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Monosodium glutamate and the Chinese Restaurant Syndrome: a review of food additive safety.

Introduction

In the spring of 1968, Dr. Robert Ho-Man Kwok wrote to The New England Journal of Medicine asking the assistance of the Journal's readership in identifying the source of a phenomenon that Dr. Kwok labeled the Chinese Restaurant Syndrome (CRS): numbness of his back and neck, palpitations, and general weakness after he consumed meals in Chinese restaurants. Dr. Kwok hypothesized that the cause of his syndrome might be a reaction to the soy sauce, the cooking wine, the high sodium content of the food, or to the flavor-enhancer monosodium glutamate (MSG) (1). Within two months, the Journal received a flurry of letters from readers who had noticed a similar phenomenon after eating restaurant-prepared Chinese food (2,3,4,5). The Chinese Restaurant Syndrome was here to stay. Since that time the majority of the research has focused on MSG as the causative agent. This paper will summarize the existing literature on CRS; on MSG toxicity in animals; as well as on the toxicity of MSG in humans.

Prevalence and Symptoms of CRS

The prevalence of the Chinese Restaurant Syndrome in the American population has been reported to be as high as 7%; however, this figure was obtained during a survey of a medical school population. Because it has been shown that individuals who are aware of the syndrome and its symptoms are more likely to report experiencing the syndrome, this figure is believed to represent overreporting. When a random sample of the American population was surveyed, only 1% reported CRS-like symptoms associated with consumption of food. This figure is believed to estimate more closely the true prevalence of the syndrome (6).

CRS is characterized by a triad of symptoms, including a "burning sensation" on the back of the neck, forearms, and chest; facial pressure or tightness; and tingling and weakness in the face, temples, upper back, neck, and arms. Chest pain, headache, nausea, and vomiting are also commonly reported. These symptoms typically begin within 25 minutes after consumption of MSG or of food containing the additive; last about 2 hours; and are self-limited (7). Case reports have also linked MSG with ventricular tachycardia (8); with rashes, depression, runny nose, and arthritis (9); and with asthma, symptoms beginning as late as 15 hours after consumption of MSG (10). Because the existing clinical research has focused primarily on the CRS triad of symptoms, this discussion is limited to this area.

History of MSG

Chemically, MSG is monosodium L-glutamate monohydrate, the sodium salt of the amino acid glutamate. Only the L-isomer acts as a flavor enhancer. It was chemically isolated in 1908, by Kikunae Ikeda, who identified it as the key agent in sea tangles which Japanese cooks had used for centuries for flavoring (9). MSG is manufactured commercially by the fermentation of starch, molasses, or sugar (11). The American food processing industry has used MSG widely since the late 1940s (9), and consumption in this country is estimated to be 28,000 tons per year (12). Consumed on its own, MSG has a unique taste which has been described as being separate from the basic tastes of sweet, sour, salty, and bitter. However, as a food ingredient MSG enhances the flavor of meat or poultry, as well as increases the "total taste intensity of food" (13). Interestingly, there is a threshold for this effect. Above 60 mg/kg, MSG decreases the palatability of food (14). Free glutamate is found as a natural component in many foods in addition to sea tangles. The fact that concentrations as high as 260 mg/100 g are found in tomato juice and 1,200 mg/100 g in parmesan cheese has led some people to speculate that free glutamate can also act as a flavor enhancer, and that this natural property has historically guided our choices of food combinations (12). Incidentally, there have been no reports of adverse effects associated with naturally-occurring glutamate (7).

Physiology of Glutamate

Physiologically, glutamate is one of the most commonly occurring amino acids. It plays a crucial role in a broad variety of metabolic processes. Glutamate acts as a donator of amino and methyl groups for the synthesis of nonessential amino acids. Glutamate is used for energy transfer in the form of alpha-ketoglutarate during the TCA cycle. Glutamate is used for transport of amino acids across cell membranes, as well as for the removal of ammonia from metabolically active cells via the urea cycle. Glutamate also plays a role in the detoxification of drugs (15). Lastly, it is a mammalian neurotransmitter. There is evidence to suggest that it is "responsible for 75% of the excitatory transmission in the brain" (16). This feature of glutamate metabolism has guided much of the search for the physiologic basis of CRS.

