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Old 06-27-2008, 11:29 AM
Rich Murray
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Default Aspartame Induced Arrhythmias and Sudden Death, HJ Roberts 2004:Murray 2008.06.26

Aspartame Induced Arrhythmias and Sudden Death, HJ Roberts 2004:
Murray 2008.06.26
http://rmforall.blogspot.com/2008_06_01_archive.htm
Thursday, June 26, 2008
http://groups.yahoo.com/group/aspartameNM/message/1544
__________________________________________________ __


Aspartame Induced Arrhythmias and Sudden Death

By H. J. Roberts, M.D., F.A.C.P., F.C.C.P.
E-Mail: HJrobertsmd@aol.com
(c)2004 by H. J. Roberts, M.D.

A recent extensive review of sudden death in young athletes (1)
made no mention of aspartame as a primary cause or suspected
contributory factor, especially when demonstrable pathology was
absent.

This issue has assumed great public health importance because
"diet" products containing this chemical are being consumed by
over two-thirds of the population -- especially weight-conscious
persons.

I have repeatedly reported the serious cardiovascular,
'neuropsychiatric, metabolic and other adverse effects of
aspartame products. (2-4)

Among the first 1200 aspartame reactors in my data base,
193 (16%) had symptomatic arrhythmia,
85 (7%) atypical chest pain, and
64 (5%) recent or aggravated hypertension.

One hypertensive patient developed complete heart block within
hours after consuming his first diet cola.

Another had undergone unsuccessful radio frequency ablations in the
heart before awareness of having aspartame disease.

Pheochromocytoma was suspected in several aspartame reactors.

The issue of sudden death related to aspartame and its breakdown
products has been raised a number of times, particularly among
previously well individuals using such products... including pilots
and drivers, (3,4,6) and athletes.

I have detailed the release of norepinephrine, epinephrine, dopamine
and free methanol by aspartame; a host of pertinent-related
pathophysiologic conditions,
(e.g., cumulative formaldehyde adducts derived from aspartame in
tissue proteins and nucleic acids; excessive insulin release);
direct oropharyngeal absorption from gum, breath fresheners and
other products; and the increasing problem of aspartame addiction.
(4-7)

The likelihood of pulmonary hypertension induced by the
vasoconstrictive effects of aspartame products also has been
considered. (5)

It is relevant that unexplained dyspnea was experienced by 110
aspartame reactors, usually with prompt improvement after
abstinence.

Moreover, primary pulmonary hypertension was found at autopsy
in a 27 year old female aspartame reactor.

The lack of familiarity of most physicians and medical examiners
with the foregoing considerations can have serious legal
consequences.

A case in point is that of a young woman (also a Sunday School
teacher) who has been sentenced to serve 50 years in a Virginia
prison for allegedly poisoning her husband with methyl alcohol.
[ Diane and Charles Fleming ]

Elevated methanol blood concentrations were found postmortem in
this body builder/basketball player who drank ten diet drinks and
other aspartame products daily.

She remains incarcerated despite affidavits indicating that 10% of
aspartame becomes free methyl alcohol after consumption.

The need for clinicians and corporate-neutral investigators to
evaluate the contributory role of aspartame in cardiopulmonary
disorders and sudden death, and drug interactions with aspartame,
is underscored by the frequency of persons dying unexpectedly
being categorized as "death due to causes yet to be determined."

One interested resident of Orange county (California) found 192
persons listed in this category between July 11 and November 15,
2003 according to the Orange county Register.

References:

Maron BJ,
Sudden death in young athletes,
N Engl J Med 2003; 349: 1064-1075

Roberts HJ,
Reactions to aspartame containing products: 551 cases,
J Appl Nutr l988; 40: 86-94

Roberts HJ, Aspartame (NutraSweet): Is It Safe?
Philadelphia, The Charles Press, 1989.

Roberts HJ,
Aspartame Disease: An Ignored Epidemic.
West Palm Beach, Sunshine Sentinel Press, 2001

Roberts HJ,
Aspartame-induced dyspnea and pulmonary hypertension,
Townsend Letter for Doctors & Patients 2003; 237 (January): 64-65

Roberts HJ,
Ignored Health Hazards for Pilots and Drivers.
West Palm Beach, Sunshine Sentinel Press, 1998.

Roberts HJ, Aspartame (NutraSweet) addiction,
Townsend Letter for Doctors & Patients, 2000; 198 (January): 52-57

H. J. Roberts, MD, FACP, FCCP
Palm Beach Institute for Medical Research
P. O. Box 17799
West Palm Beach, Florida 33416 USA
__________________________________________________ __


http://www.dorway.com/tldaddic.html 5-page review
Roberts HJ Aspartame (NutraSweet) addiction.
Townsend Letter 2000 Jan; HJRobertsMD@aol.com
http://www.sunsentpress.com/ sunsentpress@aol.com
Sunshine Sentinel Press P.O.Box 17799 West Palm Beach, FL 33416
800-814-9800 561-588-7628 561-547-8008 fax

http://groups.yahoo.com/group/aspartameNM/message/669
1038-page medical text "Aspartame Disease: An Ignored Epidemic"
published May 30 2001 $ 60.00 postpaid data from 1200 cases
available at http://www.amazon.com
over 600 references from standard medical research

http://groups.yahoo.com/group/aspartameNM/message/790
Moseley: review Roberts "Aspartame Disease: An Ignored Epidemic":
Murray 2002.02.07

Roberts, Hyman J., 1924- ,
Useful insights for diagnosis, treatment and public heath: an updated
anthology of original research, 2002, 798 pages,
aspartame disease, pages 627-685, 778-780

http://groups.yahoo.com/group/aspartameNM/message/859
Roberts: the life work of a brilliant clinician: aspartame toxicity:
Murray 2002.08.02
__________________________________________________ __


re "A Few too Many", Joan Acocella, The New Yorker, long review of
hangover
research 2008.05.26 -- same levels of formaldehyde and formic acid in
FEMA
trailers and other sources (aspartame, dark wines and liquors, tobacco
smoke): Murray 2008.06.05
http://rmforall.blogspot.com/2008_06_01_archive.htm
Thursday, June 5, 2008
http://groups.yahoo.com/group/aspartameNM/message/1541


formaldehyde and formic acid in FEMA trailers and other sources
(aspartame,
dark wines and liquors, tobacco smoke): Murray 2008.01.30
http://rmforall.blogspot.com/2008_01_01_archive.htm
Wednesday, January 30, 2008
http://groups.yahoo.com/group/aspartameNM/message/1508

The FEMA trailers give about the same amount of formaldehyde and
formic acid
daily as from a quart of dark wine or liquor, or two quarts (6 12-oz
cans)
of aspartame diet soda, from their over 1 tenth gram methanol impurity
(one
part in 10,000), which the body quickly makes into formaldehyde and
then
formic acid -- enough to be the major cause of "morning after" alcohol
hangovers.

Methanol and formaldehyde and formic acid also result from many fruits
and
vegetables, tobacco and wood smoke, heater and vehicle exhaust,
household
chemicals and cleaners, cosmetics, and new cars, drapes, carpets,
furniture,
particleboard, mobile homes, buildings, leather... so all these
sources add
up and interact with many other toxic chemicals.

methanol impurity in alcohol drinks [ and aspartame ] is turned into
neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol
Syndrome,
BM Kapur, DC Lehotay, PL Carlen at U. Toronto, Alc Clin Exp Res 2007
Dec.
plain text: detailed biochemistry, CL Nie et al. 2007.07.18: Murray
2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524

"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 126 members, 1,544 posts in a public archive

http://groups.yahoo.com/group/aspartame/messages
group with 1,119 members, 22,762 posts in public archive

http://www.newyorker.com/reporting/2...urrentPage=all

Annals Of Drinking
A Few Too Many
Is there any hope for the hung over?
by Joan Acocella May 26, 2008 themail@newyorker.com

"Wayne Jones, of the Swedish National Laboratory of Forensic Medicine"
[ http://groups.yahoo.com/group/aspartameNM/message/1469
highly toxic formaldehyde, the cause of alcohol hangovers, is
made by the body from 100 mg doses of methanol from
dark wines and liquors, dimethyl dicarbonate, and aspartame:
Murray 2007.08.31 ]

http://groups.yahoo.com/group/aspartameNM/message/1286
methanol products (formaldehyde and formic acid) are main cause
of alcohol hangover symptoms [same as from similar amounts of
methanol, the 11% part of aspartame]: YS Woo et al, 2005 Dec:
Murray 2006.01.20

Addict Biol. 2005 Dec;10(4): 351-5.
Concentration changes of methanol in blood samples during
an experimentally induced alcohol hangover state.
Woo YS, Yoon SJ, Lee HK, Lee CU, Chae JH, Lee CT, Kim DJ.
Chuncheon National Hospital, Department of Psychiatry,
The Catholic University of Korea, Seoul, Korea.
[ 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 ]
[ for more, see URL..... ]
__________________________________________________ __
Reply With Quote
  #2  
Old 06-27-2008, 07:01 PM
psevetson
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Posts: n/a
Default Re: Aspartame Induced Arrhythmias and Sudden Death, HJ Roberts 2004:Murray 2008.06.26

This article, published in 1999 in _the Lancet_, should also be read
by anyone concerned about the supposed toxicity of aspartame.

http://www.aspartame.net/rumors/Aspa...e_Internet.asp


On Jun 27, 12:54*am, Rich Murray <rmfor...@comcast.net> wrote:
> Aspartame Induced Arrhythmias and Sudden Death, HJ Roberts 2004:
> Murray 2008.06.26http://rmforall.blogspot.com/2008_06_01_archive.htm
> Thursday, June 26, 2008http://groups.yahoo.com/group/aspartameNM/message/1544

[due to size, original posting is snipped]

Reply With Quote
  #3  
Old 06-27-2008, 11:11 PM
Mąck©®
Guest
 
Posts: n/a
Default Re: Aspartame Induced Arrhythmias and Sudden Death, HJ Roberts 2004: Murray 2008.06.26

No sane person takes anything rich murray has to say as valid.
Everyone already knows he is a nutball troll.



