Scientific Abuse in Seizure Research Related to Aspartame
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Summary of Aspartame-Induced Seizures Issue
As of 1995 more than 7% of the aspartame toxicity reactions reports sent to the U.S.
Food and Drug Administration (FDA) involve seizures and convulsions (DHHS 1995).
The FDA stopped accepting aspartame toxicity reaction reports
in 1995 (Food 1995). In a study looking at 551 aspartame reactors, Roberts (1988)
found that grand mal, petit mal, and absence seizures occurred in 18% of the
In 1986, Food and Chemical News reported that 80 cases of aspartame-induced
seizures had been reported to Dr. Richard Wurtman at M.I.T. (Food 1986). Dr.
Wurtman reported three cases in The Lancet (Wurtman 1985). Walton (1986, 1988)
published reports of nine cases of seizures linked to aspartame use.
Both the U.S. Air Force's magazine "Flying Safety" and the U.S. Navy's magazine,
"Navy Physiology" published articles warning about the many dangers
of aspartame including that the ingestion of aspartame may make pilots more
susceptible to seizures and vertigo (US Air Force 1992)
In an independent double-blind study of aspartame in children with generalized absence epilepsy,
Camfield showed that a single dose of 40 mg/kg of aspartame mixed in liquid exacerbated EEG
spike-wave discharge. The authors stated:
"Aspartame appears to significantly increase the duration of time that children with absence
epilepsy have spike wave on their EEG. In this study, the children spent 40% more time in
spike wave after aspartame than after sucrose."
The subjects were not on anti-seizure medication during the study. The authors called for a
longer study to be conducted.
I believe that the aspartame-induced seizures are at least partially caused by the
synergistic effects of
formaldehyde and excitotoxins derived from aspartame metabolism. However, many researchers
believe that the adverse neurological effects of aspartame may be at least partially due
to the phenylalanine derived from aspartame ingestion. 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).
This sudden "rush" of phenylalanine does not happen when ingesting food because protein is
broken down slowly and the phenylalanine is gradually absorbed. Nor does this phenylalanine
"rush" occur when ingesting aspartame in capsules (Stegink 1987).
Maher (1987) points out that increased levels of phenylalanine along with an increase ratio
of phenylalanine to other Large Neutral Amino Acids (LNAAs) can inhibit enzymes needed to
synthesize the neurotransmitters and diminish the production of brain catecholamines and
serotonin. The hypothesis is that this change in brain chemistry will lead to a lowering
of the seizure threshold and persons ingesting aspartame will become more susceptible to
Wurtman (1988) reviews the research to show that a dose of 60 times more aspartame is
needed for rodent studies to simulate the change in phenylalanine/LNAA ratio change
that occurs in humans. Based on these findings, several research teams have found that
aspartame lowers the seizure threshold in animals (Diomede 1991, Garrattini 1988, Guiso 1988,
Kim 1988, Maher 1987, Pinto 1986, Pinto 1988)
Hopelessly Flawed Double-Blind Studies Funded by Monsanto/NutraSweet
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
- 16 of the 18 subjects were taking anti-seizure medication during the study.
- 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.
- 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
- Nine out of 10 children were taking anti-seizure medication during the study.
- 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.
- 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
- 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.
- The aspartame was given with meals which would further slow the absorption of
aspartame breakdown products.
- 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?
- 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.
- The researchers should have known that given encapsulated aspartame would reduced the
toxicity of the methanol and the excitotoxic amino acid.
- These researchers must have known that allowing the subjects to take anti-seizure
medication during the study would drastically reduce the liklihood of seizures.
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
- 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.
- 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.
- 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!
- 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
- 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.
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,
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.
Benninger, C., P. Matthis, L.M.J. de Sonneville, et al. 1991. "High Dose Aspartame Has
No Effect on EEG Spectral Parameters in Phenylketonuric Heterozygotes (PKUH)," Society
for Neuroscience Abstracts, Volume 17, page 504.
