, Renal Division,
Brigham and Women's Hospital,
Harvard Medical School, Boston, Massachusetts 02115, USA.
gcurhan@partners.org
_____________________________________________________
consider co-factors (methanol, formaldehyde, and protective folic acid), re UK FSA test of aspartame in candy bars on 50 reactors, Stephen L Atkin, Hull York Medical School: Rich Murray 2009.09.29
http://rmforall.blogspot.com/2009_09_01_archive.htm
Tuesday, September 29, 2009
http://groups.yahoo.com/group/aspartameNM/message/1587
_____________________________________________________
Included herein is substantial mainstream evidence that the natural
conversion in humans of orally ingested methanol into formaldehyde
and then formic acid results in substantial, durable, cumulative
retention of toxic reaction products.
Adequate folic acid levels expedite the safe metabolism of methanol
in most people.
Ethyl alcohol and folic acid in vegetables and fruits are sufficient to
protect most people from conversion of their methanol into
formaldehyde.
Many common agents interfere with folic acid (folic acid antagonists).
Additionally, genetic variations are potent.
About 3/4 of reactors are female.
Those who rarely have alcohol hangovers may be substantially immune
to methanol and formaldehyde.
Recent exposure to alcohol beverages, tobacco and wood smoke,
and a large variety of formaldehyde sources may compromise the
clarity of aspartame reaction tests.
Aspartame reactors often report allergies to many agents, with similar
symptoms: mercury (amalgams and fish), MSG and free glutamate in
foods (for instance, hydrolyzed vegetable or yeast protein), carbon
monoxide, molds, many foods, etc. -- up to Multiple Chemical
Sensitivity.
Aspartame reactors often take many steps to exercise, reduce stress,
lower salt, emphasize organic plant foods, reduce drug and chemical
exposures, limit protein and fat intake, use vitamin and mineral
supplements, limit processed foods -- thus complicating attempts to
create a matching control group, and introducing uncertainty about
whether the reactors are as vulnerable now as in the past, when they
may have had more negative factors for years.
So, genetic background, age, sex, obesity, existing illnesses, diet,
exercise, environmental toxins, medicines and drugs, parental
exposure to all these factors, and more may corrode the "gold
standard" of a single exposure double-blind experimental test,
especially for a rather modest test group of 50.
Perhaps, a more productive research strategy would be to test 10
reactors, one at a time, for 24 hours each, using a wide range of
tests, recording the enormous individual variations that are usually
swamped by taking group data averages.
Computerized tests facilitate fast, affordable measures of cognitive
and memory effects.
Full audio and video recording is now available.
Dimethyl dicarbonate, an approved additive for reducing fungi in
wines, perhaps with a neutral taste, quickly releases about the same
level of methanol upon ingestion as aspartame drinks, making
possible studies free of any possible "excitotoxic" effects of
aspartic acid and phenylalanine, while allowing a third beverage
to be a control substance.
This approach would also contribute to the meager research literature
about the role of methanol in alcohol hangovers.
aspartame reactors may send detailed feedback to Andrew Wadge,
UK Food Standards Agency to guide new pilot study re bad
reactions: Rich Murray 2009.06.22
http://rmforall.blogspot.com/2009_06_01_archive.htm
Monday, June 22, 2009
http://groups.yahoo.com/group/aspartameNM/message/1577
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.dorway.com/products.txt
[ rearranged, 11% methanol added ]
From the Nutrasweet Web Site: (amounts in various "foods")
Product Category -- Serving Size -- aspartame -- 11% methanol
Gelatin Dessert ----------- 8 ounces -----190 mg ---- 21 mg
Carbonated Beverage --- 12 ounces ----- 180 ------- 20
" ------------------------ 48 ounces ----- 720 ------- 79
Powdered Drink -------- 12 ounces ----- 180 -------- 20
Fruit Drink (10% juice) -- 12 ounces ----- 140 -------15.4
Hot Chocolate ----------- 12 ounces ----- 100 -------11
Yogurt ------------------- 8 ounces ----- 124 --------13.6
Ice Cream ---------------- 8 ounces ----- 100 ------- 11
Pudding Dessert ---------- 8 ounces ------ 50 --------- 5.5
Frozen Novelty ----------- 2-3 ounces ---- 50 --------- 5.5
Gum ----------------------- 1 stick -------- 6-8 -------- 0.7-0.9
Vitamins ------------------ 1 vitamin ------ 4 ---------- 0.44
Breath mint ---------------- 1 mint --------- 1.5 -------- 0.17
http://groups.yahoo.com/group/aspartameNM/message/846
aspartame in Merck Maxalt-MLT worsens migraine,
AstraZeneca Zomig, Eli Lilly Zyprexa,
J&J Merck Pepcid AC (Famotidine 10mg) Chewable Tab,
Pfizer Cool Mint Listerine Pocketpaks: Murray 2002.07.16
Migraine MLT-Down: an unusual presentation of migraine
in patients with aspartame-triggered headaches.
Newman LC, Lipton RB Headache 2001 Oct; 41(9): 899-901.
[ Merck 10-mg Maxalt-MLT, for migraine, has 3.75 mg aspartame,
while 12 oz diet soda has 200 mg. ]
Headache Institute, St. Lukes-Roosevelt Hospital Center,
New York, NY
Department of Neurology newmanache@aol.com
Albert Einstein College of Medicine, Bronx, NY
Innovative Medical Research RLipton@aecom.yu.edu
http://groups.yahoo.com/group/aspartameNM/message/855
Blumenthall & Vance: aspartame chewing gum headaches
Nov 1997: Murray 2002.07.28
Harvey J. Blumenthal, MD, Dwight A Vance, RPh
Chewing Gum Headaches. Headache 1997 Nov; 37(10): 665-6.
Department of Neurology, University of Oklahoma College of
Medicine, Tulsa, USA. neurotulsa@aol.com
Aspartame, a popular dietetic sweetener, may provoke headache in
some susceptible individuals. Herein, we describe three cases of
young women with migraine who reported their headaches could be
provoked by chewing gum sweetened with aspartame.
[ 6-8 mg aspartame per stick chewing gum ]
http://groups.yahoo.com/group/aspartameNM/message/1143
antiseptic? antifungal? antiviral? methanol (formaldehyde, formic
acid) disposition: Bouchard M et al, full plain text, 2001: substantial
sources are degradation of fruit pectins, liquors, aspartame, smoke:
Murray 2005.01.05 rmforall
http://www.toxsci.oupjournals.org/cgi/content/full/64/2/169
free full text
A Biologically Based Dynamic Model for Predicting the Disposition
of Methanol and Its Metabolites in Animals and Humans.
Michèle Bouchard,
Robert C. Brunet,
Pierre-Olivier Droz,
and Gaétan Carrier.
Toxicological Sciences 64, 169-184 (2001)
Copyright © 2001 by the Society of Toxicology
[ extracts ]
"Exposure to methanol also results from the consumption of certain
foodstuffs (fruits, fruit juices, certain vegetables, aspartame
sweetener, roasted coffee, honey) and alcoholic beverages (Health
Effects Institute, 1987; Jacobsen et al., 1988).
[ It's unusual for a mainstream journal article to mention "fruits, fruit
juices, certain vegetables, aspartame sweetener" and "alcoholic
beverages" to be methanol sources.]
... little is known about the chronic effects of low exposure doses...
Systemic methanol is extensively metabolized by liver alcohol
dehydrogenase [ ADH ] and catalase-peroxidase enzymes to
formaldehyde, which is in turn rapidly oxidized to formic acid by
formaldehyde dehydrogenase enzymes...
Formaldehyde, as it is highly reactive, forms relatively stable adducts
with cellular constituents...
Primates and humans appear to be more susceptible to the acute
toxicity of methanol than rodents...
Although methanol has been reported to be metabolized mainly in
the liver, pulmonary metabolism is also likely to occur. Indeed,
the catalase-peroxidase system responsible for a major fraction of
methanol metabolism in rats is widely distributed in mammalian
tissues...
The model included a constant background whole body methanol
burden of 2.133 mmol, which corresponds to the mean blood
concentration of 0.5 mg/L of methanol measured by Osterloh et al.
(1996) in control subjects at the end of an 8-h frequent blood
sampling period...
... once formed, a substantial fraction of formaldehyde is converted
to unobserved forms. This pathway contributes to a long-term
unobserved compartment. The latter, most plausibly, represents
either the formaldehyde that ( directly or after oxidation to formate )
binds to various endogenous molecules (Heck et al., 1983; Roe,
1982)...
That substantial amounts of methanol metabolites or by-products
are retained for a long time is verified by Horton et al. (1992)
who estimated that 18 h following an iv injection of 100 mg/kg
of 14C-methanol in male Fischer-344 rats, only 57% of the
dose was eliminated from the body. From the data of Dorman
et al. (1994) and Medinsky et al. (1997), it can further be
calculated that 48 h following the start of a 2-h inhalation
exposure to 900 ppm of 14C-methanol vapors in female
cynomolgus monkeys, only 23% of the absorbed 14C-methanol
was eliminated from the body. These findings are corroborated by
the data of Heck et al. (1983) showing that 40% of a
14C-formaldehyde inhalation dose remained in the body 70 h
postexposure...
Experimental studies on the detailed time profiles following
controlled repeated exposures to methanol are lacking...
Thus, in monkeys and plausibly humans, a much larger fraction of
body formaldehyde is rapidly converted to unobserved forms
rather than passed on to formate and eventually CO2."
If we assume 30% retention of durable cumulative toxic products of
formaldehyde and formic acid, then a 12-oz can diet drink gives 200
mg aspartame, 22 mg methanol, and 7 mg formaldehyde and formic
acid at 30% cumulative retention. We may add that well known
sources of formaldehyde include both wood and tobacco smoke,
and, notoriously, mobile homes. Two teams give evidence that
formaldehyde and formic acid from methanol in ethanol drinks
(often far above the 100 mg/L methanol in red wines, two times the
level in aspartame drinks) are the main cause of the many symptoms
of "morning after" hangovers.
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
Furthermore, BM Kapur et al, 2007 give evidence that formic acid
from methanol in ethanol drinks is a major cause of Fetal Alcohol
Syndrome, readily preventable by adequate levels of folic acid,
which expedites the safe metabolism of formaldehyde, in most
people.
"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." ...
"MeOH concentrations between 4 and 4500 mg/l can be present
in various alcoholic beverages (Sprung et al., 1988)."
A variety of mutations, as well as aspirin and many painkillers,
impede folic acid. However, fruits and vegetables give enough folic
acid to mitigate harm from their methanol. Then again, formaldehyde
may in many people treat infections by fungi, bacteria, and virusus.
All these unexamined co-factors have confused attempts to study
aspartame toxicity for three decades.
http://groups.yahoo.com/group/aspartameNM/message/1141
Nurses Health Study can quickly reveal the extent of aspartame
(methanol, formaldehyde, formic acid) toxicity: Murray 2004.11.21
The Nurses Health Study is a bonanza of information about the health of
probably hundreds of nurses who use 6 or more cans daily of diet soft
drinks -- they have also stored blood and tissue samples from their
immense pool of subjects, over 100,000 for decades.
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
A widely proclaimed NIH-AARP mass survey by U Lim et al. 2006,
while failing to show specific cancers with feeble diet drink
consumption data for a year for seniors, did find that 4% of a
half-million seniors drank 3 and more cans daily diet soda
[ 12-oz can gives 200 mg aspartame, 22 mg methanol,
7 mg formaldehyde and formic acid at 30% cumulative retention ]
aspartame mg/d
0 ---- under 100 - 100-200 - 200-400 - 400-600 - 600-1200 -
cohort %
46 ------- 25 ------ 13 ------- 7 --------- 5 ------ about 3 ----
over 1200 mg/d
under 1%
This is the first good data about the percentage of aspartame users
who use over 3 cans daily, averaging 5 cans daily at 200 mg per 12
oz can diet soda.
About 4% of 473,984 is 19,000 people, with a peak intake of 17
cans daily, and average 5 cans daily.
It would be worthwhile to investigate a wide variety of symptoms for
the 0.1 % of highest level users, about 500 people.
For about 200 million USA aspartame users, this would be 200,000
people.
The highest level 3400 mg aspartame [ 17 12-oz cans ] gives
11% = 374 mg methanol, 48 times the recommended daily limit of
consumption of 7.8 mg as recommended by the
Environmental Protection Agency (EPA).3
At 30% retention of cumulative toxic products of formaldehyde and
formic acid, these would be 125 mg, 60 times higher than the 1999
EPA alarm level for formaldehyde in daily drinking water of
1 ppm = 2 mg for average daily drinking water of 2 L daily.
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
40 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@catholic.ac.kr
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@RMV.se;
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
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
[ extracts ]
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
[ Extract ]
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.
Case Series
Six patients (ages 16 to 75 years) were referred for evaluation of
recalcitrant dermatitis. By history, five of the patients were noted to
have developed migraines following aspartame consumption; the
sixth reported dermatitis flares associated with diet cola
consumption of >2 liters/day.
All six patients had current environmental exposures to formaldehyde
or formaldehyde-releasing preservatives in their personal hygiene
products and/or regular consumption of "sugar-free food" artificially
sweetened with aspartame.
Based on their histories and clinical presentations, these patients
were patch-tested with the North American Contact Dermatitis
Group 65-allergen Standard Screening Series and selected
chemicals from the University of Miami vehicle, fragrance, bakery,
and textile trays.
All six patients had positive reactions to formaldehyde, and four had
additional positive reactions to formaldehyde-releasing preservatives
(FRPs). Expert counseling on allergen avoidance (including
avoidance of formaldehyde, FRPs, and aspartame) and alternative
product recommendations were provided to the patients.
At their follow-up appointments (between 8 and 12 weeks), all the
patients showed clearance of their dermatitis. Four patients (two
inadvertently) resumed their consumption of aspartame and
subsequently returned for an additional follow-up visit. Three of the
first five patients had recurrences of both their migraines and their
dermatitis; the sixth patient (who had no migraines) had a positive
rechallenge dermatitis. These four patients were again counseled on
avoidance regimen.
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
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@contactderm.net;
Sarah A. Stechschulte, BA sstechschulte@gmail.com
_____________________________________________________
Rich Murray, 1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298 rmforall@comcast.net
http://RMForAll.blogspot.com new primary archive
http://groups.yahoo.com/group/aspartameNM/messages
group with 143 members, 1,588 posts in a public archive
http://groups.yahoo.com/group/aspartame/messages
group with 1204 members, 23,945 posts in a public archive
http://groups.yahoo.com/group/rmforall/messages
http://groups.yahoo.com/group/AstroDeep/messages
participant, Santa Fe Complex www.sfcomplex.org
_____________________________________________________
http://rmforall.blogspot.com/2009_11_01_archive.htm
Monday, November 2, 2009
http://groups.yahoo.com/group/aspartameNM/message/1588
_____________________________________________________
"Lin's team looked at the cumulative average beverage intake,
derived from food questionnaires completed in 1984, 1986,
and 1990.
The women replied whether they drank the beverages less than
once a month, one to four times a month, two to six times weekly,
once daily but less than twice, or twice a day or more often."
[ Aspartame, approved in the USA for beverages in July, 1983,
was by far the dominant artificial sweetener in beverages
in 1984 to 1990. ]
3,267 women, median age 67 in 2000, in Nurses Health Study:
"When the researchers compared kidney function of the women
in 1989 and 2000, they found that 11.4% or 372 women
had a kidney function decline of 30% or more.
When they looked at the diet information, they found that the 30%
decline in kidney function was associated with drinking two or more
artificially sweetened sodas a day.
This was true even after taking into account factors such as age,
high blood pressure, diabetes, and physical activity."
http://www.modernmedicine.com/modernmedicine/Modern+Medicine+Now/ASN-Sodium-Sweeteners-and-Fructose-Raise-Health-Ri/ArticleNewsFeed/Article/detail/638324?contextCategoryId=40137
study presented at the American Society of Nephrology's
42nd Annual Meeting and Scientific Exposition,
held from Oct. 27 to Nov. 1 in San Diego
In separate studies, Julie Lin, M.D., and Gary Curhan, M.D.,
of Brigham and Women's Hospital in Boston, and colleagues
examined the effects of sodium and artificial sweeteners
on kidney function among more than 3,000 women
in the Nurses Health Study.
Higher dietary sodium intake was found to be associated
with a greater kidney function decline in women
with well-preserved kidneys, while the odds for kidney decline
doubled for women consuming two or more daily servings
of artificially sweetened soda.
"While more study is needed, our research suggests that higher
sodium and artificially sweetened soda intake are associated
with greater rate of decline in kidney function,"
Lin said in a statement.
http://www.webmd.com/news/20091102/diet-sodas-hard-on-the-kidneys
Diet Sodas May Be Hard on the Kidneys
Women Who Drink 2 or More Diet Sodas Daily Double
Their Risk of Kidney Function Decline, Study Shows
By Kathleen Doheny
WebMD Health News Reviewed by Louise Chang, MD
Nov. 2, 2009 -- Diet soda may help keep your calories in check,
but drinking two or more diet sodas a day may
double your risk of declining kidney function, a new study shows.
Women who drank two or more diet sodas a day had a 30% drop
in a measure of kidney function during the lengthy study follow-up,
according to research presented Saturday at the annual meeting
of the American Society of Nephrology in San Diego.
