"The Tentative Report arrived last week....
FASEB did not address the question of risk....
[instead] FASEB focused on subjects that would obscure the issue."
March 26, 1993
Kenneth D. Fisher, Ph.D.
Life Sciences Research Office
9650 Rockville Pike
Bethesda, MD 20814
Life Sciences Research Office
9650 Rockville Pike
Bethesda, MD 20814
FDA Docket No. 92N-0391
Dockets Management Branch (HFA-305)
Food and Drug Administration
12420 Parklawn Drive
Rockville, MD 20857
RE: Analysis of Adverse Reactions to Monosodium Glutamate (MSG); FDA Docket No. 92N-0391Dear Dr. Fisher:
The way to determine whether or not MSG is safe for human ingestion is to identify all products containing manufactured, free glutamate through labeling, instead of hiding MSG in food. Labeling would make it possible for people to identify their MSG sensitivities if they had them, or to know that their sensitivities were due to something else.
You know this, I know this, The Glutamate Association and the International Glutamate Technical Committee know this, and so does the Food and Drug Administration (FDA). What FASEB has done, purposely or in error, in creating the Tentative Report on the above referenced issue, is to participate in a smoke screen operation designed to obscure the real issues of MSG sensitivity, contribute to the escalating health care costs of all Americans, and prevent millions of Americans from being well.
Additionally, I believe that you are aware that under the law, it is not the responsibility of the consumer to prove that MSG (or any substance) is unsafe; but, rather, it is the responsibility of industry to prove that MSG is safe, and the responsibility of the FDA to identify any food or drug that engenders risk for the American people.
The Tentative Report arrived last week, and I still can not find the words to adequately express how disappointed I was when I read it. FASEB did not address the question of risk. In fact, FASEB focused on subjects that would obscure the issue.
As you well know, I criticized the FDA Request for Proposal (RFP) before the FDA contract was given to FASEB. The text of my May 8, 1992 letter to Thomas H. Vargo on that subject follows:
"I reviewed the RFP Contract Number 223-92-2185 that you sent me at my request on April 3, 1992, and, as you suggested, am forwarding my comments on to you for further forwarding to the authors of the RFP. You will note that I have paid particular attention to Attachment 1: COMPREHENSIVE REVIEW TASK NO. 1 CONTRACT NUMBER: 223-92-2185 ANALYSIS OF ADVERSE REACTIONS TO MONOSODIUM GLUTAMATE.
"The proposal for a literature review is both 1) unnecessary, and 2) constructed to serve the ends of the food industry. The questions asked which might serve the needs of consumers if answered are, for the most part, presently unanswerable. They are unanswerable because little or no data presently exist which address them. I find it hard to believe that the authors of the RFP were not aware of that fact when they drafted the RFP.
"Further, no reference has been made to reviewing the literature on the relation of neurodegenerative disease to brain glutamate levels; no mention has been made of evaluating studies based on whether they are industry sponsored or independently conducted; and there is no mention that a qualified neuroscientist be part of the review team.
"On the other hand, we would not be surprised to learn that industry studies designed to provide industry-friendly answers to some of the questions asked are already in progress.
"The proposal for a literature review is unnecessary, for the literature has been reviewed a number of times in the last two decades, and although industry sponsored studies 'guided' or actually reviewed by persons with strong ties to the food and/or drug industries have purported to demonstrate that MSG is safe, a review of those industry sponsored activities suggests that the data presented are questionable at best; and a review of studies done by persons outside of the food industry suggests that use of MSG is not safe.
"An efficient way to determine whether or not MSG is safe for human ingestion would be to identify all products containing MSG through labeling. (Presently most of the manufactured free glutamic acid is hidden in food.) Such labeling would make it possible for people to identify MSG sensitivities if they had them.
"The questions asked in the RFP suggest that reviewers will be encouraged to look at the work of Stegink, and the work of Reynolds and Filer--all beneficiaries of food and drug industry dollars. Filer, who worked for the drug industry, was appointed to an academic chair at the University of Iowa when Mead-Johnson & Co. Foundation funded that chair. Filer has, for many years, been a spokesperson for The Glutamate Association.
"Reviewers will also be encouraged to look at the findings of 'other authoritative organizations.' However, reviewers are not alerted to the fact that the World Health Organization and the European Communities, termed 'authoritative organizations' by The Glutamate Association and the International Food Information Council (IFIC), drew their conclusions on the 'safety' of MSG primarily, if not solely, from data provided by The Glutamate Association and the International Glutamate Technical Committee (IGTC). To quote from a June 14, 1991 letter from Andrew G. Ebert of the IGTC to Lawrence J. Lin of the FDA, 'Many of the questions raised have been previously addressed in Scientific Literature Reviews prepared by the IGTC presented to FDA and which were evaluated by FDA, FASEB, JECFA, and the EC Scientific Committee for Food.' (The underlining is mine.) There is little or nothing in the bibliographies of any of these 'authoritative organizations' to suggest that they looked at studies conducted separate and apart from studies sponsored by the food industry or reviewed the literature on neurodegenerative disease, much less considered the opinion of a qualified neuroscientist. It has already been mentioned that the industry sponsored studies that they considered were fraught with flaws. Because I have the evidence in front of me, I do not hesitate to say that some were flawed to the point of being fraudulent.
"I fear that this RFP might be nothing more than a ploy to: 1) placate consumers who are being told that through the review of the literature the FDA is 'doing something about the MSG controversy;' and 2) stall for at least two years, during which time industry will have time to find new, and possibly more devious ways, of hiding MSG. 'Clean labels' industry calls them: labels for foods that contain manufactured glutamic acid with 'clean' (unrecognizable) names.
"Again, the way to determine whether or not MSG is safe for human ingestion is to identify all products containing manufactured free glutamic acid through labeling, instead of hiding MSG in food. Labeling would make it possible for people to identify their MSG sensitivities if they had them, or to know that their sensitivities were due to something else."
After the FDA contract was awarded to FASEB, I spoke to you, Dr. Fisher; and on one occasion, you mentioned that the 18 questions raised by the FDA in their RFP would be evaluated as FASEB proceeded with the study. It was made clear that FASEB was in no way bound to answer the questions posed in the RFP by the FDA in their evaluation of the safety/toxicity of MSG; but would do whatever might be most appropriate for evaluating its safety. I came away with the impression that FASEB would evaluate the safety/toxicity of MSG fairly: that FASEB would evaluate the proof of safety provided by industry, and the suggestion of risk provided by independent scientists and MSG-sensitive consumers.