Benninger, C., P. Matthis, L.M.J. de Sonneville, et al. 1993a. "Chronic High-Dose Aspartame
Ingestion Does Not Affect Electro-Encephalogram (EEG) Spectral Parameters in Phenylketonuric
Heterozygotes," Journal of Clinical and Experimental Neuropsychology, Volume 15, page 407
Benninger, C., et al., 1993b. "Electroencephalographic Evaluation of Chronic Aspartame Ingestion in
Phenylketonuric Heterozygoes (PKUH)," Electroencephalography and Clinical Neurolophysiology,
Volume 87, page S58.
Blaylock, Russell L., 1994. "Excitotoxins: The Taste That Kills," Health Press, Santa Fe,
New Mexico, c1994.
Butchko, Harriet, Frank Kotsonis, 1994. "Postmarketing Surveillance in the Food Industry:
The Aspartame Case Study," Nutritional Toxicology, edited by Frank Kotsonis, Maureen Mackey,
and Jerry Hjelle, Raven Press, Ltd., New York, pages 235-249.
Cain, D.P., et al., 1989. "Failure of Aspartame to Affect Seizure Susceptibility in Kindled Rats,"
Neuropharmacology, Volume 28, No. 4, pages 433-435.
Caballero, Benjamin, et al., 1986. "Plasma Amino Acid Levels After Single-Dose Aspartame
Consumption in Phenylketonuria, Milk Hyperphenylalaninemai, and Heterozygous State for
Phenylketonuria," Journal of Pediatrics, Volume 190, No. 4, page 668-671.
Camfield, PR, et al., 1992. "Aspartame exacerbates EEG spike- wave discharge in children with generalized absence
epilepsy: a double-blind controlled study." Neurology, Volume 42, page 1000-1003.
Carroll, Polly, Kelsy Caplinger, Gene France, 1992. "Guidelines for Counseling Parents of
Young Children with Food Sensitivities," Journal of the American Dietetic Association,
Volume 92, No. 5, page 602-603.
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,
CNI 1984. Letter from Rodney E. Leonard and James S. Turner of Community Nutrition
Institute (CNI) to Dr. Frank E. Young, Commissioner, Food and Drug Administration,
Reprinted in Congressional Record 1985b, page S10841.
Congressional Record 1985b. "Aspartame Safety Act," Congressional Record, Volume 131, No. 106,
August 1, 1985, page S10820-10847.
Dailey, J.W., S.M. Lasley, J. Frasca, P.C. Jobe, 1987. "Aspartame (APM) is Not Proconvulsant
in the Genetically Epilepsy-Prone Rat (GERP)," Pharmacologist, Volume 29, page 142.
Dailey, J.W., S.M. Lasley, A.F. Bettendorf, R.L. Burder, P.C. Jobe, 1988. "Aspartame Does
Not Facilitate Pentylenetetrazol Induced Seizures in Genetically Epilepsy Prone Rats,"
Epilepsia, Volume 29, page 651
Dailey, J.W., S.M. Lasley, P.K. Mishra, A.F. Bettendorf, R.L. Burger, P.C. Jobe, 1989. "Aspartame
Fails to Facilitate Pentylenetetrazol-Induced Convulsions in CD-1 Mice," Toxicology and Applied
Pharmacology, Volume 98, pages 475-486.
Dailey, J.W., S.M. Lasley, R. L. Burger, A.F. Bettendorf, P.K. Mishra, P.C. Jobe, 1991. "Aspartame
Failes to Facilitate Pentylenetetrazol-Induced Convulsions in CD-1 Mice," Toxicology and
Applied Pharmacology, Volume 98, pages 475-486.
Dews, P.B., 1987. "Summary Report of an International Aspartame Workshop," Food and Chemical
Toxicology, Volume 25, No. 7, pages 549-552.
DHHS 1995. Department of Health and Human Services. "Report on All Adverse Reactions in the
Adverse Reaction Monitoring System." (April 20, 1995).
Dietary Phenylalanine and Brain Function, 1987. 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,
Diomede, L., et al., 1991. "Interspecies and Interstrain Studies on the Increased Susceptibility
to Metrazol-Induced Convulsions in Animals Given Aspartame," Food and Chemical Toxicology,
Volume 29, pages 101-106.
Food 1986. Food Chemical News, July 28, 1986, page 44.
Food 1995. "Aspartame Adverse Reaction Reports Down in 1994 From 1985 Peak: FDA," Food
Chemical News, June 12, 1995, page 27.
