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Research that says that
ingestion of "monosodium glutamate"
places humans at risk

The scientific literature relevant to the safety/toxicity of "processed free glutamic acid" (MSG) falls into two categories:

a) Those studies done by independent researchers - studies wherein "processed free glutamic acid" is almost always found to be toxic.

b) Those studies underwritten by Ajinomoto, its International Glutamate Technical Committee (IGTC), various other associations, agents, and friends in the food and drug industries -- studies wherein "processed free glutamic acid" is invariably alleged to be "safe." (A partial list of those studies is given in Table 1 of "The Toxicity/Safety of Processed Free Glutamic Acid (MSG): A Study in Suppression of Information.")

Animal studies

Animal feeding studies done by independent researchers have demonstrated that "processed free glutamic acid" causes brain lesions in the area of the hypothalamus; that animals fed "processed free glutamic acid" as infants express neuroendocrine disorders, including reproductive disorders and gross obesity, as the animals approached or reached puberty; and that 100 per cent of the offspring of studied rats fed "processed free glutamic acid" while pregnant had clearly evident learning disabilities.

The first published report of human adverse reactions to "processed free glutamic acid" appeared in The New England Journal of Medicine in 1968.(1) That report had been preceded by published studies demonstrating that processed free glutamic acid caused retinal degeneration(10-20)  It was followed by published confirmations of adverse reactions;(2-9) studies that demonstrated that processed free glutamic acid, whether laboratory grade or found in "monosodium glutamate," caused brain lesions when given to immature animals after either subcutaneous(21-43) or oral (29,35-36,38,44-48) doses; studies detailing neuroendocrine disorders,(21,30,32,48-66) possible locomotor and learning deficits either immediately or in later life,(52,55-56,67-76) learning and memory, (77-80) behavioral reactions including somnolence and seizures,(81-91) tail automutilation,(54,81) learned taste aversion,(92) and conspicuous emotional change.(54) In addition, there were epidemiologic studies completed in the 1970s demonstrating that at least 25 per cent of the population react to "processed free glutamic acid," the substance popularly referred to as MSG.(93-96)

Later, there were studies that demonstrated that free glutamic acid (including "processed free glutamic acid") can cross the placenta during pregnancy,(91,97-98) can cross the blood brain barrier in an unregulated manner during development, and can pass through the five circumventricular organs, which are "leaky" at best at any stage of life.(99-102) Moreover, the blood brain barrier is easily damaged by fever, stroke, trauma to the head, seizures, ingestion of processed free glutamic acid, and the normal process of aging.(85,102) It is generally accepted that the young are particularly at risk from ingestion of MSG.

The reader should note that most of the neuroendocrine studies cited here are from 1980 or before. By 1980, the consensus that processed free glutamic acid causes brain lesions and neuroendocrine disorders was so clear that there was little need to repeat the phenomenon.(103-107) Therefore, from 1980 to the present time, studies of the effects of processed free glutamic acid on neuroendocrine function were undertaken primarily to answer questions having to do with function, histology, or histopathology of parts of the endocrine system. The following is an example taken from a 1995-2001 Medline search:

Miskowiak, B; Partyka, M. Neonatal treatment with monosodium glutamate (MSG):structure of the TSH-immunoreactive pituitary cells. Histology and Histopathology. 15(2):415-9, 2000.
Indeed, since the 1980s, "processed free glutamic acid" has been used as an ablative tool to selectively kill brain cells to facilitate study of, and develop drugs for, endocrine dysfunction, neurodegenerative disease, and other disorders involving the brain.104 The following are examples taken from a 1995-2001 Medline search:
Ishikawa, K, Kubo, T, Shibanoki, S, Matsumoto, A, Hata, H, Asai, S. Hippocampal degeneration inducing impairment of learning in rats: model of dementia? Behavioural Brain Research 83(1-2):39-44, 1997.

Arletti, R, Benelli, A, Mazzaferro, M, Calza, L. The effect of oxytocin on feeding, drinking, and make copulatory behavior is not diminished by neonatal monosodium glutamate. Hormones & Behavior. 4:499-510, 1993.

Herrmann, G., Steunitz, H., Nitsch, C. Composition of ibotenic acid-induced calcifications in rat substantia nigra. Brain Research 786:(1-2)205-14, 1998.

The reader should also note that because independent study of glutamic acid was being done by neuroscientists trying to understand amino acids, neurotransmitters, and glutamic acid in particular, as opposed to selling a food additive/ingredient, in the majority of these studies "processed free glutamic acid" was administered to laboratory animals by gavage or subcutaneously. There were only a few oral feeding studies done by independent psychologists and neuroscientists; but there were oral feeding studies, and the studies done demonstrated that brain lesions, neuroendocrine disorders, and behavioral disorders could be caused by feeding animals "monosodium glutamate."