The Chinese Restaurant Syndrome

Published case reports suggest that there is a correlation between CRS and the consumption of MSG (9,10,17). However, clinical challenge studies provide contradictory results. In 1969 Schaumberg et al. conducted a series of tests in which they administered MSG in a variety of vehicles such as wonton soup, water, chicken broth, and intravenously. Dosages ranged from 1 g-12 g; tests were double-blind, single-blind, and unblinded. The largest group studied was 56 individuals. The researchers noted symptoms of a burning sensation on the neck, shoulders, and arms; of a tightness in the muscles of the face; and of substernal chest pressure. Symptoms were noted in all individuals; however, some individuals required massive doses before symptoms could be produced. Schaumherg et al. concluded that there was a dose-response effect seen in the severity of the symptoms and that there was no correlation with age, sex, or body weight (18).

However, in 1970 Morselli and Garattini concluded that there was no statistical difference between the number of individuals who reported reactions to 3 g MSG administered in beef broth and those who reported symptoms associated with a placebo (19).

In 1972 Kenney and Tidball expanded on previous study designs. Using an initial group of 77 individuals, they used a dose of 5 g MSG in tomato juice to identify MSG-sensitive individuals. Twenty-two of the 25 individuals who reacted to this high dose were then challenged with doses ranging from 1 g-4 g. Kenney observed a dose-response relationship in the symptom of stiffness/tightness in the face and neck, and a less clearly defined dose-response relationship in the symptoms of tingling, pressure, and warmth. However, there was a threshold dose of 2 g-3 g before any symptoms occurred. Also, at the 1 g level, a greater number of subjects reported adverse reactions to the placebo than to MSG. Kenney and Tidball also analyzed plasma glutamate levels of the test subjects. They concluded that, while the rise in plasma glutamate levels after ingestion of MSG was significant, there was no significant difference in the level of plasma glutamate between individuals reporting symptoms and that of non-reactors (20).

Kenney continued his work in 1979, finding in a double-blind placebo-controlled challenge of 16 known reactors that at doses of 1 g-5 g MSG, a reaction could be provoked in only one out of every six trials. He found there was a significantly greater percentage of female subjects who reacted to MSG (50%) than male subjects (33%), a direct contradiction of Schaumberg's findings. In the same paper, Kenney reported a refinement to his previous experimental design. Because some subjects had reported that MSG gave the tomato juice a "spoiled" flavor, Kenney felt the need to design a test vehicle which would more adequately mask the distinctive taste of MSG. He formulated a "soft drink," theorizing that since test subjects would have no base of reference for the taste of the drink, they would be less able to detect the MSG aftertaste and thereby be less likely to bias their reactions. Using this soft drink test vehicle, Kenney challenged three known reactors with 6 g of MSG. Surface electrodes to measure muscle activity/tightness, as well as temperature monitors, blood pressure, and EKG were monitored and recorded. Although all three subjects reported symptoms of warmth, weakness, tightness, and palpitation, there was no change in the objective signs being monitored (21).

As of the early 1990s, existing clinical data suggested the following: 1) subjective symptom s could be produced at high doses; 2) contradictory results were achieved at low dosages; and 3) no changes in objective symptoms could be detected. But, these early studies contained flaws which make the validity of their data questionable. Portions of Schaumberg's study were only single-blind, while other portions were unblinded. As previously mentioned, many of these early studies used vehicles that did not mask the flavor of MSG. In addition, these studies used salted placebos, which it has been argued do not replicate the taste of MSG closely enough to act as a true placebo (22). These studies also used the same subjects over the course of multiple trials. While this assures a test group comprised of individuals that in the general population are rare, it also has the potential of "training" the study group to associate the taste of MSG with a report of the symptoms under investigation (21). Most questionable, though, is the fact that these studies either recruited individuals who reported symptoms of CRS or informed the subjects in the notice of consent of the purpose of the study and the possible symptoms. Although this may be ethically correct, it has the effect of providing a script for the subjects to recite, and Kerr has shown that individuals who are aware of CRS and its symptoms are 10 times more likely than the general population to report CRS-like symptoms (6). The combined result of these flaws would be to overestimate the magnitude of the effect of CRS.