"Thirty percent is considered significant,'' says researcher
Julie Lin, MD, MPH, assistant professor of medicine
at Harvard Medical School and a staff physician at
Brigham and Women's Hospital in Boston.
That's especially true, she says, because most study participants
had well-preserved kidney function at the start of the study.
Diet Soda and Kidneys: Study Details
The researchers evaluated 3,256 women already participating in
the Nurses' Health Study who had submitted dietary information,
including their intake of sugary beverages -- sugar-sweetened
drinks, sugar-sweetened soda, and artificially sweetened soda.
Sugar-sweetened drinks included soda, fruit juices, punch,
and iced tea.
Information was also available on measures of kidney function.
Their median age was 67.
Lin's team looked at the cumulative average beverage intake,
derived from food questionnaires completed in 1984, 1986,
and 1990.
The women replied whether they drank the beverages less than
once a month, one to four times a month, two to six times weekly,
once daily but less than twice, or twice a day or more often.
Diet Soda and Kidneys: Study Results
When the researchers compared kidney function of the women
in 1989 and 2000, they found that 11.4% or 372 women had
a kidney function decline of 30% or more.
When they looked at the diet information, they found that the 30%
decline in kidney function was associated with drinking two or more
artificially sweetened sodas a day.
This was true even after taking into account factors such as age,
high blood pressure, diabetes, and physical activity.
Put another way: the women who drank two or more diet sodas
a day had a decline in their glomerular filtration rate, a measure of
kidney function, of 3 milliliters per minute per year.
''With natural aging, kidney function declines
about 1 mL per minute per year after age 40," Lin says.
No link was found with the other beverages.
And less than two sodas a day didn't seem to hurt.
"We didn't see any association up to two artificially sweetened
beverages a day," Lin says.
''A serving was reported as either a glass, a can, or a bottle
of a beverage," Lin tells WebMD.
''It was not more specific than that."
''The mechanisms aren't clear," Lin says of the association
she found.
In another study she presented at the meeting, she found higher
salt intake is also associated with faster kidney function decline.
All of the participants were women, so Lin can't say for sure
that the association holds for men, although she says there is
''no biological reason to think it wouldn't."
About 20 million Americans have some evidence of chronic
kidney disease, according to the society.
Kidney disease diagnoses have doubled
each of the last two decades. [4X more in 20 years ]
Diet Soda and Kidney Function: Industry Input
Asked to review the study findings, Maureen Storey,
senior vice president of science policy for the
American Beverage Association, says in a prepared statement:
"It's important to remember that this is an abstract presented
at an annual meeting."
She notes that the research needs further scrutiny by researchers.
She acknowledges that kidney disease is serious
but that diabetes and high blood pressure account for the majority
of kidney disease cases, ''not consumption of diet soda."
Diet Soda and Kidney Function: Dietitian's View
In reviewing the study, Connie Diekman, RD,
director of university nutrition for Washington University, St. Louis,
wonders if the link might have come about because of long-term
consumption, as many of the participants were older adults.
The link found, she says, "calls for more studies where
actual intake can be assessed, rather than taking the information
from food frequency questionnaires, which could be subject
to mistakes."
Diet drinks, she says, are ''generally low in important
health-promoting nutrients, so keeping them as a small part
of your eating plan would be a smart step."
Abstract - FC342 (login required)
Abstract - PO2751 (login required)
Abstract - FC037 (login required)
SOURCES:
Julie Lin, MD, MPH, assistant professor of medicine,
Harvard Medical School, staff physician,
Brigham and Women's Hospital, Boston.
American Society of Nephrology annual meeting,
San Diego, Oct 27-Nov. 1, 2009.
Connie Diekman, RD, director of university nutrition,
Washington University, St. Louis.
News release, American Beverage Association.
© 2009 WebMD, LLC. All rights reserved.
Kathleen Doheny
Kathleen Doheny is a Los Angeles-based journalist
specializing in health, fitness, and behavior topics.
In addition to writing for WebMD, her articles have appeared
in the Los Angeles Times, Shape, Natural Health,
and many other magazines and web sites.
Louise Chang, MD
Louise Chang, MD, is part of the WebMD medical editing team
and is responsible for reviewing WebMD news and feature
stories to ensure their medical accuracy.
She has always considered herself a patient advocate and
educator at heart.
She has had broad experience of both inpatient and outpatient
practice in urban and suburban settings.
Dr. Chang shares the WebMD mission to provide the most
accurate and useful medical information for people.
Dr. Chang completed her undergraduate degree at
Stanford University and attended medical school at
New York Medical College.
She completed her internal medicine residency at
Saint Vincent's Hospital in New York City,
where she also served as a chief resident from 2001-2002.
Immediately prior to joining WebMD, Dr. Chang worked as
an attending physician and clinical instructor at
Grady Memorial Hospital as part of the
Emory School of Medicine in downtown Atlanta,
seeing patients and working with and
teaching medical residents and students.
Dr. Chang is board-certified in internal medicine.
She is a member of both the American College of Physicians
and the Society of General Internal Medicine.
Her prior research work has been published and presented
at regional and national conferences.
http://www.scienceblog.com/cms/help-your-kidneys-pass-salt-and-diet-soda-26792.html
Help your kidneys: Pass on salt and diet soda
Individuals who consume a diet high in sodium or artificially
sweetened drinks are more likely to experience a decline in
kidney function, according to two papers being presented
at the American Society of Nephrology's annual meeting in
San Diego, California.
Julie Lin MD, MPH, FASN and Gary Curhan, MD, ScD, FASN
of Brigham and Women's Hospital studied more than 3,000
women participating in the Nurses Health Study to identify the
impact of sodium and sweetened drinks on kidney function.
"There are currently limited data on the role of diet in
kidney disease," said Dr. Lin. "While more study is needed,
our research suggests that higher sodium and artificially sweetened
soda intake are associated with greater rate of decline
in kidney function."
The first study,
"Associations of Diet with Kidney Function Decline," examined
the influence of individual dietary nutrients on kidney function
decline over 11 years in more than 3,000 women participants
of the Nurses Health Study. The authors found that
"in women with well-preserved kidney function,
higher dietary sodium intake was associated with greater kidney
function decline, which is consistent with experimental animal data
that high sodium intake promotes progressive kidney decline."
The second study, also conducted by Dr. Lin and Dr. Curhan,
"Associations of Sweetened Beverages with Kidney Function Decline,"
examined the influence of sugar-sweetened and artificially sweetened
beverages on kidney function decline in the same group
of Nurses Health Study participants.
An analysis of the nationally representative NHANES III participants
had previously reported an association between sugar-sweetened soda
and urinary protein, but data on kidney function change
was not available.
This investigation reported "a significant two-fold increased odds,
between two or more servings per day of artificially sweetened soda
and faster kidney function decline;
no relation between sugar-sweetened beverages and kidney
function decline was noted" said Dr. Lin.
This association persisted even after the study authors accounted
for age, caloric intake, obesity, high blood pressure, diabetes,
cigarette smoking, physical activity, and cardiovascular disease.
The mechanisms for kidney decline in the setting of high intake of
artificial sweetenters have not been previously studied
and deserve further investigation.
The study participants were older Caucasian women and the authors
note that the findings may not be directly applicable to men or people
of other ethnicities.
The authors report no financial disclosures.
EDITOR:
"Associations of Diet with Kidney Function Decline," (SA-FC342)
will be presented as part of a Free Communication Session at the
American Society of Nephrology's 42nd Annual Meeting and
Scientific Exposition on Oct. 31 at 4:24 pm in Room 25 of the
San Diego Convention Center in San Diego, CA.
"Associations of Sweetened Beverages with Kidney Function Decline,"
(SA-PO2751) will be presented as part of a Poster Session
from 10:00 am -- 12:00 pm in the Scientific Exposition Hall of the
San Diego Convention Center also on Oct. 31.
Both abstracts will be presented as part of a Press Briefing
on Oct. 30 at 12:15 pm in Room 12.
ASN Renal Week 2009, the largest nephrology meeting of its kind,
will provide a forum for 13,000 professionals to discuss the latest
findings in renal research and engage in educational sessions related
to advances in the care of patients with kidney and related disorders.
Renal Week 2009 will take place October 27 -- November 1
at the San Diego Convention Center in San Diego.
Founded in 1966, the American Society of Nephrology (ASN)
is the world's largest professional society devoted to the study
of kidney disease.
Comprised of 11,000 physicians and scientists, ASN continues
to promote expert patient care, to advance medical research,
and to educate the renal community.
ASN also informs policymakers about issues of importance to
kidney doctors and their patients.
ASN funds research, and through its world-renowned meetings
and first-class publications, disseminates information
and educational tools that empower physicians.
http://www.eurekalert.org/multimedia/pub/17613.php?from=147059
[ large photo ]
Contact: Shari Leventhal sleventhal@asn-online.org 202-558-8423
American Society of Nephrology
http://www.brighamandwomens.org/renal/Research/JLinClinProt.aspx
Dr. Lin’s research interests focuses on proteinuric renal diseases
and glomerulopathies.
Her current research examines associations between diet, lipids,
and inflammatory biomarkers and the development of nephropathy
in adult-onset diabetes mellitus using subjects participating in the
Nurses Health Study and Health Professionals Follow-Up Study.
10 studies listed 2001-2004
Julie Lin, M.D.,M.P.H.. Associate Physician.
Phone, (617) 732-6383. Fax, (617) 975-0840.
Office Address, Brigham and Women's Hospital, Renal Division
BWH, 75 Francis Street Boston, MA 02115 617-732-5500
http://www.brighamandwomens.org/renal/Research/clinical_research_faculty.aspx#jlin
Assistant Professor
Diabetic nephropathy, CKD and cardiovascular disease
Dr. Lin is a renal epidemiologist whose research interests focus
on proteinuric renal diseases, glomerulopathies, and chronic kidney
disease progression.
Research includes analyses of diet, lipids, genetics and
inflammatory biomarkers and nephropathy
in type 2 diabetes mellitus in participants of the Nurses Health Study
and Health Professionals Follow-Up Study.
Another area of interest is associations of chronic kidney disease
with quality of life measures in cognitive and physical functioning.
As the lead living kidney donor advocate
for Brigham and Women’s Hospital, Dr. Lin is also studying
outcomes and quality of life in living kidney donors in
collaboration with the Division of Transplantation Surgery.
She also has on-going collaborations with other investigators
within and outside of Harvard Medical School in projects that
examine cardiovascular disease risk in the setting
of chronic kidney disease.
3 previous studies published with GC Curhan
Channing Laboratory, Department of Medicine,
Brigham and Women's Hospital, Harvard Medical School,
Boston, MA, USA. jlin11@partners.org
http://www.brighamandwomens.org/renal/Research/clinical_research_faculty.aspx#gcurhan
Gary C. Curhan, MD, ScD Associate Professor
Epidemiology of CKD, nephrolithiasis, gout, hypertension
Dr. Curhan’s research focuses on the prevention of common
diseases by investigating scientifically and clinically important
questions and exploring the role of modifiable factors, chiefly
in the areas of nephrology and urology.
The synergy between his clinical training in nephrology and
doctoral work in epidemiology has produced a strong interest
in ‘metabolic epidemiology.’
In an effort to clarify and refine our insight into several prevalent
conditions, much of his work has examined and challenged
existing beliefs and commonly accepted practices,
often motivating important changes in clinical practice and
understanding.
Major ongoing areas or research include:
1) epidemiology of nephrolithiasis -- we are studying dietary
and lifestyle factors as well as the genetics of stone disease;
2) epidemiology of hypertension;
3) risk factors for renal function decline and change in albuminuria;
4) epidemiology of gout;
5) epidemiology of hearing loss;
6) mineral metabolism and risk of cardiovascular disease;
7) risk factors for community acquired pneumonia;
8) epidemiology of incontinence;
9) epidemiology of hyponatremia.
Dr. Curhan works closely with several faculty members
in the Renal Division and their efforts will hopefully lead to new
approaches to prevention and treatment of these common conditions.
Publications
Taylor EN, Fung TT, Curhan GC.
DASH-style diet and the risk of incident kidney stones.
J Am Soc Nephrol. 2009; (in press). (PMC Journal – In Process)
Forman JP, Stampfer MJ, Curhan GC.
Diet and lifestyle risk factors associated with incident hypertension
in women.
JAMA. 2009 Jul 22; 302(4):401-11
Choi HK, Curhan GC.
Soft drinks, fructose consumption, and the risk of gout in men –
A Prospective Cohort Study.
BMJ. 2008 Feb 9; 336(7639):309-12. PMCID: PMC2234536
Waikar SS, Mount DB, Curhan GC.
Mortality after hospitalization with mild, moderate,
and severe hyponatremia.
Am J Med. 2009; (in press).
Curhan SG, Eavey R, Shargorodsky J, Curhan GC.
Analgesic use and the risk of hearing loss in men.
Am J Med. 2009; (in press).
Department of Medicine, Renal Division,
Brigham and Women's Hospital,
Harvard Medical School, Boston, Massachusetts 02115, USA.
gcurhan@partners.org
_____________________________________________________
consider co-factors (methanol, formaldehyde, and protective folic acid), re UK FSA test of aspartame in candy bars on 50 reactors, Stephen L Atkin, Hull York Medical School: Rich Murray 2009.09.29
http://rmforall.blogspot.com/2009_09_01_archive.htm
Tuesday, September 29, 2009
http://groups.yahoo.com/group/aspartameNM/message/1587
_____________________________________________________
Included herein is substantial mainstream evidence that the natural
conversion in humans of orally ingested methanol into formaldehyde
and then formic acid results in substantial, durable, cumulative
retention of toxic reaction products.
Adequate folic acid levels expedite the safe metabolism of methanol
in most people.
Ethyl alcohol and folic acid in vegetables and fruits are sufficient to
protect most people from conversion of their methanol into
formaldehyde.
Many common agents interfere with folic acid (folic acid antagonists).
Additionally, genetic variations are potent.
About 3/4 of reactors are female.
Those who rarely have alcohol hangovers may be substantially immune
to methanol and formaldehyde.
Recent exposure to alcohol beverages, tobacco and wood smoke,
and a large variety of formaldehyde sources may compromise the
clarity of aspartame reaction tests.
Aspartame reactors often report allergies to many agents, with similar
symptoms: mercury (amalgams and fish), MSG and free glutamate in
foods (for instance, hydrolyzed vegetable or yeast protein), carbon
monoxide, molds, many foods, etc. -- up to Multiple Chemical
Sensitivity.
Aspartame reactors often take many steps to exercise, reduce stress,
lower salt, emphasize organic plant foods, reduce drug and chemical
exposures, limit protein and fat intake, use vitamin and mineral
supplements, limit processed foods -- thus complicating attempts to
create a matching control group, and introducing uncertainty about
whether the reactors are as vulnerable now as in the past, when they
may have had more negative factors for years.
So, genetic background, age, sex, obesity, existing illnesses, diet,
exercise, environmental toxins, medicines and drugs, parental
exposure to all these factors, and more may corrode the "gold
standard" of a single exposure double-blind experimental test,
especially for a rather modest test group of 50.
Perhaps, a more productive research strategy would be to test 10
reactors, one at a time, for 24 hours each, using a wide range of
tests, recording the enormous individual variations that are usually
swamped by taking group data averages.
Computerized tests facilitate fast, affordable measures of cognitive
and memory effects.
Full audio and video recording is now available.
Dimethyl dicarbonate, an approved additive for reducing fungi in
wines, perhaps with a neutral taste, quickly releases about the same
level of methanol upon ingestion as aspartame drinks, making
possible studies free of any possible "excitotoxic" effects of
aspartic acid and phenylalanine, while allowing a third beverage
to be a control substance.
This approach would also contribute to the meager research literature
about the role of methanol in alcohol hangovers.
aspartame reactors may send detailed feedback to Andrew Wadge,
UK Food Standards Agency to guide new pilot study re bad
reactions: Rich Murray 2009.06.22
http://rmforall.blogspot.com/2009_06_01_archive.htm
Monday, June 22, 2009
http://groups.yahoo.com/group/aspartameNM/message/1577
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.dorway.com/products.txt
[ rearranged, 11% methanol added ]
From the Nutrasweet Web Site: (amounts in various "foods")
Product Category -- Serving Size -- aspartame -- 11% methanol
Gelatin Dessert ----------- 8 ounces -----190 mg ---- 21 mg
Carbonated Beverage --- 12 ounces ----- 180 ------- 20
" ------------------------ 48 ounces ----- 720 ------- 79
Powdered Drink -------- 12 ounces ----- 180 -------- 20
Fruit Drink (10% juice) -- 12 ounces ----- 140 -------15.4
Hot Chocolate ----------- 12 ounces ----- 100 -------11
Yogurt ------------------- 8 ounces ----- 124 --------13.6
Ice Cream ---------------- 8 ounces ----- 100 ------- 11
Pudding Dessert ---------- 8 ounces ------ 50 --------- 5.5
Frozen Novelty ----------- 2-3 ounces ---- 50 --------- 5.5
Gum ----------------------- 1 stick -------- 6-8 -------- 0.7-0.9
Vitamins ------------------ 1 vitamin ------ 4 ---------- 0.44
Breath mint ---------------- 1 mint --------- 1.5 -------- 0.17
http://groups.yahoo.com/group/aspartameNM/message/846
aspartame in Merck Maxalt-MLT worsens migraine,
AstraZeneca Zomig, Eli Lilly Zyprexa,
J&J Merck Pepcid AC (Famotidine 10mg) Chewable Tab,
Pfizer Cool Mint Listerine Pocketpaks: Murray 2002.07.16
Migraine MLT-Down: an unusual presentation of migraine
in patients with aspartame-triggered headaches.