On Fri, 27 Jun 2008 10:19:02 -0700 (PDT), psevetson
<psevetson@gmail.com> wrote:

>This article, published in 1999 in _the Lancet_, should also be read
>by anyone concerned about the supposed toxicity of aspartame.
>
>http://www.aspartame.net/rumors/Aspa...e_Internet.asp
>
>
>On Jun 27, 12:54*am, Rich Murray <rmfor...@comcast.net> wrote:
>> Aspartame Induced Arrhythmias and Sudden Death, HJ Roberts 2004:
>> Murray 2008.06.26http://rmforall.blogspot.com/2008_06_01_archive.htm
>> Thursday, June 26, 2008http://groups.yahoo.com/group/aspartameNM/message/1544

>[due to size, original posting is snipped]

Reply With Quote
  #4  
Old 06-28-2008, 09:11 AM
Rich Murray
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Posts: n/a
Default Re: Aspartame Induced Arrhythmias and Sudden Death, HJ Roberts 2004:Murray 2008.06.26

http://www.aspartame.net/rumors/Aspa...e_Internet.asp

©Ajinomoto Food Ingredients LLC

Aspartame and the Internet

The following letter appeared in The Lancet on 3 July 1999. It is
reproduced here with the permission of the publishers of this
respected journal.

Sir - Patients at our diabetes clinic have raised concerns about
information on the internet about a link between the artificial
sweetener aspartame and various diseases.

Our research revealed over 6000 web sites that mention aspartame, with
many hundreds alleging aspartame to be the cause of multiple
sclerosis, lupus erythematosis, Gulf War Syndrome, chronic fatigue
syndrome, brain tumours, and diabetes mellitus, among many others.

Virtually all of the information offered is anecdotal, from anonymous
sources and is scientifically implausible.

Aspartame, a dipeptide composed of phenylalanine and aspartic acid
linked by a methyl ester bond, is not absorbed, and is completely
hydrolysed in the intestine to yield the two constituent amino acids
and free methanol.

Opponents of aspartame suggest that the phenylalanine and methanol so
released are dangerous. In particular, they assert that methanol can
be converted to formaldehyde and then to formic acid, and thus cause
metabolic acidosis and neurotoxicity.

Although a 330 ml can of aspartame-sweetened soft drink will yield
about 20 mg methanol, an equivalent volume of fruit juice produces 40
mg methanol, and an alcoholic beverage about 60-100 mg.

The yield of phenylalanine is about 100 mg for a can of diet soft
drink, compared with 300 mg for an egg, 500 mg for a glass of milk,
and 900 mg for a large hamburger (1).

Thus, the amount of phenylalanine or methanol ingested from
consumption of aspartame is trivial, compared with other dietary
sources.

Clinical studies have shown no evidence of toxic effects and no
increase in plasma concentrations of methanol, formic acid, or
phenylalanine with daily consumption of 50 mg/kg aspartame (equivalent
to 17 cans of diet soft drink daily for a 70 kg adult) (1, 2).

The anti aspartame campaign purports to offer an explanation for
illnesses that are prominent in the public eye.

By targeting a manufactured chemical agent, and combining this with
pseudo-science and selective reporting, the campaign makes complex
issues deceptively simple.

Sensational web site names (eg, aspartamekills.com) grab the browser's
attention and this misinformation is also widely disseminated via chat
groups and chain e-mail.

People consult the internet about medical issues for various reasons
and many users regard online sources as being authoritative and valid.

The medical profession has a role in teaching our patients to be
discriminating consumers of the information offered there.

Anthony Zehetner, Mark McLean

Department of Endocrinology, Westmead Hospital,
Sydney NSW 2145, Australia

References

1. Aspartame. In: Gelman C R, Rumack B H, Hess A J, eds. DRUGDEX®
System. Englewood, Colorado: MICROMEDEX, 1998. Edition expires 1999.

2. Anon. ADA position statement: use of noncaloric sweeteners.
Diabetes Care 1991.
__________________________________________________ __



mental decline in older diabetic womenm Gregg, Sherwin, Cummings,
Bennett: 2000 Jan.: Murray 2000.01.31
http://groups.yahoo.com/group/aspartameNM/message/129

Message #129 of 1544

Rich Murray rmforall@earthlink.net
Send Email Jan 31, 2000 3:50 pm

Jan 31 2000 At the end of this post is a review by H.J. Roberts,MD,
giving his clinical judgement that aspartame is an added problem for
many diabetics, who use this controversial sweetener in lieu of sugar.
As a neurotoxin, we may expect older white women with diabetes who
often use it to incur significant neurotoxic pathologies. Wouldn't
it be effective to telephone these 682 women and find roughly how much
aspartame they use, and correlate it with the extensive measures of
their mental functioning? Rich Murray rmforall@earthlink.net

Bennett DA. Diabetes and change in cognitive function.
Arch Intern Med. 2000 Jan 24; 160(2): 141-3.
PMID: 10647749; UI: 20112275.

http://www.healthscout.com

Study finds problem in older women
By Adam Marcus HealthSCOUT Reporter

TUESDAY, Jan. 25 (HealthSCOUT) --
Diabetes may be the illness of insulin shots and candy bar fixes, but
doctors are finding that it's also a disease of the mind.

A new study shows that women with type II (adult-onset) diabetes are
more likely to lose cognition as they age than those without the blood
sugar problem. And the longer the duration of the disease, the greater
the odds of serious mental decline.

"I think [the finding] tells patients that diabetes is a serious
problem
that needs to be treated aggressively rather than ignored," says Dr.
Robert Sherwin, a Yale University diabetes expert and president-elect
of
the American Diabetes Association.

An estimated 16 million Americans suffer from type II diabetes, a
condition in which the body becomes resistant to the sugar-processing
hormone insulin. About one-third of patients don't know they have the
disease.

Diabetes can cause a wide range of serious physical complications,
from
blindness to stroke. Some studies also suggest that the inability to
control one's blood sugar may also lead to neurological impairment and
dementia.

The latest work, published in the current issue of Archives of
Internal
Medicine, involved nearly 10,000 women over age 65 who were enrolled
in
a separate investigation of fracture risks from osteoporosis. Of
those,
682 had been diagnosed with type II diabetes.

Slow, steady decline
When the study started in 1986, women with diabetes scored worse than
those without the condition on three standard measures of mental
acuity
-- a general test, one to gauge brain processing speed and one to
assess the ability to decode scrambled information.

That gap worsened slightly but perceptibly over time, as diabetics
suffered greater cognitive losses than their non-diabetic counterparts
-- even after factoring smoking habits, age and educational levels.

Women who had diabetes for more than 15 years were up to 114 percent
more likely than those without the illness to have some form of major
mental decay. While the changes in cognitive agility were too subtle
to
be observed individually, researchers detected them across the wide
population of subjects.

"Doctors so far have been pretty narrow on their focus of what may be
consequences of diabetes," says Dr. Steven Cummings, a University of
California at San Francisco hormone specialist and co-author of the
study.

This work indicates that "there may be many other and broader
implications of diabetes and many ways that treatment may help,"
Cummings says. As people -- and especially women -- live longer, he
says, understanding the impact of chronic diseases like diabetes will
become increasingly important.

The physiological link between diabetes and dementia isn't well
understood, says Edward Gregg, an epidemiologist at the Centers for
Disease Control and Prevention and lead author of the study. But he
says uncontrolled blood sugar or faulty insulin receptors could
somehow
damage brain cells. Diabetes also is linked to blood vessel problems
such as clogged arteries and strokes, both of which can cause brain
damage.

The researchers caution that the study group, which included only
white
women over age 65, might not be representative. More work is needed,
they say, to see if the findings apply to younger diabetics, men and
ethnic minorities such as African-Americans, who have a particularly
high risk of the disease.

What To Do
Dr. David Bennett, who directs the Rush Alzheimer's Disease Center at
Rush Presbyterian-St. Luke's Medical Center in Chicago, says the
latest
finding is more important from a public health perspective than for
individual patients.

"There's plenty of reasons to be taking insulin and watching your diet
if you've got diabetes. You don't need this," says Bennett.

He says doctors who treat diabetics should be on the lookout for signs
of mental lapses.

To learn more about the disease, visit the American Diabetes
Association or the National Institute of Diabetes and Digestive and
Kidney Diseases.