In 1993, Tarasoff and Kelley published a study, which was highly critical of all previously published work, criticizing the experimental designs as well as the statistical corroborating evidence. Tarasoff and Kelley claimed to remedy the previous flaws by: using MSG in capsules and a soft drink to prevent aftertaste bias; eliminating data from individuals who did report an aftertaste, also to eliminate bias; using more rigorous statistical analysis; and most of all, reducing the possibility of symptom suggestion by telling subjects they were participating in the "evaluation of a new soft drink," thereby avoiding all mention of the terms MSG, or Chinese Restaurant Syndrome. Their study challenged 71 individuals with doses of 1 g-3.15 g and found no significant difference between the number of reactions reported in the test and placebos (22).

The Federation of American Societies for Experimental Biology (FASEB) has stated that "due to inconsistencies in experimental design," such as route of administration, dosages, and nutritional status of test subjects, it is difficult to compare the various challenge studies (7). These difficulties notwithstanding, it is possible to make several conclusions concerning MSG and CRS: 1) There are a number of case reports describing individuals who have experienced an adverse food reaction, characterized by a distinct set of self-limiting symptoms known collectively as the Chinese Restaurant Syndrome; and 2) Symptoms resembling those of CRS can be provoked in a laboratory setting by the administration of large doses of MSG. Further research is necessary before the final chapter can be written regarding CRS, because there is still not a definite causal link with MSG, a defined physiologic mechanism, or an answer to the lack of reactions linked to natural glutamate.

MSG in Animals

After Dr. Kwok's initial report, several researchers began to reexamine MSG toxicity in animals. In 1969 Olney reported that neonatal mice, when given subcutaneous doses of MSG, developed brain lesions. These lesions were characterized by "intracellular edema and neuronal necrosis" in the hypothalamus. In addition, when mice treated neonatally with MSG were followed to adulthood, they were found to be obese and, in the case of females, sterile (23). These findings have been confirmed by several different researchers, using rats as well as other rodent species (11,24,25). In addition, when administered by a gavage, oral doses have also been observed to cause similar lesions. The damage appears to be dose-related, as well as age and species specific; hybrid strains of mice have been observed to be more susceptible than inbred strains (24). In 1985 Daabees et al. concluded that in mice the plasma concentration of glutamate must exceed a threshold of 75 micromol/dl for neuronal damage to occur (25).

The presence of hypothalamic lesions has prompted several researchers to investigate the effect of MSG on pituitary hormones. Injections of MSG result in decreases in the size of rat gonads, adrenal and thyroid glands, as well as a "marked decrease in growth hormone and lutenizing hormone content in the anterior pituitaries" (26,27). Studies in humans have shown no change in the levels of growth hormone, thyroid stimulating hormone, or lutenizing hormone; however, there was an increase in the levels of prolactin and cortisol when massive doses of glutamic acid (10 g) were administered in a capsule form (28).

While the evidence linking MSG with brain lesions in mice is fairly convincing, studies of brain lesions in non-human primates are still highly controversial. Olney and Sharpe have reported finding neuronal damage in infant monkeys treated with MSG both subcutaneously and by nasogastric tube at doses ranging from 1 g/kg to 4 g/kg. These hypothalamic lesions included the previously observed intracellular edema, as well as lysis of cytoplasmic organelles (29). The lesions, even in animals receiving the highest dosages, were described as being "quite inconspicuous," with a maximum of 10 damaged cells being found per 1 micron section observed (30). However, other researchers have been unable to duplicate Olney's results and have observed no abnormal structures in non-human primate brains after administration of MSG via gastric tube (31,32). The debate in the literature concerning this contradictory data is quite heated. Olney attributes the lack of findings by Reynolds and others to improper experimental procedures (33). Reynolds, who believes that the lesions seen in infant mice are due to lesser physiologic maturity in rodents, has suggested that Olney's findings were caused by the poor conditions of his experimental animals or were fixation artifacts (31,32). This professional dispute aside, there is relatively little data on the subject, so the verdict is out regarding the effect of MSG on the non-human primate brain. In their 1993 Tentative Report on MSG, FASEB located only 11 studies concerning MSG and non-human primates. Of these, only one, a study of taste preferences, was published after 1980; and only four of the 11 studied the presence or absence of brain lesions. FASEB concluded that, as of the time of its report, "more studies are needed to assess the impact of L-glutamate in this animal model (non-human primates)," and that, "there is insufficient evidence...to make any definitive conclusions about the relative sensitivities of rodents and non-human primates" (7).