Newman LC, Lipton RB Headache 2001 Oct; 41(9): 899-901.
[ Merck 10-mg Maxalt-MLT, for migraine, has 3.75 mg aspartame,
while 12 oz diet soda has 200 mg. ]
Headache Institute, St. Lukes-Roosevelt Hospital Center,
New York, NY
Department of Neurology newmanache@aol.com
Albert Einstein College of Medicine, Bronx, NY
Innovative Medical Research RLipton@aecom.yu.edu
http://groups.yahoo.com/group/aspartameNM/message/855
Blumenthall & Vance: aspartame chewing gum headaches
Nov 1997: Murray 2002.07.28
Harvey J. Blumenthal, MD, Dwight A Vance, RPh
Chewing Gum Headaches. Headache 1997 Nov; 37(10): 665-6.
Department of Neurology, University of Oklahoma College of
Medicine, Tulsa, USA. neurotulsa@aol.com
Aspartame, a popular dietetic sweetener, may provoke headache in
some susceptible individuals. Herein, we describe three cases of
young women with migraine who reported their headaches could be
provoked by chewing gum sweetened with aspartame.
[ 6-8 mg aspartame per stick chewing gum ]
http://groups.yahoo.com/group/aspartameNM/message/1143
antiseptic? antifungal? antiviral? methanol (formaldehyde, formic
acid) disposition: Bouchard M et al, full plain text, 2001: substantial
sources are degradation of fruit pectins, liquors, aspartame, smoke:
Murray 2005.01.05 rmforall
http://www.toxsci.oupjournals.org/cgi/content/full/64/2/169
free full text
A Biologically Based Dynamic Model for Predicting the Disposition
of Methanol and Its Metabolites in Animals and Humans.
Michèle Bouchard,
Robert C. Brunet,
Pierre-Olivier Droz,
and Gaétan Carrier.
Toxicological Sciences 64, 169-184 (2001)
Copyright © 2001 by the Society of Toxicology
[ extracts ]
"Exposure to methanol also results from the consumption of certain
foodstuffs (fruits, fruit juices, certain vegetables, aspartame
sweetener, roasted coffee, honey) and alcoholic beverages (Health
Effects Institute, 1987; Jacobsen et al., 1988).
[ It's unusual for a mainstream journal article to mention "fruits, fruit
juices, certain vegetables, aspartame sweetener" and "alcoholic
beverages" to be methanol sources.]
... little is known about the chronic effects of low exposure doses...
Systemic methanol is extensively metabolized by liver alcohol
dehydrogenase [ ADH ] and catalase-peroxidase enzymes to
formaldehyde, which is in turn rapidly oxidized to formic acid by
formaldehyde dehydrogenase enzymes...
Formaldehyde, as it is highly reactive, forms relatively stable adducts
with cellular constituents...
Primates and humans appear to be more susceptible to the acute
toxicity of methanol than rodents...
Although methanol has been reported to be metabolized mainly in
the liver, pulmonary metabolism is also likely to occur. Indeed,
the catalase-peroxidase system responsible for a major fraction of
methanol metabolism in rats is widely distributed in mammalian
tissues...
The model included a constant background whole body methanol
burden of 2.133 mmol, which corresponds to the mean blood
concentration of 0.5 mg/L of methanol measured by Osterloh et al.
(1996) in control subjects at the end of an 8-h frequent blood
sampling period...
... once formed, a substantial fraction of formaldehyde is converted
to unobserved forms. This pathway contributes to a long-term
unobserved compartment. The latter, most plausibly, represents
either the formaldehyde that ( directly or after oxidation to formate )
binds to various endogenous molecules (Heck et al., 1983; Roe,
1982)...
That substantial amounts of methanol metabolites or by-products
are retained for a long time is verified by Horton et al. (1992)
who estimated that 18 h following an iv injection of 100 mg/kg
of 14C-methanol in male Fischer-344 rats, only 57% of the
dose was eliminated from the body. From the data of Dorman
et al. (1994) and Medinsky et al. (1997), it can further be
calculated that 48 h following the start of a 2-h inhalation
exposure to 900 ppm of 14C-methanol vapors in female
cynomolgus monkeys, only 23% of the absorbed 14C-methanol
was eliminated from the body. These findings are corroborated by
the data of Heck et al. (1983) showing that 40% of a
14C-formaldehyde inhalation dose remained in the body 70 h
postexposure...
Experimental studies on the detailed time profiles following
controlled repeated exposures to methanol are lacking...
Thus, in monkeys and plausibly humans, a much larger fraction of
body formaldehyde is rapidly converted to unobserved forms
rather than passed on to formate and eventually CO2."
If we assume 30% retention of durable cumulative toxic products of
formaldehyde and formic acid, then a 12-oz can diet drink gives 200
mg aspartame, 22 mg methanol, and 7 mg formaldehyde and formic
acid at 30% cumulative retention. We may add that well known
sources of formaldehyde include both wood and tobacco smoke,
and, notoriously, mobile homes. Two teams give evidence that
formaldehyde and formic acid from methanol in ethanol drinks
(often far above the 100 mg/L methanol in red wines, two times the
level in aspartame drinks) are the main cause of the many symptoms
of "morning after" hangovers.
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
Furthermore, BM Kapur et al, 2007 give evidence that formic acid
from methanol in ethanol drinks is a major cause of Fetal Alcohol
Syndrome, readily preventable by adequate levels of folic acid,
which expedites the safe metabolism of formaldehyde, in most
people.
"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." ...
"MeOH concentrations between 4 and 4500 mg/l can be present
in various alcoholic beverages (Sprung et al., 1988)."
A variety of mutations, as well as aspirin and many painkillers,
impede folic acid. However, fruits and vegetables give enough folic
acid to mitigate harm from their methanol. Then again, formaldehyde
may in many people treat infections by fungi, bacteria, and virusus.
All these unexamined co-factors have confused attempts to study
aspartame toxicity for three decades.
http://groups.yahoo.com/group/aspartameNM/message/1141
Nurses Health Study can quickly reveal the extent of aspartame
(methanol, formaldehyde, formic acid) toxicity: Murray 2004.11.21
The Nurses Health Study is a bonanza of information about the health of
probably hundreds of nurses who use 6 or more cans daily of diet soft
drinks -- they have also stored blood and tissue samples from their
immense pool of subjects, over 100,000 for decades.
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
A widely proclaimed NIH-AARP mass survey by U Lim et al. 2006,
while failing to show specific cancers with feeble diet drink
consumption data for a year for seniors, did find that 4% of a
half-million seniors drank 3 and more cans daily diet soda
[ 12-oz can gives 200 mg aspartame, 22 mg methanol,
7 mg formaldehyde and formic acid at 30% cumulative retention ]
aspartame mg/d
0 ---- under 100 - 100-200 - 200-400 - 400-600 - 600-1200 -
cohort %
46 ------- 25 ------ 13 ------- 7 --------- 5 ------ about 3 ----
over 1200 mg/d
under 1%
This is the first good data about the percentage of aspartame users
who use over 3 cans daily, averaging 5 cans daily at 200 mg per 12
oz can diet soda.
About 4% of 473,984 is 19,000 people, with a peak intake of 17
cans daily, and average 5 cans daily.
It would be worthwhile to investigate a wide variety of symptoms for
the 0.1 % of highest level users, about 500 people.
For about 200 million USA aspartame users, this would be 200,000
people.
The highest level 3400 mg aspartame [ 17 12-oz cans ] gives
11% = 374 mg methanol, 48 times the recommended daily limit of
consumption of 7.8 mg as recommended by the
Environmental Protection Agency (EPA).3
At 30% retention of cumulative toxic products of formaldehyde and
formic acid, these would be 125 mg, 60 times higher than the 1999
EPA alarm level for formaldehyde in daily drinking water of
1 ppm = 2 mg for average daily drinking water of 2 L daily.
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
40 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@catholic.ac.kr
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@RMV.se;
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
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
[ extracts ]
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
[ Extract ]
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.
Case Series
Six patients (ages 16 to 75 years) were referred for evaluation of
recalcitrant dermatitis. By history, five of the patients were noted to
have developed migraines following aspartame consumption; the
sixth reported dermatitis flares associated with diet cola
consumption of >2 liters/day.
All six patients had current environmental exposures to formaldehyde
or formaldehyde-releasing preservatives in their personal hygiene
products and/or regular consumption of "sugar-free food" artificially
sweetened with aspartame.
Based on their histories and clinical presentations, these patients
were patch-tested with the North American Contact Dermatitis
Group 65-allergen Standard Screening Series and selected
chemicals from the University of Miami vehicle, fragrance, bakery,
and textile trays.
All six patients had positive reactions to formaldehyde, and four had
additional positive reactions to formaldehyde-releasing preservatives
(FRPs). Expert counseling on allergen avoidance (including
avoidance of formaldehyde, FRPs, and aspartame) and alternative
product recommendations were provided to the patients.
At their follow-up appointments (between 8 and 12 weeks), all the
patients showed clearance of their dermatitis. Four patients (two
inadvertently) resumed their consumption of aspartame and
subsequently returned for an additional follow-up visit. Three of the
first five patients had recurrences of both their migraines and their
dermatitis; the sixth patient (who had no migraines) had a positive
rechallenge dermatitis. These four patients were again counseled on
avoidance regimen.
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
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@contactderm.net;
Sarah A. Stechschulte, BA sstechschulte@gmail.com
_____________________________________________________
Rich Murray, 1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298 rmforall@comcast.net
http://RMForAll.blogspot.com new primary archive
http://groups.yahoo.com/group/aspartameNM/messages
group with 143 members, 1,588 posts in a public archive
http://groups.yahoo.com/group/aspartame/messages
group with 1204 members, 23,945 posts in a public archive
http://groups.yahoo.com/group/rmforall/messages
http://groups.yahoo.com/group/AstroDeep/messages
participant, Santa Fe Complex www.sfcomplex.org
_____________________________________________________
Tuesday, September 29, 2009
consider co-factors (methanol, formaldehyde, and protective folic acid), re UK FSA test of aspartame in candy bars on 50 reactors, Stephen L Atkin
consider co-factors (methanol, formaldehyde, and protective folic acid), re UK FSA test of aspartame in candy bars on 50 reactors, Stephen L Atkin, Hull York Medical School: Rich Murray 2009.09.29
http://rmforall.blogspot.com/2009_09_01_archive.htm
Tuesday, September 29, 2009
http://groups.yahoo.com/group/aspartameNM/message/1587
_____________________________________________________
Included herein is substantial mainstream evidence that the natural
conversion in humans of orally ingested methanol into formaldehyde
and then formic acid results in substantial, durable, cumulative
retention of toxic reaction products.
Adequate folic acid levels expedite the safe metabolism of methanol
in most people.
Ethyl alcohol and folic acid in vegetables and fruits are sufficient to
protect most people from conversion of their methanol into
formaldehyde.
Many common agents interfere with folic acid (folic acid antagonists).
Additionally, genetic variations are potent.
About 3/4 of reactors are female.
Those who rarely have alcohol hangovers may be substantially immune
to methanol and formaldehyde.
Recent exposure to alcohol beverages, tobacco and wood smoke,
and a large variety of formaldehyde sources may compromise the
clarity of aspartame reaction tests.
Aspartame reactors often report allergies to many agents, with similar
symptoms: mercury (amalgams and fish), MSG and free glutamate in
foods (for instance, hydrolyzed vegetable or yeast protein), carbon
monoxide, molds, many foods, etc. -- up to Multiple Chemical
Sensitivity.
Aspartame reactors often take many steps to exercise, reduce stress,
lower salt, emphasize organic plant foods, reduce drug and chemical
exposures, limit protein and fat intake, use vitamin and mineral
supplements, limit processed foods -- thus complicating attempts to
create a matching control group, and introducing uncertainty about
whether the reactors are as vulnerable now as in the past, when they
may have had more negative factors for years.
So, genetic background, age, sex, obesity, existing illnesses, diet,
exercise, environmental toxins, medicines and drugs, parental
exposure to all these factors, and more may corrode the "gold
standard" of a single exposure double-blind experimental test,
especially for a rather modest test group of 50.
Perhaps, a more productive research strategy would be to test 10
reactors, one at a time, for 24 hours each, using a wide range of
tests, recording the enormous individual variations that are usually
swamped by taking group data averages.
Computerized tests facilitate fast, affordable measures of cognitive
and memory effects.
Full audio and video recording is now available.
Dimethyl dicarbonate, an approved additive for reducing fungi in
wines, perhaps with a neutral taste, quickly releases about the same
level of methanol upon ingestion as aspartame drinks, making
possible studies free of any possible "excitotoxic" effects of
aspartic acid and phenylalanine, while allowing a third beverage
to be a control substance.
This approach would also contribute to the meager research literature
about the role of methanol in alcohol hangovers.
aspartame reactors may send detailed feedback to Andrew Wadge,
UK Food Standards Agency to guide new pilot study re bad
reactions: Rich Murray 2009.06.22
http://rmforall.blogspot.com/2009_06_01_archive.htm
Monday, June 22, 2009
http://groups.yahoo.com/group/aspartameNM/message/1577
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.dorway.com/products.txt
[ rearranged, 11% methanol added ]
From the Nutrasweet Web Site: (amounts in various "foods")
Product Category -- Serving Size -- aspartame -- 11% methanol
Gelatin Dessert ----------- 8 ounces -----190 mg ---- 21 mg
Carbonated Beverage --- 12 ounces ----- 180 ------- 20
" ------------------------ 48 ounces ----- 720 ------- 79
Powdered Drink -------- 12 ounces ----- 180 -------- 20
Fruit Drink (10% juice) -- 12 ounces ----- 140 -------15.4
Hot Chocolate ----------- 12 ounces ----- 100 -------11
Yogurt ------------------- 8 ounces ----- 124 --------13.6
Ice Cream ---------------- 8 ounces ----- 100 ------- 11
Pudding Dessert ---------- 8 ounces ------ 50 --------- 5.5
Frozen Novelty ----------- 2-3 ounces ---- 50 --------- 5.5
Gum ----------------------- 1 stick -------- 6-8 -------- 0.7-0.9
Vitamins ------------------ 1 vitamin ------ 4 ---------- 0.44
Breath mint ---------------- 1 mint --------- 1.5 -------- 0.17
http://groups.yahoo.com/group/aspartameNM/message/846
aspartame in Merck Maxalt-MLT worsens migraine,
AstraZeneca Zomig, Eli Lilly Zyprexa,
J&J Merck Pepcid AC (Famotidine 10mg) Chewable Tab,
Pfizer Cool Mint Listerine Pocketpaks: Murray 2002.07.16
Migraine MLT-Down: an unusual presentation of migraine
in patients with aspartame-triggered headaches.
Newman LC, Lipton RB Headache 2001 Oct; 41(9): 899-901.
[ Merck 10-mg Maxalt-MLT, for migraine, has 3.75 mg aspartame,
while 12 oz diet soda has 200 mg. ]
Headache Institute, St. Lukes-Roosevelt Hospital Center,
New York, NY
Department of Neurology newmanache@aol.com
Albert Einstein College of Medicine, Bronx, NY
Innovative Medical Research RLipton@aecom.yu.edu
http://groups.yahoo.com/group/aspartameNM/message/855
Blumenthall & Vance: aspartame chewing gum headaches
Nov 1997: Murray 2002.07.28
Harvey J. Blumenthal, MD, Dwight A Vance, RPh
Chewing Gum Headaches. Headache 1997 Nov; 37(10): 665-6.
Department of Neurology, University of Oklahoma College of
Medicine, Tulsa, USA. neurotulsa@aol.com
Aspartame, a popular dietetic sweetener, may provoke headache in
some susceptible individuals. Herein, we describe three cases of
young women with migraine who reported their headaches could be
provoked by chewing gum sweetened with aspartame.
[ 6-8 mg aspartame per stick chewing gum ]
http://groups.yahoo.com/group/aspartameNM/message/1143
antiseptic? antifungal? antiviral? methanol (formaldehyde, formic
acid) disposition: Bouchard M et al, full plain text, 2001: substantial
sources are degradation of fruit pectins, liquors, aspartame, smoke:
Murray 2005.01.05 rmforall
http://www.toxsci.oupjournals.org/cgi/content/full/64/2/169
free full text
A Biologically Based Dynamic Model for Predicting the Disposition
of Methanol and Its Metabolites in Animals and Humans.
Michèle Bouchard,
Robert C. Brunet,
Pierre-Olivier Droz,
and Gaétan Carrier.
Toxicological Sciences 64, 169-184 (2001)
Copyright © 2001 by the Society of Toxicology
[ extracts ]
"Exposure to methanol also results from the consumption of certain
foodstuffs (fruits, fruit juices, certain vegetables, aspartame
sweetener, roasted coffee, honey) and alcoholic beverages (Health
Effects Institute, 1987; Jacobsen et al., 1988).