Was I wrong? First, I observed that two of the three consultants appointed by FASEB to this Expert Panel had benefited from funding by a company that would be adversely affected if MSG were found to be unsafe. On February 26, 1993, I wrote to you, to FASEB, and to FDA Docket No. 92N-0391, with copies to President Clinton, Secretary Shalala, and Commissioner Kessler, requesting that those two gentlemen be removed from the FASEB expert panel. Now I read a Tentative Report that responds to the 18 questions suggested in the FDA's RFP and essentially looks no farther; and in so doing has set the stage for a final report from FASEB that says "there is not enough data on the subject of the safety/toxicity of MSG to draw a conclusion, and we recommend that additional study be done."
Study? We don't need additional study. FASEB has in its files a copy of MSG: A Review of the Literature and Critique of Industry Sponsored Research, that amply demonstrates that industry has failed to demonstrate that MSG is safe. I have, in the past, offered to meet with FASEB and members of the Expert Panel to clarify and/or elaborate on the points that I made in that paper. I also asked to be allowed to defend that paper before FASEB to demonstrate my credibility. You told me that such a meeting would be outside the scope of the above referenced study.
FASEB also has access to numerous scientific studies that unequivocally demonstrate that ingestion of MSG causes brain lesions and neuroendocrine disorders in laboratory animals. FASEB has access to the files of the FDA wherein there are numerous complaints of adverse reactions to MSG. Thus, FASEB has considerable evidence available to it that ingestion of MSG places humans at risk.
We don't need additional study. We need labeling so people can know what they are eating and identify substances that make them ill. I realize that FASEB does not have the authority to cause such labeling; but FASEB does have the authority to recommend full labeling to assist in the determination of the extent to which MSG makes people ill.
We need an admission that MSG is a hazardous material, or, if you are not yet convinced that it poses a threat to all Americans, an admission that MSG may be a hazardous material. Given the data that you have in hand, you can not deny that use of MSG in food places humans at risk.
It was clear to me when I read the RFP, that the 18 questions raised by the FDA were designed to obscure the issue of the toxicity of MSG, not elucidate it. Very few of those questions are relevant to a study of the safety/toxicity of MSG. Very few of the questions asked can be answered with available data. The facts that need to be set before any group evaluating the safety of MSG must come from information available to us 1) from animal research that suggests that humans can be harmed by the ingestion or other use of neurotoxic amino acids such as MSG, and 2) from understanding the adverse reactions experienced by MSG-sensitive consumers. The 18 questions, as used by FASEB, appear to have been designed expressly to obscure that focus.
Focus on the 18 questions in the first place; then use of industry-friendly concepts and phraseology--phraseology that blends half-truths and innuendoes in a subtle effort to misdirect readers' perceptions of the safety/toxicity of MSG; and, finally, the highlighting of industry-friendly data while minimizing data that might point to the risk involved in the ingestion of MSG, all suggest that FASEB may not be an independent evaluator of the safety/toxicity of MSG as the FDA told us it would be.
In a later section of this letter, I will review the 18 questions, not
because I think they are worth answering, but because doing so will help
expose the bias that FASEB has brought to this study by focusing on them.
I do this in an effort to help FASEB understand precisely what my criticisms
are. Moreover, since the Tentative Report fails to ask a number of
questions that need to be asked to better understand the toxicity of MSG,
I will address that issue, also, even though it does not directly address
the subject of risk.
First, however, I would like to discuss the approach that FASEB has taken for this study. It is clear that FASEB has ignored the issues of industry proof and consumer risk. It is also clear from the phraseology of the Tentative Report, that FASEB intends to find that there is not enough data to make a determination on the toxicity of MSG, and that there needs to be further study. Let me elaborate, starting with questions. Not rhetorical questions, but questions that need to be addressed by anyone who is objectively evaluating the safety/toxicity of MSG.
QUESTIONS THAT NEED TO BE ANSWERED BY FASEB IN RELATION TO THE PHRASEOLOGY OF THE TENTATIVE REPORT
1. FASEB must be well aware that under the law, it is not the responsibility of the consumer to prove that MSG (or any substance) is unsafe; but, rather, that it is the responsibility of industry to prove that MSG is safe, and the responsibility of the FDA to identify any food or drug that engenders risk for the American people. Yet, FASEB has focused on 18 questions that, for the most part, address all sorts of interesting, but irrelevant issues. Why has FASEB not focused on risk?
2. As I understand it, the FASEB study is supposed to evaluate possible adverse reactions to MSG (free glutamate found in food as a consequence of manufacture). The first reaction identified in the literature as being an adverse reaction to MSG was actually three reactions: numbness, tingling, and tightness, all of which were observed in a single individual at the same time. That triad of symptoms was dubbed "Chinese restaurant syndrome (CRS)" in 1968 by the New England Journal of Medicine. Since that time, glutamate industry representatives have attempted to convince the public that the only "legitimate" reaction to MSG is those three distinct reactions occurring all at the same time, while MSG-sensitive consumers have reported a whole spate of neurotoxic reactions as occurring after ingestion of MSG. Why does FASEB distinguish between "CRS" and "other reactions?"
On page 8 of the Tentative Report, FASEB reports on the Reif-Lehrer questionnaire survey of the prevalence of CRS. I quote from FASEB: "Twenty-five percent of the adult population sampled reported adverse reactions to Chinese restaurant food or food containing exogenous MSG. Most commonly, the 'tightness-burning sensation-headache' triad of symptoms predominated." (The emphasis is mine.)
First, let me suggest that the number given by Reif-Lehrer was 30 percent--not 25 percent. Second, let me suggest that Reif-Lehrer reported that headache was the most prevalent symptom found in her study. She spoke of the "tightness-burning sensation-headache grouping" of symptoms, not a triad of symptoms as FASEB reported. I would submit to you that this subtle change is purposefully misleading. When I first read FASEB's statement, I thought I had read that Reif-Lehrer was saying that the most prevalent symptom was the triad of symptoms that were associated with CRS. Only because I had read her study and knew that such was not the case, did I question my interpretation of FASEB's statement. Why did FASEB choose to blend half-truth and innuendo in referring to a "triad of symptoms" when in fact "headache" was the most often reported symptom?
3. As I understand it, the study is supposed to be concerned with the ultimate welfare of consumers. Why was consumer input not solicited by FASEB?
4. I would expect that we will be told that FASEB solicits nothing from anyone. If that is true, we can expect that the only materials that will be volunteered will be from people with something to gain from providing data. For members of industry, the gain would be monetary. For consumers and independent physicians, if they happened to know about the study, the gain would be in better health for themselves and their patients. Certainly FASEB must understand that. So why has FASEB not solicited input from independent physicians, and scientists? Admittedly that may not be FASEB's normal policy; but FASEB is not prohibited from doing so by the terms of its contract.
5. Why was an announcement of the FASEB study made in the Federal Register and nowhere else? Consumers don't usually read the Federal Register, although food industry representatives do. That doesn't provide much of an opportunity for non-industry people to respond to announcement of the study, but alerts industry interests to respond.