Safety of MSG

Are any of these studies relevant to the question of CRS and the safety of MSG? CRS is a subjective set of symptoms. Lemkey-Johnston noted that after a massive dose (4 g/kg by gastric tube) infant mice became "markedly quiet, and ceased motion" (24). However, Olney reported a "lack of symptoms" in infant primates after a subcutaneous dose of 2.7 g/kg (29). The lack of signs, even at high doses in primates, calls into question whether these animal lesions are related to the human syndrome.

More significantly, the animal studies involve dosages and routes of administration that are not applicable to the normal human usage of MSG. MSG is a flavor enhancer; it is more reasonable to test its effects when administered in the diet. It has been shown that the route of administration of glutamate has an effect on the concentration of glutamate in the blood. The highest plasma concentration is achieved when the dose is given by injection; lower concentrations of glutamate are seen in the blood when the same dose is administered by feeding tube (34). The lowest plasma concentrations occur when the dose is given with food as a normal part of the diet, although dietary consumption in water produces slightly higher concentrations. In addition, there is evidence to show that peak plasma levels in man are much lower than in rodents given an equivalent dose by body weight and that humans metabolize glutamate more slowly than either rodents or monkeys (35).

The bottom line regarding animal studies of MSG is that in studies that assess effects of MSG as a food additive, no adverse effects are observed. Dietary MSG has been shown to be non-carcinogenic and non-mutagenic, and to have no long-term toxicity (11,33). In a multigenerational study, when MSG was administered in the diet at a dose of 2-7 g/kg body weight to three generations of mice (the species widely acknowledged as being the most sensitive to MSG) there were no adverse effects observed. There was no obesity, no reproductive difficulties, and no evidence of brain lesions (36). This presents strong evidence in support of the safety of MSG when consumed with food.

Proposed Mechanisms for CRS

Although the bulk of the research has focused on MSG's effects on the hypothalamus, no mechanism linking the observed lesions and CRS has been described. However, other mechanisms have been suggested. Although CRS resembles a Type I, anaphylactic, allergic reaction, it has not been demonstrated to be an Ig-E mediated reaction; therefore, the syndrome is not a true allergic reaction (11,37).

Other nonallergic mechanisms that have been suggested as the cause of CRS include acetylcholine imbalance, vitamin deficiency, vasospasm, gastric reflux, and histamine toxicity. In 1971 Ghadmi et al. suggested that CRS was the result of an increase in acetylcholine caused by the ingestion of MSG in large doses. They observed a similarity between the symptoms of CRS and the symptoms occurring after injection of acetylcholine (flushing, a feeling of warmth, throbbing in the head, palpitation, and substernal constriction). They also observed experimentally that in humans there is a 28% decrease in cholinesterase after MSG is ingested (38). Folkers et al. have suggested that the reactions experienced by MSG-sensitive individuals are a result of vitamin B6 deficiency. They found that when MSG responders received supplemental B6, CRS symptoms were prevented (39). Kenney has suggested that the symptoms seen in CRS are caused by MSG but are not a neurological reaction. He has suggested that CRS is actually a case of gastric reflux, with MSG acting as an esophageal irritant (21). Lastly, Chin et al. suggested that there were similarities between CRS and scombroid poisoning, caused by naturally-occurring histamine in foods. They assayed several common Chinese dishes and condiments for histamine content and concluded that although the amounts of histamine contained in any given dish sampled did not exceed the level of toxicity, a diner could conceivably consume toxic amounts of histamine during the course of a Chinese meal, resulting in CRS symptoms (40). Although interesting to consider, there has been very little research to support these theories.

