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From: Rich Murray <[EMAIL PROTECTED]>
Newsgroups: alt.health,alt.health.diabetes,alt.support.depression
Date: Fri, 23 Jun 2000 19:59:37 -0600
To: [EMAIL PROTECTED], [EMAIL PROTECTED], Alan Raetz
<[EMAIL PROTECTED]>, [EMAIL PROTECTED], [EMAIL PROTECTED],
[EMAIL PROTECTED]
Subject: Murray: Gold: Schiffman: Spiers: aspartame toxicity 2.18.00


Murray: Gold: Schiffman: Spiers: aspartame toxicity 2.18.00

N Engl J Med 1987 Nov 5;317(19):1181-5
Aspartame and susceptibility to headache.
Schiffman SS, Buckley CE 3d, Sampson HA, Massey EW, Baraniuk JN, Follett
JV, Warwick ZS
Department of Psychiatry, Duke University, Durham, N.C. 27710.

Dr. Susan S. Schiffman  Dept. of Psychiatry   Duke University
www.duke edu  [EMAIL PROTECTED]    919-684-3303, 660-5657.
She has over 100 obviously competent experimental studies and
reviews since 1971 in PubMed.  Her major field is the deterioration
of smell and taste in seniors and AIDS patients from exposure to
drugs, chemicals, and pollutants-- one wonders if she ever considered
the effects of aspartame, since smell and tase impairment are known to
result from exposure to aspartame or formaldehyde.

"Loss of taste" is one of 90 symptoms from many case reports of
aspartame toxicity, summarized in:
Department of Health and Human Services.  "Report on All Adverse
Reactions in the Adverse Reaction Monitoring System." (February 25
and 28, 1994).

Abstract (Schiffman et al, 1987):
We performed a double-blind crossover trial of challenges with 30 mg of
aspartame per kilogram of body weight or placebo in 40 subjects who
reported having headaches repeatedly after consuming products containing
aspartame. The incidence rate of headache after aspartame (35 percent)
was not significantly different from that after placebo (45 percent)
(P less than 0.50). No serious reactions were observed, and the
incidence of symptoms other than headache following aspartame was also
equivalent to that after placebo. No treatment-related effects were
detected in vital signs, blood pressure, or plasma concentrations of
cortisol, insulin, glucagon, histamine, epinephrine, or norepinephrine.
Most of the subjects were well educated and overweight and had a family
or personal history of allergic reactions. The subjects who had
headaches had lower plasma concentrations of norepinephrine (P less than
0.0002) and epinephrine (P less than 0.02) just before the development
of headache. We conclude that in this population, aspartame is no more
likely to produce headache than placebo.  PMID: 3657889, UI: 88014077

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

http://www.holisticmed.com/aspartame/abuse/migraine.html  :

"Scientific Abuse in Migraine/Headache Research Related to Aspartame":

"Other industry researchers have cited this study as evidence that
aspartame does not induce headaches (Butchko 1994, Leon 1989, Moser
1994). In addition, Yost (1989) claimed that aspartame is not more
likely to cause headache than placebo. Tollefson (1992) of the FDA
cited this Schiffman study as evidence that aspartame does not cause
headaches. (The Tollefson review was discussed in detail in the
Seizure Research Abuse section).

"What these researchers fail to mention is that the Schiffman (1987)
research is useless because of major design flaws. It is also
particularly troubling that none of the above-mentioned authors
cited the Koehler (1988) double-blind study!

"Before we discuss the major flaws of the Schiffman study, I will
present some background information.  The study was partially funded
by Monsanto/NutraSweet and conducted at the Searle Center at Duke
University. (G.D. Searle is owned by Monsanto.) Susan Schiffman
performed her research at the "Searle Center" at Duke University.
The Searle Center is under the guidance of William Anlyan, a former
G.D. Searle director. Schiffman is a former General Foods and G.D.
Searle consultant. The FDA helped design the study protocol.
[Gordon 1987, page 500 of US Senate 1987; Shapiro 1987, page 403
of US Senate 1987].)

"Schiffman (1987) major flaws:

  1.The aspartame was given for only one day.

  2.The aspartame was given in encapsulated form which would lower the
toxicity by eliminating the sudden absorption of the excitotoxic amino
acid and methanol (Stegink 1987). The absorption of the excitotoxin is
gradual, somewhat closer to what happens when ingesting food. The
methanol is absorbed more slowly and that may significantly reduce
toxicity as happens when food in the stomach slows methanol absorption
(Posner 1975).

  3.There was no baseline frequency of headaches determined before
administering aspartame or placebo.

"It is very important to note the main distinction between the Koehler
(1988) study and the Schiffman (1987) study. While both studies used
capsules, which would be expected to significantly reduce aspartame
toxicity, and both studies used subjects who claimed to have headaches
from aspartame, the Koehler (1988) study administered aspartame for
four weeks, while the Schiffman (1987) study administered the
aspartame for only one day!