SOURCES: Interviews with Steven R. Cummings, M.D., professor of
medicine and epidemiology, University of California, San Francisco
stevec@medicine.ucsf.edu 415-597-9114

Edward Gregg, Ph.D., epidemiologist, Centers for Disease Control and
Prevention, Atlanta; egregg@moose.uvm.edu http://www.cdc.gov/
Public Inquiries (404) 639-3534 (800) 311-3435
National Center for Disease Control and Health Promotion
1600 Clifton Rd. Atlanta, GA 30333 404-639-3311
National Center for Chronic Disease Prevention and Health Promotion
Division of Diabetes Translation, Centers for Disease Control and
Prevention, 4770 Buford Highway, N.E., Mailstop K-10,
Atlanta, GA 30341. 770-488-1273

David Bennett, M.D., director, Rush Alzheimer's Disease Center
Rush Presbyterian-St. Luke's Medical Center, Chicago,
1645 W. Jackson Suite 675 Chicago, Il 60612
(312) 942-3350 (312) 942-2861 Fax
www.resh.edu/patients/radc medcol@rush.edu 312-942-5000
Department of Neurological Sciences, Rush University
Chicago 60612, USA. dbennett@rush.edu

National Institute of Diabetes and Digestive and Kidney Diseases
National Institute of Health http://www.niddk.nih.gov/

Robert S. Sherwin, M.D., professor of medicine, Yale
University School of Medicine, New Haven, Conn., and president-elect,
American Diabetes Association http://www.diabetes.org/
customerservice@diabetes.org 800-342-2383 robert.sherwin@yale.edu
************************************************** **********************

Also, see the excellent 5-page review by H.J. Roberts in "Townsend
Letter", Jan 2000, "Aspartame (NutraSweet) Addiction":
http://www.dorway.com/tldaddic.html

Diabetes & aspartame: a clinical appraisal Aug 9 1994

http://presidiotex.com/aspartame/Fac...and_Aspartame/
diabetes_and_aspartame.html

H. J. ROBERTS, M.D.,F.A.C.P., F.C.C.P., PA

H.J. Roberts, M.D. hroberts@bp.seflin.org sunpress@gate.net
Sunshine Sentinel Press http://members.icanect.net/~sunpress/index.htm
6708 Pamela Lane West Palm Beach, Florida 33405 800-814-9800
561-588-7628 561-547-8008 fax

Dr. Roberts is on the Staff of Good Samaritan Hospital and
St. Mary's Hospital in West Palm Beach, Director of the Palm Beach
Institute for Medical Research (since 1964), and a member of many
prestigious medical and scientific organizations such as the American
College of Physicians, The Endocrine Society and the American Academy
of Neurology. His publications include nine acclaimed texts and more
than 220 original articles and letters. Many deal with original
researches on challenging metabolic and neurological disorders.
The Order of St. George knighted Dr. Roberts for his professionalism
and humanitarian efforts.

STATEMENT OF H. J. ROBERTS, M.D., CONCERNING THE USE OF PRODUCTS
CONTAINING ASPARTAME (NUTRASWEET) BY PERSONS WITH DIABETES AND
HYPOGLYCEMIA.

I have treated many patients with diabetes mellitus and hypoglycemia
(low blood sugar) in my capacity as a Board-certified internist and an
endocrinologist (member of the Endocrine Society). Since both groups
should abstain from sugar, I initially rejoiced that these persons
had an acceptable and presumably safe sugar substitute in aspartame.

Unfortunately, many patients in my practice, and others seen in
consultation, developed serious metabolic, neurologic and other
complications that could be specifically attributed to using aspartame
products. This was evidenced by:

*The loss of diabetic control, the intensification of hypoglycemia,
the
occurrence of presumed insulin reactions (including convulsions) that
proved to be aspartame reactions, and the precipitation, aggravation
or
simulation of diabetic complications (especially impaired vision and
neuropathy) while using these products.

*Dramatic improvement of such features after avoiding aspartame, AND
the
prompt predictable recurrent of these problems when the patient
resumed
aspartame products, knowingly or inadvertently. I have cited many
instances of severe complications in patients with diabetes and
hypoglycemia caused by the use of aspartame products in my books and
scientific articles. Here are few illustrations:

A 21 year-old insulin-dependent teacher suffered more frequent insulin
reactions both at school and at home, while drinking many aspartame
colas daily. He reported: When we cut down on aspartame, I stopped
having so many reactions.

A diabetic man suffered severe changes in vision when he was drinking
four liters of aspartame soft drinks daily. An opthalmologist assured
him that there was no detectable diabetic retinopathy. The patient
then
chanced to read an article about aspartame-related eye problems. He
promptly improved after avoiding these beverages, an unlikely event if
the problem was primarily a diabetic retinopathy.

A 46 year-old man with insulin-dependent diabetes had been in good
control for three decades until he began using several aspartame sodas
and packets of tabletop sweetener daily. He summarized his experience
in these terms: My diabetes went haywire, and I had terrible insulin
reactions. His diabetes was fully controlled within one week after
abstaining from aspartame products.

A 12 year-old boy with known diabetes required multiple
hospitalizations
for diabetic coma while consuming considerable aspartame products.
Physicians at a university hospital had difficulty in stabilizing his
insulin requirements while he used them.

In the light of this experience, I now advise ALL my patients with
diabetes and hypoglycemia to avoid aspartame products. A number of
alternatives are available.

I regret the failure of other physicians and the American Diabetes
Association (ADA) to sound appropriate warnings to patients and
consumers based on these repeated fininds which have been described in
my corporate-neutral studies and publications. This is largely due to
these factors:

1) It has been virtually impossible to get on the programs for
national
meetings of diabetologists and other professional groups in order to
describe these observations. Indeed, the ADA (of which I have been a
member for over three decades) even refused to print an abstract of
adverse reactions I encountered in 58 diabetic patients that was
submitted for its 1987 annual meeting.

This abstract subsequently appeared in CLINICAL RESEARCH (Vol. 3:
489A,
1988)...six years ago.

2) Journals devoted to diabetes and internal medicine have refused to
publish my manuscripts on this subject due to negative comments from
peer review. The likelihood that some of these reviewer-authorities
had
self-serving interests in denying publication is suggested below.

3) The AMA, the FDA, and the ADA dogmatically continue to express the
unequivocal opinion that aspartame is completely safe for diabetics--
and nearly everyone else.

4) Manufacturers and producers accomplished the marketing miracle of
the 1980s through highly effective PR campaigns, the underwriting of
numerous research projects (a number involving flawed protocols) by
investigators they granted on contracted with, and enormous
biopolitical clout in order to protect their billion-dollar market.

I detailed these matters in my two books on the subject: ASPARTAME
(NUTRASWEET): IS IT SAFE? (Philadelphia, 1989, the Charles Press) and
SWEETNER DEAREST: BITTERSWEET VIGNETTES ABOUT ASPARTAME (NUTRASWEET)
(West Palm Beach, 1992, Sunshine Sentinel Press, PO Box 8697,
1-800-814-9800). They are also summarized in my two-tape lecture, IS
ASPARTAME (NUTRASWEET) SAFE? A MEDICAL, PUBLIC HEALTH AND LEGAL
OVERVIEW
(West Palm Beach, 1992, Sunshine Sentinel Press, PO Box 8697,
1-800-814-9800).

I have discussed some of the reasons aspartame might aggravate
diabetes
and hypoglycemia in these books. The possible mechanisms include the
following:

* Marked changes in appetite and weight as reflected by paradoxic
weight
gain or severe loss of weight.

* Excessive insulin secretion and depletion of the insulin reserve

* Possible alteration of cellular receptor sites for insulin, with
ensuing insulin resistance

* Neurotransmitter alterations within the brain and peripheral nerves

* The toxicity of each of the three components of aspartame
(phenylalanine; aspartic acid; the methylester, which promptly becomes
methyl alcohol or methanol), and their multiple breakdown products
after
exposure to heat or during prolonged storage

I have asserted in my publications, and in testimony both to Congress
and FDA advisory group, that the current wholesale ingestion of
aspartame products by over half the adult population constitutes an
imminent public health hazard. Yet, this warning continues to be
ignored by the medical profession and the FDA.

Accordingly, informed and concerned consumers are justified in
criticizing the industrial-medical complex that 1) refuses to
acknowledge the problem of aspartame disease, and 2) fails to warn
high-risk groups about the potential dangers. In addition to patients
with diabetes and hypoglycemia, they include pregnant women, children,
patients with epilepsy, liver, kidney disease and eating disorders,
older persons with memory impairment, and the relatives of aspartame
reactors, diabetics and patients with phenylketonuria.

Many also correctly ask: Why is aspartame still on the market?
Their concern is intensified by the high incidence of brain tumors in
animals (known before FDA approval), and the reasonable doubt I have
documented about the apparent contributory role of aspartame in human
brain tumors.

1994 H.J. Roberts, M.D., F.A.C.P.,F.C.C.P. August 9, 1994
************************************************** *******************

http://www.thelancet.com/cgi-bin/new...pg_discuss.cgi
The Lancet Interactive discussion group:
Aspartame Toxicity: fact or fiction? 8.15.99

The Lancet Interactive offers discussion groups on articles in
The Lancet, and also an Electronic Research Archive:
www.thelancet.com . The Westmead Hospital and Community Health
Service has 975 beds, and is affifiated with the Universtiy of
Sidney: www.westmead.nsw.gov.au/ www/usyd.edu.au/

Aspartame and the internet
Correspondence Copyright 1999 The Lancet July 3, 1999

Sir--Patients at our diabetes clinic have raised concerns
about information on the Internet about a link between the artificial
sweetener aspartame and various diseases. Our research revealed over
6000 websites that mention aspartame, with many hundreds alleging
aspartame to be the cause of multiple sclerosis, lupus erythematosis,
Gulf War syndrome, chronic fatigue syndrome, brain tumours, and
diabetes mellitus, among many others. Virtually all of the information
offered is anecdotal, from anonymous sources and is scientifically
implausible.

Aspartame, a dipeptide composed of phenylalanine and aspartic
acid linked by a methyl ester bond, is not absorbed, and is
completely hydrolysed in the intestine to yield the two constituent
amino acids and free methanol. Opponents of aspartame suggest that
the phenylalanine and methanol so released are dangerous. In
particular, they assert that methanol can be converted to formaldehyde
and then to formic acid, and thus cause metabolic acidosis and
neurotoxicity.

Although a 330 mL can of aspartame-sweetened soft drink will
yield about 20 mg methanol, an equivalent volume of fruit juice
produces 40 mg methanol, and an alcoholic beverage about 60-100 mg.
The yield of phenylalanine is about 100 mg for a can of diet soft
drink, compared with 300 mg for an egg, 500 mg for a glass of milk,
and 900 mg for a large hamburger. (1) Thus, the amount of
phenylalanine or methanol ingested from consumption of aspartame
is trivial, compared with other dietary sources. Clinical studies
have shown no evidence of toxic effects and no increase in plasma
concentrations of methanol, formic acid, or phenylalanine with daily
consumption of 50 mg/kg aspartame (equivalent to 17 cans of diet
soft drink daily for a 70 kg adult). (1,2)

The antiaspartame campaign purports to offer an explanation for
illnesses that are prominent in the public eye. By targeting a
manufactured chemical agent, and combining this with pseudoscience
and selective reporting, the campaign makes complex issues
deceptively simple. Sensational website names
(eg, aspartamekills.com) grab the browser's attention and this
misinformation is also widely disseminated via chat groups and
chain e-mail.