Current Regulatory Status of MSG

What is the opinion of the regulatory community regarding the safety of MSG? The answer is simple; in the United States and abroad, MSG has been given the green light as a food additive. In 1987 the World Health Organization Joint Expert Committee on Food Additives reviewed the literature and concluded that: "the total dietary intake of glutamates...at the levels necessary to achieve the desired technological effect...do not, in the opinion of the Committee, represent a hazard to health." In 1992 the American Medical Association issued a statement that MSG did not "pose a significant public health hazard" (7). Also the U.S. Food and Drug Administration has placed MSG on the list of food additives which are considered to be "Generally Recognized as Safe" (GRAS). In fact, MSG is cited as an example in the definition of GRAS substances, along with other common food ingredients such as salt, pepper, and sugar (CFR 21 182.1). This status is currently under review. In 1992, because of consumer concerns about the safety of MSG and because of complaints about apparent side effects like CRS, the FDA contracted with FASEB to assess the safety of MSG and whether or not restrictions on its labeling and use were needed (CFR 57 FR 57467). This report, which was scheduled for publication in the spring of 1994, has not yet been released; however, a tentative report has been issued. Although not yet released, the final report is already controversial. Self-proclaimed anti-MSG activists are concerned about FASEB's decision to exclude parenteral animal studies from the body of the final report. The activists argue for inclusion because these are the only studies showing brain damage associated with MSG (41). FASEB intends to place the parenteral studies in the appendix of the final report because parenteral administration is not relevant to the normal usage of MSG (42).

Conclusion

Is it safe to use MSG as a food additive? Summarizing 26 years of research and 87 years of use, the answer is "Yes." Arguments to the contrary are overwhelmed by evidence in support of MSG.

Case reports have linked MSG and CRS. However, postprandial reactions are not unusual. One researcher has concluded that 43% of his study population experienced unpleasant sensations of one sort or another after eating (6). In addition, the symptoms linked to MSG in the majority of case reports are not life threatening. No deaths or other long-term adverse effects have been reported associated with MSG (7). To quote Kenney, "the typical MSG reaction that can be provoked with high doses in the laboratory, while uncomfortable, is transient and benign" (43).

A proportion of the existing body of research indicates that MSG causes brain lesions in rodents (14,23,24,25,33,34). However, these lesions were observed under extreme circumstances, using unrealistically large doses, and under forms of administration that are not applicable to MSG's role as a food additive (24,34,35,36).

If for a moment, we grant that these studies may be relevant, the data still support MSG as a safe food additive. It is customary to use less than 1% MSG, by weight, in food (44). Brain lesions are observed in sensitive newborn mice when they receive a 20% solution of MSG by gavage (500 mg/kg). Even when humans are given doses of 60 mg/kg, an unpalatable dose 30 times greater than the average U.S. daily intake, their plasma levels of glutamate are 57 times less than the levels at which damage occurs in mice. This difference becomes even more striking when MSG is given in conjunction with other nutrients. When the same massive dose is given in tomato juice, plasma levels are 110 times below the neurotoxic concentration (14). MSG toxicity is only seen in animals under circumstances that do not replicate its use by humans.

Based on current data, it is possible to conclude that it is safe to use MSG as a food additive. For nearly a century, it has been used with no adverse effects in Oriental countries at a rate that is, in some cases, more than double the consumption in this country (12). Although some individuals experience sensations, collectively referred to as the Chinese Restaurant Syndrome, there is no clinical data that links MSG, when used as a food additive, with any long-term adverse consequences.

References

1. Kwok, R. (1968), Chinese Restaurant Syndrome (letter). N Engl J Med, 278:796.

2. Shaumberg, H. (1968), letter, N Engl J Med, 278:1122.

3. McCaghren, T. (1968), letter, N Engl J Med, 278:1123.

4. Menken, M. (1968), letter, N Engl J Med, 278:1123.

5. Rath, J. (1968), letter, N Engl J Med, 278:1123.

6. Kerr, G., et al. (1979), "Food-Symptomology Questionnaires: Risks of Demand Bias Questions and Population-Biased Surveys," In: Filer, L.J., et al. (eds.), Glutamic Acid: Advances in Biochemistry and Physiology, Raven Press, New York, pp, 375-387.