Review of studies financed by the glutamate industry demonstrates that the individual studies are badly flawed. Taken as a whole, the studies are flawed to the point of being fraudulent. The glutamate industry's animal studies can be characterized as looking for the wrong thing, at the wrong time, in the wrong place, using poor technique. The comments of John W. Olney, M.D. made in April, 1993, address the integrity of the glutamate industry's animal studies.(108)  (John W. Olney is a neuroscientist of international reputation. He has published hundreds of articles in leading medical journals and has won numerous awards.)(109)

Historically, glutamate industry researchers, led by Andrew G. Ebert of the IGTC and the Robert H. Kellen Company, have focused on research designed with the single purpose of convincing the public that "processed free glutamic acid" is "safe." To accomplish this, they compared two groups of subjects, a test group and a control, and chose their subjects, methodology, and statistics to find no difference between the two groups. Probably their most productive researchers have been L.D. Stegink, Lloyd J. Filer, and W. Ann Reynolds, who together did a number of studies designed to refute the findings of Olney and others of brain lesions and neuroendocrine disorders, and thus quell any concerns the public might have had about the toxic potential of their product, the flavor enhancer called "monosodium glutamate." It can be said of the Stegink/Reynolds/Filer group that they studied Olney's procedures carefully, having sent a representative to Olney's laboratory in the early 1970s, where every courtesy was afforded her. It is particularly bothersome, therefore, that subsequent studies coming from the Stegink/Reynolds/Filer laboratory looked for evidence of brain lesions in areas of the brain that would not, according to Olney, have been affected by monosodium glutamate; waited to examine the brain samples taken for 24 hours or more after insult - after which time all evidence of lesions would have been obscured; and used inappropriate methods of fixation and staining.(108)

Examination of the methodology sections of representative industry-sponsored studies(110-112) will demonstrate that subjects, test materials, overall procedures, and/or methods of analysis differed from the studies being "replicated." For example, although it had been established that brain lesions could not be identified if examination was not done within 24 hours after insult, glutamate-industry researchers routinely examined the brains of test animals after 24 hours had elapsed. They also used inappropriate methods and materials for staining the material they were examining.

Of particular interest were a study by Stegink et al.(112) and a study by Reynolds, Butler, and Lemkey-Johnston.(113) Careful examination will show that researchers used a single slide of the brain of one animal as evidence that free glutamic acid failed to produce brain damage in two different monkeys.

Those industry studies were underwritten by Ajinomoto, Gerber, International Minerals and Chemical Company, Nestle, and others, in cooperation with the IGTC.

Feeding studies were of particular concern to the defenders of the safety of "monosodium glutamate." One of their prime defenses on behalf of the "safety" of "monosodium glutamate" was that animal studies that showed that "monosodium glutamate" was toxic to animals did not reflect the human condition.

As always, the industry-sponsored feeding studies were badly flawed. In these animal feeding studies, researchers accounted for the amount of food consumed by experimental and control groups, but did not account for the amount of "processed free glutamic acid" consumed as opposed to being left on the table. According to the few methodology sections that covered the subject, "processed free glutamic acid" was added to each test animal's diet. Most studies outlined, in great detail, the amount of food given to test and control animals, the name (but not the components) of the basic diet (which might very well have contained "processed free glutamic acid" or some other neurotoxic amino acid like aspartic acid or L-cysteine), and the amount of "processed free glutamic acid" added to the diets of each animal or test group.

One industry-sponsored study provided an unusual amount of detail, including detail of the exact nature of the basal diet provided wherein "yeast food" was listed as a component of the protein.(114)  In 1990, yeast food invariably contained either protease (which creates processed free glutamic acid during manufacture) or L-cysteine which produces neurotoxic effects(115) somewhat different from, but more extensive than, the effects of "processed free glutamic acid." In this study, as well as in industry-sponsored studies from literature submitted by Auxein Corporation (now known as Emerald BioAgriculture) to the EPA in support of their application to register "processed free glutamic acid" for use in pesticide, fungicides, and plant "growth enhancers," failure to find differences in animals' growth or the adverse reactions of control and experimental groups may very well have been due, in part, to the fact that control groups were receiving neurotoxic substances in their basal diets.