People consult the internet about medical issues for various
reasons and many users regard online sources as being authoritative
and valid. The medical profession has a role in teaching our
patients to be discriminating consumers of the information offered
there.

*Anthony Zehetner, Mark McLean

Department of Endocrinology, Westmead Hospital, Sydney NSW 2145,
Australia

1 Aspartame. In: Gelman CR, Rumack BH, Hess AJ, eds. DRUGDEX®
System. Englewood, Colorado: MICROMEDEX, 1998. Edition expires 1999.

2 Anon. ADA position statement: use of noncaloric sweeteners.
Diabetes Care 1991; 14 (suppl 2): 28-29.
************************************************** ************

Re: Aspartame toxicity From: hroberts@pb.seflin.org
Date Tue, 10 Aug 1999 16:20:00 GMT

I disagree with the assertion by Zehetner and McLean (1) that concern
about the adverse health effects of aspartame products is
"scientifically implausible", and largely represents anecdotal
information from "anonymous" sources. I am not anonymous.

My opinion represents 15 years of corporate-neutral study of
aspartame disease in practice, consultation, and research (2-11),
based on over 1300 persons so afflicted. I now regard these products
as a probably imminent public health threat because of the
serious neurologic, psychiatric, metabolic, ocular, and allergic
reactions encountered, coupled with apparent fetotoxic and oncologic
consequences. Specific examples are seizures (4), headache (10),
depression (2), severe confusion (9), loss of diabetes control (5),
the aggravation or simulation of diabetic complications (5) and
multiple sclerosis (6), gross weight loss or gain (3,8), accident
proneness (11), aspartame addiction, and the perceived
causation/acceleration of Alzheimer's disease (9) and brain
tumors (7).

My diagnostic criteria for aspartame disease, and the grounds for
the foregoing assertions are detailed in articles and books (2-11).
They challenge the misleading attitudes of Zehetner and McLean
concerning "trivial" amounts of free methanol, of the sequelae from
flooding the body with large amounts of phenylalanine, aspartic acid
and their stereoisomers, and failure to appreciate chronic
methanol-derived formaldehyde toxicity.

The public health significance of this matter is compounded by the
fact that over half the United States population currently consumes
aspartame products. The dangers of excessive heat, prolonged storage,
aspartame gum, and the incorporation of aspartame in pediatric
preparations are underscored.

Inasmuch as the authors are in Australia, I refer them to my
solicited critique of the official position by the Australia and
New Zealand Food Authority (ANZFA) on aspartame (12).

REFERENCES
1. Zehetner A, McLean M. Lancet 1999, 354:78.
2. Roberts HJ. Neurological, psychiatric, and behavioral reactions
to aspartame in 505 aspartame reactors.
Chapter 45 in Dietary Phenylalanine and Brain Function ed by R.
Wurtman and E. Ritter-Walker, Birkhauser Boston, Inc., 1988, 373-376.
3. Roberts HJ. Reactions to aspartame-containing products: 551 Cases.
J Appl Nutr 1988: 40:85-94.
4. Roberts HJ. Aspartame (NutraSweet7)-associated epilepsy.
Clin Res 1988, 36:349A.
5. Roberts HJ. Complications associated with aspartame (NutraSweet7)
in diabetics. Clin Res 1988: 3-489A.
6. Roberts HJ. Aspartame (NutraSweet7): Is it safe?
Philadelphia, The Charles Press, 1989.
7. Roberts HJ. Does aspartame cause human brain cancer?
J. Advanc M 1991; 4 (Winter):231-241.
8. Roberts HJ. Sweet'ner Dearest: Bittersweet Vignettes About
Aspartame (NutraSweet7).
West Palm Beach, Sunshine Sentinel Press 1992.
9. Roberts HJ. Defense Against Alzheimer's Disease.
West Palm Beach, Sunshine Sentinel Press, 1995.
10. Roberts HJ. Aspartame and headache. Neurology 1995; 45:1631-1633.
11. Roberts HJ. Ignored Health Hazards for Pilots and Drivers.
West Palm Beach, Sunshine Sentinel Press, 1998.
12. Roberts HJ. Critique of the official Australia and New Zealand
Authority (ANZFA) position on aspartame.
Soil & Health 1997; July/September 15.
************************************************** ***********

Blalock: The Lancet: aspartame issues 7.29.99

http://www.thelancet.com/cgi-bin/new...pg_discuss.cgi
The Lancet Interactive dissussion group:
Aspartame Toxicity: fact or fiction?

Re: Aspartame toxicity From russell@misnet.com
Date: Thu, 29 Jul 1999 23:07:04 +0100 (BST)

Russell L. Blaylock Neurosurgeon

In reviewing the available literature on aspartame toxicity I have
developed several concerns. First, is the results of the GD Searle
study itself in 1977 which indicated a significant increase in brain
tumor induction in the aspartame fed animals. This appeared to be
secondary to a breakdown product, DKP. Follow up studies with DKP
were seriously flawed, as demonstrated by the Bressler report. It
should also be noted that other tumors appeared in the NutraSweet
group including breast tumors, pancreatic tumors, testicular tumors,
ovarian tumors and other tissues. Aspartame has been reported in
association with a cutaneous panniculitis as well in human cases.

The recent study using radiolabeled aspartame that indicated
attachment of the formaldehyde breakdown product to DNA and that the
formaldehyde was cumulative with each dose should cause all of us
concern. This is especially so in relation to oncogene activation and
in disorders associated with elevated rates of DNA damage, such as
lupus and the neurodegenerative disorders. I have found no studies
relating to possible elevation of free radicals with aspartame
exposure, but this certainly deserves review.

Shephard, et al found that aspartame was nitrosated in the GI tract
and that in this form was significantly mutagenic. Such nitrosation,
according to their findings, could also occur in endothelial cells
and stimulated macrophages. This would raise concern not only of
carcinogenic potential but also the stimulation of free radical
generation in blood vessels associated with atherosclerosis. Related
to this finding is another report by Hardcastle and Bruch, in which
they found that macrophages treated with aspartame produced an excess
of leukotrienes and other arachidonic acid metabolites. Yamada, et al
found that aspartic acid inhibited melatonin secretion from the pineal
gland. It has been shown that aspartame consumption does increase
aspartic acid blood levels, especially when consumed with MSG.

Another concern is the formation of stereoisomer when aspartame is
heated. Jeffry Bada has shown that when aspartame is heated there is
a significant conversion of the L-phenylalanine and aspartate to the
D-form. In addition, he found 6 to 10 decomposition products, some of
which are known to have deleterious neurological effects. Elevated
levels of D-aspartate have been described in several of the
neurodegenerative diseases.

The effect of aspartame feeding on blood phenylalanine is of concern
to the pregnant mother and those with newborns as well, since
phenylalanine has been associated with abnormal neural connectivity
in the immature brain. It has been established that PKU carriers
develop phenylalanine blood levels double that of normals. Further,
it has been shown that the placenta concentrates phenylalanine on
the fetal side of the circulation. Matalon, et al demonstrated that
in the human a loading dose of 34mg/kg increased phenylalanine levels
greater than 6mg/dl in 14% of normals and 35% of PKU carriers. Of
even more concern 5% of normals and 12% of carriers had blood Phe
levels exceeding 10mg/dl. The National Collaborative Study for
Maternal PKU has recommended that during pregnancy blood Phe should
not exceed 6mg/dl. This means that 14% of the general public could
exceed this level when consuming high intakes of aspartame and that
5% of normal people could exceed 10mg/dl. One in fifty persons
carries a heterozygous gene for PKU. Up to 35% of such unfortunate
individuals, and their babies, would be at risk without knowing it.
Especially, since the babies brain levels would even exceed that of
the mother.

With the complexity of the central nervous system it would be
irresponsible for the FDA to allow the widespread selling o
aspartame without further independent study of the
neurophysiological, neurobehavioral and neurochemical effects
of high intakes of this drug at all ages using chronic studies.
I think it is foolish to ignore the complaints of millions of
individuals reporting difficulties with this substance.

Russell L. Blaylock Neurosurgeon 601-982-1175 russell@misnet.com
9 Lakeland Circle Jackson, Mississippi 39216

Blaylock RL. Hydrosyringomyelia of the conus medullaris associated
with a thoracic meningioma: case report.
J Neurosurg. 1981 Jun;54(6):833-5.
************************************************** *******************


April 21, 1999 Richard T. Murray, M.A. rmforall@earthlink.net
Here is research in 1998 at a very low level of aspartame ingestion,
10 mg/kg, for rats, which have a much greater tolerance for aspartame
than humans. The same level for humans would be about 1 or 2 mg/kg.
Many headache studies in humans used doses of about 30 mg/kg daily.
A daily dose of 2100mg aspartame, about 4 L diet soda, used in many
experimental tests on humans, supplies 210mg methanol into the body.
Many cases report a typical serious symptom syndrome at this level.

This report shows that aspartame causes binding of methanol's product,
formaldehyde, a potent, cumulative toxin, into tissues.

Life Sci 1998;63(5):337-49 From PubMed
Formaldehyde derived from dietary aspartame binds to tissue components
in vivo. Trocho C, Pardo R, Rafecas I, Virgili J, Remesar X,
Fernandez-Lopez JA, Alemany M, Departament de Bioquimica i Biologia
Molecular, Facultat de Biologia, Universitat de Barcelona, Spain.

