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Thursday, August 7, 2014

FROM #FDA DOCUMENT FILES (Washington DC) re: #ASPARTAME RECALL /#PARKINSON'S DISEASE RESEARCH

Date: January 12, 2002 
Please find below Evidence File #6: Aspartame & Parkinson's Disease
                  Scientific Abuse in Parkinson's                      Disease Research Related to                              Aspartame    Table of Contents           Summary of Aspartame Effects on Parkinson's Disease         Meaningless Industry Research         References    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 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 aspartame (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.
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Subject: Docket # 02P-0317  To: FDA Dockets Submittal  From: Mark D. Gold - Concord, NH
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Mary Nash Stoddard
marystod@airmail.net