6. On page iii, the Tentative Report states that "FASEB's resources are particularly suited to marshaling the opinions of knowledgeable scientists..." Who are those scientists? Are they people with close ties to the food industry, or are they independent of conflict of interest? Are there neuroscientists among them? From which scientists has FASEB marshaled opinions?
7. If FASEB is marshaling the opinions of knowledgeable scientists, as stated on page iii of the Tentative Report, why does the Tentative Report not mention solicited reports giving the opinions of those eminent scientists? I would expect that the list of eminent scientists would include physicians engaged in the treatment of environmental illness, for example, and I do not see any.
8. On page 1 of the Tentative Report we read that "...the information and data received from FDA have been supplemented by searches of scientific and statistical reference sources..." What data searches have been made? I have identified a number of sources that I would consider significant sources of data missing from the Tentative Report bibliography. For example, more than 100 references found in MSG: A Review of the Literature and Critique of Industry Sponsored Research are missing from the Tentative Report.
9. The contract between FASEB and the FDA provides for evaluation of data held by the FDA. There is, however, no citation in the bibliography to indicate that FASEB has reviewed the case studies on file with the Adverse Reactions Monitoring System (ARMS) of the FDA. I believe that analyses of reviews done by ARMS director Linda Tollefson, D.V.M., M.P.H., demonstrate so much pro-industry, anti-consumer bias, that their use by the FDA is tantamount to fraud. (An analysis of Tollefson's work is enclosed.) To objectively review all available data on MSG-induced adverse reactions, FASEB must evaluate each and every report of MSG-induced sensitivity on file at ARMS. Why has FASEB not done that?
10. As the 18 questions have been reviewed by FASEB, and an evaluation has been made as to whether or not there is sufficient data to respond to them, research is cited that has been criticized by Samuels(1) as being methodologically unsound or making use of assumptions inappropriate to the statistics used. That leads me to believe that MSG: A Review of the Literature and Critique of Industry Sponsored Research, although listed in the bibliography of the current FASEB study, has not been carefully studied. In what manner was that particular study presented to members of the ad hoc Expert Panel or members of the FASEB staff working on the study?
11. On page 3 of the Tentative Report, FASEB asks whether "...[MSG] contributes to the presentation of a complex of symptoms after oral ingestion of levels up to or beyond 5 g/occasion, referred to as the Chinese Restaurant Syndrome, and/or the elicitation of other reactions including more serious adverse reactions that reportedly occur following ingestion of MSG at levels of 25 to 100 mg per eating occasion..."
Why does FASEB make a distinction between "Chinese Restaurant Syndrome" and "more serious adverse reactions?" And where did FASEB get the notion that reactions other than "Chinese Restaurant Syndrome" occur only with doses of MSG between 25 and 100 mg per eating occasion? The reactions reported by consumers to FASEB, and those on file at the FDA consist of a variety of reactions ranging from simple skin rash, a tingling sensation, etc., to tachycardia, asthma, anxiety attacks, depression, etc. The severity of each of those overt reactions can range from mild and short lived to debilitating over a long period of time, and, even, to death. MSG-induced migraine headaches can incapacitate a person for days at a time, and MSG-induced asthma can cause asthma attacks as severe and life threatening as any other asthma trigger.
I know of no MSG-sensitive person who has quantified, or had quantified for him, the amount of MSG needed to induce an adverse reaction. I do know that highly sensitive people react to MSG in skim milk, i.e., to milk solids containing hydrolyzed protein; and to malted barley, a product almost always listed as an ingredient of white flour, but present only occasionally. It would seem to me that the amounts of free glutamate consumed at one meal from either of those sources must be very, very small. I don't believe, however, that anyone has as yet measured the amount of MSG in either of those products.
On the other hand, I know of a number of people who react to MSG with life-threatening reactions only after ingesting high levels of the substance. I am thinking of a person who told me that although he is not sensitive to MSG, he did empathize with MSG-sensitive people because when he ate TVP (textured vegetable protein), he lost consciousness, experienced a precipitous drop in blood pressure, and was rushed to the hospital for treatment which, doctors told him, came within minutes of being too late to revive him. As you well know, MSG is a constituent of TVP. If you'd like to interview my acquaintance, I'd be pleased to call him and ask him to talk to you. I think he'd make the trip to Washington to do so.
12. Why has FASEB not evaluated the relevancy of each of the 18 questions asked in the RFP? FASEB attended to redundancies but not irrelevancies. I would suggest that for most of the questions it matters little, if any, that there might be insufficient data to answer them; for answering most of them would have no immediate benefit for MSG-sensitive consumers; and we are dealing with an issue that has great urgency.
13. On page 6 of the Tentative Report, it is stated that "Chapter V lists the references collected, collated, and examined for the Phase I study." The Tentative Report states that "As of February 17, 1993, LSRO received 59 letters from individuals describing reactions..." I am concerned because no references are made in Chapter V to data from people writing to FASEB about their sensitivities. This suggests to me that FASEB will not consider data from individual MSG-sensitive consumers, except, possibly, to summarize them as "complaints" as has been done in Tables 1 and 2 of the Tentative Report. How does FASEB intend to treat the reports of MSG-sensitive consumers? Why are those letters not included in the references listed in Part V of the Tentative Report?
Following this reasoning, I note that individual reports on file with ARMS are not listed in Chapter V either. That suggests that FASEB will not consider data (data as opposed to a biased summary of those data) on file at the FDA, either.
14. FASEB's discussion of "Reports of Adverse Effects" is particularly bothersome. It is bothersome because of the extent to which half-truths are blended with innuendo, and objectivity is obscured. It is also bothersome because any semblance of a focus on risk occurs in only two places in the Tentative Report, and this is one of them.
I note, first, that in a number of instances, FASEB has used terms provided for it by the FDA, taking conjecture and treating it as fact. Question 1, discussed on page 7 of the Tentative Report, contains the words "temporary," and "self-limited," referring to classes of adverse reaction reported to occur with ingestion of MSG. FASEB contrasts "temporary" and "self-limited" to "serious (life-threatening)." The work of Olney and others has exposed the fact that ingestion of MSG by laboratory animals causes not only brain lesions, but neuroendocrine problems that remain unresolved for a lifetime. If MSG caused brain lesions and neuroendocrine disorders in animals, wouldn't you be concerned that MSG might cause brain lesions and neuroendocrine disorders in humans, too? But FASEB has provided no category for these unremitting conditions. Certainly, brain lesions and neuroendocrine disfunction would not be considered "temporary" or "self-limited," would they?
I know that there has been no systematic study of MSG-induced brain damage and/or neuroendocrine disfunction in humans; but animal research plus the reports of MSG-sensitive people tell us that those conditions exist. Why has FASEB not discussed them?