In studies submitted by Auxein Corporation to the EPA, detail pertaining to the amount of food consumed was also given. But sorely lacking was any discussion of the amount of "processed free glutamic acid" consumed by animals in various test groups. The casual reader may assume that "processed free glutamic acid" would be ingested in proportion to the amount of basic diet ingested by test animals. But that is not true. Every animal owner knows that animals are quite adept at ferreting out and rejecting (not eating) pills or other goodies "hidden" in their food, and in avoiding food in which they have no interest. Thus, the "processed free glutamic acid" could have been left on the table by the test animals, causing there to be no difference in reactions expressed by test and control animals. Had this not been the case, both the form of the "processed free glutamic acid" added to each animal's diet and the consumption of "processed free glutamic acid" would certainly have been discussed in research reports.

By 1980, those studies done by glutamate-industry funded researchers in the 1970s that alleged to demonstrate that the food additive "monosodium glutamate" failed to cause brain lesions in laboratory animals had been refuted. Today, the neurotoxic effects of processed free glutamic acid are so clear cut that scientists use "processed free glutamic acid" as an ablative tool to selectively kill brain cells in order to study brain function and the effects of drugs on brain function.(116)

Glutamate-industry sponsored researchers never actually replicated the work of Olney and others who had demonstrated that processed free glutamic acid causes brain lesions and subsequent neuroendocrine disorders. In a 1981 review of the literature, Nemeroff stated unequivocally that "...not one single [primate] study has truly replicated the methods utilized by Olney, making evaluation of the available data impossible."(107)

Human experimental studies

Human studies of the safety/toxicity of "monosodium glutamate" are rarely done by independent researchers, because no one from industry will support them. From time to time, however, a physician will investigate the relationship between "monosodium glutamate" and his or her area of interest such as skin problems, irritable bowel, asthma, cardiac arrhythmia, or migraine headache.

The asthma studies of Allen and Baker are of particular interest because their finding, that as little as .5 grams "monosodium glutamate" would trigger an "MSG" reaction, caused Ajinomoto a great deal of embarrassment. That embarrassment was evidently exacerbated when the Federation of American Societies for Experimental Biology (FASEB), in its 1995 report on "The Safety of Monosodium Glutamate (MSG) in Food," commented on the Allen et al. study, noting that "The studies of Allen et al. (1987)(117) provide scientific evidence for a role of MSG in the onset of severe asthma in selected asthmatic patients."(118)

The study on hydrolyzed vegetable protein induced headache done by Alfred Scopp, published in 1991, is also of particular interest because that study is never mentioned by the defenders of the "safety" of "monosodium glutamate." Neither is it mentioned in the 1995 FASEB Report. In 1991, Alfred Scopp published a study entitled; "MSG and hydrolyzed vegetable protein induced headache: review and case studies." In 1993, Martinez et al.(119) measured glutamic and aspartic acid levels in plasma and cerebrospinal fluid (CSF) of patients with common and classic migraine during attacks, making comparisons with controls suffering from stress. Plasma levels of amino acids in migraine patients were lower than in controls, while CSF concentrations of glutamic acid were higher in migraineurs than in controls. The authors concluded that "... results suggest an excess of neuroexcitatory amino acids in the [central nervous system] of migraine patients during attacks, possibly favoring a state of neuronal hyperexcitability." Martinez et al. had found a relationship between glutamate levels in the CSF of the central nervous system and migraine headache. But neither Scopp's article, the Martinez et al. article, nor the subject of migraine headache are discussed in the August 31, 1995 FASEB report.

In 1992, the FDA had commissioned FASEB to do an independent review of research on the safety (never toxicity) of MSG. The FDA has admitted, in reports of adverse reactions on file at the FDA, that migraine headache (they call it headache) has been reported as an adverse reaction by over 43 per cent of the people reporting reactions to MSG. Moreover, with possible rare exception, "monosodium glutamate" is acknowledged as a migraine headache trigger by every headache clinic in the United States. Yet the subject of migraine headache is not even mentioned in the August 31, 1995 FASEB report. In the FASEB report, reports of migraine headache are reported as reports of headache.

On June 16, 2002, the Migraine Information Center page (http://www.ama-assn.org/special/migraine/support/educate/causes.htm) of the Web page of the Journal of the American Medical Association stated that "There are a number of dietary triggers that have been reported, these include: alcohol, especially red wine; foods with monosodium glutamate (MSG) (see Table2); foods that contain tyramine...and preserved meats with nitrates and nitrites (see Table 3)."(120)

It must be noted that FASEB's failure to discuss "monosodium glutamate" as a migraine headache trigger is consistent with the tone of the entire 1995 FASEB report which, in its verbiage, minimizes the severity and extent of "monosodium glutamate" induced adverse reactions. Tachycardia and atrial fibrillation, for example, are described as "change in heart rate;" asthma is described as "difficulty breathing;" and depression is described as "change in mood quality or level." The ultimate we have seen of this sort of thing from the FDA is, in their list of adverse reactions reported following ingestion of aspartame, to list each of the reported deaths under "other."