7. Life Science Research Office (1993), "Tentative Report: Adequacy of Existing Scientific Information on Possible Adverse Reactions to Monosodium Glutamate," Prepared for the Food and Drug Administration under Contract No. FDA223-92-2185.

8. Gann, D. (1977), "Ventricular Tachycardia in a Patient with the 'Chinese Restaurant Syndrome," South Med J, 70(7):879-881.

9. Schwartz, G. (1988), In Bad Taste: The MSG Syndrome, Signet Books, New York.

10. Allen, D., J. Delohery, and G. Baker (1987), "Monosodium L-glutamate Induced Asthma," J Allergy Clin Immunol, 80(4):530-7.

11. Pulce, C. et al. (1992), "The Chinese Restaurant Syndrome: A Reappraisal of Monosodium Glutamate's Causative Role," Adverse Drug React Toxicol Rev, 11: 19-39.

12. Giacometti, T. (1979), "Free and Bound Glutamate in Natural Products," In: Filer, L.J., et al. (eds.) Glutamic Acid: Advances in Biochemistry and Physiology, Raven Press, New York, pp. 25-33.

13. Yamaguchi, S. and A. Kimizuka (1979), "Psychometric Studies on the Taste of Monosodium Glutamate," In: Filer, L.J., et al. (eds.) Glutamic Acid: Advances in Biochemistry and Physiology, Raven Press, New York, pp. 35-54.

14. Airoldi, L., et al. (1979), "Attempts to Establish the Safety Margin for Neurotoxicity of Monosodium Glutamate," In: Filer, L.J., et al. (eds.) Glutamic Acid: Advances in Biochemistry and Physiology, Raven Press, New York, pp. 321-331.

15. Meister, A. (1979), "Biochemistry of Glutamate: Glutamine and Glutathione," In: Filer, L.J., et al. (eds.) Glutamic Acid: Advances in Biochemistry and Physiology, Raven Press, New York, pp. 69-84.

16. Ganong, W. (1991), Review of Medical Physiology, 15th ed., Appleton and Lange, East Norwalk, Conn.

17. Scopp, A. (1991), "MSG and Hydrolyzed Vegetable Protein Induced Headache: Review and Case Studies," Headache, 31: 107-110.

18. Schaumberg, H., et al. (1969), "Monosodium L-glutamate: Its Pharmacology and Role in the Chinese Restaurant Syndrome," Science, 163:826-828.

19. Morselli, P., and S. Garattini (1970), "Monosodium Glutamate and the Chinese Restaurant Syndrome," Nature, 227:611-12.

20. Kenney, R., and C. Tidball (1972), "Human Susceptibility to Oral Monosodium L-glutamate," Am J Clin Nutr, 25:140-46.

21. Kenney, R. (1979), "Placebo-controlled Studies of Human Reaction to Oral Monosodium L-glutamate," In:Filer, L.J., et al. (eds.) Glutamic Acid: Advances in Biochemistry and Physiology, Raven Press, New York, pp. 363-373.

22. Tarasoff, L., and M. Kelley (1993), "Monosodium L-glutamate: A Double Blind Study and Review," Food Chem Toxic, 31(12):1019-35.

23. Olney, J. (1969), "Brain Lesions, Obesity, and Other Disturbances in Mice Treated with Monosodium Glutamate," Science, 164:719-721.

24. Lemkey-Johnston, N., and W. Reynolds (1974), "Nature and Extent of Brain Lesions in Mice Related to Ingestion of Monosodium Glutamate," J Neuropath Exp Neuro, 33:74-97.

25. Daabees, T., et al. (1985), "Correlation of Glutamate Plus Aspartate dose, Amino Acid Concentration and Neuronal necrosis in Infant Mice," Food Chem Toxic, 23(10):887-893.

26. Redding, T. (1971), "Effect of Monosodium Glutamate on some Endocrine Functions," Neuroendocrinology, 8:245-255.

27. Millard, W. (1981), "Light-Dark Entrainment of the Growth Hormone Ultradian Rhythm in the Rat is Mediated by the Arcuate Nucleus," Endocrinology, 108:2393-2397.