"When one examines the double-blind studies funded by the aspartame
industry, a pattern develops.  Industry-supported research on subjects
who have reported serious reactions to aspartame is almost always
one day long and the aspartame is administered in capsules (e.g.,
Hertelendy 1993, Rowen 1995, Schiffman 1987). Industry-supported
research that lasts several weeks is usually performed on individuals
that might be expected to experience adverse reactions after at least
several months of aspartame use (e.g., Shaywitz 1994) or on individuals
even less susceptible to short-term aspartame toxicity, but where more
sensitive neurological tests were conducted (e.g., Spiers 1998). The
longer (but still relatively short) industry-supported research
(3-6 months) usually uses healthy subjects who would likely only
experience serious adverse reactions after many months or several
years of aspartame use (e.g., Leon 1989, Trefz 1994). While the length
of the study is not the only flaw in these industry-sponsored studies,
there appears to be an obvious pattern of exceptionally short studies
used on more susceptible subjects. It would appear that the
manufacturer funds research with protocol designs virtually guaranteed
to find no adverse reactions!" [end of Gold quote]

Am J Clin Nutr 1998 Sep; 68(3): 531-7
Aspartame: neuropsychologic and neurophysiologic evaluation of acute
and chronic effects.
Spiers PA, Sabounjian L, Reiner A, Myers DK, Schomer DL
Clinical Research Center, Massachusetts Institute of Technology,
Cambridge 02139, USA.
Paul A. Spiers  [EMAIL PROTECTED]  617-253-6797
and 978-887-6220  Neurological Associates
Donald L. Schomer, M.D., Assc. Prof. Neurology, Beth Israel Deaconess
Medical Center, Harvard Medical Sch., [EMAIL PROTECTED],
617-667-3999

This study, done on or before 1993, was described in an abstract in
1993: then Richard J. Wurtman, Ph.D., Director of the CRC, was
listed as an author, but not in 1998. It was paid for by NutraSweet
Co. It used 48 healthy college students, half male and half female in
each group of 24, high-dose and low-dose aspartame, also tested with
placebo and sucrose, who took 20 days each of daily aspartame, sucrose,
or placebo, and were tested clinically on the morning of the 20th day,
before the last dose.  The study is summarized by Schomer, Spiers, and
Sabounjian on pages 225-31 in "The Clinical Evaluation of a Food
Additive: Assessment of Aspartame," 1996, CRC Press, 308 pages, Ed. by
Tschanz C, Butchko H, Stargel WW, Kotsonis FN, all employees of
Monsanto/NutraSweet.

High-dose, 45, and low-dose, 15 mg/kg daily, groups had 24 subjects
each. The results showed that the total number of headaches was about
the same for low dose, sucrose, and placebo, at 11,14, and 11, but only
4 headaches for the 24 high-dose subjects in 20 days.  The probability
of this is not given.  The numbers for fatigue were 3, 4, 2, and 1,  for
nausea 1, 3, 4, and  1, for acne 1, 4, 3, and 2. For these 4 symptoms,
the most common reported, the high-dose group is far less than sucrose
or placebo.  This indicates that some sort of confounding processes were
indeed operating, and that the study is therefore meaningless, unless we
are to start proclaiming aspartame as the newest aspirin.

Wouldn't a few students simply stop taking pills, if they thought it
caused headache, and wouldn't they also start taking regular aspirin?
Wouldn't a few students continue their favored diet drinks and foods?
Wouldn't exposure to MSG, claimed by many researchers to have similar
toxic biochemistry and symptoms, also confound the results?  Only a few
malfunctions like this suffice to eliminate statistical significance in
a group of only 24.

"Complaints of adverse experiences were recorded in blinded fashion."
It is not clear whether a symptom log was kept on a daily basis, or
if symptoms were discussed only at day 10 and 20. The scientific
community should have access to the actual raw data for daily symptoms
for each subject.

"We were clearly able to distinguish the subjects in the high-dose
aspartame group when they received the aspartame treatment because
they had significantly elevated fasting plasma phenylalanine
concentrations (Figures 3 and 4)..."  This was about a 30% higher value
at 85 minutes after the 3 PM dose on day 10, compared to placebo or
sucrose.  Is this kind of rise seen from consumption of phenylalanine
in ordinary foods?

Since aspartame and its products, methanol, formaldehyde, and aspartic
acid are cumulative toxins, we would expect symptoms to increase over
the 20 days, and to continue afterwards when the subjects were given
sucrose and placebo.  Since vulnerability varies greatly, we would
expect a few subjects to be providing most of the symptoms.  It might
be illuminating to have the raw data on each of the subjects.

Moreover, when aspartame is given in capsules and at meals, then it
is released gradually into the body, along with foods that mitigate
its effects, while diet soda, the main source of aspartame, allows
aspartame to be absorbed quickly, often with little food.  In many
cases, symptoms may not develop until after months and years of daily
exposure, as in the case of tobacco.  Finally, the sample of 24 in
the high-dose group allows us to infer, at best, even if the study
had inpecably consistent results, that the incidence of harm within 3
weeks in healthy college students is perhaps less than 5 or 10% at
the 95% confidence level.
***********************************************************************

Rich Murray  Room For All  [EMAIL PROTECTED]
1943  Otowi Drive
Santa Fe, NM 87505  505-986-9103  505-920-6130
***********************************************************************






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