[ It's unusual for a mainstream journal article to mention "fruits, fruit
juices, certain vegetables, aspartame sweetener" and "alcoholic
beverages" to be methanol sources.]
... little is known about the chronic effects of low exposure doses...
Systemic methanol is extensively metabolized by liver alcohol
dehydrogenase [ ADH ] and catalase-peroxidase enzymes to
formaldehyde, which is in turn rapidly oxidized to formic acid by
formaldehyde dehydrogenase enzymes...
Formaldehyde, as it is highly reactive, forms relatively stable adducts
with cellular constituents...
Primates and humans appear to be more susceptible to the acute
toxicity of methanol than rodents...
Although methanol has been reported to be metabolized mainly in
the liver, pulmonary metabolism is also likely to occur. Indeed,
the catalase-peroxidase system responsible for a major fraction of
methanol metabolism in rats is widely distributed in mammalian
tissues...
The model included a constant background whole body methanol
burden of 2.133 mmol, which corresponds to the mean blood
concentration of 0.5 mg/L of methanol measured by Osterloh et al.
(1996) in control subjects at the end of an 8-h frequent blood
sampling period...
... once formed, a substantial fraction of formaldehyde is converted
to unobserved forms. This pathway contributes to a long-term
unobserved compartment. The latter, most plausibly, represents
either the formaldehyde that ( directly or after oxidation to formate )
binds to various endogenous molecules (Heck et al., 1983; Roe,
1982)...
That substantial amounts of methanol metabolites or by-products
are retained for a long time is verified by Horton et al. (1992)
who estimated that 18 h following an iv injection of 100 mg/kg
of 14C-methanol in male Fischer-344 rats, only 57% of the
dose was eliminated from the body. From the data of Dorman
et al. (1994) and Medinsky et al. (1997), it can further be
calculated that 48 h following the start of a 2-h inhalation
exposure to 900 ppm of 14C-methanol vapors in female
cynomolgus monkeys, only 23% of the absorbed 14C-methanol
was eliminated from the body. These findings are corroborated by
the data of Heck et al. (1983) showing that 40% of a
14C-formaldehyde inhalation dose remained in the body 70 h
postexposure...
Experimental studies on the detailed time profiles following
controlled repeated exposures to methanol are lacking...
Thus, in monkeys and plausibly humans, a much larger fraction of
body formaldehyde is rapidly converted to unobserved forms
rather than passed on to formate and eventually CO2."
If we assume 30% retention of durable cumulative toxic products of
formaldehyde and formic acid, then a 12-oz can diet drink gives 200
mg aspartame, 22 mg methanol, and 7 mg formaldehyde and formic
acid at 30% cumulative retention. We may add that well known
sources of formaldehyde include both wood and tobacco smoke,
and, notoriously, mobile homes. Two teams give evidence that
formaldehyde and formic acid from methanol in ethanol drinks
(often far above the 100 mg/L methanol in red wines, two times the
level in aspartame drinks) are the main cause of the many symptoms
of "morning after" hangovers.
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
Furthermore, BM Kapur et al, 2007 give evidence that formic acid
from methanol in ethanol drinks is a major cause of Fetal Alcohol
Syndrome, readily preventable by adequate levels of folic acid,
which expedites the safe metabolism of formaldehyde, in most
people.
"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." ...
"MeOH concentrations between 4 and 4500 mg/l can be present
in various alcoholic beverages (Sprung et al., 1988)."
A variety of mutations, as well as aspirin and many painkillers,
impede folic acid. However, fruits and vegetables give enough folic
acid to mitigate harm from their methanol. Then again, formaldehyde
may in many people treat infections by fungi, bacteria, and virusus.
All these unexamined co-factors have confused attempts to study
aspartame toxicity for three decades.
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
A widely proclaimed NIH-AARP mass survey by U Lim et al. 2006,
while failing to show specific cancers with feeble diet drink
consumption data for a year for seniors, did find that 4% of a
half-million seniors drank 3 and more cans daily diet soda
[ 12-oz can gives 200 mg aspartame, 22 mg methanol,
7 mg formaldehyde and formic acid at 30% cumulative retention ]
aspartame mg/d
0 ---- under 100 - 100-200 - 200-400 - 400-600 - 600-1200 -
cohort %
46 ------- 25 ------ 13 ------- 7 --------- 5 ------ about 3 ----
over 1200 mg/d
under 1%
This is the first good data about the percentage of aspartame users
who use over 3 cans daily, averaging 5 cans daily at 200 mg per 12
oz can diet soda.
About 4% of 473,984 is 19,000 people, with a peak intake of 17
cans daily, and average 5 cans daily.
It would be worthwhile to investigate a wide variety of symptoms for
the 0.1 % of highest level users, about 500 people.
For about 200 million USA aspartame users, this would be 200,000
people.
The highest level 3400 mg aspartame [ 17 12-oz cans ] gives
11% = 374 mg methanol, 48 times the recommended daily limit of
consumption of 7.8 mg as recommended by the
Environmental Protection Agency (EPA).3
At 30% retention of cumulative toxic products of formaldehyde and
formic acid, these would be 125 mg, 60 times higher than the 1999
EPA alarm level for formaldehyde in daily drinking water of
1 ppm = 2 mg for average daily drinking water of 2 L daily.
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
40 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@catholic.ac.kr
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@RMV.se;
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
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
[ extracts ]
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
[ Extract ]
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.
Case Series
Six patients (ages 16 to 75 years) were referred for evaluation of
recalcitrant dermatitis. By history, five of the patients were noted to
have developed migraines following aspartame consumption; the
sixth reported dermatitis flares associated with diet cola
consumption of >2 liters/day.
All six patients had current environmental exposures to formaldehyde
or formaldehyde-releasing preservatives in their personal hygiene
products and/or regular consumption of "sugar-free food" artificially
sweetened with aspartame.
Based on their histories and clinical presentations, these patients
were patch-tested with the North American Contact Dermatitis
Group 65-allergen Standard Screening Series and selected
chemicals from the University of Miami vehicle, fragrance, bakery,
and textile trays.
All six patients had positive reactions to formaldehyde, and four had
additional positive reactions to formaldehyde-releasing preservatives
(FRPs). Expert counseling on allergen avoidance (including
avoidance of formaldehyde, FRPs, and aspartame) and alternative
product recommendations were provided to the patients.
At their follow-up appointments (between 8 and 12 weeks), all the
patients showed clearance of their dermatitis. Four patients (two
inadvertently) resumed their consumption of aspartame and
subsequently returned for an additional follow-up visit. Three of the
first five patients had recurrences of both their migraines and their
dermatitis; the sixth patient (who had no migraines) had a positive
rechallenge dermatitis. These four patients were again counseled on
avoidance regimen.
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
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@contactderm.net;
Sarah A. Stechschulte, BA sstechschulte@gmail.com
_____________________________________________________
http://www.guardian.co.uk/science/2009/sep/23/sweetener-aspartame-side-effects
Sweetener aspartame to be investigated for possible side-effects
The Food Standards Agency is calling for volunteers to help test
claims that the artificial sweetener aspartame, used in more than
4,000 products, causes illnesses
Ian Sample, science correspondent
guardian.co.uk, Wednesday 23 September 2009 00.05 BST
Food and drinks containing aspartame
Just some of the thousands of products containing the artificial
sweetener aspartame. Photograph: Graham Turner/Guardian
The Food Standards Agency is launching an investigation into the
artificial sweetener aspartame amid claims that some people
experience side-effects after consuming the substance.
Scientists funded by the agency will test whether certain people
develop a range of illnesses after eating food prepared with the
sweetener.
Aspartame is around 200 times sweeter than sugar and is used in
more than 4,000 products, including diet drinks, cereal bars,
yogurt and chewing gum.
Previous reviews by the Food Standards Agency (FSA) and the
http://www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_home.htm
European Food Safety Authority
[ http://www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_home.htm ]
have concluded that aspartame is safe, but some people complain
they develop headaches, dizziness, vomiting, diarrhoea and fatigue
after eating food containing the chemical.
Researchers led by Professor Stephen Atkin, head of endocrinology,
diabetes and metabolism at the Hull York Medical School,
will look for signs of illness in volunteers after
they consume cereal bars made with or without aspartame.
Atkin's group is recruiting 50 people who believe they are sensitive
to aspartame. The volunteers will be matched by age and sex to 50
volunteers who are happy to eat the sweetener.
In the study, individuals will be randomly assigned an aspartame or
aspartame-free cereal bar and given psychological and medical
checks up to four hours after consuming it.
The following week, the experiment will be repeated with each
volunteer receiving the other type of cereal bar.
The scientists will take blood and urine samples before and after
each test.
Aspartame breaks down in the digestive system into aspartic acid,
methanol and phenylalanine
Some individuals believe it is these chemicals that cause their
symptoms.
The tests will allow scientists to link any ill effects to levels of the
chemicals in the volunteers' blood and urine.
"This is a fundamental study for the people who believe they are
sensitive to aspartame, because it will hopefully prove or disprove
whether or not aspartame can cause problems," Prof Atkin said.
The study is expected to be completed next year and will be
published as a report to the FSA.
A spokesman for the agency said: "We know that aspartame can
be consumed safely but some people consider that they react badly
to it.
We've commissioned this research because it's important to increase
our knowledge about what is happening.
The study will address consumer concerns, including these
anecdotal reports."
Food safety officials are expected to fund a larger investigation if the
study finds evidence that people can be sensitive to the sweetener.
A spokeswoman for the Aspartame Information Service, an industry
body, [ http://www.aspartame.info/ ] said:
"Aspartame has been on the market for more than 25 years
and studies have been done on it from every angle.
We get more of these breakdown products from the
rest of our diets than we get from aspartame.
"The whole anecdotal area [of sensitivity] has been looked at before,
so why start another round of research?
Our concern is that people might be attributing to aspartame
something that might have a more serious cause."
Patience Purdy, honorary vice president of the
National Council of Women of Great Britain,
[ http://fp.ncwgb.f9.co.uk/
http://www.slotfilms.com/NCW/contact.htm
The National Council of Women Of Great Britain
36 Danbury Street, Islington, London N1 8JU
Telephone: 071-354 2395 Fax No. 071-354 9214
Registered Charity No. 1001015 ]
which campaigns for aspartame to be banned on health grounds,
said: "It's good the FSA are taking this seriously, but our concern is
that the study is inadequate. We all react differently to aspartame."
Contact the Science editor: science@guardian.co.uk
Letters for publication should be sent to: letters@guardian.co.uk
Call the main Guardian and Observer switchboard:
+44 (0)20 3353 2000
http://nutnewstoday.blogspot.com/2009/09/aspartame-sensitivity-probe-is-funded.html
Friday, September 25, 2009
Aspartame sensitivity probe is funded in the UK
Scientists are to assess whether the artificial sweetener aspartame
causes health problems in people unusually sensitive to it.
Expert advice is that aspartame -- found in more than 4,000
products -- is safe to consume.
However, a number of people have reported sensitivity to the
product including headaches, dizziness, vomiting, diarrhoea
and fatigue.
The University of Hull study is funded by the
Food Standards Agency (FSA).
Aspartame, 150 times sweeter than sugar, is found in products
such as diet soft drinks, cereal bars, yogurts and chewing gum.
There have long been concerns that the sweetener is linked to a
raft of health problems, including a greater risk of cancer,
fertility issues, nausea, double vision and an effect on appetite.
However, after reviewing the available scientific literature, both
the FSA and the European Food Safety Authority decided there
was no firm evidence of any impact on health, and ruled that
aspartame was safe to consume.
Professor Stephen Atkin, who will lead the new research, said:
"This study is not to determine whether aspartame can be
consumed safely; this has already been established, but rather
to see whether certain people are sensitive to it."
Read more of Aspartame sensitivity probe is funded in the UK
at BBC News site.
http://news.bbc.co.uk/2/hi/health/8266707.stm
Published: 2009/09/25 16:33:14 GMT
BBC NEWS
Sensitivity to aspartame probed
...The Hull team hope their work will lead to a larger
international study to pin down the issue once and for all.
Body chemistry
Professor Atkin also hopes to secure funding to analyse the
chemical breakdown of aspartame in the body.
The sweetener can be broken down to produce
methanol and formaldehyde,
both of which have been previously linked to cancer.
However, it is not clear whether this process takes place in the
body, or, if it does, whether the metabolites are absorbed into the
blood in sufficient quantity to produce any biological effect.
Andrew Wadge, Chief Scientist at the Food Standards Agency said:
"The study will address consumer concerns, including anecdotal
reports that have linked a range of conditions to aspartame.
'The Agency's view remains that aspartame can be consumed safely
and we are not recommending any changes to its current use.
"However, we know that some people consider that they react
badly to consuming this sweetener so we think it is important
to increase our knowledge about what is happening."
One hundred people will take part in the Hull study,
half of who have complained of side effects from aspartame.
The study is expected to take 18 months.
At present the Acceptable Daily Intake (ADI) for aspartame is set
by the European Commission's Scientific Committee on Food (SCF)
at 40 milligrams per kilogram of body weight.
An adult would have to drink about 14 cans a day of diet soft drink,
or consume about 80 sachets of sweetener to reach this amount.
© BBC MMIX
http://www2.hull.ac.uk/news/2009newsarchive/september/studytoinvestigateallegeds.aspx
Study to investigate alleged side effects of aspartame
23 September 2009
...The national study will be carried out by Professor Stephen Atkin
at the University of Hull, in collaboration with colleagues at the
Hull York Medical School and Hull
and East Yorkshire Hospitals NHS Trust.
He explains: “This study is not to determine whether aspartame can
be consumed safely; this has already been established by the FSA
and EFSA, but rather to see whether certain people are sensitive to it.
“We will look at the effects of eating a snack bar which may
or may not contain aspartame in people who say they have a problem
eating aspartame and people who normally consume foods containing
aspartame with no problems.
The study is a double blind placebo crossover,
which is the gold standard of studies.”
It is hoped that this study will help to design a larger international
study, which will provide the information needed to inform
governments and the European Union on whether the consumption
of aspartame is related to symptoms.
Andrew Wadge, Chief Scientist at the Food Standards Agency
said: ‘The study will address consumer concerns, including
anecdotal reports that have linked a range of conditions to
aspartame.
‘The Agency’s view remains that aspartame can be consumed
safely and we are not recommending any changes to its current use.
However, we know that some people consider that they react
badly to consuming this sweetener so we think it is important
to increase our knowledge about what is happening.’
The research is expected to take 18 months and the results will be
published as a report to be delivered to the Food Standards Agency.
A summary of this information will be available on the FSA website.
Ends
Notes to Editors
For press enquiries, or to request an interview with
Prof Stephen Atkin, please contact Claire Mulley
on 01482 466943 or 07809 585965. [ c.mulley@hull.ac.uk ]
Potential volunteers for the study should contact a member of the
clinical trial team on 01482 675372 or 01482 675387
from 9am to 5pm weekdays, or the
Hull Royal Infirmary switchboard on 01482 328541 out of hours.
This is a pilot study involving 100 volunteers; 50 of them have
complained of side-effects from aspartame and they will be
matched in gender and age by people who have no side effects.
Prof Stephen Atkin will be available for interview on
21 and 22 Sept; contact Claire Mulley to request an interview slot.
Prof Stephen Atkin is the Head of Diabetes and Endocrinology
at the University of Hull’s Postgraduate Medical Institute (PGMI).
He has a BSc Biochemistry and MD from Newcastle University.
Prof Atkin completed a PhD at Liverpool University
where he was also an MRC training fellow.
He was appointed in October 2005 as Professor of
Diabetes, Endocrinology and Metabolism
at Hull York Medical School (HYMS).
He is based and leads the pharmaceutical and nutritional
clinical trials teams for these studies at the
Clinical Research Centre based at the
Michael White Diabetes Centre at Hull Royal Infirmary.
The laboratory focusing on molecular and a cellular research is
based within the medical research unit at the University of Hull.
Translational clinical trials for both the food and pharmaceutical
industry are a major focus of the work undertaken and part of
the overall research portfolio on modulation of insulin resistance
and cardiovascular risk in these conditions that are associated
with a high morbidity and mortality.
Read more about Hull York Medical School (HYMS).
http://www.hyms.ac.uk/
© The University of Hull,
Cottingham Road, Hull. HU6 7RX, +44 (0)1482 346311
HYMS STAFF
Professor Stephen L. Atkin
Primary organisation:
Michael White Diabetes Centre
Head, Academic Endocrinology, Diabetes and Metabolism
Additional affiliation:
HYMS
Teaching role(s) within HYMS:
Clinical Placement Tutor
Phase 2 Curriculum Group
Plenary Lecturer - Phase 1
Plenary Lecturer - Phase 2
http://www.hyms.ac.uk/research/
Insulin (blue) encapsulated within a pollen exine [ photo ]
Endocrinology and Diabetes
Stephen Atkin is HYMS Professor of Endocrinology and Metabolism.
His section of the PGMI at Hull incorporates bone metabolism,
and has a specific interest in the cardiovascular risk factors associated
with the metabolic syndrome that encompasses polycystic ovarian
syndrome, impaired glucose tolerance and type 2 diabetes.
The group is collaborating with the University of Hull's
Department of Chemistry to develop the use of pollen and spore
coatings that can deliver orally ingested material into the blood stream.
