Scientific Abuse in Parkinson's Disease Research Related to Aspartame
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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 Mission Possible International and the
Aspartame Consumer Safety Network.
These organizations have received numerous case reports of aspartame worsening
Parkinson's Disease patients (Martini 1995, 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 aspertane (Nutrasweet) or any food or beverage
containing it due to what I have seen as side effects in patients with
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:
- 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
- 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!
- 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 authos 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
Whenever one sees statements implying that aspartame is "safe" in 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.
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,
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.
Martini, Betty, 1995. Conversations between Betty Martini of Mission Possible and Mark D. Gold.
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.