The 1995 FASEB study has been criticized for conflicts of interests of Expert Panel members, for failure to consider all data relevant to the safety/toxicity of MSG, for dismissing, or attempting to dismiss, data that did not fit well with a conclusion that MSG is safe, and more.(121),(122),(123),(124),(125),(126)

Those criticisms plus the names and addresses of over 650 people who wrote to FASEB about their sensitivities to "monosodium glutamate" and "processed free glutamic acid" appear on the log sheets relevant to FDA Docket No. 92N-0391. All are public record and names, addresses, and testimony can be accessed through the FDA.

Interestingly enough, IGTC studies, themselves, have added to the weight of evidence that says that humans react to "monosodium glutamate." In the epidemiological study done by Kerr et al.,(95) 43 per cent of the people studied claimed to have reactions that are known to be produced by "monosodium glutamate."  In the double blind study done by Tarasoff and Kelly, approximately 33 per cent of the subjects in the study reacted to "monosodium glutamate" test material, and almost that same number reacted to the placebos laced with "processed free glutamic acid" or aspartic acid (in aspartame).(132)

In the 1980s, in the face of overwhelming evidence that monosodium glutamate kills brain cells in laboratory animals,(103-104) industry researchers changed their original strategy. They began to claim that animal studies were not relevant to humans. They initiated a series of double-blind human studies that, they would claim, "proved" that "monosodium glutamate" was safe.

Detailed analysis of those double-blind studies revealed that subjects, materials used, and protocols for administering test and placebo material, minimized the chance that subjects would react to the MSG test material; and that if subjects did react to the MSG test material, they would also react to the placebo.

The primary strategy used in most, if not all, glutamate-industry-sponsored research is to look for evidence of toxicity in subjects least likely to be sensitive to "processed free glutamic acid" (eg. "well subjects" -- people who had never in their lives had any of the adverse reactions attributable to "monosodium glutamate"); to use test materials least likely to produce observable reactions; to use placebos laced with neurotoxic amino acids and/or other substances that will cause identical or similar reactions to those caused by "processed free glutamic acid" test material; to serve "drinks," or a "standard breakfast" laced with neurotoxins with both test material and "placebo" material; to set up protocols that will obscure evidence of toxicity (eg. accepting as adverse reactions only those that occurred within two hours of testing, and those that might be considered mild and transitory, while excluding such reactions as heart irregularities, migraine headache, seizures, nausea and vomiting, and asthma); to allege that finding no evidence of toxicity constitutes proof that their product is "safe;" and to allege that adverse reactions to their reactive "placebos" constituted evidence that reactions to the test material are not reactions to "processed free glutamic acid."

Industry researchers:

1. Use variables and methods known to minimize or be irrelevant to identification of the toxic effects of glutamic acid; then conclude that glutamic acid never produces adverse effects. Studies have focused on the relationship between "objective" parameters such as blood pressure and body temperature and ingestion of MSG.

Unless MSG sensitive people are studied, one can not legitimately draw conclusions about the relationship of the variables being studied (no matter how objective they are) to people who are sensitive to MSG. Often, these studies are used to allegedly "prove" that people who are not sensitive to MSG are not sensitive to MSG.

2. Limit the recorded adverse effects to a few generally mild and transitory reactions occurring simultaneously, such as those first reported in 1968 by Kwok and dubbed "Chinese- restaurant syndrome" (CRS): "...numbness at the back of the neck, gradually radiating to both arms and the back, general weakness and palpitation." Industry researchers do not consider migraine headache, asthma, seizures, tachycardia, arrhythmia, depression, anxiety attacks or other obviously debilitating and/or life-threatening reactions to "monosodium glutamate" reported since 1968, when they tally up the reactions to MSG.

3. Make no attempt during a study to prevent subjects from ingesting food to which they might be allergic or sensitive.

4. Record reactions as reactions to "monosodium glutamate" or placebo material only if they occur 2 hours or less following ingestion of test or placebo material, even though many symptoms are commonly expressed much later, and reactions may persist for much longer periods.

5. Fail to report all data.

6. Draw conclusions that do not follow from the results of the study. The IGTC researchers have inappropriately concluded, for example, that because approximately one third of their subjects reacted adversely to placebos containing MSG and/or aspartame, they have "proved" that reactions to MSG-containing test material are not reactions to MSG.