I know of no research that has even attempted to evaluate whether a human adverse reaction that is objectively visible for only a short length of time has any long term affects on humans. Do repeated asthma attacks, for example, weaken any system of the body, making it increasingly more susceptible to asthma attacks or other disorders? If they do, then one could not say that an adverse reaction was solely "temporary" or "self-limited." Why is FASEB using these terms?
15. Still looking at the particularly bothersome section on "Reports of Adverse Effects," I note that if one were to read this portion of the report without knowing the data, an entirely erroneously picture of the nature of the reactions to MSG would be drawn.
There are three parts to the answer to the first question: Reported symptoms and signs of adverse reactions (acute, temporary, and self-limited). The first part summarizes data from the literature. At this point, the first data are presented; and an incomplete summary is given (pages 7 and 8). That summary omits a number of reactions that should be of interest and/or concern.
The list of adverse reactions reported on pages 7 and 8 of the Tentative Report does not include migraine headache, tachycardia, depression, hyperactivity in children, attention deficit disorders, skin rash, or orofacial granulomatosis, even though they have all been reported in the literature [Scopp,(2) Gann,(3) Coleman,(4) Buist,(5) Oliver(6)]. Is it because they sound more serious than the reactions that were mentioned? An omission of this sort is an example of the kind of half-truth so often given by representatives of the glutamate industry. How does FASEB justify this sort of half-truth?
Being both an educator and an experimental psychologist by training, I am aware that readers often skim materials such as the Tentative Report, looking at the first part of any defined section, and ignoring detail laid out in figures and tables. Thus, I would expect that readers of the Tentative Report will notice only this first, incomplete, list of adverse reactions and not notice that it differs from the list of adverse reactions reported by consumers, appearing a page later.
Setting up the Tentative Report in this way also gives glutamate industry representatives an opportunity to quote from one section of the Tentative Report without having to tell the whole story. I find it hard to believe that FASEB would make this kind of error.
The second part of "Reports of Adverse Effects" talks about consumer "complaints." I find it interesting that from the literature we get "reports," but from consumers we get "complaints." Subtle bias? Yes, subtle bias, and another example of the sort of half-truths and innuendo used by representatives of the glutamate industry. How does FASEB justify this use of innuendo?
Note also in "Reports of Adverse Effects" the use of the words "alleged" as in "alleged MSG-induced symptoms..." and "reportedly" as in "complaints reportedly resulting from ingestion of MSG." There is a section of the report called "Category IV: Statements of Authoritative Organizations." I would guess that the information in that section comes directly (or indirectly through the FDA) from The Glutamate Association, for I have seen that material used in things that they distribute. But FASEB has not used the term "alleged" to refer to "Authoritative organizations." Why?
16. If you read the section on consumer complaints, you will note that demographics are given, but no report of the time frame within which reactions occur. Thus we have only a summary of data from the literature that leaves one with the impression that symptoms typically occur within 20 to 25 minutes of consuming foods containing glutamates and that they last for about 1 to 2 hours. The truth of the matter, however, is that researchers, for the most part, only tracked possible reactions to MSG for an hour or two after MSG was given, and, using the definition of CRS as their guide to what was or was not a true MSG reaction, did not consider later reactions, or non CRS reactions, as being induced by MSG. Consumers have reported reactions occurring immediately after MSG ingestion or as late as 48 or 72 hours after eating; but FASEB presents no information taken from MSG-sensitive consumers on onset or duration of reactions. We have here another example of the sort of half-truths used by representatives of the glutamate industry. How does FASEB justify this sort of half-truth?
17. The Tentative Report also states on page 8 that in the literature, symptoms ranged from mild to moderate, rarely severe. How are the words "rarely" and "severe" defined?
On page 8 of the Tentative Report it says that "Mild or moderate symptoms were reported by 66 percent of complainants, severe reactions by 8.2 percent." Why are there 25.8 percent unaccounted for?
18. What does "The average number of symptoms per person was 1 to 4" mean? (The emphasis is mine.)
19. On page 8 of the Tentative Report, FASEB mentioned one study done by Reif-Lehrer and one study done by Kerr et al. FASEB's imprecise treatment of the Reif-Lehrer study was discussed in some detail on page 11. In discussing the Kerr, et al. study, FASEB stated that "About 3 to 7 percent reported symptoms that were compatible with a diagnosis of CRS," and further commented that "These investigators estimated the prevalence of CRS in the general population at less than 7 percent." Why is FASEB citing research on "CRS" (defined on page 7 as the Chinese Restaurant Syndrome reported by Kwok in 1968) and ignoring the whole range of other reactions attributed to ingestion or other use of MSG? Why has FASEB not noted that Kerr found MSG type reactions in 43 percent of his subjects but chose to eliminate all reactions except the triad known as CRS, occurring all at the same time, and within a highly restricted time frame, in presenting his conclusions?
20. Table 1 on page 9 lists cumulative MSG consumer "complaints" to FDA by Reported Symptoms. Don't you think that 19.9 percent is an awfully large category for "Other?" I know that in classifying complaints about aspartame, the FDA classifies death under "Other." Does the FDA do that for MSG, too? What complaints are in the category "Other?"
21. Table 2 on pages 10 and 11 classifies 27.6 percent of the symptoms under "Other." Table 2 is a list of cumulative MSG consumer complaints received by FASEB. How can FASEB justify a category for "Other" constituting 27.6 percent of its sample? What complaints are in the category "Other?"
22. On page 12 there is discussion of types of serious reactions reported. Who has determined what is "serious" and what is not? I know a women who was told that her otherwise undiagnosed reactions (irritability, nausea, and vomiting) occurred because she was under a great deal of stress, and that the solution would be to dissolve her marriage. She followed the advice of her physician, got a divorce, but had no reduction in adverse reactions--until she stopped eating food that contained MSG. I think her state of chronic illness: her irritability, nausea, and vomiting; constituted a "serious" reaction. I also know an airplane pilot who becomes dizzy and disoriented when he ingests MSG. I think that "pilot error" is a "serious" reaction.
23. A distinction has been made between MSG and PH (protein hydrolysates). Why is that distinction made by FASEB? I have letters from the FDA dated March 3, 1981 and October 4, 1991 stating that MSG (glutamate) is a constituent of hydrolyzed protein. The FDA does not dispute the fact that all protein hydrolysates contain MSG (glutamate). I read it in the January 6, 1993 Federal Register.
24. FASEB uses the terms "accessory" and "predisposing factors." What is meant by "accessory?" Why is there discussion of "predisposing factors?" Any event, any happening, can be reviewed for the factors or conditions that preceded it. For any event or happening there are predisposing factors. If MSG is a toxic substance (and there can be no dispute about that), then it should be identified as such, regardless of whether or not there is some subgroup in the population that is more sensitive to the substance than others. Certainly it is of value to understand the correlates of MSG-induced adverse reactions; but don't you find that a discussion of "accessory" and "predisposing factors" detracts from an evaluation of risk?
