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Tuesday, January 21, 2014

Scientific Abuse in Parkinson's Disease Research Related to Aspartame:
Summary of Aspartame and Parkinson's Disease Issue

Severe adverse effects of regular aspartame use by Parkinson's Disease
patients has not been reported in the scientific literature. However,
researchers and physicians know that case histories are rarely reported in
the scientific literature, but instead, reported to the U.S. Food and Drug
Administration and to independent organizations such as the Aspartame Consumer Safety Network. These
organizations have received numerous case reports of aspartame worsening
Parkinson's Disease patients  (Stoddard 1995). In addition,
professionals familiar with aspartame use and Parkinson's Disease have
reported adverse effects (Morris 1995):

 "[At] the state psychiatric hospital where I worked in quality assurance
  the psychiatrists [stated] that patients exhibiting Parkinsonian tremors
  should not receive any food or beverage containing Nutrasweet as it
  increased the tremors.
  ....
 "I NEVER use aspertame (Nutrasweet) or any food or beverage
  containing it due to what I have seen as side effects in patients with
  Parkinsonian tremors."

The adverse effects of aspartame on Parkinson's Disease patients may be
due to the damaging effects of aspartame-released excitotoxins in
combination with the formaldehyde metabolite. Excitotoxins have been
implicated in the development and worsening of Parkinson's Disease
symptoms (Blaylock 1994, Choi 1992, Kurland 1988). [Note: Scientific abuse
related to excitotoxins and aspartame will be discussed in another
chapter.] Formaldhyde would be expected to exacerbate the toxic effects of
the excitotoxins and discussed in the Methanol / Formaldehyde Research
section.

Another theory as to adverse effects of aspartame on Parkinson's Disease
patients has been put forth by Pardridge (1986):

 "Blockade of the therapeutic effects of some drugs would also be a
  complication associated with hyperphenylalaninemia. The on-off effects
  seen in L-DOPA therapy of Parkinson patients have been attributed to
  the effects of the amino acids in dietary protein on L-DOPA uptake
  into the brain [Nutt 1984]. Since L-DOPA, a neutral amino acid, is
  transported into the brain on the same phenylalanine transport system
  [Wade 1975], it would be expected that L-DOPA levels in the brain are
  inversely related to plasma neutral amino acid levels."

Because the phenylalanine from aspartame is in free-form (unbound to
protein), it is absorbed suddenly and can spike the blood plasma levels of
phenylalanine (Caballero 1986, Matalon 1988, Stegink 1987). Pardridge's
theory is that this sudden rise in phenylalanine levels interferes with
L-DOPA used to treat Parkinson's Disease. Unfortunately, Dr. Pardrige was
(like many others) fooled by flawed and nearly fraudulent industry
research related to methanol and excitotoxins.

There is admitedly a lack of long-term research on the effects of
aspartame on Parkinson's Disease patients. But given the exposure to
formaldehyde, free-form excitotoxic amino acids, and free-form
phenylalanine, there is plenty of reasons for Parkinson's Disease patients
to avoid aspartame until long-term independent research is performed.


Meaningless Industry Research

Industry research (Karstaedt 1993) has concluded that:

 "Aspartame consumption in amounts well in excess of what would be
  consumed by heavy users of aspartame-sweetened products has no
  adverse effects on PD [Parkinson's Disease] patients."

It sounds very convincing until the study is examined and it becomes clear
that the researchers were not testing anything related to aspartame
toxicity. The researchers were not even testing their own hypothesis
because of the severely-flawed study deisgn.

Karstaedt (1993) flaws:

 1. The study lasted only one day. It is difficult to imagine how any
    researcher could proclaim the safety of aspartame after a single day
    test. It has been known for many years that the neurological effects
    of aspartame usually take medium-term or long-term use to appear in
    patients (CDC 1984, Roberts 1988). This proves that they were not
    testing adverse effects as they happen in the real world.

 2. The aspartame was given in capsules. Capsule administration of
    aspartame has been proven to eliminate the sudden absorption of the
    aspartame breakdown products (Stegink 1987). This is particularly
    disturbing because the researchers were attempting to test whether the
    spike of plasma phenylalanine levels (normally seen from aspartame
    consumption) affects Parkinson's Disease patients. Yet they
    administered aspartame in such a way as to eliminate the plasma
    phenylalanine spike!

 3. The authors claim that a high dose of aspartame was administered. In
    reality, the dose was approximately 20-40% of the FDA acceptable
    daily intake of 50 mg/kg/day. The dose given in this experiment been
    shown to be equaled or exceeded on a daily basis by regular users
    (CDC 1984, Frey 1976, Porikos 1984). The authors based their estimate
    of a high dose on a projected estimate of daily intake published
    shortly after aspartame was approved for use in carbonated beverages
    (Roak-Folz 1984).

Whenever one sees statements implying that aspartame is "safe" for
Parkinson's Disease patients, it should be understood that such statements
are based soley on this single-day, poorly-designed study. People who cite
this study as evidence of aspartame's "safety" are usually either
Monsanto/NutraSweet consultants or persons completely unfamiliar with the
scientific literature.