7. Use test material that will minimize the effect of any stated amount of glutamic acid test material in producing adverse reactions. One gram monosodium glutamate encased in capsules, and therefore guaranteeing slow release, will cause less effect than 1g monosodium glutamate sprinkled on food; and 1g monosodium glutamate modified with sucrose will cause less effect than otherwise because sucrose is known to slow monosodium glutamate uptake(127)

8. Continue subjects on medications that might block the effects of MSG.

9. Use placebos to which MSG-sensitive people would react (placebos containing MSG, aspartame, carageenan or enzymes, for example), test potential subjects for sensitivity to those placebos, and eliminate any subjects who react to placebos. Researchers can be fairly certain that those who do not react to their reactive placebos will not react to monosodium glutamate test material.

10. Advertise for, and presumably use, "well subjects" - people who had never experienced any of the symptoms with which reactions to MSG are associated. (If 50 per cent of the population were sensitive to MSG, but research design precluded inclusion of that 50 per cent who were sensitive, a study claiming to assess the number of people sensitive to MSG would be invalid.)

11. Refer to studies as "randomized double-blind crossover design studies," which gives the casual reader the impression that subjects were drawn randomly from the general population. In fact, subjects are often carefully selected people who tell researchers that they have never experienced any of the adverse reactions associated with monosodium glutamate, and, under those conditions, are paid to participate in the studies. Other subjects are people, often students, paid for participating in industry-sponsored studies only if they say that they are sensitive to monosodium glutamate. In either case, the only thing in those studies that is "random" is whether subjects get their monosodium glutamate test trial first and their placebo second, or vice versa. Subjects recruited in 1993 for an IGTC-sponsored studies begun in 1992 by Harvard Medical School, Northwestern University Medical School, and UCLA Medical School, were paid hundreds of dollars each--only if the applying subjects (many of them students) claimed that they were sensitive to monosodium glutamate.

12. Use placebos virtually guaranteed to produce as many reactions as might be produced following ingestion of the "monosodium glutamate" test material. Using toxic material in both test material and placebo, researchers argue that the reactions to MSG-containing test material are not reactions to MSG because subjects also react to placebos, which are assumed to be inert. However, the use of toxic material in placebos, particularly when it is identical or similar to the "monosodium glutamate" in the test material, makes it virtually inevitable that there will be approximately as many reactions to placebos as there are reactions to "monosodium glutamate" test material.

Sometimes glutamate-industry researchers use "processed free glutamic acid" in placebos, but use sources of "processed free glutamic acid" different than the ingredient called "monosodium glutamate." Gelatin, which always contains "processed free glutamic acid," has been a favorite. Beginning in 1978, even before aspartame was approved by the FDA for use in food, glutamate-industry researchers used aspartame in placebos.(128)

Over and above the fact that use of aspartame in placebos is grossly inappropriate, the fact that aspartame-containing products are supposed to carry a warning on their labels did not deter industry from using the substance, or the FDA from allowing its use. Aspartame contains phenylalanine (which adversely affects one in 15,000 Americans); aspartic acid (an excitatory amino acid); and a methyl esther. Aspartic acid and glutamic acid load on the same receptors in the brain, cause the same brain damage and neuroendocrine disorders in experimental animals, and, with the exception of blindness related to aspartame ingestion, cause virtually the same adverse reactions in humans. In addition, aspartic acid and glutamic acid act in an additive fashion. There are over 7,000 unsolicited reports of adverse reactions to aspartame filed with the FDA. It should surprise no one, therefore, that glutamate industry researchers find as many reactions following ingestion of an aspartame-containing placebo as they find following ingestion of monosodium glutamate test material.

Strong, in a study entitled "Why do some dietary migraine patients claim they get headaches from placebos?" tested the hypothesis that it was the gelatin capsules used to conceal placebo material that caused headaches from placebos, and concluded that capsules may give headaches to dietary migraine patients that are similar to those from foods.(129) This, Strong said, would explain some of the headaches of patients from placebos.

In a previous study, Strong had found that 18 per cent of his subjects reported headaches from placebos which were all concealed in gelatin capsules. Glutamate-industry double-blind studies of the "safety" of "processed free glutamic acid" almost always use gelatin capsules. Of interest is the fact that a gelatin capsule is over 11 per cent "processed free glutamic acid."

It should be noted that placebo reactions have also been noted in industry-sponsored animal studies. It was noted by Nemeroff(107) that Abraham, Doughtery, Goldberg, and Coulston(37) and Abraham, Swart, Goldberg, and Coulston(130) found in both control and glutamic acid treated monkeys a "very small proportion of necrotic or damaged neuronal cells and oligodendrocytes... in the arcuate nuclear region of the hypothalamus." This might happen if the placebo, as well as the test material, contained small amounts of an excitotoxin identical or similar to glutamic acid.