25. Time after time, the Tentative Report discusses the conclusions (or lack thereof) of "investigators," but fails to take into account data available to FASEB in the files of ARMS or data provided to FASEB in letters sent by physicians and consumers. Discussion of "Dose Responsiveness," on page 13, is a case in point. According to the Tentative Report, "this topic has not been thoroughly studied, and the available data are insufficient to warrant firm conclusions." Were FASEB to review the reports of MSG-sensitive people, however, it would be abundantly clear that reactions vary with the amount of MSG ingested. Unfortunately, since MSG is so often hidden in food and, even if labeled as such, is identified without specification of the amount of MSG to be found in the end product of a food item, neither the consumer or physician would have any way to estimate the amount of MSG it takes to cause various reactions in MSG-sensitive people. Why has FASEB not included data from consumers in the Tentative Report?
26. Why does FASEB have a section on "other authoritative organizations?" Was the concept of "other authoritative organizations" developed so that glutamate industry interests could come up with a list of "authorities" to suite their needs? I know that the Institute of Food Technologists (IFT), the World Health Organization (WHO), the American Medical Association Council on Scientific Affairs (AMA), and the Commission of the European Communities (EC) all obtained their data either directly or indirectly from The Glutamate Association, the International Glutamate Technical Committee (IGTC), and/or ARMS, and came to the same conclusion that The Glutamate Association and the IGTC came to. Is that what makes them "authoritative?" They are listed in your section on "other authoritative organizations."
FASEB forgot to include the Ad Hoc Advisory Committee on Hypersensitivity to Food Constituents convened by the FDA in or about 1985 to its list of "other authoritative organizations." Did FASEB fail to mention them because it is common knowledge that the materials that they reviewed were hand carried to committee members by The Glutamate Association? FASEB also forgot to include the opinions of the Social Issues Committee of the Society for Neuroscience. They sound authoritative (much more so than the Helen Keller Institute). Why did FASEB overlook them? Why did FASEB include the Helen Keller International?
FASEB also neglected to include FASEB, 1992 as an "authoritative organization," even though it included FASEB, 1978 and FASEB, 1980 (identified as SCOGS, 1978 and SCOGS, 1980, respectively). Could that slight be attribute to the fact that FASEB, 1992 concluded, in part that:
"...it is prudent to avoid the use of dietary supplements of L-glutamic acid by pregnant women, infants, and children.... and...by women of childbearing age and individuals with affective disorders."(7)27. On page 25, the Tentative Report states that "The Expert Panel concluded that the most appropriate group for the investigation of potential adverse effects of MSG or PH used as food ingredients in the food supply would be healthy adults with no preexisting medical conditions."
If I were investigating the safety/toxicity of MSG, and I wanted to
be certain that I could come up with a study wherein few people, if any,
reacted to MSG, I would choose to study people who had no history of adverse
reactions--to anything. By identifying "healthy adults with no preexisting
medical conditions" as FASEB would do, FASEB would be essentially eliminating
all of the people who had experienced headache, migraine headache, asthma,
tachycardia, depression, seizures, gastric distress, anxiety attacks, sleep
disorders, etc., i.e., many, if not all, of the people who had ever had
reactions induced by MSG. Who proposed that the most appropriate group
for the investigation would be people who could not possibly be sensitive
There are a number of significant questions that need to be asked by anyone attempting to understand the toxic effects of MSG. Admittedly there is little known in many of these areas, and not all of the questions focus on risk. But this is true, also, of other areas where FASEB has chosen to ask questions. Is it possible that FASEB has not asked the following questions because raising those questions would prove to be embarrassing for the glutamate industry?
1. It has been documented that elevated levels of brain glutamate are found in people who die with a variety of neurodegenerative diseases including ALS, Huntington's disease, and Alzheimer's disease. What do we know about the relationship of ingestion of MSG and incidence of such neurodegenerative diseases? What is the relationship of MSG ingestion to Parkinson's disease?
2. In his studies on ALS, Spencer has described the toxic effects of the neurotoxic cycad plant. According to Spencer, et al., "A latent period of years or decades seems to intervene between cycad exposure and clinical expression of disease."(8) Spencer now refers to this phenomenon as a "slow neurotoxin." If there is a substance that can act as a slow neurotoxin, is there any evidence to suggest that glutamate can not act in the same way? What do we know about the workings of a slow neurotoxin?
3. It is often noted in glutamate industry supported literature that the adult brain is protected by a blood-brain barrier, impervious to the penetration of excess quantities of excitatory amino acids. The fact is, however, that there are circumventricular organs in the brain without efficient blood-brain barriers.(9,10) What are the areas of the brain that are without efficient blood-brain barriers? What functions do they control? What do we know about effects of MSG on these areas?
4. There are a number of analogs of glutamate that appear in the food supply. Aspartic acid or aspartate is an example. What analogs are known to exist? Are there reports of adverse reactions association with some or all of the them? What do we know about the mechanisms underlying the toxicity of these substances?
5. We know that MSG causes brain lesions and neuroendocrine disorders in laboratory animals. What is the potential for using MRI or PET SCAN techniques for examining the hypothalamus in general or some of the circumventricular organs in the brains of highly MSG-sensitive people to determine whether MSG causes brain lesions in humans, too? Do we have the sophistication to study brain activity during or immediately following ingestion of MSG?
6. We know that glutamate is both a neurotransmitter and a neurotoxic substance. We suspect that most, if not all, of the human adverse reactions might be neurologically induced. In what way(s) are the adverse reactions reported following ingestion of MSG similar to reactions or side effects of other neurotropic drugs?
7. Highly sensitive MSG-sensitive consumers report that cosmetics, soaps, and shampoos containing hydrolyzed proteins cause MSG-induced adverse reactions. What might be the mechanisms that facilitate such response?
8. Stegink and others have failed to find a relationship between such things as blood glutamate levels, blood pressure, heart rate, blood glucose levels, etc, and ingestion of MSG. I would expect that if blood glutamate levels, blood pressure, etc. were influenced by MSG-ingestion, people who demonstrated MSG-induced adverse reactions might express different blood glutamate levels, blood pressure, blood glucose, etc., than would people who demonstrate no overt reactions to ingestion of MSG. Most, if not all of the studies done to date that purport to examine these correlations can be criticized because MSG-sensitive people have not been used in the studies. There has never been systematic and comprehensive study of known MSG-sensitive people, much less of acutely MSG-sensitive people, to determine if blood glutamate levels, blood pressure, blood glucose levels, etc., might be affected--either increased or reduced--by ingestion of MSG. What do we know about the body function of acutely sensitive MSG-sensitive people?