GAO 1986. "Six Former HHS Employees' Involvement in Aspartame's Approval," United States
General Accounting Office, GAO/HRD-86-109BR, July 1986.
Garrattini, Silvo, et al., 1988. "Studies on the Susceptibility to Convulsions in Animals
Receiving Abuse Doses of Aspartame," 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 131-143.
Gold, Mark, 1996. "Reported Aspartame Toxicity Effects" (Referenced Analysis of Reported Toxicity
From Aspartame and Reporting Rate). Aspartame (NutraSweet) Toxicity Information Center Web Page,
Gordon, Gregory, 1987. "NutraSweet: Questions Swirl," UPI Investigative Report, 10/12/87.
Reprinted in US Senate (1987, page 483-510), page 497.
Guiso, G., et al. 1988. "Effect of Aspartame on Seizures in Various Models of Experimental
Epilepsy," Toxicology and Applied Pharmacology, Volume 96, No. 3, pages 485-493.
Inouye, M., 1976. "Selective Distribution of Radioactivity in the Neonatal Mouse Brain
Following Subcutaneous Administration of 14 C-Labeled Monosodium Glutamate,"
Congenital Anomolies (Journal Serial # 0914-3505, Japan), Volume 16, page 79-84.
Jobe, P.C., A.F. Bettendorf, S.M. Lasley, J.W. Daily, 1988. "Effects of Aspartame on
Pentylenetetrazol (PTZ)-Induced Convulsions in CD1 Mice," Toxicologist, Volume 8, page 85.
Kim, K.C., M.D. Tasch, S.H. Kim, 1988. "The Effect of Aspartame on 50% Convulsion Doses of
Lidocaine," 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 127-130.
Koehler, SM, A. Glaros, 1988. "The Effect of Aspartame on Migraine Headache," Headache,
Volume 28, page 10-14.
Lajtha, Abel, Margaret Reilly, David Dunlop, 1994. "Aspartame Consumption: Lack of Effects
on Neural Function," Journal of Nutritional Biochemistry, Volume 5, page 266-283.
Maher, Tomothy J., Richard Wurtman, 1987. "Possible Neurologic Effects of Aspartame, a Widely
Used Food Additive," Environmental Health Perspectives, Volume 75, page 53-57.
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.
Meldrum, B.S., N. Nanji, 1988. "Lack of Effect of Large Doses of Aspartame on Photically-Induced
Seizures in the Baboon (Papio papio)," FASEB Journal, Volume 2, page A434.
Nevins, M.E., S.M. Arnolde, H.J. Haigler, 1986. "Aspartame: Lack of Effect on Convulsant
Thresholds in Mice," Federal Proceedings, Volume 45, page 1096
Olney, John W., et al., 1980. "Brain Damage in Mice From Voluntary Ingestion of Glutamate and
Aspartate," Neurobehavioral Toxicology and Teratology, Volume 2, page 125-129.
Olney, John W., 1988. "Excitotoxic Food Additives: Functional Teratological Aspects,"
In Progress in Brain Research, Volume 73 -- Biochemical Basis of Functional Neuroteratology:
Permanent Effects of Chemicals on the Developing Brain, Edited by Boer, G.J., et al., Elsevier,
New York, c1988.
Perego, C., et al., 1988. "Aspartame and the Rat Brain Monoaminergic System," Toxicology Letters,
Volume 44, page 331-339.
Pinto, Judith M.B., Timothy J. Maher, 1986. "High Dose Aspartame Lowers the Seizure Threshold
to Subcutaneous Pentylenetetrazol in Mice," The Pharmacologist, Volume 28, page 155.
Pinto, Judith M.B., Timmothy J. Maher, 1988. "Administration of Aspartame Potentiates
Pentylenetetrazole- and Fluorothyl-Induced Seizures in Mice," Neuropharmacology,
Volume 27, No. 1, page 51-55.
Roberts, H.J., 1988. "Reactions Attributed to Aspartame-Containing Products: 551 Cases,"
Journal of Applied Nutrition, Volume 40, page 85-94.
Roe, O., 1982. "Species Differences in Mehtanol Poisoning," CRC Critical Reviews In Toxicology,
October 1982, page 275-286.