In response to studies that demonstrated that ingestion of "monosodium glutamate" places humans at risk, Ajinomoto, their IGTC, and their agents produced studies alleging the "safety" of "monosodium glutamate." By and large, the human studies were described as double blind placebo controlled studies to evaluate alleged reactions to monosodium glutamate (MSG).

The hallmark of the glutamate industry double blind human studies has been use of a neurotoxic amino acid in their "placebos." Sometime it was aspartic acid (found in aspartame). Sometimes it was "processed free glutamic acid" in some food additive or ingredient other than "monosodium glutamate." Upon being confronted with questions about their placebos, Andrew G. Ebert, Chairman of the IGTC, admitted (in 1991) that since 1978, studies underwritten by the IGTC have used aspartame in "placebos."(131) In response to suggestions from this author that materials used in double-blind tests of the safety of "monosodium glutamate" contained free amino acids, Ebert responded that "the only glutamate or other free amino acids ingested in these controls would have been from natural sources."(132) According to the FDA, both "monosodium glutamate" and aspartame come from "natural sources."

Never were the contents of the glutamate industry's "placebos" disclosed in any publication before Jack Samuels wrote to the FDA in 1993, telling the FDA that the alleged "placebos" contained "processed free glutamic acid" and aspartic acid (in aspartame), and that as such, the IGTC was responsible for scientific fraud.

Typical of the IGTC's human studies is a study done by Tarasoff and Kelly from the Faculty of Business and Technology, University of Western Sydney, Australia, Macarthur Campus, published in Food and Chemical Toxicology in 1993.(133) The first hint that there was something seriously wrong with the study was the fact that 16 out of 38 subjects (42 per cent) reacted to "placebos."

The Tarasoff and Kelly study embodies most of the 12 flaws elaborated earlier in this section. A critique of the Tarasoff and Kelly study was published in January, 1994.(134)

In 1993, Tarasoff and Kelly were still using neurotoxic amino acids in placebos, but the contents of the placebos were elaborated -- as they had not been previously. In June, 1994, Harvard University Medical School, Northwestern University Medical School, and UCLA Medical School were engaged in an IGTC sponsored study designed to convince the public that "monosodium glutamate" was "safe."(135) On June 16,1994, when Adrienne Samuels, Ph.D., wrote to Vice Dean Donald Nutter, M.D., Northwestern University School of Medicine about the impropriety of participating in a study wherein neurotoxic amino acids were being used in placebos, study protocols called for using aspartame in placebos. After I spoke to, and wrote to Dr. Nutter, who told me he would do nothing to interfere with any study that had been reviewed and approved by the appropriate School and University bodies, the protocols were changed to exclude the use of aspartame. Protocols did, however, use a source of "processed free glutamic acid" that would not be recognized as such by most people.

As part of our submission to FASEB during the study that was published in 1995, we alerted FASEB to the fact that those human studies that pretended to have demonstrated that "monosodium glutamate" was "safe," had used neurotoxic amino acids in their placebos. FASEB did not find that such use of neurotoxic amino acids invalidated the glutamate sponsored studies. FASEB did, however, suggest that in the future, neurotoxic amino acids should not be used in placebo materials.

These little stories are told here because they tell me that those School and University bodies, once alerted to the fact that neurotoxic amino acids were being used in studies being carried on in their schools, found such protocols inappropriate; and so did FASEB. But since the rich and powerful glutamate industry did not want their studies questioned, there were no questions raised.

The IGTC has amassed a number of double-blind studies concluding--but not demonstrating--that "monosodium glutamate" is "safe." The fact that these studies are often done at generally respected universities or medical schools, all of which required that the research be approved by medical research review committees, has public relations value. Often, studies are eventually published in peer reviewed journals--accepted by editors who, themselves, may have ties to the food and/or drug industries; and who may not accept comments in the form of letters to the editor from those who would criticize their friends in industry. If not published in their entirety, abstracts of these studies, which have been presented at professional meetings, are finally published. They then appear in the Medline data base, and that has public relations value.

In years past, reports of glutamate industry sponsored research that claimed to offer evidence that MSG is "safe" appeared in a wide range of journals.  Today it would appear that only the Journal of Nutrition and the Journal of Allergy and Clinical Immunology are publishing such work.

In years past, studies allegedly demonstrating that MSG is "safe" were carried out at prestigeous American universities and medical schools such as Harvard, Northwestern University, UCLA, and Scripps Research Institute in LaJolla, California.  Presently, they seem to come from Australia (Alfred Hospital and Monash University Medical School, Melbourne, Australia and Department of Chemistry, Faculty of Business & Technology, University of Western Sydney, Campbelltown, NSW, Australia for example).