Sra. Carme Trocho, Sra. Rosario Pardo, Dra. Immaculada Rafecas,
Sr. Jordi Virgili, X. Remesar, Dr. Jose Antonio Fernandez-Lopez,
Dr. Marią Alemany Fac. Biologia Tel.: (93)4021521, FAX: (93)4021559
alemany@porthos.bio.ub.es bioq@sun.bq.ub.es

Abstract:
Adult male rats were given an oral dose of 10 mg/kg aspartame,
14C-labelled in the methanol carbon. At timed intervals of up to 6
hours, the radioactivity in plasma and several organs was
investigated.
Most of the radioactivity found (>98% in plasma, >75% in liver) was
bound to protein. Label present in liver, plasma and kidney was in the
range of 1-2% of total radioactivity administered per g or mL,
changing
little with time. Other organs (brown and white adipose tissues,
muscle, brain, cornea and retina) contained levels of label in the
range of 1/12th to 1/10th of that of liver. In all, the rat retained,
6 hours after administration, about 5% of the label, half of it in the
liver. The specific radioactivity of tissue protein, RNA and DNA was
quite uniform. The protein label was concentrated in amino acids,
different from methionine, and largely coincident with the result of
protein exposure to labelled formaldehyde. DNA radioactivity was
essentially in a single different adduct base, different from the
normal bases present in DNA. The nature of the tissue label
accumulated was, thus, a direct consequence of formaldehyde binding to
tissue structures. The administration of labelled aspartame to a group
of cirrhotic rats resulted in comparable label retention by tissue
components, which suggests that liver function(or its defect) has
little effect on formaldehyde formation from aspartame and binding to
biological components. The chronic treatment of a series of rats with
200 mg/kg of non-labelled aspartame during 10 days resulte in the
accumulation of even more label when given the radioactive bolus,
suggesting that the amount of formaldehyde adducts coming from
aspartame in tissue proteins and nucleic acids may be cumulative.
It is concluded that aspartame consumption may constitute a hazard
because of its contribution to the formation of formaldehyde adducts.
PMID: 9714421, UI: 98378223

Mark D. Gold has an excellent, detailed analysis, "Scientific Abuse in
Methanol / Formaldehyde Research Related to Aspartame" at:

http://www.holisticmed.com/aspartame...tml#discussion .

In short, biochemical evidence exists to motivate us to seriously and
respectfully consider anecdotal evidence of aspartame toxicity.

Mark D. Gold gives another detailed review, "Scientific Abuse in
Seizure Research Related to Aspartame", at:

http://www.holisticmed.com/aspartame.../seizures.html .

"If the seizures from aspartame are caused by the combination of
methanol/formaldehyde and the excitotoxic amino acid from aspartame,
as
I believe may be the case, it is important to note that methanol is 10
times more acutely toxic in humans than in rodents (Roe 1982), and it
takes five times more excitotoxins given to rodents to simulate human
ingestion (Olney 1988, Stegink 1979, page 90)."
************************************************** *********************

Aspartame (NutraSweet, Equal, Canderel, Benevia) is reported by many
scientific studies and case histories to be toxic: headaches, all
kinds of body and joint pain (or burning, tingling, tremors,
twitching,
spasms, cramps, or numbness); "mind fog", "feel unreal", poor
memory, confusion, anxiety, irritability, depression, mania, insomnia,
dizziness, slurred speech, ringing in ears, sexual problems, nausea,
seizures, poor vision, hearing, or taste; fatigue; red face,
itching, rashes, burning eyes or throat, dry mouth or eyes, mouth
sores;
hair loss; obesity, bloating, poor or excessive hunger or thirst,
anorexia; coldness; diarrhea or constipation; breathing problems;
racing
heart, high blood pressure, erratic blood sugar levels; birth defects;
brain cancers.

Three careful double-blind experimental studies prove asp.
causes headaches: Koehler SM et al, 1988, Headache, 28(1), 10-14.
Shirley Koehler, PhD 904-858-7651 skoehler@brookshealth.org
Walton RG et al, 1993, Biological Psychiatry, 34(1), 13-17.
Prof. Ralph G. Walton 330-740-3621 rwalton193@aol.com
Van Den Eeden SK et al, 1994, Neurology, 44, 1787-93.
Steven K. Van Den Eeden,PhD 550-450-2202 skv@dor.kaiser.org

Woodrow C. Monte, Director, Food Science and Nutrition Laboratory
602-965-6938 Arizona State University, woody.monte@asu.edu,
"Aspartame: Methanol and the Public Health," 1984,
J. Applied Nutrition, 36(1), 42-54 (62 references):
The methanol from 2 L of diet soda, 5.6 12-oz cans, 20 mg/can, is
112 mg, 10% of the asp. 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.) This study is at: http://www.dorway.com/wmonte.txt

Who pays the piper, calls the tune. Ralph G. Walton, Prof.
of Clinical Psychology, Northeastern Ohio Universities, Youngstown,
OH 44501, 330-740-3621 rwalton193@aol.com , in an unpublished
66-page study (1998), listed 166 studies about asp. and health. All
74 studies funded by the industry were favorable, whereas 84 of the 92
non-industry studies identified a problem. Moreover, many industry
studies were published repeatedly with slight changes, from 2 to 6
times each, violating scientific ethics.
This study is available at: http://www.dorway.com/peerrev.html

Aspartame Toxicity Information Center Mark D. Gold
www.HolisticMed.com/aspartame 603-225-2100
"Scientific Abuse in Aspartame Research"
http://www.holisticmed.com/aspartame.../methanol.html
mgold@tiac.net 12 East Side Drive #2-18 Concord, NH 03301

Aspartame Victims Support Group Home Page and also Spanish
translations
http://www.presidiotex.com/aspartame/

Mission-Possible-USA Betty Martini 770-242-2599
www.dorway.com Bettym19@mindspring.com

Aspartame Consumer Safety Network 800-969-6050 214-352-4268
http://web2.airmail.net/marystod/index.html marystod@airmail.net
Mary Nash Stoddard, "The Deadly Deception"

Geoff.Brewer@clara.net United Kingdom Mission Possible International
63 Downlands Road DEVIZES SN10 5EF Tel: 01380 728059
http://www.connectotel.com/missionpossible/

H.J. Roberts, M.D. hroberts@bp.seflin.org sunpress@gate.net
Sunshine Sentinel Press http://members.icanect.net/~sunpress/index.htm
6708 Pamela Lane West Palm Beach, Florida 33405 800-814-9800
561-588-7628 561-547-8008 fax

http://www.truthinlabeling.org/ Truth in Labeling Campaign [MSG]
Adrienne and Jack Samuels P.O. Box 2532 Darien, Illinois 60561
858-481-9333 adandjack@aol.com "The Toxicity/Safety of Processed
Free Glutamic Acid (MSG): A Study in Suppression of Information."

Health Press hlthprs@trail.com 505-982-9373 505-474-0303
http://www.healthpress.com/in-bad-taste.html "In Bad Taste: The MSG
Symptom Complex," George R. Schwartz, M.D. drgschwartz@yahoo.com
http://www.healingresearch.org/ Healing Research Institute

The Aspartame Homepage (pro-asp.) http://www.aspartame.org/

Many long, referenced posts are in the archive at:
www.onelist.com/community/aspartameNM

The eminent British journal: The Lancet Interactive Discussion Group:
"Aspartame Toxicity: fact or fiction?" http://www.thelancet.com/

You may search among 9 million medical citations on PubMed for any
topic or author, and for many studies get an abstract summary:
http://www.ncbi.nlm.nih.gov/PubMed/

The great health advantages of a no-fat vegetarian diet are well
described by Dr. John A. McDougall at www.drmcdougall.com ,
which has copious scientific references and Net links.
************************************************** ********************

Rich Murray Room For All
1943 Otowi Drive, Santa Fe, New Mexico 87505
505-986-9103 505-920-6130 cell rmforall@earthlink.net
[B.A., M.I.T. 1964, M.A., Boston U. 1967: a layman committed to
facilitating civil debate on aspartame toxicity]
************************************************** ********************
__________________________________________________ __


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"

"We present a case of a medical student who presented with
erythematous eczematoid plaques on her trunk and legs and
fine vesiculation of her scalp, 3 weeks after starting anatomy class.

Of note, she routinely washed her face and arms after leaving the
anatomy lab, but remained in her scrubs for the rest of the day.

Formaldehyde and Quaternium-15 positive reactions
in the same patient."

"Our patient underscores the importance of appropriate patch
testing and education.
Once we identified the allergy to formaldehyde and quaternium-15,
we provided patient education materials regarding the common and
not-so-common locations of these chemicals and cross-reactors.
We also gave the patient information on avoidance
and safe alternatives (see Table 5).

Fortunately, with technical advances, this student completed the
anatomy section via electronic learning tools.

By avoiding formaldehyde, including anatomy lab, FRP
in her shampoo and cosmetics,
and aspartame in her diet, this patient dramatically improved.

As with all contact dermatitides, the mainstay of treatment for
allergic contact dermatitis is avoidance."


http://www.skinandaging.com/article/5158Skin & Aging Journal
Skin & Aging - ISSN: 1096-0120 - Volume 13 - Issue 12_2005 -
December 2005 - Pages: 22 - 27

Allergen Focus:
Focus on T.R.U.E. Test Allergens #21, 13 and 18:
Formaldehyde and Formaldehyde-Releasing Preservatives
-- By Sharon E. Jacob, M.D., Tace Steele, B.A., [now MD]
and Georgette Rodriguez, M.D., M.P.H.

[ See also:

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 ]


Allergic Contact Dermatitis is an important disease with a high
impact both in terms of patient morbidity and economics.

The contact dermatitides include irritant contact dermatitis,
contact urticaria and allergic contact dermatitis.

