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Remove _pooperscooper_ from email if you reply

Disclaimer: "I don't know what I'm talking about. I just read some stuff off
the Internet." If there is irrefutable proof that the below is a bunch of
bs, please let me know.

According to http://www.holisticmed.com/aspartame/abuse/seizures.html
Shaywitz's and Trefz's work was part of "Hopelessly Flawed Double-Blind
Studies Funded by Monsanto/NutraSweet", and there are important points as to
why it was flawed, including the fact that the children were already on
anti-seizure medication while they were being administered Aspartame....

Shaywitz (1994) concludes that "our findings indicate that, in this group of
vulnerable children, APM [aspartame] does not provoke seizures." Rowen
(1995) concludes that "aspartame, in acute dosage of ~50 mg/kg, is no more
likely than placebo to cause seizures in individuals who reported that their
seizures were provoked by aspartame consumption." Trefz (1994) reports that
doses of 15 mg/kg and 45 mg/kg of aspartame in PKU heterozygotes does not
change EEG spectral parameters. (The Trefz (1994) study appears to have been
published in summary form as Benninger (1991), Benninger (1993a) and
Benninger (1993b) ). Others have cited these studies as evidence that
aspartame does not cause seizures (Lajtha 1994, Butchko 1994).

These results appear very convincing, but these industry-sponsored studies
are so flawed so as to be nearly worthless. Below are a selection of major
problems with these studies.

Rowen (1995) Flaws

 a.. 16 of the 18 subjects were taking anti-seizure medication during the
study.

 b.. The aspartame was given in capsules so that instead of spiking the
plasma phenylalanine level and significantly changing the phenylalanine/LNAA
ratio the phenylalanine was absorbed very slowly -- more like what happens
when ingesting food (Stegink 1987). These researchers discussed in detail
the issue of plasma phenylalanine and LNAA levels. It was particularly
absurd is that they gave the aspartame in capsules even though they cited
industry research (Burns 1990) which proves capsule administration of
aspartame eliminates the spike in plasma phenylalanine levels! Simply
stated, the researchers were pretending to test the hypothesis that
phenyalalnine/LNAA ratio changes would cause seizures, but they knowingly
administered aspartame in a way that eliminated the possibility of a large
change in plasma phenylalanine levels and phenylalanine/LNAA ratios.

 Capsule administration of aspartame slows the absorption of methanol and
may reduce its toxicity somewhat similar to the way ingestion of food with
methanol may slightly reduce its toxicity (Posner 1975). Capsule
administration of aspartame also eliminates the quick absorption of the
excitotoxin, aspartic acid (Stegink 1987). When aspartic acid is absorbed
quickly, it can be excitotoxic (Blaylock 1994, Olney 1980) especially in
conjunction with formaldehyde derived from methanol as discussed in the
Methanol article.

 c.. The study consisted of only single dose of aspartame ingestion!

This results of this study only apply to people who ingest a single dose of
encapsulated aspartame while taking anti-seizure medication. Not only is
this study worthless, but key information was not put in the abstract,
namely, the fact that the subject were on anti-seizure medication and that
the aspartame was given in capsules.

Shaywitz (1994) Flaws

 a.. Nine out of 10 children were taking anti-seizure medication during the
study.

 b.. Again the aspartame was given in capsules at a dose of 34 mg/kg per
day. This makes the experiment worthless since they were testing the
hypothesis of changes in plasma phenylalanine to LNAA ratios as described
above. It also reduces the toxicity of other aspartame breakdown products as
described above.

 c.. The experiment lasted only two weeks. The Rowen (1995) study used
individuals who had experienced aspartame-induced seizures and it was only
one day long (with other flaws described above). This short study used
epileptic children who had not reported aspartame-induced seizures. A cynic
might wonder if the researchers were able to make this study slightly longer
than the Rowen (1995) study because the subjects had not reported
aspartame-induced seizures.

Trefz (1994) Flaws

 a.. Like the other studies, aspartame was given in slow-dissolving
capsules despite the fact that the researchers were claiming to test the
effects of the spike in phenylalanine levels and the change in phenylalanine
to LNAA ratios.

 b.. The aspartame was given with meals which would further slow the
absorption of aspartame breakdown products.

 c.. This study was longer than the others, ~ 3 months. However, an
analysis of seizure cases by the U.S. Centers for Disease Control (CDC 1984)
shows that most seizures linked to aspartame do not begin to appear until
after 3 or more months of real-world (i.e., non-encapsulated) aspartame.

What did industry scientists know or should have known?

 1.. These researchers must have known that administering the aspartame in
capsules would mean that they were not testing the phenylalanine and LNAA
changes as they claimed.

 2.. The researchers should have known that given encapsulated aspartame
would reduced the toxicity of the methanol and the excitotoxic amino acid.

 3.. These researchers must have known that allowing the subjects to take
anti-seizure medication during the study would drastically reduce the
liklihood of seizures.

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FDA Gift to Monsanto
In 1992, the FDA published an analysis of reports of seizures associated
with consumption of aspartame (Tollefson 1992). The report concludes:

 "In most cases, information obtained from the complaintants' medical
records as well as data on consumption patterns, temporal relationships, and
challenge tests did not support the claim that the occurrences of the
seizures were linked to consumption of aspartame."

Monsanto scientists repeated the FDA conclusion in their postmarketing
surveillance report published in 1994 (Butchko 1994). Shaywitz (1994) also
used this FDA report to bolster their conclusion.

What they do not mention is that this FDA analysis has major flaws and is
provably biased, rendering it useless.