Given the methodological flaws inherent in their work, and their unwillingness to change their protocols after flaws are pointed out to them, we can only conclude that IGTC researchers move from a predetermined conclusion (that their product is "safe") to design and implementation of research guaranteed to bring the reader to that predetermined conclusion.

Human epidemiologic studies

Studies done in the 1970s demonstrated that 25 to 30 percent of the population of the United States reacted to "processed free glutamic acid" at that time. In 1969, Schaumburg et al. determined that approximately 30% of the population of the United States suffered adverse reactions when fed "monosodium glutamate" in an ordinary diet.(96) Reif-Lehrer(93) and Kenney and Tidball(94) confirmed their findings.

Those studies were challenged by Kerr et al. in a 1979 glutamate industry sponsored study.(95) Kerr et al. found that 43 per cent of respondents reported one or more unpleasant symptoms associated with eating, but concluded that only 1.8 per cent of the population might be sensitive to "monosodium glutamate." To accomplish this, Kerr et al. decreed that the only true symptoms of MSG-sensitivity (called "Chinese restaurant syndrome"), were "burning, tightness, and numbness," experienced simultaneously, that commenced between 10 minutes and 2 hours after the start of a meal, and lasted 4 hours or less. Kerr et al. had to ignore all other reported symptoms, even migraine headache,(136) in order to come up with this 1.8 per cent figure. They also had to ignore the fact that MSG-sensitive people react from immediately to 48 hours following ingestion of "MSG."

Given increased use of "monosodium glutamate" and other food additives/ingredients that contain "processed free glutamic acid" since 1979, we would now expect more than 30% of the population to suffer adverse reactions from time to time.


The FDA has admitted, and even pretended to address the fact, that "processed free glutamic acid" created by acid hydrolysis contains carcinogenic mono and dichloro propanols.(137)

The FDA has also admitted that "processed free glutamic acid" found in reaction flavors which are produced from a combination of specific amino acids, reducing sugars, and animal or vegetable fats or oils, and optional ingredients including hydrolyzed vegetable protein is also carcinogenic.(138-139)

Adverse reactions caused by "monosodium glutamate" and other food additives/ingredients that contain "processed free glutamic acid" are the same reactions recognized as side effects of other neurotropic drugs

Ingestion of "processed free glutamic acid" causes adverse reactions in susceptible individuals. Those reactions are diverse, but no more diverse than reactions to other neurotropic drugs such as Valium. The fairly recent discovery of glutamate receptors in many locations outside of the central nervous system(140) suggests that the readily observable toxic effects of processed free glutamic acid, referred to as adverse reactions, are facilitated by glutamate receptors in the mouth, lungs, intestines, and muscle, for example; and that the fate of ingested "processed free glutamic acid," at least in some cases, is not to come to rest in the plasma as elevated plasma glutamate and from there to be excreted by the liver. Rather, it would appear that the fate of ingested "processed free glutamic acid" may be to move with dispatch to any glutamate receptors available to it; and to create an adverse or toxic reaction if any one of those peripheral glutamate receptors is weak, crippled, diseased, or otherwise unhealthy.

Today, virtually every headache clinic in the United States acknowledges that "processed free glutamic acid" (popularly referred to as MSG) is one of the triggers of migraine headache. According to Alfred Scopp of the Northern California Headache Clinic, at least 33 per cent of migraine patients have some migraine headaches triggered by "MSG."(141)

A report from the Federation of American Societies for Experimental Biology (FASEB) on the safety of amino acids in dietary supplements reads, in part:

"The continuing controversy over the potential effects of glutamate on growth and development of neonatal animal models suggests that it is prudent to avoid the use of dietary supplements of L-glutamic acid by pregnant women, infants, and children. The existence of evidence of potential endocrine responses, i.e., elevated cortisol and prolactin, and differential responses between males and females, would also suggest a neuroendocrine link and that supplemental L-glutamic acid should be avoided by women of childbearing age and individuals with affective disorders."(142)
There is government prohibition against producing or importing "monosodium glutamate" in Myanmar.(143)

Today, reports of adverse reactions submitted to the FDA are on file in FDA Dockets including Docket # 96N-0244 and Docket # 92N-0391. The FDA, which discourages consumer reports of reactions to "processed free glutamic acid," has reports of reactions to "processed free glutamic acid" on file in its Adverse Reactions Monitoring Section (ARMS). The FDA's ARMS accepts (but does not solicit) reports of MSG-sensitivity. Neither does the FDA record all comments received regarding "processed free glutamic acid."