Irritant contact dermatitis, the most common form, accounts for
approximately 80% of environmental-occupational based
dermatoses.

Contact urticaria (wheal and flare reaction) represents an IgE and
mast cell-mediated immediate-type hypersensitivity reaction
that can lead to anaphylaxis,
the foremost example of this would be latex hypersensitivity.
While this is beyond the scope of this section, we acknowledge this
form of hypersensitivity due to the severity of the potential
reactions
and direct the reader to key sources. 1,2

Allergic contact dermatitis, on the other hand, is a delayed type IV
hypersensitivity reaction. The primary focus of this section is to
highlight the educational component of allergic contact dermatitis.

Clinical Illustration

We present a case of a medical student who presented with
erythematous eczematoid plaques on her trunk and legs
and fine vesiculation of her scalp,
3 weeks after starting anatomy class.
Of note, she routinely washed her face and arms after leaving the
anatomy lab, but remained in her scrubs for the rest of the day.

Formaldehyde and Quaternium-15 positive reactions
in the same patient.

History of Formaldehyde
and the Formaldehyde-Releasing Preservatives

The desire to improve one's appearance with topical applications
dates back to the Egyptian Queen, Cleopatra, who was fond of
using creams and make-up for skin beautification. 3

What once was fit for a queen has become a $30 billion a year
cosmetic industry. 4

With the cosmetic boom came the concern of microorganisms
in cosmetic creams introduced during manufacture or transferred
to the product through use. 5

A variety of reports of cosmetic contamination from
Klebsiella pneumoniae have been reported.

In addition, this bacterium has been linked to septicemia
after contact with a contaminated hand cream dispenser. 6,7

Consequently, considerable attention has been given to topical
pharmaceutical preparations
with effective methods of antimicrobial preservation.

Preservatives are biocidal chemicals added to cosmetics,
topical medicaments and foods to protect against spoilage,
bacterial and fungal contamination, and biological degradation. 7

The ideal preservative should be stable, antimicrobial, nontoxic,
non-irritating and active over a broad range of pH values.

In 1938, the FDA passed the Food, Drug and Cosmetic Act
requiring the cosmetic industry to prove product safety
before marketing to consumers. 8

Prior to that, products such as Lash-Lure
(by the Los Angeles-based company)
containing paraphenylenediamine had caused blindness,
and a whitening foundation containing lead oxide
had caused muscle paralysis. 9

Soon thereafter, formaldehyde preservation of cosmetics was being
streamlined for its many advantages.
It was cheap and effective in eliminating a wide range of
microorganisms and aggressively destroying degradation enzymes,
thus slowing product decomposition.
Formaldehyde remains a commonly used preservative in cosmetics
today with an average concentration between 0.02% and 0.3%. 10

How It Was Discovered

A formaldehyde-based white brittle material, polyformaldehyde was
discovered
during the incomplete combustion of carbon in 1859
by the Russian chemist, Alexander Mikhailovich Butlerov.
This leader in isomer chemistry (and synthesizer of the first
artificial
sugar) has had a crater on the moon named after him to
commemorate his work. 11,12

Ten years after the polymer discovery, the German chemist,
August Wilhem von Hofman, found that by passing methanol
and air over a heated platinum spiral, he could create pure
formaldehyde (a technique is still used today). 13

In 1892, the year of Hofman's death, Friedrich August Kekule von
Stradonitz,
the scientist who introduced the concept of chemical
bonds, isolated pure formaldehyde by the catalytic oxidation of
methanol.

First Commercial Uses

One of the first mass commercial uses of formaldehyde was in
medical embalming (a practice known to be utilized during the
Civil War). 14

Interestingly, formaldehyde use evolved with medical advancement.
In 1883, Robert Koch made a landmark discovery with a weighty
economic impact to the food industry.
He found that the bacterium, Vibrio cholerae, the cause of cholera,
could be transmitted via food and water.
This discovery initiated the demand for government regulation
of food industry sanitation and the necessitation of antimicrobial
food additives. 8

In 1900, San Franciscan Chinese immigrants suffered from an
outbreak of the bubonic plague. The city board of health quarantined
Chinatown and dusted the district with a mixture of lime and
formaldehyde to control the spread of disease. 15

In 1912, Dr. Harvey Wiley, Head of the Department of Chemistry
in Washington D.C. (Predecessor to the Food and Drug
Administration), founded the "poison squad".
This squadron of volunteers ate food to test the safety of added
preservatives (for example, borax, benzoic acid, sulfuric acid and
formaldehyde).
The poison squad was so popular with the public that minstrel
shows sang about it:

"Next week he'll give them mothballs, a la Newburgh or else plain;
O, they may get over it, but they'll never look the same." 8

After 5 years of experiments, vomiting and stomach pain,
Dr. Wiley publicly resolved that preservatives in food and medications
should "only be used when absolutely necessary,"
despite big business fighting him "tooth and nail". 8

In the 1950s, formaldehyde again made its mark in the medical
news. Jonas Salk's team created a polio vaccine.
This was made possible through the use
of formaldehyde to kill the poliovirus. 15

Success with Plastics

Although the medical and food industries had mixed experiences
with formaldehyde, the plastics industry thrived because of it.

Prior to innovation of formaldehyde-derived plastics, the
celluloid plastics had been highly flammable and not suitable for mass
marketing. 16 At the turn of the century,
the International Galalith Gesellschaft Hoff and Company
compounded formaldehyde and fat-free milk curd to formulate
a new synthetic plastic (casein-formaldehyde),
which became a main constituent of buttons. 16,17

The biggest landmark in formaldehyde-based plastics
came in 1910.
Leo H. Baekeland condensed phenol and formaldehyde to make
the first non-flammable synthetic plastic, Bakelite, which had high
utility as an electronics insulator. 10,18
Bakelite sales skyrocketed, as it was marketed in toys,
jewelry and cameras.
The Bakelite Museum in England even boasts a Bakelite coffin! 19

Its amber color contributed to its popularity in jewelry, but limited
its
potential when transparency was needed. 10
During the Bakelite heyday, circa 1912, scientists, Daniel J. O'Conor
and Herbert Faber, added formaldehyde to a urea polymer to
develop a novel insulation substitute for mica, aka formica. 18

The 1920s and '30s, saw the explosive age of the urea
formaldehyde resins whose colorless properties allowed new lines
of plastic products in bright colors, i.e the trendy plastic versions
of marble dishes, bandalasta. 11,21

Today, urea-formaldehyde resins and melamine-formaldehyde
laminates dominate the commercial market.
What began as a reach for a new plastic alternative and preservative
has become a $500 billion industry,
representing 5% of the United States' gross national product. 11

Formaldehyde is used to make plywood, asphalt shingles, car gears
and bearings.

Specifically, p-tert-Butylphenol formaldehyde resin is used in
bonded leather, construction materials and waterproof glues.

In addition, fertilizers and photographic developers are also known to
contain formaldehyde. 11

A Powerful Allergen

The rates of sensitization to formaldehyde have risen to 9.2%. 22,23

Formaldehyde is second only to fragrances as the most common
sources of cosmetic-associated contact dermatitis. 24

To decrease sensitization and lower the concentration of
formaldehyde, the formaldehyde-releasing-preservatives (FRPs)\
are often used in place of frank formaldehyde, for example
quaternium-15 (see Table 1). 7,22,25


Herbert and Rietschel explain that if the concentration of
formaldehyde that is released by FRPs is below the threshold
of reactivity for virtually all formaldehyde-sensitive patients
(somewhere between 30 and 250 ppm), there would not be
an allergy to the FRP. 25

Many cases of contact dermatitis to formaldehyde/FRPs present
as eyelid dermatitis associated with the use of cosmetics
(mascara, blush and foundation), shampoos, medical creams
or nail hardeners, to name a few.

Other important sources of exposure include permanent press clothing,
cleaning agents, baby wipes, disinfectants, paper
and even cigarette smoke. 22

As is often the case in contact dermatitis, the distribution of the
dermatitis can provide insight into the exposure.
For example, patients sensitized to formaldehyde from adorned
permanent-press clothing tend to present with a chronic dermatitis
around their body folds, where the clothes rub against the skin. 22

Patients sensitized to formaldehyde in clothing textiles have been
found
to become secondarily sensitized to quaternium-15, presenting with a
diffuse nummular dermatitis or erythroderma. 24

Systematized dermatitis is seen with both formaldehyde and the FRPs.

Inhalation (smoking) and ingestion of formaldehyde containing foods
are important systemic sensitization sources (see Table 2) .27-30


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

Formaldehyde-Releasing Preservatives

The formaldehyde releasers are reversible polymers
of formaldehyde. 31

Formaldehyde is formed in different amounts based on the pH,
temperature, and amount of water. 31,32
The antibacterial effects are independent of the
amount of formaldehyde released. 29

An allergic reaction can be seen specifically to the FRP,
formaldehyde or both. 31

Quaternium-15, a colorless, odorless, biocidal FRP
is highly water-soluble, stable, and active over a broad range of pH.

It has broad antimicrobial activity, particularly Pseudomonas
aeruginosa,
yeasts, and molds. 22

As the most common sensitizer among the formaldehyde-releasers,
it is included on the T.R.U.E. test and has many alternative names
(see Table 3). 23

Occupational sources

Occupation is one of the biggest risk factors
for quaternium-15 exposure.
Occupations such as hair dressing, painting, printing, textile dyeing,
paper processing and working with disinfectants all have greater risks
of developing allergies to quaternium-15, according to Haz-Map,
an organization that evaluates occupational risks for exposures to
hazardous chemicals.

Formaldehyde is both an irritant and a contact allergen.

Contact urticaria and anaphylaxis to formalin have been described
in a patient after a root canal and in a hemodialysis patient,
respectively
(see list of systemic formaldehyde effects in Table 4). 28,33

Garment industry workers, hemodialysis nurses, embalmers,
pathologists, and dermatologists are at great occupational risk for
occupational-based formaldehyde allergy.