9. MSG-sensitive people often report that more than one symptom or reaction occurs following ingestion of MSG. But there appear to be no "sets" of symptoms or reactions that always occur together. MSG-sensitive people would gladly share information on their reactions with people interested in understanding the etiology of MSG-induced adverse reactions. What kinds of researchers would be interested in looking into this question? Is there any information on "sets" of symptoms?
10. Samuels1 has presented evidence that, by and large, industry sponsored studies are methodologically unsound and that conclusions drawn from statistical analyses are unwarranted. Have other statisticians, people with no ties to the food industry, studied those data, and if so, have they found the same thing?
11. The literature suggests that ingestion and uptake of MSG (a free form amino acid) is different than ingestion/digestion/ metabolism of amino acids released following their ingestion as protein.1 Certainly we know that the flavor enhancing effects of MSG are immediate, having no relation to our traditional understanding of digestion and metabolism. There is no reason to believe that the uptake of MSG is the same as the digestion of amino acids released from protein in the stomach and lower intestines. What do we know about the uptake of MSG?
12. Why do books on pregnancy and child birth advise against using MSG and aspartame during pregnancy and during breast feeding?
13. What causes headache clinics to cite MSG as a migraine headache trigger?
14. Why do MSG-sensitive people react to MSG that occurs in food as a consequence of manufacture but not to the glutamate (non-manufactured) in such things as unadulterated tomatoes, mushrooms, and old fashioned parmesan cheese?
15. What are the mechanisms that cause MSG-sensitive people to react to MSG?
16. We know that neucleotides work synergistically with MSG to enhance
flavor. Do they also work synergistically with MSG to promote neurotoxicity?
THE 18 QUESTIONS
The FDA listed 18 core questions in its request for proposal, and FASEB has responded to them all. I have written out each of the questions (in bold print) and commented briefly on them, even though, for the most part, attempting to answer them has little value for MSG-sensitive people, but rather serves to distract those reading the Tentative Report from the question of risk.
1. What are the symptoms and signs of acute, temporary and "self-limited" adverse reactions that have been reported to occur with oral ingestion of MSG? These are listed in Table 1 of this paper.
Do these reports provide a basis for establishing causality by MSG? Dr. Linda Tollefson, Dr. Fred Shank, and Dr. David Kessler of the FDA say they do not. Representatives of the glutamate industry say they do not. MSG-sensitive people say that when they avoid ingestingingesting or otherwise using MSG, adverse reactions (Table 1) no longer express themselves. Some MSG-sensitive people have been diagnosed as being MSG-sensitive by physicians.
Do these reports indicate a dose-related response or a requirement for accessory factors, such as predisposing medical or dietary conditions, in the occurrence or relative severity of the adverse reactions? There are reports that the MSG reaction is dose-related. There are reports that the consumption of small amounts of alcohol and/or physical stress serve to intensify adverse reactions in some cases, and that the reaction to MSG is greater when MSG is consumed "on an empty stomach." There is also a theory that MSG attacks the weakest organ or system in a person's body.
2. What serious (life-threatening) reactions have been reported to occur with oral ingestion of MSG? From the list enclosed we would consider asthma, tachycardia, arrhythmias, vaso-vagal reactions, loss of blood pressure, and depression potentially directly life threatening. Extended vomiting that leads to dehydration and swelling that leads to a closing of the throat would be life threatening, too.
Reactions like fatigue, dizziness, disorientation, migraine headache, nausea and vomiting could easily result in what we call "human error"--the kind of errors that cause car accidents and air plane crashes. Depression can lead to murder and/or suicide.
What is the quantity and quality of these reports? The quantity of these reports is small, for the FDA discourages receiving them. There is no "form" to guide consumers in the preparation of reports, so the quality will very likely be considered poor.
How do dose and time relationships compare with "self-limited" adverse reactions? I don't know what "self-limited" reactions are. There are overt reactions to MSG--we can feel them or see them. We also suspect that there are lasting effects that we do not immediately see. Peter Spencer talks about a "slow neurotoxin" associated with ingestion of the cycad seed.8 There is good reason to suspect that the concept of "slow neurotoxin" may apply to the neurotoxic amino acid MSG, too. We have no evidence that it does. Neither do we have evidence that it doesn't.
Are there predisposing medical conditions associated with specific reactions? It has been suggested that any insult to the system predisposes an individual to sensitivity to MSG. We are aware that a number of people who suffer adverse reactions to MSG also have mitral-valve prolapse. A doctor friend told me that all of his patients with hiatal hernia are MSG-sensitive. Whether there might be cause or effect here, we do not know.
It would appear that the vagus nerve possibly plays a roll in some, if not all, MSG-induced reactions. Scher and Scher(11) have suggested that nitric oxide transport might have a role in the expression of MSG-induced toxicity. To my knowledge, however, no one has studied these, or any other relationships. There is no volume of data on this general subject.
3. Assuming that reproducible association with MSG ingestion can be demonstrated, what is a reasonable classification scheme for the various types of adverse reactions to MSG that have been reported? As long as the studies that purport to examine reproducible associations with MSG ingestion administer ineffective amounts of MSG, in such things as capsules (which is not the way MSG is presented in food), fail to control subjects' diets for a period of days prior to and after administration of test materials, use placebo materials that contain MSG in the form of hydrolyzed proteins or use highly allergenic substances, and arbitrarily limit reaction time to less than 48 hours, there will be no reproducible reactions recorded in the laboratory.
MSG-sensitive people who do not know about the hidden sources of MSG reproduce their reactions every day.
Reproducible associations or not, the adverse reactions to MSG can be classified just as reactions to other neurotropic drugs are classified.
4. Is it possible to classify adverse reactions based upon [a variety of factors]? It would be possible, if there were data, but as of this date there have been no data gathered to fill this function. Hypotheses need to be generated and data gathered to test them. It would not be difficult, for there exists a large base of MSG-sensitive people. It is my understanding, however, that the contractors are explicitly prohibited from collecting data by the terms of the contract; and because the FDA tells physicians and scientists that MSG is safe, there is no motivation to fund such a project.
5. Is it possible to determine the mechanism whereby any glutamate-based adverse reaction might occur? Of course it is possible. But with the FDA telling physicians and scientists that MSG is safe, it is unlikely that research money will be made available to do so. Industry appears to have research money, but it is spent on double-blind studies designed to "prove" that MSG is safe.
We have already indicated that there appears to be a great deal of mitral-valve prolapse associated with severe sensitivity to MSG. It would also appear that the vagus nerve is implicated in most, if not all, of the MSG adverse reactions. Scher and Scher11 have suggested that nitric oxide might be implicated. As of this date, no one has looked carefully at these questions.