The Truth in Labeling Campaign, a nonprofit organization that champions the identification of "processed free glutamic acid" in food and on food, has compiled a list of the adverse reactions to "processed free glutamic acid" reported to it.  The Truth in Labeling Campaign receives daily correspondence, primarily by e-mail and telephone, from people looking for help in avoiding ingesting "processed free glutamic acid."

A list of the adverse reactions reported to and collected by the Truth in Labeling Campaign will be found in the table titled "Collected Reports of Adverse Reactions to MSG Ingestion" at www.truthinlabeling.org/adversereactions.html.

Adverse reactions to "monosodium glutamate" and other food additives/ingredients that contain "processed free glutamic acid" include reactions that are debilitating and/or life-threatening.

One of the core strategies of the defenders of the safety of "monosodium glutamate" is to insist that the alleged "few" reactions to "monosodium glutamate" are "mild and transitory." Originally, there was only one reaction recognized by the defenders of the safety of "monosodium glutamate:" Chinese restaurant syndrome" ("burning," "tightness," and "numbness," all occurring at the same time, and commencing between 10 minutes and 2 hours after the start of a meal). In 1995, with the publication of the 1995 FASEB "Analysis of Adverse Reactions to Monosodium Glutamate (MSG)," the glutamate industry, with the cooperation of the FDA, gave up the term "Chinese restaurant syndrome" for the term "MSG Symptom Complex, and expanded the "industry approved list" of reactions to "processed free glutamic acid" to include:

burning sensation back of neck, forearms, chest
facial pressure/tightness
chest pain
numbness in back of neck radiating to arms and back
tingling, warmth, weakness in face, temples, upper back, neck and arms
bronchospasm (observed in asthmatics only)
In contrast, the Truth in Labeling Campaign knows that adverse reactions to "monosodium glutamate" include all of the adverse reactions listed in the table titled "Collected Reports of Adverse Reactions to MSG Ingestion" referred to previously. Clearly, any one of the cardiac, circulatory, gastrointestinal, neurological, visual, respiratory or urological/genital reactions could be debilitating and/or life-threatening.

Not listed in the table of Collected Reports of Adverse Reactions to MSG Ingestion, but of equal, if not greater concern, are conditions that we know stem directly from brain lesions and subsequent neuroendocrin disorders caused by injecting MSG into the system (as would be true of the many vaccines that contain MSG) and by eating MSG.  Those conditions include retinal degeneration, obesity, behavior and learning dirorders, stunted growth, and reproductive disorders. Of additional concern is the acknowledged, but little understood, relationship between being the role that glutamic acid plays in a number of pathological conditions such as addiction, stroke, epilepsy, brain trauma, neuropathic pain, multiple sclerosis, schizophrenia, anxiety, depression, and degenerative disorders such as Parkinson's disease, Alzheimer's disease, Huntington's disease, and amyotrophic lateral sclerosis (ALS).

Small amounts of "processed free glutamic acid" cause adverse reactions in some people

Human adverse reactions to ingestion of as little as 1.5 g and .5 g of processed free glutamic acid have been reported in the literature.(96,144) The Truth in Labeling Campaign has received reports of adverse reactions to the minute amounts of processed free glutamic acid that would be contained in products such as vitamin and mineral enrichments, gelatin capsules, and produce treated with fertilizers, pesticides, fungicides, and plant "growth enhancers" that contain "processed free glutamic acid." A number of those reports are on file with the FDA and the EPA. In both the 1995 FASEB report and in a 1992 report on the safety of amino acids in dietary supplements, FASEB concluded that there is insufficient evidence to determine safe concentrations of dietary supplements of L-glutamic acid in the diets of normal healthy humans.(141,145) And no study of the least amount of processed free glutamic acid needed to trigger reactions in MSG-sensitive people has ever been done. Thus, while there are data to suggest that as little as .5g of processed free glutamic acid will trigger an adverse reaction, and there are anecdotal reports that reactions are triggered by much lesser amounts, there are no data to even suggest what the least amount of processed free glutamic acid needed to cause an adverse reaction in an MSG-sensitive person might be.

It is common knowledge that minute amounts of certain allergens will trigger adverse reactions, including anaphylaxis, in people who are acutely sensitive to those allergens.(146-148)  There is nothing in the literature that says that similarly minute amounts of neurotoxic amino acids such as glutamic acid, aspartic acid, and L-cysteine will not trigger adverse reactions, including anaphylaxis, in people who are acutely sensitive to those neurotoxins. "Monosodium glutamate" contains neurotoxic "processed free glutamic acid."


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