A short summary is in order for those who have not yet read the History of
Aspartame Frequently Asked Questions (FAQs) report. During the FDA approval
process, a number of government officials were rewarded with jobs connected
to the aspartame industry (GAO 1986). This included two US Attorneys
investigating the manufacturer for pre-approval research fraud who were
hired by the manufacturer's law firm (one during the investigation itself).
The Director of the FDA's Bureau of Foods was given a job as the Vice
President of the National Soft Drink Associaton (GAO 1986). The FDA
Commissioner was rewarded with a high-paying consulting position with the
public relations company of the manufacturer (Burston Marsteller) not long
after approving aspartame (GAO 1986). After these and other employees were
given jobs related to the aspartame industry, the FDA supported the
manufacturer unconditionally. The FDA redirected aspartame reaction reports
to the AIDS Hotline (Turner 1987). In addition, the FDA told its regional
offices to not report aspartame toxicity reactions to the Washington, D.C.
headquarters (CNI 1984). The extreme FDA bias continues to this day leading
some people to refer to the FDA as a Monsanto subsidiary.

Tollefson (1992) Flaws

 a.. Tollefson inappropriately classified seizures as "Group D -- highly
unlikely" related to aspartame if the subjects refused to release their
medical records. This shows extreme bias as such cases would obviously be
more appropriately categorized in a "possible aspartame reaction" category
since the cases may or may not be caused by aspartame -- more information
was needed.

 b.. Tollefson inapropriately classified seizures as "Group D -- highly
unlikely" related to aspartame if there was any possible factor in the
patient's life that could have caused or contributed to those seizures. This
is akin as categorizing smoking or stress as "highly unlikely" for
contributing to heart disease if the patient eats a diet which could
contribute to heart disease! Clearly, these patients should have been
classified in a "possible aspartame reaction" category.

 c.. The authors inappropriately declared ineligable, 35% of the non-Group
D seizure victims because the seizures occured more than 13 hours after
ingestion of aspartame. This is absurd because 1) it is thought that
aspartame may lower the seizure threshold and therefore, aspartame-caused
seizures could occur long after phenylalanine levels return to normal; 2) an
animal study has shown that excitotoxins can accumulate in areas of the
brain not protected by the blood brain barrier and remain there for as much
as 24 hours (Inouye 1976); 3) formaldehyde adducts appear to accumulate from
aspartame ingestion (Trocho 1998); and 4) a journal article immediately
following this biased analysis, Carroll (1992), points out that food
reactions can be delayed up to 48 hours after ingestion!

 d.. The authors claim that only 251 cases of seizures due to aspartame
ingestion have been reported to the FDA. In reality, the FDA splits the
categories into: "Seizures and Convulsions," "Grand Mal," "Petit Mal,"
"Complex Partial Seizures," and "Simple Partial Seizures." The 251 cases
quoted by the authors referred only to the "Seizures and Convulsions"
category as of 1995. There have been over 500 seizures reported to the FDA
(DHHS 1995) at probably a reporting rate of far less 1% (Gold 1996) leading
to well over 50,000 cases of seizures which have already been linked to
aspartame consumption.

 e.. Even with the major flaws in classifying adverse reaction reports, 76
of 251 cases were still categorized as Group A and Group B meaning that a
rechallenge with aspartame lead to furthur seizures. Clearly, one cannot
possibly conclude that this analysis shows no link between aspartame and
seizures as implied in the abstract.

What is particularly disturbing about this analysis -- aside from its major
flaws -- is that independent research was totally ignored in favor of
aspartame industry-sponsored research. For example, the one-day industry
study of aspartame and headache (Schiffman 1987) was listed, but not the
much longer independent study (Koehler 1988). An aspartame
industry-sponsored International Workshop was cited (Dews 1987), but the
authors completely ignored an International Conference which invited both
independent and industry researchers and which focused largely on the
aspartame and seizure issue (Wurtman 1988). Most of the rest of the
citations are from publications of aspartame industry-funded scientists.

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Aspartame Industry Pumps Out Its Own Animal Research
Not surprisingly, the aspartame industry has its own selection animals
studies which claim that aspartame does not lower the seizure threshhold
(Cain 1989, Dailey 1987, Dailey 1988, Dailey 1989, Dailey 1991, Jobe 1988,
Lasley 1988, Meldrum 1988, Nevins 1986, Thai 1988, Tilson 1989). The
discussion sections of some of these studies and the review by Sze (1989)
points to the huge doses of aspartame in rodents needed to lower the seizure
threshold in many of the independent studies. The implication is that normal
doses of aspartame ingested by humans could not possibly cause lower the
seizure threshold.

What these researchers fail to mention is that Wurtman (1988) showed that it
takes approximately 60 times more phenylalanine given to rodents to cause
the changes in phenylalanine/LNAA ratio seen in humans. Therefore, the
aspartame doses given to the rodents in these experiments are really not
very high after adjusting for differences between rodent and human
metabolism. 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).

It is also not surprising that Monsanto/NutraSweet attempted to challenge
the Wurtman (1988) conclusion that it takes 60 times the dose of
phenyalanine given to rodents to change the phenylalanine to LNAA ratio
similar to what happens in humans (Hjelle 1992). The results in this study
are ridiculous and do not even come close to matching the results of other,
independent research (Perego 1988, Pinto 1988, Wurtman 1983, Yokogoshi
1984). The numerous studies that Hjelle (1992) claims their results are
similar to actually have results far different. This will be discussed in
more detail when the research abuses related to aspartame and phenylalanine
are looked at.

----------------------------------------------------------------------------
----

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