6. What have other authoritative organizations concluded regarding the potential of MSG to elicit adverse clinical reactions? What is the basis for their decisions? It would appear from a review of the bibliographies of the "other authoritative organizations" that those selected by FASEB have based their conclusions on materials provided to them by The Glutamate Association and/or the International Glutamate Technical Committee. A letter from Andrew G. Ebert of the International Glutamate Technical Committee to Lawrence J. Lin of the FDA tends to confirm this appraisal. These are authoritative organizations vis-a-vis MSG only in the eyes of representatives of the glutamate industry.
7. What are the free glutamate levels in food containing hydrolyzed vegetable protein (HVP) as used in the range of products manufactured for consumption by American consumers? We have no meaningful data on free glutamate levels in any of the products that contain MSG. The range appears to be broad; and many products contain multiple sources of MSG.
What is the evidence that HVP ingestion is associated with adverse reactions similar to those reported to occur after MSG ingestion? The product called "monosodium glutamate"("MSG") by the FDA for purposes of labeling, is the result of protein hydrolysis and refinement resulting in a product containing 98 percent or more L-glutamate. It is L-glutamate that causes both brain lesions and neuroendocrine disorders in laboratory animals, and adverse reactions in humans [(Olney(12,13) and Schaumburg(14)]. All hydrolyzed protein contains some free L-glutamate. Therefore, if "MSG" causes adverse reactions, other hydrolyzed proteins do, too. The Federal Register of January 6, 1993, states clearly that "All hydrolyzed protein contains MSG."(15) Consumers who are MSG-sensitive have reported that they react to food labeled with the words "monosodium glutamate," "hydrolyzed protein," "sodium caseinate," "yeast extract," "autolyzed yeast," "flavoring," "broth," "natural flavoring," "seasonings," and more. All are sources of hydrolyzed protein. All contain MSG.
Have life-threatening adverse reactions been verified to occur with the levels of glutamate reported to be used in this range of products? Since the FDA refuses to accept clinical reports of MSG reactions as having any basis in fact, and many products that contain hydrolyzed proteins are unlabeled, how would life-threatening adverse reactions to HVP possibly be verified?
8. Are there any defined human subgroups that are more susceptible to glutamate than the general population? There has been no research on the question.
9. Are there clinical adverse reaction reports of physiological mechanisms that would explain why a glutamate sensitive individual might respond adversely to "synthetic" or added MSG but not to comparable levels of free glutamates that occur naturally in such food products as tomato juice and parmesan cheese? There is little or nothing "in the literature" to suggest that MSG-sensitive people respond any differently to free glutamates that are manufactured as opposed to non-manufactured. MSG-sensitive people, however, report that they react only to glutamate freed as a consequence of manufacture. The figures given in industry sponsored reports of free glutamate in food such as tomato and parmesan cheese have been grossly overstated, and thus it is entirely possible that MSG-sensitive people do not respond to this "natural" free glutamate because there is very little of it. It is also possible that when nature produces free glutamate, it produces it in a particular balance with other amino acids.
It must be noted that "tomato juice" and "parmesan cheese" are processed products. It would be very easy for industry interests to produce high levels of free glutamate in tomato juice and parmesan cheese if they desired to do so.
Is there evidence that adverse reactions similar to those reported for MSG occur when foods naturally high in glutamates are consumed? No. MSG sensitive people report that they can eat protein (in which glutamate is found bound in the protein chain) without ill effect.
10. During testing for MSG-mediation of adverse reactions, what is a reasonable range of doses to be administered to assure that potentially MSG-sensitive individuals would be detected for each class of adverse reaction while assuring patient safety? What study designs are appropriate for testing MSG mediation of different types of reported adverse reactions?
11. During testing for MSG-mediation of each class of adverse reactions, what is the best manner to control for various possible disease triggers? What are the appropriate subject selection criteria? Can the test solution be adequately blinded? When is it appropriate to use MSG in capsules rather than in solution or in food matrices? What sample size is needed to assure that adequate sensitivity is present to detect an effect or the absence of an effect?
Questions 10 and 11 focus on experimental design. The glutamate industry has a history of attempting to "guide" people to focus on the results of industry sponsored double-blind studies that appear to be purposefully designed to obscure the fact that there is sufficient data in the literature and on file at the FDA to demonstrate that MSG ingestion poses risk to the American people. We have considerable evidence that tells us that some, if not all, of those studies have made use of inappropriate placebo materials,1 which guarantees them that placebos will be responded to. That fact, combined with faulty reasoning, enables them to then contend that MSG has not been found to be unsafe.
It would appear that questions 10 and 11 are directed at aiding and abetting the glutamate industry in maintaining a focus on such studies, and legitimizing the fact that at present they are busy setting up more double-blind studies.
The need to test for MSG sensitivity using double blind procedures and glutamate industry protocols, is a need of industry to obscure the fact that MSG poses a hazard to human health. Blinding is done all the time by consumers. They eat food they think is safe; they get sick; and then they discover that what they ate contained MSG.
12. What are the relative sensitivities of rodents and nonhuman primates to the acute central nervous system (CNS) effects of MSG?
13. Are there any studies conducted "in vivo" during the 1980's or 1990's that provide additional insight concerning the capacity of orally-administered MSG to mediate acute damage (lesion) of the arcuate nucleus of the anterior hypothalamus or of other circumventricular structures in the CNS of nonhuman primates?
Questions 12 and 13 come from interest in extrapolation of data from animal studies to a consideration of the safety of MSG for humans. Animal studies are widely used in drug testing where use of drugs on humans might be dangerous; yet representatives of the glutamate industry spend a lot of time and money attempting to convince people that MSG-induced brain lesions and neuroendocrine disorders in laboratory animals have no relevance to humans. Questions 12 and 13 are typical of questions used by industry to detract from the relevancy of animal studies.
14. What evidence is available concerning the ability of exogenously administered MSG to mediate changes in pituitary function following acute oral or parenteral dosing. What controls were used to demonstrate that this effect was specific to MSG and not related to non-specific changes in such factors as plasma pH or osmolarity? What evidence is provided that specific excitatory neurotransmitter receptors are involved in any effect observed?
When legitimate areas of concern give rise to questions that truly appear to be interesting, such as those that would appear to underlie questions 13, 14, and possibly 15, representatives of the glutamate industry have raised questions that sound important, but are not vital to assessing human risk. Because no data are available in these areas (such as new "in vivo" studies or nonhuman primates), and the questions sound important, one is left with the impression that we don't have enough data to assess human risk; and that simply is not so. That tactic appears to have been applied here.
15. What are the comparative blood levels of glutamate and aspartate that are produced from large orally administered doses of MSG from solutions (such as in clear soups) and the blood levels inducing the release of luteinizing hormone in non-human primates? What is the probability of MSG ingestion with foods influencing the release of pituitary hormones?