References

Blaylock, Russell L., 1994. "Excitotoxins: The Taste That Kills," Health
Press, Santa Fe, New Mexico, c1994.

Caballero, Benjamin, et al., 1986. "Plasma Amino Acid Levels After
Single-Dose Aspartame Consumption in Phenylketonuria, Milk
Hyperphenylalaninemia, and Heterozygous State for Phenylketonuria,"
Journal of Pediatrics, Volume 190, No. 4, page 668-671.

CDC 1984. "Evaluation of Consumer Complaints Related to Aspartame Use,"
Division of Nutrition, Center for Health Promotion and Education, Centers
for Disease Control, Atlanta, GA 30333, November 1984.

Choi, Dennis W., 1992. "Amyotrophic Lateral Sclerosis and Glutamate -- Too
Much of a Good Thing," Science, Volume 326, No. 22, page 1493-1495.

Frey, Gunther H., 1976. "Use of Aspartame By Apparently Healthy Children
and Adolescents," Journal of Toxicology and Environmental Health, Volume
2, page 401-415.

Karstaedt, Patricia, Jonathan Pincus, 1993. "Aspartame Use in Parkinson's
Disease," Neurology, Volume 43, pages 611-613.

Kurland, L.T., 1988 "Amyotrophic Lateral Sclerosis and Parkinson's Disease
Complex on Guam Linked to an Environmental Neurotoxin," Trends in
Neuroscience, Volume 11, page 51-54.

Matalon, Reuben, et al., 1988. "Aspartame Consumption in Normal
Individuals and Carriers for Phenylketonuria (PKU)," Presented at "Dietary
Phenylalanine and Brain Function." Proceedings of the First International
Meeting on Dietary Phenylalanine and Brain Function, Washington, D.C., May
8-10, 1987. Center for Brain Sciences and Metabolism Charitable Trust,
P.O. Box 64, Kendall Square, Cambridge, MA 02142. Reprinted in "Dietary
Phenyalalnine and Brain Function," c1988, Birkhauser, Boston, MA USA, page
41-52.

Morris, Rosemary, 1995. Post to USENET Group sci.med.nutrtion on July 5,
1995. Found on the Internet at:
http://x16.dejanews.com/getdoc.xp?AN=105653826&CONTEXT=917226403.236126282&hitnum=1

Nutt, J.G., et al. 1984. "The 'on-off' Phenomenon in Parkinson's Disease.
Relation to Levodopa Absorption and Transport," New England Journal of
Medicine, Volume 310, pages 483-488.

Pardridge, William M., 1986. "Potential Effects of the Dipeptide Sweetener
Aspartame on the Brain," In "Nutrition and the Brain, Volume 7," Edited by
R.J. Wurtman and J.J. Wurtman, Raven Press, New York, c1986, page 199-241.

Porikos, Katherine P., Theodore B. Van Italie, 1984. "Efficacy of
Low-Calorie Sweeteners in Reducing Food Intake: Studies with Aspartame"
IN Stegink, L., Filer L., 1984. "Aspartame: Physiology and Biochemistry,"
Marcel Dekker, Inc., N.Y., page 273-286.

Roak-Foltz, R., Leveille, G., 1984. "Projected Aspartame Intake: Daily
Ingestion of Aspartic Acid, Phenylalanine, and Methanol," in Stegink, L.,
Filer L., 1984. "Aspartame: Physiology and Biochemistry," Marcel Dekker,
Inc., N.Y.

Roberts, H.J., 1988. "Reactions Attributed to Aspartame-Containing
Products:  551 Cases," Journal of Applied Nutrition, Volume 40, page
85-94.

Stegink, Lewis D., et al. 1987. "Plasma Amino Acid Concentrations in
Normal Adults Administered Aspartame in Capsules or Solution: Lack of
Bioequivalence," Metabolism, Volume 36, No. 5, page 507-512.

Stoddard, Mary Nash, 1995. Conversations between Mary Nash Stoddard of the
Aspartame Consumer Safety Network and Mark D. Gold.

Wade, L.A., R. Katzman, 1975. "Rat Brain Regional Uptake and
Decarboxylation of L-DOPA Following Carotid Injection," American Journal
of Physiology, Volume 228, page 352-359.



From: Mark D. Gold
      Aspartame Toxicity Information Center
      12 East Side Dr., Suite 2-18
      Concord, NH 03301
      603-225-2110


Date: January 12, 2002

Please find below Evidence File #6: Aspartame & Parkinson's Disease

From: Mark Gold [mgold@shelltown.net]
Sent: Sunday, January 12, 2003 11:14 PM
To: fdadockets@oc.fda.gov
Subject: Docket # 02P-0317 Recall Aspartame as a Neurotoxic Drug: File
#6: Aspartame and Parkinson's Disease

Subject: Docket # 02P-0317

To: FDA Dockets Submittal