Read more about the Food Standards Agency.
http://www.food.gov.uk/
http://www.timesonline.co.uk/tol/news/uk/health/article6845119.ece
If you want to submit your material to TimesOnline,
please email feedback@thetimes.co.uk
http://www.foodmanufacture.co.uk/news/printpage.php/aid/9424/Experts_challenge_pilot_aspartame_study.html
Food Manufacture
News & Features » Latest news
Experts challenge pilot aspartame study
By Rick Pendrous
Published: 14 September, 2009
The pilot study launched by the Food Standards Agency (FSA) into
the health effects of individuals “self-reporting as sensitive” to
aspartame has been criticised for being an unnecessary waste of
precious research resources.
A spokeswoman for aspartame supplier Ajinomoto argued that the
safety of aspartame had been proven time and again in various
robust studies over the years. Consequently, she said, there was no
scientific justification for the FSA embarking on the latest pilot.
Her comments followed a meeting last week of the FSA’s
General Advisory Committee on Science (GACS).
She also argued that the number of people reporting adverse side
effects following consumption of aspartame was so small that
money would be better spent counselling these people individually.
Some members of the GACS committee also expressed concerns
about the study. Jeya Henry, professor of human nutrition at
Oxford Brookes University, questioned the scientific approach of
the pilot study, in particular the use of high numbers of volunteers
with self-diagnosed sensitivity issues.
“I really think the sensitivity issue may need to be rethought because
the model that you are using is going to be loaded against you proving
what you want to prove,” said Henry. His concerns about using people
who were “self-reporting” were echoed by Dr Ian Brown, chair of the
Advisory Committee on Animal Feedstuffs.
However, professor sir Roger Jowell, chair of the FSA’s Social
Sciences Research Committee, added: “My worry was the description
of the study -- to investigate anecdotal claims -- it is actually more than
that and of course it is less than a randomised control trial. I think it is
important to describe it as a limited controlled trial. But what you are
doing is effectively putting your toe in the water, and as a first stage
that is perfectly acceptable.”
Even if the study gave a green light to aspartame, this might make little
difference to people who were convinced that it did adversely affect
them, said GACS chairman, professor Colin Blakemore.
However, he noted that: “The fact is that somatization
[a psychological condition in which some people persistently complain
of varied physical symptoms that have no identifiable physical origin]
is a very real phenomenon.”
“Aspartame is a controversial issue,” admitted FSA chief scientist
Andrew Wadge. “And, indeed, the idea of doing a study like this is
controversial. Whenever there is a scientific evaluation on safety,
the answer comes back that this product is safe to consume … and
yet we have the situation where a significant number of people who
are convinced that they react to this particularly product.”
The FSA’s latest pilot aims to recruit 50 individuals “self-diagnosed”
as sensitive to aspartame and 50 age/sex matched controls, who are
normal, healthy volunteers. Volunteers will be asked to consume a
product which may or may not contain aspartame and any resulting
health effects will be recorded.
According to Wadge the study aims to investigate anecdotal claims
made by individuals and test the suitability of a food product
developed by the FSA for use in ‘blinded’ trials. “I personally think
it is something that is interesting and worthwhile doing,” said Wadge.
The pilot study will inform the design and feasibility of a larger-scale
study that could be done at European level, he added.
The European Food Safety Authority (EFSA) recently provided a
clean bill of health to aspartame. However, it is reported to be
undertaking a further review of published reports and “some
anecdotal reports” since the Scientific Committee on Foods issued
an opinion on aspartame in 2002.
© William Reed Business Media Ltd 2009. All rights reserved.
Registered Office: Broadfield Park, Crawley, RH11 9RT.
Tel: +44 (0) 1293 613400 Registered in England
No. 2883992 VAT No. 644 3073 52.
_____________________________________________________
Rich Murray, 1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298 rmforall@comcast.net
http://groups.yahoo.com/group/rmforall/messages
http://groups.yahoo.com/group/AstroDeep/messages
http://RMForAll.blogspot.com new primary archive
http://groups.yahoo.com/group/aspartameNM/messages
group with 141 members, 1,587 posts in a public archive
http://groups.yahoo.com/group/aspartame/messages
group with 1199 members, 23,909 posts in a public archive
participant, Santa Fe Complex www.sfcomplex.org
_____________________________________________________
http://rmforall.blogspot.com/2009_09_01_archive.htm
Tuesday, September 29, 2009
http://groups.yahoo.com/group/aspartameNM/message/1587
_____________________________________________________
Included herein is substantial mainstream evidence that the natural
conversion in humans of orally ingested methanol into formaldehyde
and then formic acid results in substantial, durable, cumulative
retention of toxic reaction products.
Adequate folic acid levels expedite the safe metabolism of methanol
in most people.
Ethyl alcohol and folic acid in vegetables and fruits are sufficient to
protect most people from conversion of their methanol into
formaldehyde.
Many common agents interfere with folic acid (folic acid antagonists).
Additionally, genetic variations are potent.
About 3/4 of reactors are female.
Those who rarely have alcohol hangovers may be substantially immune
to methanol and formaldehyde.
Recent exposure to alcohol beverages, tobacco and wood smoke,
and a large variety of formaldehyde sources may compromise the
clarity of aspartame reaction tests.
Aspartame reactors often report allergies to many agents, with similar
symptoms: mercury (amalgams and fish), MSG and free glutamate in
foods (for instance, hydrolyzed vegetable or yeast protein), carbon
monoxide, molds, many foods, etc. -- up to Multiple Chemical
Sensitivity.
Aspartame reactors often take many steps to exercise, reduce stress,
lower salt, emphasize organic plant foods, reduce drug and chemical
exposures, limit protein and fat intake, use vitamin and mineral
supplements, limit processed foods -- thus complicating attempts to
create a matching control group, and introducing uncertainty about
whether the reactors are as vulnerable now as in the past, when they
may have had more negative factors for years.
So, genetic background, age, sex, obesity, existing illnesses, diet,
exercise, environmental toxins, medicines and drugs, parental
exposure to all these factors, and more may corrode the "gold
standard" of a single exposure double-blind experimental test,
especially for a rather modest test group of 50.
Perhaps, a more productive research strategy would be to test 10
reactors, one at a time, for 24 hours each, using a wide range of
tests, recording the enormous individual variations that are usually
swamped by taking group data averages.
Computerized tests facilitate fast, affordable measures of cognitive
and memory effects.
Full audio and video recording is now available.
Dimethyl dicarbonate, an approved additive for reducing fungi in
wines, perhaps with a neutral taste, quickly releases about the same
level of methanol upon ingestion as aspartame drinks, making
possible studies free of any possible "excitotoxic" effects of
aspartic acid and phenylalanine, while allowing a third beverage
to be a control substance.
This approach would also contribute to the meager research literature
about the role of methanol in alcohol hangovers.
aspartame reactors may send detailed feedback to Andrew Wadge,
UK Food Standards Agency to guide new pilot study re bad
reactions: Rich Murray 2009.06.22
http://rmforall.blogspot.com/2009_06_01_archive.htm
Monday, June 22, 2009
http://groups.yahoo.com/group/aspartameNM/message/1577
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.dorway.com/products.txt
[ rearranged, 11% methanol added ]
From the Nutrasweet Web Site: (amounts in various "foods")
Product Category -- Serving Size -- aspartame -- 11% methanol
Gelatin Dessert ----------- 8 ounces -----190 mg ---- 21 mg
Carbonated Beverage --- 12 ounces ----- 180 ------- 20
" ------------------------ 48 ounces ----- 720 ------- 79
Powdered Drink -------- 12 ounces ----- 180 -------- 20
Fruit Drink (10% juice) -- 12 ounces ----- 140 -------15.4
Hot Chocolate ----------- 12 ounces ----- 100 -------11
Yogurt ------------------- 8 ounces ----- 124 --------13.6
Ice Cream ---------------- 8 ounces ----- 100 ------- 11
Pudding Dessert ---------- 8 ounces ------ 50 --------- 5.5
Frozen Novelty ----------- 2-3 ounces ---- 50 --------- 5.5
Gum ----------------------- 1 stick -------- 6-8 -------- 0.7-0.9
Vitamins ------------------ 1 vitamin ------ 4 ---------- 0.44
Breath mint ---------------- 1 mint --------- 1.5 -------- 0.17
http://groups.yahoo.com/group/aspartameNM/message/846
aspartame in Merck Maxalt-MLT worsens migraine,
AstraZeneca Zomig, Eli Lilly Zyprexa,
J&J Merck Pepcid AC (Famotidine 10mg) Chewable Tab,
Pfizer Cool Mint Listerine Pocketpaks: Murray 2002.07.16
Migraine MLT-Down: an unusual presentation of migraine
in patients with aspartame-triggered headaches.
Newman LC, Lipton RB Headache 2001 Oct; 41(9): 899-901.
[ Merck 10-mg Maxalt-MLT, for migraine, has 3.75 mg aspartame,
while 12 oz diet soda has 200 mg. ]
Headache Institute, St. Lukes-Roosevelt Hospital Center,
New York, NY
Department of Neurology newmanache@aol.com
Albert Einstein College of Medicine, Bronx, NY
Innovative Medical Research RLipton@aecom.yu.edu
http://groups.yahoo.com/group/aspartameNM/message/855
Blumenthall & Vance: aspartame chewing gum headaches
Nov 1997: Murray 2002.07.28
Harvey J. Blumenthal, MD, Dwight A Vance, RPh
Chewing Gum Headaches. Headache 1997 Nov; 37(10): 665-6.
Department of Neurology, University of Oklahoma College of
Medicine, Tulsa, USA. neurotulsa@aol.com
Aspartame, a popular dietetic sweetener, may provoke headache in
some susceptible individuals. Herein, we describe three cases of
young women with migraine who reported their headaches could be
provoked by chewing gum sweetened with aspartame.
[ 6-8 mg aspartame per stick chewing gum ]
http://groups.yahoo.com/group/aspartameNM/message/1143
antiseptic? antifungal? antiviral? methanol (formaldehyde, formic
acid) disposition: Bouchard M et al, full plain text, 2001: substantial
sources are degradation of fruit pectins, liquors, aspartame, smoke:
Murray 2005.01.05 rmforall
http://www.toxsci.oupjournals.org/cgi/content/full/64/2/169
free full text
A Biologically Based Dynamic Model for Predicting the Disposition
of Methanol and Its Metabolites in Animals and Humans.
Michèle Bouchard,
Robert C. Brunet,
Pierre-Olivier Droz,
and Gaétan Carrier.
Toxicological Sciences 64, 169-184 (2001)
Copyright © 2001 by the Society of Toxicology
[ extracts ]
"Exposure to methanol also results from the consumption of certain
foodstuffs (fruits, fruit juices, certain vegetables, aspartame
sweetener, roasted coffee, honey) and alcoholic beverages (Health
Effects Institute, 1987; Jacobsen et al., 1988).
[ It's unusual for a mainstream journal article to mention "fruits, fruit
juices, certain vegetables, aspartame sweetener" and "alcoholic
beverages" to be methanol sources.]
... little is known about the chronic effects of low exposure doses...
Systemic methanol is extensively metabolized by liver alcohol
dehydrogenase [ ADH ] and catalase-peroxidase enzymes to
formaldehyde, which is in turn rapidly oxidized to formic acid by
formaldehyde dehydrogenase enzymes...
Formaldehyde, as it is highly reactive, forms relatively stable adducts
with cellular constituents...
Primates and humans appear to be more susceptible to the acute
toxicity of methanol than rodents...
Although methanol has been reported to be metabolized mainly in
the liver, pulmonary metabolism is also likely to occur. Indeed,
the catalase-peroxidase system responsible for a major fraction of
methanol metabolism in rats is widely distributed in mammalian
tissues...
The model included a constant background whole body methanol
burden of 2.133 mmol, which corresponds to the mean blood
concentration of 0.5 mg/L of methanol measured by Osterloh et al.
(1996) in control subjects at the end of an 8-h frequent blood
sampling period...
... once formed, a substantial fraction of formaldehyde is converted
to unobserved forms. This pathway contributes to a long-term
unobserved compartment. The latter, most plausibly, represents
either the formaldehyde that ( directly or after oxidation to formate )
binds to various endogenous molecules (Heck et al., 1983; Roe,
1982)...
That substantial amounts of methanol metabolites or by-products
are retained for a long time is verified by Horton et al. (1992)
who estimated that 18 h following an iv injection of 100 mg/kg
of 14C-methanol in male Fischer-344 rats, only 57% of the
dose was eliminated from the body. From the data of Dorman
et al. (1994) and Medinsky et al. (1997), it can further be
calculated that 48 h following the start of a 2-h inhalation
exposure to 900 ppm of 14C-methanol vapors in female
cynomolgus monkeys, only 23% of the absorbed 14C-methanol
was eliminated from the body. These findings are corroborated by
the data of Heck et al. (1983) showing that 40% of a
14C-formaldehyde inhalation dose remained in the body 70 h
postexposure...
Experimental studies on the detailed time profiles following
controlled repeated exposures to methanol are lacking...
Thus, in monkeys and plausibly humans, a much larger fraction of
body formaldehyde is rapidly converted to unobserved forms
rather than passed on to formate and eventually CO2."
If we assume 30% retention of durable cumulative toxic products of
formaldehyde and formic acid, then a 12-oz can diet drink gives 200
mg aspartame, 22 mg methanol, and 7 mg formaldehyde and formic
acid at 30% cumulative retention. We may add that well known
sources of formaldehyde include both wood and tobacco smoke,
and, notoriously, mobile homes. Two teams give evidence that
formaldehyde and formic acid from methanol in ethanol drinks
(often far above the 100 mg/L methanol in red wines, two times the
level in aspartame drinks) are the main cause of the many symptoms
of "morning after" hangovers.
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
Furthermore, BM Kapur et al, 2007 give evidence that formic acid
from methanol in ethanol drinks is a major cause of Fetal Alcohol
Syndrome, readily preventable by adequate levels of folic acid,
which expedites the safe metabolism of formaldehyde, in most
people.
"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." ...
"MeOH concentrations between 4 and 4500 mg/l can be present
in various alcoholic beverages (Sprung et al., 1988)."
A variety of mutations, as well as aspirin and many painkillers,
impede folic acid. However, fruits and vegetables give enough folic
acid to mitigate harm from their methanol. Then again, formaldehyde
may in many people treat infections by fungi, bacteria, and virusus.
All these unexamined co-factors have confused attempts to study
aspartame toxicity for three decades.
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
A widely proclaimed NIH-AARP mass survey by U Lim et al. 2006,
while failing to show specific cancers with feeble diet drink
consumption data for a year for seniors, did find that 4% of a
half-million seniors drank 3 and more cans daily diet soda
[ 12-oz can gives 200 mg aspartame, 22 mg methanol,
7 mg formaldehyde and formic acid at 30% cumulative retention ]
aspartame mg/d
0 ---- under 100 - 100-200 - 200-400 - 400-600 - 600-1200 -
cohort %
46 ------- 25 ------ 13 ------- 7 --------- 5 ------ about 3 ----
over 1200 mg/d
under 1%
This is the first good data about the percentage of aspartame users
who use over 3 cans daily, averaging 5 cans daily at 200 mg per 12
oz can diet soda.
About 4% of 473,984 is 19,000 people, with a peak intake of 17
cans daily, and average 5 cans daily.
It would be worthwhile to investigate a wide variety of symptoms for
the 0.1 % of highest level users, about 500 people.
For about 200 million USA aspartame users, this would be 200,000
people.
The highest level 3400 mg aspartame [ 17 12-oz cans ] gives
11% = 374 mg methanol, 48 times the recommended daily limit of
consumption of 7.8 mg as recommended by the
Environmental Protection Agency (EPA).3
At 30% retention of cumulative toxic products of formaldehyde and
formic acid, these would be 125 mg, 60 times higher than the 1999
EPA alarm level for formaldehyde in daily drinking water of
1 ppm = 2 mg for average daily drinking water of 2 L daily.
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
40 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@catholic.ac.kr
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@RMV.se;
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
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
[ extracts ]
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
[ Extract ]
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.
Case Series
Six patients (ages 16 to 75 years) were referred for evaluation of
recalcitrant dermatitis. By history, five of the patients were noted to
have developed migraines following aspartame consumption; the
sixth reported dermatitis flares associated with diet cola
consumption of >2 liters/day.
All six patients had current environmental exposures to formaldehyde
or formaldehyde-releasing preservatives in their personal hygiene
products and/or regular consumption of "sugar-free food" artificially
sweetened with aspartame.
Based on their histories and clinical presentations, these patients
were patch-tested with the North American Contact Dermatitis
Group 65-allergen Standard Screening Series and selected
chemicals from the University of Miami vehicle, fragrance, bakery,
and textile trays.
All six patients had positive reactions to formaldehyde, and four had
additional positive reactions to formaldehyde-releasing preservatives
(FRPs). Expert counseling on allergen avoidance (including
avoidance of formaldehyde, FRPs, and aspartame) and alternative
product recommendations were provided to the patients.
At their follow-up appointments (between 8 and 12 weeks), all the
patients showed clearance of their dermatitis. Four patients (two
inadvertently) resumed their consumption of aspartame and
subsequently returned for an additional follow-up visit. Three of the
first five patients had recurrences of both their migraines and their
dermatitis; the sixth patient (who had no migraines) had a positive
rechallenge dermatitis. These four patients were again counseled on
avoidance regimen.
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
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@contactderm.net;
Sarah A. Stechschulte, BA sstechschulte@gmail.com
_____________________________________________________
http://www.guardian.co.uk/science/2009/sep/23/sweetener-aspartame-side-effects
Sweetener aspartame to be investigated for possible side-effects
The Food Standards Agency is calling for volunteers to help test
claims that the artificial sweetener aspartame, used in more than
4,000 products, causes illnesses
Ian Sample, science correspondent
guardian.co.uk, Wednesday 23 September 2009 00.05 BST
Food and drinks containing aspartame
Just some of the thousands of products containing the artificial
sweetener aspartame. Photograph: Graham Turner/Guardian
The Food Standards Agency is launching an investigation into the
artificial sweetener aspartame amid claims that some people
experience side-effects after consuming the substance.
Scientists funded by the agency will test whether certain people
develop a range of illnesses after eating food prepared with the
sweetener.
Aspartame is around 200 times sweeter than sugar and is used in
more than 4,000 products, including diet drinks, cereal bars,
yogurt and chewing gum.
Previous reviews by the Food Standards Agency (FSA) and the
http://www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_home.htm
European Food Safety Authority
[ http://www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_home.htm ]
have concluded that aspartame is safe, but some people complain
they develop headaches, dizziness, vomiting, diarrhoea and fatigue
after eating food containing the chemical.
Researchers led by Professor Stephen Atkin, head of endocrinology,
diabetes and metabolism at the Hull York Medical School,
will look for signs of illness in volunteers after
they consume cereal bars made with or without aspartame.
Atkin's group is recruiting 50 people who believe they are sensitive
to aspartame. The volunteers will be matched by age and sex to 50
volunteers who are happy to eat the sweetener.
In the study, individuals will be randomly assigned an aspartame or
aspartame-free cereal bar and given psychological and medical
checks up to four hours after consuming it.
The following week, the experiment will be repeated with each
volunteer receiving the other type of cereal bar.
The scientists will take blood and urine samples before and after
each test.
Aspartame breaks down in the digestive system into aspartic acid,
methanol and phenylalanine
Some individuals believe it is these chemicals that cause their
symptoms.
The tests will allow scientists to link any ill effects to levels of the
chemicals in the volunteers' blood and urine.
"This is a fundamental study for the people who believe they are
sensitive to aspartame, because it will hopefully prove or disprove
whether or not aspartame can cause problems," Prof Atkin said.
The study is expected to be completed next year and will be
published as a report to the FSA.
A spokesman for the agency said: "We know that aspartame can
be consumed safely but some people consider that they react badly
to it.
We've commissioned this research because it's important to increase
our knowledge about what is happening.
The study will address consumer concerns, including these
anecdotal reports."
Food safety officials are expected to fund a larger investigation if the
study finds evidence that people can be sensitive to the sweetener.
A spokeswoman for the Aspartame Information Service, an industry
body, [ http://www.aspartame.info/ ] said:
"Aspartame has been on the market for more than 25 years
and studies have been done on it from every angle.
We get more of these breakdown products from the
rest of our diets than we get from aspartame.
"The whole anecdotal area [of sensitivity] has been looked at before,
so why start another round of research?
Our concern is that people might be attributing to aspartame
something that might have a more serious cause."
Patience Purdy, honorary vice president of the
National Council of Women of Great Britain,
[ http://fp.ncwgb.f9.co.uk/
http://www.slotfilms.com/NCW/contact.htm
The National Council of Women Of Great Britain
36 Danbury Street, Islington, London N1 8JU
Telephone: 071-354 2395 Fax No. 071-354 9214
Registered Charity No. 1001015 ]
which campaigns for aspartame to be banned on health grounds,
said: "It's good the FSA are taking this seriously, but our concern is
that the study is inadequate. We all react differently to aspartame."
Contact the Science editor: science@guardian.co.uk
Letters for publication should be sent to: letters@guardian.co.uk
Call the main Guardian and Observer switchboard:
+44 (0)20 3353 2000
http://nutnewstoday.blogspot.com/2009/09/aspartame-sensitivity-probe-is-funded.html
Friday, September 25, 2009
Aspartame sensitivity probe is funded in the UK
Scientists are to assess whether the artificial sweetener aspartame
causes health problems in people unusually sensitive to it.
Expert advice is that aspartame -- found in more than 4,000
products -- is safe to consume.
However, a number of people have reported sensitivity to the
product including headaches, dizziness, vomiting, diarrhoea
and fatigue.
The University of Hull study is funded by the
Food Standards Agency (FSA).
Aspartame, 150 times sweeter than sugar, is found in products
such as diet soft drinks, cereal bars, yogurts and chewing gum.
There have long been concerns that the sweetener is linked to a
raft of health problems, including a greater risk of cancer,
fertility issues, nausea, double vision and an effect on appetite.
However, after reviewing the available scientific literature, both
the FSA and the European Food Safety Authority decided there
was no firm evidence of any impact on health, and ruled that
aspartame was safe to consume.
Professor Stephen Atkin, who will lead the new research, said:
"This study is not to determine whether aspartame can be
consumed safely; this has already been established, but rather
to see whether certain people are sensitive to it."
Read more of Aspartame sensitivity probe is funded in the UK
at BBC News site.
http://news.bbc.co.uk/2/hi/health/8266707.stm
Published: 2009/09/25 16:33:14 GMT
BBC NEWS
Sensitivity to aspartame probed
...The Hull team hope their work will lead to a larger
international study to pin down the issue once and for all.
Body chemistry
Professor Atkin also hopes to secure funding to analyse the
chemical breakdown of aspartame in the body.
The sweetener can be broken down to produce
methanol and formaldehyde,
both of which have been previously linked to cancer.
However, it is not clear whether this process takes place in the
body, or, if it does, whether the metabolites are absorbed into the
blood in sufficient quantity to produce any biological effect.
Andrew Wadge, Chief Scientist at the Food Standards Agency said:
"The study will address consumer concerns, including anecdotal
reports that have linked a range of conditions to aspartame.
'The Agency's view remains that aspartame can be consumed safely
and we are not recommending any changes to its current use.
"However, we know that some people consider that they react
badly to consuming this sweetener so we think it is important
to increase our knowledge about what is happening."
One hundred people will take part in the Hull study,
half of who have complained of side effects from aspartame.
The study is expected to take 18 months.
At present the Acceptable Daily Intake (ADI) for aspartame is set
by the European Commission's Scientific Committee on Food (SCF)
at 40 milligrams per kilogram of body weight.
An adult would have to drink about 14 cans a day of diet soft drink,
or consume about 80 sachets of sweetener to reach this amount.
© BBC MMIX
http://www2.hull.ac.uk/news/2009newsarchive/september/studytoinvestigateallegeds.aspx
Study to investigate alleged side effects of aspartame
23 September 2009
...The national study will be carried out by Professor Stephen Atkin
at the University of Hull, in collaboration with colleagues at the
Hull York Medical School and Hull
and East Yorkshire Hospitals NHS Trust.
He explains: “This study is not to determine whether aspartame can
be consumed safely; this has already been established by the FSA
and EFSA, but rather to see whether certain people are sensitive to it.
“We will look at the effects of eating a snack bar which may
or may not contain aspartame in people who say they have a problem
eating aspartame and people who normally consume foods containing
aspartame with no problems.
The study is a double blind placebo crossover,
which is the gold standard of studies.”
It is hoped that this study will help to design a larger international
study, which will provide the information needed to inform
governments and the European Union on whether the consumption
of aspartame is related to symptoms.
Andrew Wadge, Chief Scientist at the Food Standards Agency
said: ‘The study will address consumer concerns, including
anecdotal reports that have linked a range of conditions to
aspartame.
‘The Agency’s view remains that aspartame can be consumed
safely and we are not recommending any changes to its current use.
However, we know that some people consider that they react
badly to consuming this sweetener so we think it is important
to increase our knowledge about what is happening.’
The research is expected to take 18 months and the results will be
published as a report to be delivered to the Food Standards Agency.
A summary of this information will be available on the FSA website.
Ends
Notes to Editors
For press enquiries, or to request an interview with
Prof Stephen Atkin, please contact Claire Mulley
on 01482 466943 or 07809 585965. [ c.mulley@hull.ac.uk ]
Potential volunteers for the study should contact a member of the
clinical trial team on 01482 675372 or 01482 675387
from 9am to 5pm weekdays, or the
Hull Royal Infirmary switchboard on 01482 328541 out of hours.
This is a pilot study involving 100 volunteers; 50 of them have
complained of side-effects from aspartame and they will be
matched in gender and age by people who have no side effects.
Prof Stephen Atkin will be available for interview on
21 and 22 Sept; contact Claire Mulley to request an interview slot.
Prof Stephen Atkin is the Head of Diabetes and Endocrinology
at the University of Hull’s Postgraduate Medical Institute (PGMI).
He has a BSc Biochemistry and MD from Newcastle University.
Prof Atkin completed a PhD at Liverpool University
where he was also an MRC training fellow.
He was appointed in October 2005 as Professor of
Diabetes, Endocrinology and Metabolism
at Hull York Medical School (HYMS).
He is based and leads the pharmaceutical and nutritional
clinical trials teams for these studies at the
Clinical Research Centre based at the
Michael White Diabetes Centre at Hull Royal Infirmary.
The laboratory focusing on molecular and a cellular research is
based within the medical research unit at the University of Hull.
Translational clinical trials for both the food and pharmaceutical
industry are a major focus of the work undertaken and part of
the overall research portfolio on modulation of insulin resistance
and cardiovascular risk in these conditions that are associated
with a high morbidity and mortality.
Read more about Hull York Medical School (HYMS).
http://www.hyms.ac.uk/
© The University of Hull,
Cottingham Road, Hull. HU6 7RX, +44 (0)1482 346311
HYMS STAFF
Professor Stephen L. Atkin
Primary organisation:
Michael White Diabetes Centre
Head, Academic Endocrinology, Diabetes and Metabolism
Additional affiliation:
HYMS
Teaching role(s) within HYMS:
Clinical Placement Tutor
Phase 2 Curriculum Group
Plenary Lecturer - Phase 1
Plenary Lecturer - Phase 2
http://www.hyms.ac.uk/research/
Insulin (blue) encapsulated within a pollen exine [ photo ]
Endocrinology and Diabetes
Stephen Atkin is HYMS Professor of Endocrinology and Metabolism.
His section of the PGMI at Hull incorporates bone metabolism,
and has a specific interest in the cardiovascular risk factors associated
with the metabolic syndrome that encompasses polycystic ovarian
syndrome, impaired glucose tolerance and type 2 diabetes.
The group is collaborating with the University of Hull's
Department of Chemistry to develop the use of pollen and spore
coatings that can deliver orally ingested material into the blood stream.
Read more about the Food Standards Agency.
http://www.food.gov.uk/
http://www.timesonline.co.uk/tol/news/uk/health/article6845119.ece
If you want to submit your material to TimesOnline,
please email feedback@thetimes.co.uk
http://www.foodmanufacture.co.uk/news/printpage.php/aid/9424/Experts_challenge_pilot_aspartame_study.html
Food Manufacture
News & Features » Latest news
Experts challenge pilot aspartame study
By Rick Pendrous
Published: 14 September, 2009
The pilot study launched by the Food Standards Agency (FSA) into
the health effects of individuals “self-reporting as sensitive” to
aspartame has been criticised for being an unnecessary waste of
precious research resources.
A spokeswoman for aspartame supplier Ajinomoto argued that the
safety of aspartame had been proven time and again in various
robust studies over the years. Consequently, she said, there was no
scientific justification for the FSA embarking on the latest pilot.
Her comments followed a meeting last week of the FSA’s
General Advisory Committee on Science (GACS).
She also argued that the number of people reporting adverse side
effects following consumption of aspartame was so small that
money would be better spent counselling these people individually.
Some members of the GACS committee also expressed concerns
about the study. Jeya Henry, professor of human nutrition at
Oxford Brookes University, questioned the scientific approach of
the pilot study, in particular the use of high numbers of volunteers
with self-diagnosed sensitivity issues.
“I really think the sensitivity issue may need to be rethought because
the model that you are using is going to be loaded against you proving
what you want to prove,” said Henry. His concerns about using people
who were “self-reporting” were echoed by Dr Ian Brown, chair of the
Advisory Committee on Animal Feedstuffs.
However, professor sir Roger Jowell, chair of the FSA’s Social
Sciences Research Committee, added: “My worry was the description
of the study -- to investigate anecdotal claims -- it is actually more than
that and of course it is less than a randomised control trial. I think it is
important to describe it as a limited controlled trial. But what you are
doing is effectively putting your toe in the water, and as a first stage
that is perfectly acceptable.”
Even if the study gave a green light to aspartame, this might make little
difference to people who were convinced that it did adversely affect
them, said GACS chairman, professor Colin Blakemore.
However, he noted that: “The fact is that somatization
[a psychological condition in which some people persistently complain
of varied physical symptoms that have no identifiable physical origin]
is a very real phenomenon.”
“Aspartame is a controversial issue,” admitted FSA chief scientist
Andrew Wadge. “And, indeed, the idea of doing a study like this is
controversial. Whenever there is a scientific evaluation on safety,
the answer comes back that this product is safe to consume … and
yet we have the situation where a significant number of people who
are convinced that they react to this particularly product.”
The FSA’s latest pilot aims to recruit 50 individuals “self-diagnosed”
as sensitive to aspartame and 50 age/sex matched controls, who are
normal, healthy volunteers. Volunteers will be asked to consume a
product which may or may not contain aspartame and any resulting
health effects will be recorded.
According to Wadge the study aims to investigate anecdotal claims
made by individuals and test the suitability of a food product
developed by the FSA for use in ‘blinded’ trials. “I personally think
it is something that is interesting and worthwhile doing,” said Wadge.
The pilot study will inform the design and feasibility of a larger-scale
study that could be done at European level, he added.
The European Food Safety Authority (EFSA) recently provided a
clean bill of health to aspartame. However, it is reported to be
undertaking a further review of published reports and “some
anecdotal reports” since the Scientific Committee on Foods issued
an opinion on aspartame in 2002.
© William Reed Business Media Ltd 2009. All rights reserved.
Registered Office: Broadfield Park, Crawley, RH11 9RT.
Tel: +44 (0) 1293 613400 Registered in England
No. 2883992 VAT No. 644 3073 52.
_____________________________________________________
Rich Murray, 1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298 rmforall@comcast.net
http://groups.yahoo.com/group/rmforall/messages
http://groups.yahoo.com/group/AstroDeep/messages
http://RMForAll.blogspot.com new primary archive
http://groups.yahoo.com/group/aspartameNM/messages
group with 141 members, 1,587 posts in a public archive
http://groups.yahoo.com/group/aspartame/messages
group with 1199 members, 23,909 posts in a public archive
participant, Santa Fe Complex www.sfcomplex.org
_____________________________________________________
Monday, September 28, 2009
A Cure For Cancer? Eating A Plant-Based Diet, Kathy Freston interviews Dr. T. Colin Campbell, Cornell University: Rich Murray 2009.09.28
A Cure For Cancer? Eating A Plant-Based Diet, Kathy Freston interviews Dr. T. Colin Campbell, Cornell University: Rich Murray 2009.09.28
http://rmforall.blogspot.com/2009_09_01_archive.htm
Monday, September 28, 2009
http://groups.yahoo.com/group/aspartameNM/message/1586
_____________________________________________________
http://www.huffingtonpost.com/kathy-freston/a-cure-for-cancer-eating_b_298282.html
The Huffington Post, September 28, 2009
Kathy Freston
Author, Health and Wellness Expert
Posted: September 24, 2009 08:34 AM
A Cure For Cancer? Eating A Plant-Based Diet
466 Comments
I have been working closely recently with a few extraordinary
nutritional researchers, and I find that the information they
have compiled is quite eye opening. Interestingly, what these
highly esteemed doctors are saying is just beginning to be
understood and accepted, perhaps because what they are
saying does not conveniently fit in with or support the
multi-billion dollar food industries that profit from our
"not knowing". One thing is for sure: we are getting sicker
and more obese than our health care system can handle,
and the conventional methods of dealing with disease often
have harmful side effects and are ineffective for some patients.
As it is now, one out of every two of us will get cancer or
heart disease and die from it -- an ugly and painful death as
anyone who has witnessed it can attest.
And starting in the year 2000, one out of every three children
who are born after that year will develop diabetes -- a disease
that for most sufferers (those with Type 2 diabetes) is largely
preventable with lifestyle changes.
This is a rapidly emerging crisis, the seriousness of which I'm
not sure we have yet recognized. The good news is, the means
to prevent and heal disease seems to be right in front of us;
it's in our food.
Quite frankly, our food choices can either kill us - which
mounting studies say that they are, or they can lift us right out
of the disease process and into soaring health.
In the next few months, I will share a series of interviews I've
conducted with the preeminent doctors and nutritional
researchers in the fields of their respective expertise.
And here it is straight out: they are all saying the same thing in
different ways and through multiple and varying studies:
animal protein seems to greatly contribute to diseases of nearly
every type; and a plant-based diet is not only good for our health,
but it's also curative of the very serious diseases we face .
Cancer
On the subject of cancer, I've asked Dr. T. Colin Campbell,
Professor Emeritus of Cornell University and author of the
groundbreaking The China Study to explain how cancer
happens and what we can do to prevent and reverse it.
Dr. Campbell's work is regarded by many as the definitive
epidemiological examination of the relationship between diet
and disease. He has received more than 70 grant years of
peer-reviewed research funding, much of which was funded
by the U.S. National Institutes of Health (NIH), and he has
authored more than 300 research papers. He grew up on a
dairy farm believing in the great health value of animal protein
in the American diet and set out in his career to investigate
how to produce more and better animal protein. Troublesome
to his preconceived hypothesis of the goodness of dairy,
Dr. Campbell kept running up against results that consistently
proved an emerging and comprehensive truth: that animal
protein is disastrous to human health.
Through a variety of experimental study designs,
epidemiological evidence, along with observation of real life
conditions which had rational biological explanation,
Dr. Campbell has made a direct and powerful correlation
between cancer (and other diseases and illnesses) and animal
protein. Following is a conversation I had with him so that
I could better understand the association.
KF: What happens in the body when cancer develops?
What is the actual process?
TCC: Cancer generally develops over a long period of time,
divided into 3 stages, initiation, promotion and progression.
Initiation occurs when chemicals or other agents attack the
genes of normal cells to produce genetically modified cells
capable of eventually causing cancer. The body generally
repairs most such damage but if the cell reproduces itself
before it is repaired, its new (daughter) cell retains this genetic
damage. This process may occur within minutes and, to some
extent, is thought to be occurring most of the time in most of our
tissues.
Promotion occurs when the initiated cells continue to replicate
themselves and grow into cell masses that eventually will be
diagnosed. This is a long growth phase occurring over months
or years and is known to be reversible.
Progression occurs when the growing cancer masses invade
neighboring tissues and/or break away from the tissue of origin
(metastasis) and travel to distant tissues when they are capable
of growing independently at which point they are considered to
be malignant.
KF: Why do some people get cancer, and other don't?
What percentage is genetic, and what percentage has to do
with diet?
TCC: Although the initiated cells are not considered to be
reversible, the cells growing through the promotion stage
are usually considered to be reversible, a very exciting concept.
This is the stage that especially responds to nutritional factors.
For example, the nutrients from animal based foods, especially
the protein, promote the development of the cancer
whereas the nutrients from plant-based foods, especially the
antioxidants, reverse the promotion stage.
This is a very promising observation because cancer proceeds
forward or backward as a function of the balance of promoting
and anti-promoting factors found in the diet, thus consuming
anti-promoting plant-based foods tend to keep the cancer
from going forward, perhaps even reversing the promotion.
The difference between individuals is almost entirely related
to their diet and lifestyle practices.
Although all cancer and other diseases begin with genes,
this is not the reason whether or not the disease actually appears.
If people do the right thing during the promotion stage, perhaps
even during the progression stage, cancer will not appear
and if it does, might even be resolved.
Most estimates suggest that not more than 2-3 percent of cancers
are due entirely to genes; almost all the rest is due to diet and
lifestyle factors.
Consuming plant based foods offers the best hope of avoiding
cancer, perhaps even reversing cancer once it is diagnosed.
Believing that cancer is attributed to genes is a fatalistic idea
but believing that cancer can be controlled by nutrition
is a far more hopeful idea.
KF: You said that initially something attacks the genes, chemicals
or other agents; like what?
TCC: Cancer, like every other biological event -- good or bad --
begins with genes. In the case of cancer, gene(s) that give rise
to cancer either may be present when we are born or, during our
lifetimes, normal genes may be converted into cancer genes by
certain highly reactive chemicals (i.e., carcinogens).
Consider 'cancer genes' as seeds that grow into tumor masses
only if they are 'fed'. The 'feeding' comes from wrongful nutrition.
It's like growing a lawn. We plant seeds but they don't grow into
grass (or weeds) unless they are provided water, sunlight and
nutrients. So it is with cancer. In reality, we are planting seeds all
of our lifetime although some may be present at birth, not only for
cancer but also for other events as well. But this mostly does not
matter unless we 'nourish' their growth.
The chemicals that create these cancer genes are called 'carcinogens'.
Most carcinogens of years past have been those that attack normal
genes to give cancer genes.
These are initiating carcinogens, or initiators. But more recently,
carcinogens also may be those that promote cancer growth.
They are promoting carcinogens, or promoters.
Our work showed that casein is the most relevant cancer promoter
ever discovered.
Aside from chemicals initiating or promoting cancer, other agents
such as cosmic rays (energetic particles) from the sun or from the
outer reaches of space may impact our genes to cause them to change
(i.e., mutate) so that they could give rise to cancer 'seeds'.
The most important point to consider is that we cannot do much
about preventing initiation but we can do a lot about preventing
promotion.
The initiating idea is fatalistic and outside of our control but the
promotion idea is hopeful because we can change our exposure to
promoting agents and reverse the cancer process,
thus is within our control.
KF: What exactly is so bad about animal protein?
TCC: I don't choose the word "exactly" because it suggests
something very specific. Rather, casein causes a broad spectrum
of adverse effects.
Among other fundamental effects, it makes the body more acidic,
alters the mix of hormones and modifies important enzyme activities,
each of which can cause a broad array of more specific effects.
One of these effects is its ability to promote cancer growth
(by operating on key enzyme systems, by increasing hormone
growth factors and by modifying the tissue acidity).
Another is its ability to increase blood cholesterol (by modifying
enzyme activities) and to enhance atherogenesis,
which is the early stage of cardiovascular disease.
And finally, although these are casein-specific effects, it should be
noted that other animal-based proteins are likely to have the same
effect as casein.
KF: Ok, so I am clear that it's wise to avoid casein,
which is intrinsic in dairy (milk and cheese),
but how is other animal protein, such as chicken, steak, or pork,
implicated in the cause and growth of cancer?
TCC: I would first say that casein is not just "intrinsic" but
IS THE MAIN PROTEIN OF COW MILK,
REPRESENTING ABOUT 87% OF THE MILK PROTEIN.
The biochemical systems which underlie the adverse effects of casein
are also common to other animal-based proteins.
Also, the amino acid composition of casein, which is the characteristic
primarily responsible for its property, is similar to most other
animal-based proteins.
They all have what we call high 'biological value', in comparison,
for example, with plant-based proteins, which is why animal
protein promotes cancer growth and plant protein doesn't.
KF: Isn't anything in moderation ok, as long as we don't overdo it?
TCC: I rather like the expression told by my friend,
Caldwell Esselstyn, Jr., MD, the Cleveland Clinic surgeon
who reversed heart disease and who says, "Moderation kills!"
I prefer to go the whole way, not because we have fool-proof
evidence showing that 100% is better than, say, 95% for every
single person for every single condition but that it is easier to
avoid straying off on an excursion that too often becomes a
slippery slope back to our old ways. Moreover, going the
whole way allows us to adapt to new unrealized tastes and
to rid ourselves of some old addictions. And finally, moderation
often means very different things for different people.
KF: Are you saying that if one changes their diet from animal
based protein to plant-based protein that the disease process
of cancer can be halted and reversed?
TCC: Yes, this is what our experimental research shows.
I also have become aware of many anecdotal claims by people
who have said that their switch to a plant-based diet stopped
even reversed (cured?) their disease. One study on melanoma
has been published in the peer-reviewed literature that shows
convincing evidence that cancer progression is substantially
halted with this diet.
KF: How long does it take to see changes?
TCC: It is not clear because carefully designed research in humans
has not been done. However, we demonstrated and published
findings showing that experimental progression of disease is at least
suspended, even reversed, when tumors are clearly present.
KF: Consider a person who has been eating poorly his whole life;
is there still hope that a dietary change can make a big difference?
Or is everything already in motion?
TCC: Yes, a variety of evidence shows that cancers and
non-cancers alike can be stopped even after consuming
a poor diet earlier in life.
This effect is equivalent to treatment, a very exciting concept.
KF: This is sounding like it's a cure for cancer; is that the case?
TCC: Yes. The problem in this area of medicine is that traditional
doctors are so focused on the use of targeted therapies
(chemo, surgery, radiation) that they refuse to even acknowledge
the use of therapies like nutrition and are loathe to even want to do
proper research in this area. So, in spite of the considerable
evidence -- theoretical and practical -- to support a beneficial
nutritional effect, every effort will be made to discredit it.
It's a self-serving motive.
KF: What else do you recommend one does to avoid, stop,
or reverse cancer?
TCC: A good diet, when coupled with other health
activities like exercise, adequate fresh air and sunlight, good water
and sleep, will be more beneficial.
The whole is greater than the sum of its parts. ***
For help on how to lean into a plant based diet,
check out my blog post here;
http://www.huffingtonpost.com/kathy-freston/one-bite-at-a-time-a-begi_b_42211.html
and for recipes click here.
For more information about diet and cancer, visit www.tcolincampbell.org ***
www.vegsource.com
www.drmcdougall.com
www.notmilk.com
http://www.notmilk.com/tudrmac.html 65 citations
The over 100 mg methanol impurity per liter wine
or two liters aspartame beverages becomes
formaldehyde and then formic acid in humans -- co-factors
for "morning after" hangovers, birth defects, cancers -- folic acid
protects most people.
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
_____________________________________________________
Rich Murray
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298 rmforall@comcast.net
http://groups.yahoo.com/group/rmforall/messages
http://groups.yahoo.com/group/AstroDeep/messages
http://RMForAll.blogspot.com new primary archive
http://groups.yahoo.com/group/aspartameNM/messages
group with 141 members, 1,586 posts in a public archive
http://groups.yahoo.com/group/aspartame/messages
group with 1199 members, 23,909 posts in a public archive
participant, Santa Fe Complex www.sfcomplex.org
_____________________________________________________
http://rmforall.blogspot.com/2009_09_01_archive.htm
Monday, September 28, 2009
http://groups.yahoo.com/group/aspartameNM/message/1586
_____________________________________________________
http://www.huffingtonpost.com/kathy-freston/a-cure-for-cancer-eating_b_298282.html
The Huffington Post, September 28, 2009
Kathy Freston
Author, Health and Wellness Expert
Posted: September 24, 2009 08:34 AM
A Cure For Cancer? Eating A Plant-Based Diet
466 Comments
I have been working closely recently with a few extraordinary
nutritional researchers, and I find that the information they
have compiled is quite eye opening. Interestingly, what these
highly esteemed doctors are saying is just beginning to be
understood and accepted, perhaps because what they are
saying does not conveniently fit in with or support the
multi-billion dollar food industries that profit from our
"not knowing". One thing is for sure: we are getting sicker
and more obese than our health care system can handle,
and the conventional methods of dealing with disease often
have harmful side effects and are ineffective for some patients.
As it is now, one out of every two of us will get cancer or
heart disease and die from it -- an ugly and painful death as
anyone who has witnessed it can attest.
And starting in the year 2000, one out of every three children
who are born after that year will develop diabetes -- a disease
that for most sufferers (those with Type 2 diabetes) is largely
preventable with lifestyle changes.
This is a rapidly emerging crisis, the seriousness of which I'm
not sure we have yet recognized. The good news is, the means
to prevent and heal disease seems to be right in front of us;
it's in our food.
Quite frankly, our food choices can either kill us - which
mounting studies say that they are, or they can lift us right out
of the disease process and into soaring health.
In the next few months, I will share a series of interviews I've
conducted with the preeminent doctors and nutritional
researchers in the fields of their respective expertise.
And here it is straight out: they are all saying the same thing in
different ways and through multiple and varying studies:
animal protein seems to greatly contribute to diseases of nearly
every type; and a plant-based diet is not only good for our health,
but it's also curative of the very serious diseases we face .
Cancer
On the subject of cancer, I've asked Dr. T. Colin Campbell,
Professor Emeritus of Cornell University and author of the
groundbreaking The China Study to explain how cancer
happens and what we can do to prevent and reverse it.
Dr. Campbell's work is regarded by many as the definitive
epidemiological examination of the relationship between diet
and disease. He has received more than 70 grant years of
peer-reviewed research funding, much of which was funded
by the U.S. National Institutes of Health (NIH), and he has
authored more than 300 research papers. He grew up on a
dairy farm believing in the great health value of animal protein
in the American diet and set out in his career to investigate
how to produce more and better animal protein. Troublesome
to his preconceived hypothesis of the goodness of dairy,
Dr. Campbell kept running up against results that consistently
proved an emerging and comprehensive truth: that animal
protein is disastrous to human health.
Through a variety of experimental study designs,
epidemiological evidence, along with observation of real life
conditions which had rational biological explanation,
Dr. Campbell has made a direct and powerful correlation
between cancer (and other diseases and illnesses) and animal
protein. Following is a conversation I had with him so that
I could better understand the association.
KF: What happens in the body when cancer develops?
What is the actual process?
TCC: Cancer generally develops over a long period of time,
divided into 3 stages, initiation, promotion and progression.
Initiation occurs when chemicals or other agents attack the
genes of normal cells to produce genetically modified cells
capable of eventually causing cancer. The body generally
repairs most such damage but if the cell reproduces itself
before it is repaired, its new (daughter) cell retains this genetic
damage. This process may occur within minutes and, to some
extent, is thought to be occurring most of the time in most of our
tissues.
Promotion occurs when the initiated cells continue to replicate
themselves and grow into cell masses that eventually will be
diagnosed. This is a long growth phase occurring over months
or years and is known to be reversible.
Progression occurs when the growing cancer masses invade
neighboring tissues and/or break away from the tissue of origin
(metastasis) and travel to distant tissues when they are capable
of growing independently at which point they are considered to
be malignant.
KF: Why do some people get cancer, and other don't?
What percentage is genetic, and what percentage has to do
with diet?
TCC: Although the initiated cells are not considered to be
reversible, the cells growing through the promotion stage
are usually considered to be reversible, a very exciting concept.
This is the stage that especially responds to nutritional factors.
For example, the nutrients from animal based foods, especially
the protein, promote the development of the cancer
whereas the nutrients from plant-based foods, especially the
antioxidants, reverse the promotion stage.
This is a very promising observation because cancer proceeds
forward or backward as a function of the balance of promoting
and anti-promoting factors found in the diet, thus consuming
anti-promoting plant-based foods tend to keep the cancer
from going forward, perhaps even reversing the promotion.
The difference between individuals is almost entirely related
to their diet and lifestyle practices.
Although all cancer and other diseases begin with genes,
this is not the reason whether or not the disease actually appears.
If people do the right thing during the promotion stage, perhaps
even during the progression stage, cancer will not appear
and if it does, might even be resolved.
Most estimates suggest that not more than 2-3 percent of cancers
are due entirely to genes; almost all the rest is due to diet and
lifestyle factors.
Consuming plant based foods offers the best hope of avoiding
cancer, perhaps even reversing cancer once it is diagnosed.
Believing that cancer is attributed to genes is a fatalistic idea
but believing that cancer can be controlled by nutrition
is a far more hopeful idea.
KF: You said that initially something attacks the genes, chemicals
or other agents; like what?
TCC: Cancer, like every other biological event -- good or bad --
begins with genes. In the case of cancer, gene(s) that give rise
to cancer either may be present when we are born or, during our
lifetimes, normal genes may be converted into cancer genes by
certain highly reactive chemicals (i.e., carcinogens).
Consider 'cancer genes' as seeds that grow into tumor masses
only if they are 'fed'. The 'feeding' comes from wrongful nutrition.
It's like growing a lawn. We plant seeds but they don't grow into
grass (or weeds) unless they are provided water, sunlight and
nutrients. So it is with cancer. In reality, we are planting seeds all
of our lifetime although some may be present at birth, not only for
cancer but also for other events as well. But this mostly does not
matter unless we 'nourish' their growth.
The chemicals that create these cancer genes are called 'carcinogens'.
Most carcinogens of years past have been those that attack normal
genes to give cancer genes.
These are initiating carcinogens, or initiators. But more recently,
carcinogens also may be those that promote cancer growth.
They are promoting carcinogens, or promoters.
Our work showed that casein is the most relevant cancer promoter
ever discovered.
Aside from chemicals initiating or promoting cancer, other agents
such as cosmic rays (energetic particles) from the sun or from the
outer reaches of space may impact our genes to cause them to change
(i.e., mutate) so that they could give rise to cancer 'seeds'.
The most important point to consider is that we cannot do much
about preventing initiation but we can do a lot about preventing
promotion.
The initiating idea is fatalistic and outside of our control but the
promotion idea is hopeful because we can change our exposure to
promoting agents and reverse the cancer process,
thus is within our control.
KF: What exactly is so bad about animal protein?
TCC: I don't choose the word "exactly" because it suggests
something very specific. Rather, casein causes a broad spectrum
of adverse effects.
Among other fundamental effects, it makes the body more acidic,
alters the mix of hormones and modifies important enzyme activities,
each of which can cause a broad array of more specific effects.
One of these effects is its ability to promote cancer growth
(by operating on key enzyme systems, by increasing hormone
growth factors and by modifying the tissue acidity).
Another is its ability to increase blood cholesterol (by modifying
enzyme activities) and to enhance atherogenesis,
which is the early stage of cardiovascular disease.
And finally, although these are casein-specific effects, it should be
noted that other animal-based proteins are likely to have the same
effect as casein.