16. What are the relative effects of treatment conditions, or circumstances of oral ingestion, on the plasma concentrations of MSG, i.e., does MSG given in water produce a different plasma level of glutamate than the same dose given in a more complex food matrix containing carbohydrates? What influence does strength of MSG concentration and mode of administration (human sipping versus animal gavage) have on plasma levels of glutamate?
17. What evidence is available concerning the relative rates of MSG metabolism in infants, children and adults? What is the evidence for altered sensitivity of the CNS to circulating levels of glutamates?
One of the favorite ploys of the glutamate industry representatives is to look in the wrong place, at the wrong time, for the wrong thing as in questions 15, 16, and 17. If, for example, human research on MSG-sensitivity is done, to be meaningful, it must be done on MSG-sensitive people. I believe that glutamate industry representatives focus on blood glutamate levels in humans because elevated levels have not been associated with adverse reactions to MSG in the people they study, i.e., non-sensitive people. To my knowledge, no proper evaluation of blood glutamate levels, using highly sensitive people, has ever been done.
18. What have other authoritative organizations concluded regarding the potential of MSG to elicit neurotoxic reactions? What are the bases for their conclusions?
Question 18, a concept being pushed particularly hard by The Glutamate Association of late, is a repeat of the same question asked earlier.
I had to laugh when I turned to page 32 of the Tentative Report: "Issues of Concern." Where did FASEB get these "issues of concern?" Is FASEB concerned that there are not enough meaningless questions asked already? Why is FASEB talking about a need to ask additional questions in order to evaluate "the potential adverse effects of MSG?" And the questions! Food grade specifications; available glutamate; demographic analysis; more double-blind studies; primate studies.
Are brain lesions and neuroendocrine disorders "potential" effects? Are migraine headache, asthma, tachycardia, etc. "potential" effects? FASEB has industry sponsored data in its hands. Does FASEB not have the expertise to read it and see that much of it is flawed to the point of being fraudulent? Industry has failed to "prove" that MSG is safe. FASEB has data from independent scientists and MSG-sensitive consumers in its hands. Does FASEB not have the expertise to look at the data and ascertain that ingestion of MSG, a substance that no scientist will deny is neurotoxic, places humans at risk?
Enclosed you will find a list of references sufficient to prove to any objective observer that MSG places humans at risk.
I have asked FASEB to ask for the resignations of the two members of the Expert Panel who have done work for the manufacturers of the neurotoxic amino acid aspartate or aspartic acid, a significant component of aspartame. I asked for their resignations solely on the basis of conflict of interest. I made my request before I received a copy of the Tentative Report.
Now that I have read the Tentative Report, I am certain that I did the right thing. I had expected FASEB to whitewash the question of MSG safety/toxicity, but I thought the whitewash would at least be subtle. FASEB has abrogated its responsibility to look beyond glutamate industry propaganda and fraudulent studies and ferret out the facts. The Tentative Report is an embarrassment to the Clinton administration and an insult to the American people.
I think you know by now, Dr. Fisher, that I make no statement of fact without data in my files to substantiate it. I would be pleased to expand upon what has been said in this submission, clarify any aspect of the submission that FASEB or the Expert Panel finds unclear, and defend any position with which FASEB and/or the Expert Panel disagrees. I would gladly make myself available during the FASEB open hearings or any time during the month of April, if that would be of value to FASEB.
I look forward to your reply.
Adrienne Samuels, Ph.D.
540 Frontage Road
Northfield, IL 60093
1. Samuels, A. MSG: A Review of the Literature and Critique of Industry Sponsored Research. Food and Drug Administration, Docket No 90N-0379, submitted by Jack L. Samuels as supplement to testimony presented to FASEB/LSRO on Evaluation of the Safety of Amino Acids and Related Products in Nutrients and Supplements, February 4, 1991. Also on file in FDA Docket No 92N-0391.
2. Scopp, A.L. MSG and hydrolyzed vegetable protein induced headache: review and case studies. Headache. 31:107-110, 1991.
3. Gann, D. Ventricular tachycardia in a patient with the "Chinese restaurant syndrome." Southern Medical J. 70: 879-880, 1977.
4. Coleman, A.D. Possible psychiatric reactions to monosodium glutamate. N Engl J Med. 299: 902, 1978.
5. Buist, R. Food Chemical Sensitivity. Garden City Park, NY: Avery, 1988.
6. Oliver, A.J., Rich, A.M., Reade, P.C., Varigos, G.A., and Radden, B.G. Monosodium glutamate-related orofacial granulomatosis. Oral Surg Oral Med Oral Pathol. 1991;71:560-564.
7. Anderson, S.A., and Raiten, D.J. Safety of amino acids used as dietary supplements. Prepared for the Food and Drug Administration under Contract No. FDA 223-88-2142 by the Life Sciences Research Office, FASEB. Available from: Special Publications, FASEB, Rockville, MD.
8. Spencer, P.S., Kisby, G.E., and Ludolph, A.C. Cycad exposure and amyotrophic lateral sclerosis and parkinsonism-dementia complex (ALS/P-D) in the Pacific zone, including Japan. Proceedings of the XIth International Congress of Neuropathology. Kyoto, September 2-8. 1990, pp219-224.
9. Price, M.T., Olney, J.W., Lowry, O.H. and Buchsbaum, S. Uptake of exogenous glutamate and aspartate by circumventricular organs but not other regions of brain. J Neurochem. 1981;36:1774-1780.
10. Weindl, A. Neuroendocrine aspects of circumventricular organs. In: Frontiers in Neuroendocrinology, ed W.F. Ganong and L. Martin. pp3-32. New York: Oxford University Press, 1973.
11. Scher, W., and Scher, B.M. A possible role for nitric oxide in glutamate (MSG)-induced Chinese restaurant syndrome, glutamate-induced asthma, 'Hot-dog headache', pugilistic Alzheimer's disease, and other disorders. Medical hypotheses. 1992;38:185-188.
12. Olney, J.W. Brain lesions, obesity, and other disturbances in mice treated with monosodium glutamate. Science. 164: 719-721, 1969.
13. Olney, J.W., Labruyere, J., and DeGubareff, T. Brain damage in mice from voluntary ingestion of glutamate and aspartate. Neurobehav Toxicol. 2: 125-129, 1980.
14. Schaumburg, H.H., Byck, R., Gerstl, R., and Mashman, J.H. Monosodium L-glutamate: its pharmacology and role in the Chinese Restaurant Syndrome. Science. 1969;163:826-828.
15. Federal Register January 6, 1993, page 2855.
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IF MSG ISN'T HARMFUL, WHY IS IT HIDDEN?