Rowen, A. James, Bennett A. Shaywitz, et al., 1995. "Aspartame and Seizure Susceptibility:
Results of a Clinical Study in Reportedly Sensitive Individuals," Epilepsia, Volume 36, No. 3,
Schiffman, Susan S., et al., 1987. "Aspartame and Susceptibility to Headache," The New
England Journal of Medicine, Volume 317, No. 19, page 1181-1185.
Shaywitz, B.A., et al., 1994a, "Aspartame Has No Effect on Seizures or Epileptiform
Discharges in Epileptic Children," Annuls of Neurology, Volume 35, page 98-103.
Stegink, Lewis D., W.A. Reynolds, L.J. Filer, et al. 1979. "Comparative Metabolism of
Glutamate in the Mouse and Man," In Filer L.J. Jr., Garattini, S., Dare MR, Reynolds WA,
Wurtman RJ (eds): "Glutamic Acid: Advances in Biochemistry and Physiology,"
Raven Press, New York 1979, pages 85-102.
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.
Sze, Paul Y., "Pharmacological Effects of Phenylalanine on Seizure Susceptibility: An Overview,"
Neurochemical Research, Volume 14, No. 2, pages 103-111.
Thai, L. H.A. Tilson, et al., 1988. "Lack of Effect of Aspartame on Kindling, Electroconvulsive
Shock (ECS) and Metrazol-Induced Seizures in Rats," Society of Neuroscience Abstracts, Volume 14,
Tilson, H.A., L. Thai, et al., 1989. "Oral Administration of Aspartame is Not Proconvulsant
in Rats," Neurotoxicology, Volume 10, pages 229-238.
Tollefson, Linda, Robert J. Barnard,1992. "An Analysis of FDA Passive Surveillance Reports of
Seizures Associated With Consumption of Aspartame," Journal of the American Dietetic Association,
Volume 92, No. 5, page 598-601.
Trefz, Friedrich, Leo de Sonneville, Peter Matthis, Christian Benninger, Brigitte Lanz-Englert,
Horst Bickel, 1994. "Neuropsychological and Biochemical Investigations in Heterozygotes for
Phenylketonuria During Ingestion of High Dose Aspartame (A Sweetener Containing
Phenylalanine)," Human Genetics, Volume 93, page 369-374.
Trocho, C., et al., 1998. "Formaldehyde Derived From Dietary Aspartame Vinds to Tissue
Components in vivo," Life Sciences, Vol. 63, No. 5, pp. 337+, 1998
Turner, James, 1987. Testimony of James Turner, Esq., Community Nutrition Institute before the
U.S. Senate Committee on Labor and Human Resources, November 3, 1987 regarding "NutraSweet Health
and Safety Concerns." Document # Y 4.L 11/4:S.HR6.100, page 316.
US Air Force 1992. "Aspartame Alert." Flying Safety 48(5): 20-21 (May 1992).
US Senate 1987. U.S. Senate Committee on Labor and Human Resources, November 3, 1987 regarding
"NutraSweet Health and Safety Concerns." Document # Y 4.L 11/4:S.HR6.100.
Walton, Ralph G., 1986. "Seizure and Mania After High Intake of Aspartame," Psychosomatics,
Volume 27, page 218-220.
Walton, Ralph G., 1988. "The Possible Role of Aspartame in Seizure Induction," 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,
Wurtman, Richard J., 1983. "Effects of Aspartame and Glucose on Rat Brain Amino Acids and Serotonin," New
England Journal of Medicine, Volume 309, No. 7, page 429-430.
Wurtman, Richard J., 1985. "Aspartame: Possible Effect on Seizure Susceptibility," The Lancet,
Volume 2, page 1060.
Wurtman, Richard J., Tomothy J. Maher, 1988. "General Discussion: Calculation of the Aspartame
Dose for Rodents that Produces Neurochemical Effects Comparable to Those Occurring in
People," 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.
Yokogoshi, H., et al., 1984. "Effects of aspartame and glocose administration on brain and plasma
levels of large neutral amino acids and brain 5-hydroxy-indoles." American Journal of Clinical
Nutrition, Volume 40, page 1-7.