Due to the notoriety it has received as a potential carcinogen,
irritant,
and sensitizer, formaldehyde use in cosmetics
has significantly decreased. Notably, formaldehyde is prohibited
in cosmetics in Sweden and Japan. 22

Testing for Allergy to Formaldehyde and FRPs

Patch testing for formaldehyde, quaternium-15,
and p-tert-Butylphenol formaldehyde resin allergy
can be accomplished with the
Thin-layer Rapid Use Epicutaneous (T.R.U.E.) test
(sites 18, 21, and 13, respectively).

The T.R.U.E. test is the commercially available, globally used,
allergen screening system.

While it is widely used, the discrepancy in allergen prevalence and
uncertain relevance has led to scrutiny of its utility.

The T.R.U.E test contains 23 allergens and one negative control.

At best, the T.R.U.E test is a minimum screening tool because
it tests only 23 of the more than 3,700 possible allergens
that can cause allergic contact dermatitis.

Krob et al. recently demonstrated that nickel, thimerosal, cobalt,
fragrance and balsam of Peru are the most prevalent allergens
detected by the T.R.U.E. test, yet a significant number of relevant
allergens, not present on the T.R.U.E. test, are potentially missed
by this screening tool used alone. 34

Value of this Patient Case

Our patient underscores the importance of appropriate
patch testing and education

Once we identified the allergy to formaldehyde and quaternium-15,
we provided patient education materials regarding the common and
not-so-common locations of these chemicals and cross-reactors.

We also gave the patient information on avoidance
and safe alternatives (see Table 5).

Fortunately, with technical advances, this student completed the
anatomy section via electronic learning tools.

By avoiding formaldehyde, including anatomy lab,
FRP in her shampoo and cosmetics,
and aspartame in her diet,
this patient dramatically improved.

As with all contact dermatitides, the mainstay of treatment
for allergic contact dermatitis is avoidance.

References:

1. Valks R, Conde-Salazar L, Cuevas M.
Allergic contact urticaria from
natural rubber latex in healthcare and non-healthcare workers.
Contact Dermatitis 2004; 50(4): 222-4.

2. Warshaw E. Latex allergy.
Skinmed. 2003; 2(6): 359-66.

3. Mehta, Surjit S, Surjit R, Belum SN.
Cosmetic dermatitis current perspectives.
International Journal of Dermatology 2003; 42(7): 533-542.

4. Geist I.
Movers & Shakers Ron's $70 Million Sale.
Forbes Accessible on the Internet at:
http://www.forbes.com/realestate/200...105movers.html

5. Behravan, J., Bazzaz, Fazly & Malaekeh, P.
Survey of bacteriological contamination
of cosmetic creams in Iran (2000).
International Journal of Dermatology 2005; 44(6): 482-485.

6. Morse LJ, Williams HL, Grenn FP, et al.
Septicemia due to Klebsiella pneumoniae
originating from a hand cream dispenser.
New Engl J Med 1967; 277: 472-473.

7. Sasseville, D.
Hypersensitivity to preservatives.
Dermatologic Therapy 2004; 17: 251-263.

8. US Food and Drug Administration.
History of the FDA: The 1938 Food, Drug, and Cosmetic Act
Accessible on the Internet at:
http://www.fda.gov/oc/history/histor.../section2.html

9. Brief History of Beauty and Hygiene Products.
Accessible on the Internet at:
http://scriptorium.lib.duke.edu/adac...s-history.html

10. Cahill J, Nixon R
Allergic contact dermatitis to quaternium-15 in a moisturizing lotion.
Australasian Journal of Dermatology. 2005; 46(4): 284-285.

11. Formaldehyde Council.
Formaldehyde: A Brief History and Its Contributions to Society
and the U.S. Economy. Accessible on the Internet at: www.formaldehyde.org
2005.

12. Biography.ms.
Aleksandr Mikhailovich Butlerov. Accessible on the Internet at:
http://aleksandr-butlerov.biography.ms/

13. Formaldehyde its history, chemistry and uses.
Accessible on the Internet at:
http://www.chm.bris.ac.uk/webproject...ome%20page.htm

14. Bedino JH.
Formaldehyde Embalming Sprays: A Modern Myth.
In: The Expanding Encyclopedia of Mortuary Practices.
Champion Company; Springfield, OH: 2001.

15. Chase M.
The Barbary Plague.
Random House; New York, NY: 2003.

16. British Plastics Federation.
History of Plastics. Accessible on the Internet at:
http://www.bpf.co.uk/bpfindustry/His...f_Plastics.cfm.

17. Plastics Historical Society.
Casein.
Accessible on the Internet at:
http://www.plastiquarian.com/casein2.htm

18. Cook P, Sleeker C.
Bakelite, An Illustrated Guide to Collectible Bakelite Objects.
Chartwell Books; Secaucus, New York: 1992.

19. Bakelite Museum. Accessible on the Internet at:
http://www.bakelitemuseum.co.uk/

20. Wikedia.
Formica (plastic).
Accessible on the Internet at:
http://en.wikipedia.org/wiki/Formica_(plastic)

21. The Bandalasta Web site.
Accessible on the Internet at:
http://www.bandalasta.com/

22. Hill AM, Belsito DV.
Systemic contact dermatitis of the eyelids
caused by formaldehyde derived from aspartame.
Contact Dermatitis. 2003; 49(5): 258-259.

23. Marks JG, Belsito DV, DeLeo VA, et al.
North American Contact Dermatitis Group
patch-test results, 1998-2000.
J Am Acad Dermatol 1998; 38: 9118.

24. Adams R M, Maibach H I.
A five-year study of cosmetic reactions.
J Am Acad Dermatol 1985; 13: 1062-1069.

25. Herbert, Courtney & Rietschel, Robert L.
Formaldehyde and formaldehyde releasers:
How much avoidance of cross-reacting agents is required?
Contact Dermatitis 2004; 50(6): 371-373.

26. Fowler JF, Jr, Skinner SM, Belsito DV.
Allergic contact dermatitis from
formaldehyde resins in permanent-press clothing.
An underdiagnosed cause of generalized dermatitis.
J Am Acad Dermatol 1992; 27: 962-968.

27. Restani P, Campagner P, Fiecchi A, et al.
Identification of spinacine as the principal reaction product of
gamma-casein with formaldehyde in cheese.
Food Chem Toxicol. 1988; 26(5): 441-6.

28. Food Standards Agency.
Analysis of formaldehyde in shiitake mushrooms
(2004) Accessible on the Internet at:
www.food.gov.uk/science/research/researchinfo/
foodcomponentsresearch/phytoestrogensresearch/
t05-t06programme/t05t06projectlist/t05027project/

29. Food and environmental Hygiene department.
The Government of Hong Kung
special administration region. Accessible on the Internet at:
http://www.fehd.gov.hk/safefood/repo...maldehyde.html

30. Agency for Toxic Substances and Disease Registry.
Medical Management Guidelines (MMGs) for Formaldehyde
(HCHO) on the Internet at:
http://www.atsdr.cdc.gov/MHMI/mmg111.html

31. Andersen K, White I, Goossens A.
Allergens from the Standard Series.
In: Rycroft R, Menne T, Frosch P, Lepoittevin JP (eds)
Textbook of Contact Dermatitis. 3rd ed.
Springer-Verlag: New York: 2001.

32. De Groot A, White I.
Cosmetics and Skin Care Products.
In: Rycroft R, Menne T, Frosch P, Lepoittevin JP (eds)
Textbook of Contact Dermatitis. 3rd ed.
Springer-Verlag: New York: 2001.

33. Kitagawa T, Katoh N, Yasuno H, Wakamori T.
A case of contact urticaria syndrome due to formalin
in root-canal dental paste (2001). Accepted for publication:
Accessible at:
http://www.fujita-hu.ac.jp/JSCD/all_...f/83-14601.pdf

34. Krob HA, Fleischer AB, D'Agostino R, et al.
Prevalence and relevance of contact dermatitis allergens:
a meta-analysis of 15 years of published T.R.U.E. test data.
J Am Acad Dermatol. 2004; 51(3): 349-53.
__________________________________________________ __



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.: eye 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
__________________________________________________ __


"It is generally recommended that exposure to products containing
formaldehyde, FRP's, and aspartame (NutraSweet) be avoided
in children."

"Through metabolism, aspartame is converted metabolically
in the liver to methanol,
which is in turn metabolized to formaldehyde. 8"


http://www.pediatricannalsonline.com....asp?rID=21306

Avoiding formaldehyde allergic reactions in children
Pediatric Annals. 2007 Jan.; 36(1): 55-6. PMID: 17269284

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;
__________________________________________________ __



On Jun 27, 4:34*pm, Mąck©® <I...@OneWithTheGoddess.org> wrote:
> No sane person takes anything rich murray has to say as valid.
> Everyone already knows he is a nutball troll.
>
> On Fri, 27 Jun 2008 10:19:02 -0700 (PDT), psevetson
>
> <psevet...@gmail.com> wrote:
> >This article, published in 1999 in _the Lancet_, should also be read
> >by anyone concerned about the supposed toxicity of aspartame.