KF: Ok, so I am clear that it's wise to avoid casein,
which is intrinsic in dairy (milk and cheese),
but how is other animal protein, such as chicken, steak, or pork,
implicated in the cause and growth of cancer?
TCC: I would first say that casein is not just "intrinsic" but
IS THE MAIN PROTEIN OF COW MILK,
REPRESENTING ABOUT 87% OF THE MILK PROTEIN.
The biochemical systems which underlie the adverse effects of casein
are also common to other animal-based proteins.
Also, the amino acid composition of casein, which is the characteristic
primarily responsible for its property, is similar to most other
animal-based proteins.
They all have what we call high 'biological value', in comparison,
for example, with plant-based proteins, which is why animal
protein promotes cancer growth and plant protein doesn't.
KF: Isn't anything in moderation ok, as long as we don't overdo it?
TCC: I rather like the expression told by my friend,
Caldwell Esselstyn, Jr., MD, the Cleveland Clinic surgeon
who reversed heart disease and who says, "Moderation kills!"
I prefer to go the whole way, not because we have fool-proof
evidence showing that 100% is better than, say, 95% for every
single person for every single condition but that it is easier to
avoid straying off on an excursion that too often becomes a
slippery slope back to our old ways. Moreover, going the
whole way allows us to adapt to new unrealized tastes and
to rid ourselves of some old addictions. And finally, moderation
often means very different things for different people.
KF: Are you saying that if one changes their diet from animal
based protein to plant-based protein that the disease process
of cancer can be halted and reversed?
TCC: Yes, this is what our experimental research shows.
I also have become aware of many anecdotal claims by people
who have said that their switch to a plant-based diet stopped
even reversed (cured?) their disease. One study on melanoma
has been published in the peer-reviewed literature that shows
convincing evidence that cancer progression is substantially
halted with this diet.
KF: How long does it take to see changes?
TCC: It is not clear because carefully designed research in humans
has not been done. However, we demonstrated and published
findings showing that experimental progression of disease is at least
suspended, even reversed, when tumors are clearly present.
KF: Consider a person who has been eating poorly his whole life;
is there still hope that a dietary change can make a big difference?
Or is everything already in motion?
TCC: Yes, a variety of evidence shows that cancers and
non-cancers alike can be stopped even after consuming
a poor diet earlier in life.
This effect is equivalent to treatment, a very exciting concept.
KF: This is sounding like it's a cure for cancer; is that the case?
TCC: Yes. The problem in this area of medicine is that traditional
doctors are so focused on the use of targeted therapies
(chemo, surgery, radiation) that they refuse to even acknowledge
the use of therapies like nutrition and are loathe to even want to do
proper research in this area. So, in spite of the considerable
evidence -- theoretical and practical -- to support a beneficial
nutritional effect, every effort will be made to discredit it.
It's a self-serving motive.
KF: What else do you recommend one does to avoid, stop,
or reverse cancer?
TCC: A good diet, when coupled with other health
activities like exercise, adequate fresh air and sunlight, good water
and sleep, will be more beneficial.
The whole is greater than the sum of its parts. ***
For help on how to lean into a plant based diet,
check out my blog post here;
http://www.huffingtonpost.com/kathy-freston/one-bite-at-a-time-a-begi_b_42211.html
and for recipes click here.
For more information about diet and cancer, visit www.tcolincampbell.org ***
www.vegsource.com
www.drmcdougall.com
www.notmilk.com
http://www.notmilk.com/tudrmac.html 65 citations
The over 100 mg methanol impurity per liter wine
or two liters aspartame beverages becomes
formaldehyde and then formic acid in humans -- co-factors
for "morning after" hangovers, birth defects, cancers -- folic acid
protects most people.
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
_____________________________________________________
Rich Murray
1943 Otowi Road, Santa Fe, New Mexico 87505
505-501-2298 rmforall@comcast.net
http://groups.yahoo.com/group/rmforall/messages
http://groups.yahoo.com/group/AstroDeep/messages
http://RMForAll.blogspot.com new primary archive
http://groups.yahoo.com/group/aspartameNM/messages
group with 141 members, 1,586 posts in a public archive
http://groups.yahoo.com/group/aspartame/messages
group with 1199 members, 23,909 posts in a public archive
participant, Santa Fe Complex www.sfcomplex.org
_____________________________________________________
Thursday, August 27, 2009
severe brain harm in obese -- aspartame a co-factor? -- body turns its methanol into formaldehyde and formic acid: Rich Murray 2009.08.27
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
_____________________________________________________
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 <5%),
while DM2 and FPI were no longer associated
with any volume differences.
In an Analysis of Covariance (ANCOVA) model
controlling for age, gender, and race,
obese subjects with a high BMI (BMI > 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
_____________________________________________________
"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@comcast.net
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 141 members, 1,585 posts in a public archive
http://groups.yahoo.com/group/aspartame/messages
group with 1208 members, 23,878 posts in a public archive
_____________________________________________________
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
_____________________________________________________
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 <5%),
while DM2 and FPI were no longer associated
with any volume differences.
In an Analysis of Covariance (ANCOVA) model
controlling for age, gender, and race,
obese subjects with a high BMI (BMI > 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
_____________________________________________________
"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@comcast.net
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 141 members, 1,585 posts in a public archive
http://groups.yahoo.com/group/aspartame/messages
group with 1208 members, 23,878 posts in a public archive
_____________________________________________________
Tuesday, August 18, 2009
Ralph Walton, MD, asks FDA to ban aspartame: Stephen Fox: Rich Murray 2009.08.18
Ralph Walton, MD, asks FDA to ban aspartame: Stephen Fox: Rich Murray 2009.08.18
http://rmforall.blogspot.com/2009_08_01_archive.htm
Tuesday, August 18, 2009
http://groups.yahoo.com/group/aspartameNM/message/1584
___________________________________________________
http://www.opednews.com/articles/New-York-Psychiatrist-Exho-by-Dr-Ralph-Walton--090812-518.html
Tag(s): Artificial Sweetener; Aspartame; Aspartame Poisoning;
Carcinogenic; Dr Russell Blaylock; Equal Merisant;
Margaret Hamburg; Merisant; Monsanto; Neurotoxic; (more...)
Psychiatrists; Ralph Walton Md (less...)
August 14, 2009 at 11:52:02
New York Psychiatrist Exhorts FDA to Rescind Artificial
Sweetener Aspartame Approval
by Dr. Ralph Walton, M.D. (Posted by Stephen Fox)
Page 1 of 1 page
www.opednews.com
Margaret Hamburg, M.D.
Commissioner, F.D.A.
5600 Fishers Lane
Rockville, Maryland 20857
Dear Dr. Hamburg:
I would like to urgently request that the F.D.A. re-visit the
approval of aspartame.
This is an issue which I have been involved with for the past 25
years -- initially because of the adverse effects experienced by
one of my patients. I had been treating a then 54 year old
woman with imipramine because of recurrent major depressive
episodes. Previous psychoanalytically based therapy had
proven ineffective, but she responded dramatically to 150 mg
of imipramine per day. She had done well for 11 years on this
medication, but was then suddenly hospitalized with a grand
mal seizure and subsequent manic episode.
One could postulate that she was bipolar and the imipramine
had triggered the mania, but she had been on the same
medication for a total of 11 years, and for the previous 5
years at the same 150 mg per day dose. Neither the seizure
nor her mania were consistent with what we know about the
clinical course of bipolar disorder or epilepsy. Careful history
revealed that the only change in her life was a recent decision
to switch from the sugar which she had always used to sweeten
her iced tea to a newly marketed product with aspartame.
I reasoned that the aspartame could have altered the
catecholamine/indoleamine balance and thus account for her
clinical difficulties.
After the publication of this case report many patients with
unexplained seizures or puzzling psychiatric presentations were
referred to me. I became increasingly convinced that aspartame
could trigger seizure activity and mimic or exacerbate a variety
of psychiatric disorders. I presented a paper based on those
patients at a 1987 MIT sponsored conference on dietary
phenylalanine and brain function.
Industry sponsored criticism was made that my conclusions
regarding aspartame's toxicity could not be accepted as valid
because my case reports were "merely anecdotal" and not
based on double-blind research. Although I personally
believe that case reports are undervalued in modern medical
literature, I was so convinced of aspartame's toxicity, and the
need to have it's hazards more widely appreciated in the
medical community, that I did undertake a double-blind study.
That study was published in Biological Psychiatry in 1993
(a copy of the paper is enclosed). It demonstrated that
individuals with mood disorders are particularly sensitive to
aspartame and experienced an accentuation of depression
and multiple physical symptoms. I had expected that the
difficulties experienced by patients receiving aspartame
would be fairly subtle (the dose of 30 mg/kg/day was well
below the 50 mg/kg/day that the F.D.A. considered "safe").
I was not prepared for the severity of the reactions and for
obvious ethical reasons cannot perform any further human
studies with aspartame.
Two years after the publication of that study I was contacted by
a producer for "60 Minutes" and asked if I would be willing to
be interviewed by Mike Wallace for a segment on aspartame.
During that interview Mike challenged me on my assertion that
there were major problems with this sweetener in view of the
fact that the bulk of the medical literature attested to its safety.
I responded that one had to look carefully at study funding --
that virtually all of the studies claiming safety were funded by
the industry, whereas independently funded studies invariably
identified one or more problems. When he challenged me to
prove this I prepared a chart correlating study outcome and
funding source. This chart was aired on the 60 Minutes
segment, and is enclosed, with further discussion of this entire
issue.
Although for obvious ethical reasons I cannot perform further
human studies with aspartame, as a busy clinician I continue
to see the multiple neurological and psychiatric consequences
of aspartame use. It can lower seizure threshold and lead to
an incorrect diagnosis of epilepsy, with subsequent
inappropriate prescription of anticonvulsants. It can mimic
or exacerbate symptoms of MS, it can paradoxically produce
carbohydrate craving and weight gain. The world-wide epidemic
of obesity and type 2 diabetes obviously has multiple causes,
but I am convinced aspartame is a major factor.
On a daily basis I see how it can both produce and aggravate
depression, in certain patients it can trigger manic episodes, it can
produce or aggravate panic attacks. Some of my patients have
experienced a complete cessation of panic attacks and needed
no further treatment after they totally eliminated aspartame from
their diet. Certain schizophrenic patients have experienced fewer
auditory hallucinations and needed less antipsychotic medication
after the elimination of aspartame consumption.
Thank you Dr. Hamburg for your attention to this urgent public
health problem.
Yours sincerely,
Ralph G. Walton, M.D.
Former Professor and Chairman,
Department of Psychiatry,
Northeastern Ohio Universities College of Medicine
___________________________________________________
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
http://groups.yahoo.com/group/aspartameNM/message/1141
Nurses Health Study can quickly reveal the extent of aspartame
(methanol, formaldehyde, formic acid) toxicity:
Murray 2004.11.21 rmforall
http://groups.yahoo.com/group/aspartameNM/message/1143
antiseptic? antifungal? antiviral? methanol (formaldehyde, formic
acid) disposition: Bouchard M et al, full plain text, 2001:
substantial sources are degradation of fruit pectins, liquors,
aspartame, smoke: Murray 2005.01.05 rmforall
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@catholic.ac.kr
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@RMV.se;
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@drthrasher.org
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
___________________________________________________
"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@comcast.net
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 141 members, 1,584 posts in a public archive
http://groups.yahoo.com/group/aspartame/messages
group with 1207 members, 23,867 posts in a public archive
___________________________________________________
http://rmforall.blogspot.com/2009_08_01_archive.htm
Tuesday, August 18, 2009
http://groups.yahoo.com/group/aspartameNM/message/1584
___________________________________________________
http://www.opednews.com/articles/New-York-Psychiatrist-Exho-by-Dr-Ralph-Walton--090812-518.html
Tag(s): Artificial Sweetener; Aspartame; Aspartame Poisoning;
Carcinogenic; Dr Russell Blaylock; Equal Merisant;
Margaret Hamburg; Merisant; Monsanto; Neurotoxic; (more...)
Psychiatrists; Ralph Walton Md (less...)
August 14, 2009 at 11:52:02
New York Psychiatrist Exhorts FDA to Rescind Artificial
Sweetener Aspartame Approval
by Dr. Ralph Walton, M.D. (Posted by Stephen Fox)
Page 1 of 1 page
www.opednews.com
Margaret Hamburg, M.D.
Commissioner, F.D.A.
5600 Fishers Lane
Rockville, Maryland 20857
Dear Dr. Hamburg:
I would like to urgently request that the F.D.A. re-visit the
approval of aspartame.
This is an issue which I have been involved with for the past 25
years -- initially because of the adverse effects experienced by
one of my patients. I had been treating a then 54 year old
woman with imipramine because of recurrent major depressive
episodes. Previous psychoanalytically based therapy had
proven ineffective, but she responded dramatically to 150 mg
of imipramine per day. She had done well for 11 years on this
medication, but was then suddenly hospitalized with a grand
mal seizure and subsequent manic episode.
One could postulate that she was bipolar and the imipramine
had triggered the mania, but she had been on the same
medication for a total of 11 years, and for the previous 5
years at the same 150 mg per day dose. Neither the seizure
nor her mania were consistent with what we know about the
clinical course of bipolar disorder or epilepsy. Careful history
revealed that the only change in her life was a recent decision
to switch from the sugar which she had always used to sweeten
her iced tea to a newly marketed product with aspartame.
I reasoned that the aspartame could have altered the
catecholamine/indoleamine balance and thus account for her
clinical difficulties.
After the publication of this case report many patients with
unexplained seizures or puzzling psychiatric presentations were
referred to me. I became increasingly convinced that aspartame
could trigger seizure activity and mimic or exacerbate a variety
of psychiatric disorders. I presented a paper based on those
patients at a 1987 MIT sponsored conference on dietary
phenylalanine and brain function.
Industry sponsored criticism was made that my conclusions
regarding aspartame's toxicity could not be accepted as valid
because my case reports were "merely anecdotal" and not
based on double-blind research. Although I personally
believe that case reports are undervalued in modern medical
literature, I was so convinced of aspartame's toxicity, and the
need to have it's hazards more widely appreciated in the
medical community, that I did undertake a double-blind study.
That study was published in Biological Psychiatry in 1993
(a copy of the paper is enclosed). It demonstrated that
individuals with mood disorders are particularly sensitive to
aspartame and experienced an accentuation of depression
and multiple physical symptoms. I had expected that the
difficulties experienced by patients receiving aspartame
would be fairly subtle (the dose of 30 mg/kg/day was well
below the 50 mg/kg/day that the F.D.A. considered "safe").
I was not prepared for the severity of the reactions and for
obvious ethical reasons cannot perform any further human
studies with aspartame.
Two years after the publication of that study I was contacted by
a producer for "60 Minutes" and asked if I would be willing to
be interviewed by Mike Wallace for a segment on aspartame.
During that interview Mike challenged me on my assertion that
there were major problems with this sweetener in view of the
fact that the bulk of the medical literature attested to its safety.
I responded that one had to look carefully at study funding --
that virtually all of the studies claiming safety were funded by
the industry, whereas independently funded studies invariably
identified one or more problems. When he challenged me to
prove this I prepared a chart correlating study outcome and
funding source. This chart was aired on the 60 Minutes
segment, and is enclosed, with further discussion of this entire
issue.
Although for obvious ethical reasons I cannot perform further
human studies with aspartame, as a busy clinician I continue
to see the multiple neurological and psychiatric consequences
of aspartame use. It can lower seizure threshold and lead to
an incorrect diagnosis of epilepsy, with subsequent
inappropriate prescription of anticonvulsants. It can mimic
or exacerbate symptoms of MS, it can paradoxically produce
carbohydrate craving and weight gain. The world-wide epidemic
of obesity and type 2 diabetes obviously has multiple causes,
but I am convinced aspartame is a major factor.
On a daily basis I see how it can both produce and aggravate
depression, in certain patients it can trigger manic episodes, it can
produce or aggravate panic attacks. Some of my patients have
experienced a complete cessation of panic attacks and needed
no further treatment after they totally eliminated aspartame from
their diet. Certain schizophrenic patients have experienced fewer
auditory hallucinations and needed less antipsychotic medication
after the elimination of aspartame consumption.
Thank you Dr. Hamburg for your attention to this urgent public
health problem.
Yours sincerely,
Ralph G. Walton, M.D.
Former Professor and Chairman,
Department of Psychiatry,
Northeastern Ohio Universities College of Medicine
___________________________________________________
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
http://groups.yahoo.com/group/aspartameNM/message/1141
Nurses Health Study can quickly reveal the extent of aspartame
(methanol, formaldehyde, formic acid) toxicity:
Murray 2004.11.21 rmforall
http://groups.yahoo.com/group/aspartameNM/message/1143
antiseptic? antifungal? antiviral? methanol (formaldehyde, formic
acid) disposition: Bouchard M et al, full plain text, 2001:
substantial sources are degradation of fruit pectins, liquors,
aspartame, smoke: Murray 2005.01.05 rmforall
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@catholic.ac.kr
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@RMV.se;
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@drthrasher.org
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
___________________________________________________
"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@comcast.net
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 141 members, 1,584 posts in a public archive
http://groups.yahoo.com/group/aspartame/messages
group with 1207 members, 23,867 posts in a public archive
___________________________________________________
Subscribe to:
Posts (Atom)