28. Carlson, H. (1989), "Stimulation of Pituitary Hormone Secretion by Neurotransmitter Amino Acids in Humans," Metabolism, 38(12): 1179-1182.

29. Olney, J., and L. Sharpe (1969), "Brain Lesions in an Infant Rhesus Monkey Treated with Monosodium Glutamate," Science, 166:386-388.

30. Olney, J., L. Sharpe, and R. Feigin (1972), "Glutamate-induced Brain Damage in Infant Primates," J Neuropathol Exp Nerol, 31:464-487.

31. Reynolds, W. (1979), "Morphology of the Fetal Monkey Hypothalamus After In Utero Exposure to Monosodium Glutamate," In: Filer, L.J., et al. (eds.) Glutamic Acid: Advances in Biochemistry and Physiology, Raven Press, New York, pp. 217-229.

32. Reynolds, W. (1980) "Aspartame Administration to the Infant Monkey: Hypothalamic Morphology and Plasma Amino Acid Levels," Anat Rec, 198:73-85.

33. Filer, L., and L. Stegink (1994), "A Report of the Proceedings of an MSG Workshop Held August 1991," Crit Rev in Food Science and Nut, 34(2): 159-174.

34. Airoldi, L. (1980), "Effect of Oral Monosodium Glutamate on Glutamic Acid Levels in the Nucleus Arcuatus of the Hypothalamus and on Serum Osmolality of Adult and Infant Mice," Toxicol Lett, 7:107-111.

35. Stegink, L. (1979), "Metabolism of Free Glutamate in Clinical Products Fed Infants," In: Filer, L.J., et al, (eds.) Glutamic Acid: Advances in Biochemistry and Physiology, Raven Press, New York, pp. 85-101.

36. Anantharaman, K. (1979), "In Utero and Dietary Administration of Monosodium L-glutamate to Mice: Reproductive Performance and Development in a Multigeneration Study," In: Filer, L.J., et al. (eds.) Glutamic Acid: Advances in Biochemistry and Physiology, Raven Press, New York, pp. 231-53.

37. Tarlo, S., and G. Sussman (1993), "Asthma and Anaphylactoid Reactions to Food Additives," Canadian Family Physician, 39:1119-23.

38. Ghadmi, H., S. Kumar, and F. Abaci (1971), "Studies on Monosodium Ingetion: I. Biochemical Explanation of Chinese Restaurant Syndrome," Biochem Med, 5:447-456.

39. Folkers, K., et al. (1981), "Biochemical Evidence of Deficiency of Vitamin B6 in Subjects Reacting to Monosodium L-glutamate by the Chinese Restaurant Syndrome," Blochem Biophys Res Comm, 100:972-976.

40. Chin, K., M. Garriga, and D. Metcalfe (1989), "The Histamine Content of Oriental Foods," Food Chem Toxic, 27(5):283-287.

41. Rothschild, L., Jr. (1994), "MSG Critic Alleges Relevant Data 'Suppressed' in FASEB Study," Food Chemical News, 36(24), 8 August:28.

42. Rothschild, L., Jr. (1994), "FASEB Study to Consider Parenteral Studies, MSG Critics Told," Food Chemical News, 36(26), 22 August:48.

43. Kenney, R. (1986), "The Chinese Restaurant Syndrome: An Anecdote Revisited," Food Chem Toxic, 24(4):351-354.

44. Life Sciences Research Office (1980), "Evaluation of the health aspects of certain glutamates as food ingredients," Supplemental review and evaluation. Prepared for the Food and Drug Administration under Contract No. FDA 223-75-2004. SCOGS-37aSuppl. Available from: NTIS, Springfield, Va., PB80-178635.

Acknowledgements

I would like to thank Dr. J.F. Borzelleca and Mr. R.E. Harrington for their assistance in the preparation of this manuscript.

Patricia J. Taliaferro, M.P.H., R.E.H.S., 8111 E. Yale Ave., Bldg. 5-202, Denver, CO 80231.
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Date:Jun 1, 1995
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