>
> >http://www.aspartame.net/rumors/Aspa...e_Internet.asp

>
> >On Jun 27, 12:54*am, Rich Murray <rmfor...@comcast.net> wrote:
> >> Aspartame Induced Arrhythmias and Sudden Death, HJ Roberts 2004:
> >> Murray 2008.06.26http://rmforall.blogspot.com/2008_06_01_archive.htm
> >> Thursday, June 26, 2008http://groups.yahoo.com/group/aspartameNM/message/1544

> >[due to size, original posting is snipped]

__________________________________________________ __

Reply With Quote
  #5  
Old 06-28-2008, 09:11 AM
Nico Kadel-Garcia
Guest
 
Posts: n/a
Default Re: Aspartame Induced Arrhythmias and Sudden Death, HJ Roberts 2004:Murray 2008.06.26

Rich Murray wrote:
> http://www.aspartame.net/rumors/Aspa...e_Internet.asp
>
> ©Ajinomoto Food Ingredients LLC
>
> Aspartame and the Internet
>
> The following letter appeared in The Lancet on 3 July 1999. It is
> reproduced here with the permission of the publishers of this
> respected journal.
>
> Sir - Patients at our diabetes clinic have raised concerns about
> information on the internet about a link between the artificial
> sweetener aspartame and various diseases.
>
> Our research revealed over 6000 web sites that mention aspartame, with
> many hundreds alleging aspartame to be the cause of multiple
> sclerosis, lupus erythematosis, Gulf War Syndrome, chronic fatigue
> syndrome, brain tumours, and diabetes mellitus, among many others.


Yes, of those over 6000, probably 5000 mention its uses in food recipes. The a
few of those 'hundreds' are Betty Martini, an even smaller number are you, and
the rest are people directly refuting and making fun of you.
Reply With Quote
  #6  
Old 06-29-2008, 02:29 PM
Rich Murray
Guest
 
Posts: n/a
Default Re: Aspartame Induced Arrhythmias and Sudden Death, HJ Roberts 2004:Murray 2008.06.26

Re: Aspartame Induced Arrhythmias and Sudden Death, HJ Roberts 2004:
Murray 2008.06.26 -- as an unqualified medical layman, since 1999 I
quote directly from abstracts and full texts of mainstream medical
research -- please copy to me any specific full texts that actually
refute the details of any of my 1544 reviews, using reason and
mainstream research: Nico Kadel-Garcia: Rich Murray 2008.06.28
__________________________________________________ __


methanol impurity in alcohol drinks [ and aspartame ] is turned into
neurotoxic formic acid, prevented by folic acid, re Fetal Alcohol
Syndrome,
BM Kapur, DC Lehotay, PL Carlen at U. Toronto, Alc Clin Exp Res 2007
Dec.
plain text: detailed biochemistry, CL Nie et al. 2007.07.18: Murray
2008.02.24
http://rmforall.blogspot.com/2008_02_01_archive.htm
Sunday, February 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1524

[ Rich Murray comments: As a medical layman volunteer information
activist for aspartame and related toxicity issues since January 1999,
I note with appreciation the remarkable exponential progress on all
fronts, including a rapidly emerging consensus about the primary
importance of all toxicity challenges for our world.

This lengthy review features in detail two quite different,
revolutionary
contributions, from Canada, and England and China.

It is indicative of our times that the CL Nie et al. study, 2007
appears in a free, open access journal-- indeed,
as all life and death information must.

Following rather vigorously, indeed blindly, the imperatives of
single-minded, profit-driven capitalist competition -- manipulating
adroitly research, education, media, citizens, governments -- many
great global corporations have inevitably created results that
oppose the common good. Alcohol and tobacco are well known.

Realistically, any further manipulations can only lead to inevitable
and even sudden corporate meltdowns, in the context of an
unfettered, cooperative, democratic global information forum,
the Internet.

Now, it is as easy and cheap to compose and instantly post a
30-page review as 3 pages a decade ago -- and such reviews
are archived forever in multiple collections, open via global search
engines to a billion Net citizens.

Perforce, and increasingly happily, all societal entities will have to
operate by high and shared voluntary universal standards
for the common good. ]


http://www.blackwell-synergy.com/doi...7.2007.00541.x

Alcoholism: Clinical and Experimental Research
Volume 31 Issue 12 Page 2114-2120, December 2007

Bhushan M. Kapur, b.kapur@utoronto.ca;
Arthur C. Vandenbroucke, PhD, FCACB
Yana Adamchik,
Denis C. Lehotay, dlehotay@health.gov.sk.ca;
Peter L. Carlen carlen@uhnres.utoronto.ca;
(2007) Formic Acid, a Novel Metabolite of Chronic Ethanol
Abuse, Causes Neurotoxicity, Which Is Prevented by Folic Acid
Alcoholism: Clinical and Experimental Research 31 (12), 2114-2120.
doi:10.1111/j.1530-0277.2007.00541.x

Abstract

Background:
Methanol is endogenously formed in the brain and is present as a
congener in most alcoholic beverages.

Because ethanol is preferentially metabolized over methanol (MeOH)
by alcohol dehydrogenase, it is not surprising that MeOH
accumulates in the alcohol-abusing population.

This suggests that the alcohol-drinking population will have higher
levels of MeOH's neurotoxic metabolite, formic acid (FA).

FA elimination is mediated by folic acid.

Neurotoxicity is a common result of chronic alcoholism.

This study shows for the first time that FA,
found in chronic alcoholics, is neurotoxic
and this toxicity can be mitigated by folic acid administration.

Objective:
To determine if FA levels are higher in the alcohol-drinking
population and to assess its neurotoxicity in organotypic
hippocampal rat brain slice cultures.

Methods:
Serum and CSF FA was measured in samples from both ethanol
abusing and control patients, who presented to a hospital emergency
department. [ CSF = Cerebral Spinal Fluid ]

FA's neurotoxicity and its reversibility by folic acid were assessed
using organotypic rat brain hippocampal slice cultures using
clinically
relevant concentrations.

Results:
Serum FA levels in the alcoholics
(mean ± SE: 0.416 +- 0.093 mmol/l, n = 23)
were significantly higher than in controls
(mean ± SE: 0.154 +- 0.009 mmol/l, n = 82) (p < 0.0002).

FA was not detected in the controls' CSF (n = 20),
whereas it was >0.15 mmol/l in CSF of 3 of the 4 alcoholic cases.

Low doses of FA from 1 to 5 mmol/l added for 24, 48 or 72 hours
to the rat brain slice cultures caused neuronal death as measured by
propidium iodide staining.

When folic acid (1 umol/l) was added with the FA,
neuronal death was prevented. [ umol = micromole ]

Conclusions:
Formic acid may be a significant factor in the neurotoxicity of
ethanol abuse.

This neurotoxicity can be mitigated by folic acid administration
at a clinically relevant dose.

Key Words:
Formic Acid, Folic Acid, Methanol, Neurotoxicity, Alcoholism.

From the Department of Clinical Pathology (BMK),
Sunnybrook Health Science Centre,
Division of Clinical Pharmacology and Toxicology,
The Hospital for Sick Children, Toronto, Ontario, Canada;

St. Michael's Hospital (ACV), Toronto, Canada;

Department of Laboratory Medicine and Pathobiology
(BMK, ACV), Faculty of Medicine,
University of Toronto, Toronto, Ontario, Canada;

Departments of
Medicine (Neurology) and Physiology (YA, PLC),
Toronto Western Research Institute,
University of Toronto, Toronto, Ontario, Canada;

and University of Saskatchewan (DLC), Saskatchewan, Canada.

Received for publication May 1, 2007;
accepted September 24, 2007.

Reprint requests: Dr. Bhushan M. Kapur,
Department of Clinical Pathology,
Sunnybrook Health Science Centre,
2075 Bayview Ave, Toronto, Ontario, M4N 3M5, Canada;
Fax: 416-813-7562; E-mail: b.kapur@utoronto.ca;

Copyright 2007 by the Research Society on Alcoholism.
DOI: 10.1111/j.1530-0277.2007.00541.x
Alcoholism: Clinical and Experimental Research 2007 Dec.
Alcohol Clin Exp Res, Vol. 31, No 12, 2007: pp 2114-2120

NEUROTOXICITY AND BRAIN damage are common
concomitants findings of chronic alcoholism
(Carlen and Wilkinson, 1987; Carlen et al., 1981; Harper,
2007).

The cause of ethanol-induced neurotoxicity is still unclear.

We present here a novel hypothesis for neurotoxicity:
increased formic acid (FA) levels produced from methanol
(MeOH), whose catabolism is blocked by ethanol.

Axelrod and Daly (1965) demonstrated the endogenous formation
of MeOH from S-adenosylmethionine (SAM) in the pituitary
glands of humans and various other mammalian species.

Presence of MeOH in the breath of human subjects was
reported by Ericksen and Kulkarni (1963).

Most alcoholic beverages also have a small amount of MeOH
as a congener (Sprung et al., 1988).

As ethanol (EtOH) has a higher affinity for
alcohol dehydrogenase (ADH) than MeOH,
EtOH is preferentially metabolized (Mani et al., 1970).

As a result, MeOH accumulation from endogenously produced
MeOH, and/or, that consumed as part of an alcoholic beverage,
has been reported in concentrations up to 2 mmol/l in heavy
drinkers (Majchrowicz and Mendelson, 1971).

Toxicity resulting from MeOH consumption is extensively
documented in both humans and animals and has been
attributed to its metabolite, FA (Benton and Calhoun, 1952;
Roe, 1946, 1955; Wood, 1912; Wood and Buller, 1904).

The rate of formate oxidation and elimination is dependent on
adequate levels of hepatic folic acid, particularly hepatic
tetrahydrofolate (THF)
(Johlin et al., 1987; Tephly and McMartin, 1974).

Significantly higher formate levels were obtained when
folate-deficient animals were exposed to MeOH as compared
with folate-sufficient animals (Lee et al., 1994;
McMartin et al., 1975; Noker et al., 1980).

To understand ethanol's toxicity, one must consider FA
produced from MeOH, and its elimination mediated by folic acid.

We postulate that in the chronically drinking patient,
we will find higher levels of FA than in the nondrinking population,
and that formate is neurotoxic.

We also hypothesize that treatment with folic acid, which is a
critical factor in the catabolism of FA, can prevent or
diminish FA neurotoxicity.....

DISCUSSION

There are at least 2 sources of MeOH: