Printed May 1994
(Reprinted from the International Food Information Council Foundation, 1994)
Because of the evolving science, researchers rarely, if ever, close the book on studying various foods or food ingredients. Such is the case with monosodium glutamate (MSG), which, even though it has been used extensively for nearly a century, continues to be examined in light of current scientific knowledge and methods of testing.
Over the last several years, experts in the fields of pediatrics, allergy, pharmacology, medical psychology, toxicology and food science have reviewed the scientific data on glutamate. This issue of IFIC Review examines the scientific research conducted on MSG and summarizes the latest findings.
MSG is the sodium salt of glutamic acid. Glutamic acid, or glutamate, is one of the most common amino acids found in nature. It is the main component of many proteins and peptides, and is present in most tissues. Glutamate is also produced in the body and plays an essential role in human metabolism. (1,2) Virtually every food contains glutamate. It is a major component of many protein-rich food products such as meat, fish, milk and some vegetables. In the early 1900s scientists isolated the ingredient - MSG - in plants that was responsible for greatly enhancing flavor. (1, 2)
In the early part of this century, MSG was extracted from seaweed and other plant sources. Today, MSG is produced in many countries around the world through a fermentation process of molasses from sugar cane or sugar beets, as well as starch and corn sugar. (1,3)
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When present in its "free" form - not bound together with other amino acids in protein - glutamate has a flavor enhancing effect in foods. When MSG is added to foods, it provides a flavoring function similar to the naturally occurring free glutamate. MSG contains only one-third the amount of sodium as salt and is used to enhance the natural flavors of meats, poultry, seafood, snacks, soups and stews. (1, 3)
Multidimensional scaling experiments, which are used in sensory research, indicate that MSG falls outside the region occupied by the four classic tastes of sweet, sour, salty and bitter. (3, 4) This distinctive taste is known as "umami," a word coined by the Japanese to describe the taste imparted by glutamate. Westerners often describe this flavor as savory, broth-like or meaty. (3, 4)
Emerging dietary research also points to MSG's potential to enhance food intake in the elderly. (5, 6 ) Over the years, research has shown that losses in taste and smell are major contributors to poor nutritional status in the elderly, sometimes even leading to anorexia. Losses of taste and smell generally occur around 60 years of age and become more pronounced in persons in their 70s. (6)
Deterioration in the senses of both taste and smell that accompany aging often contributes to poor nutritional status. Studies find that moderate levels of added MSG in certain foods, such as mushroom soup and mashed potatoes, increased food intake in an institutionalized elderly population, ensuring sufficient intake of necessary vitamins, minerals and proteins. (2, 6)
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Current consumption data from the United Kingdom shows that per capita consumption of MSG is 4 grams (less than one teaspoon) per week. (7) This is comparable to U.S. estimates of roughly 0.55 grams for the average consumer, spread out through an entire day. (8) In Taiwan, for example, per capita consumption figures are much higher, averaging 3 grams daily. (9)
Still, the human body metabolizes glutamate added to foods in the same manner it metabolizes glutamate found naturally in many foods. Once glutamate is ingested, our bodies make no distinction between the origins of the glutamate. The body cannot distinguish between free glutamate from tomatoes or added MSG in tomato sauce. (2)
In 1958 the U.S. Food and Drug Administration (FDA) designated MSG as a Generally Recognized As Safe (GRAS) substance, along with many other common food ingredients such as salt, vinegar and baking powder. (10)
Consumers continue to have questions regarding MSG's safety and efficacy. However, there is general agreement in the scientific community, based on numerous biochemical, toxicological and medical studies over the last twenty years, that MSG is safe for the general population, including pregnant and lactating women, and children.
It is common practice for expectant women to eat a varied and well-balanced diet and consume enough calories to ensure a healthy pregnancy.
To facilitate fetal growth and development, most amino acids are actively transported across the placenta. Research indicates that amino acid concentrations are higher in the fetus, regardless of what the mother consumes. (11)
Because it is difficult to increase blood glutamate to significantly higher levels through dietary intake of MSG, scientists injected glutamate directly into the bloodstream to observe any effect.
Pitkin et al intravenously administered large amounts of MSG into pregnant monkeys to increase glutamate levels in the mother's bloodstream. On examination, no increases in the fetal glutamate levels were found with doses up to 220 mg/kg of maternal weight. The authors further concluded that the placenta is virtually impermeable to glutamate, even at high levels. (12)
In rodent studies, researchers investigated effects of dietary intake of MSG on reproduction and birth. The study looked at three generations of mice that were fed a daily intake of up to 7.2 g/kg of MSG. No adverse effect was observed in each generation, nor was there evidence of any incident of brain lesions in the neonates. (13)
Besides research on the fetus, scientists also investigated the effect of MSG ingestion on lactation and breast-fed infants. Upon examination of lactating women who consumed MSG at 100 mg/kg of body weight, researchers noticed no increase in the level of glutamate in human milk, and no effect on the infant's intake of glutamate. (2)
Likewise, studies show that breast feeding infants are able to detect the taste of naturally occurring free glutamate, which is 10 times more plentiful in human breast milk than cow's milk. (14) According to Baker et al, a newborn infant, through breast feeding, ingests more free glutamate per kilogram of body weight than during any other period of its life. (15)
Additionally, in December 1993 the American Academy of Pediatrics Committee on Drugs reviewed the effects of food and environmental agents on breast feeding. In the report, the Committee stated that MSG has no effect on lactation and poses no risk to the consuming infant. (16)
It has been speculated that children would metabolize oral MSG more slowly than adults. However, research conducted by Stegink et al at the University of Iowa showed that children as young as one year old metabolize glutamate as effectively as adults.
In the study, infants were fed beef consomme providing MSG at various dosage levels of 0, 25 and 50 mg/kg of body weight. Researchers measured the infant's plasma glutamate levels and, after comparing the children's plasma levels to those of adults, found no higher plasma glutamate values for children. (17) Additionally, scientific evidence has not implicated MSG in attention deficit hyperactivity disorder or other behavioral problems in children.
For the general population, MSG does not pose a health risk. Based on the scientific evidence upholding the safety and efficacy of MSG, the Select Committee on GRAS Substances (SCOGS) concluded in 1980 that there is no evidence that demonstrates reasonable grounds to suspect a hazard to the public when glutamic acid or its salts are used at current levels and manners now practiced. (18)
In the brain, glutamate serves as a neurotransmitter in addition to its general role in protein and energy metabolism. Neurotransmitters are stored in nerve endings and are used by nerve cells to inhibit or excite target cells, such as muscle or endocrine cells.
Concerns were raised in the late 1960s by John Olney, M.D., of Washington University, that high doses of MSG may adversely affect brain function. Dr. Olney examined the possibility of MSG-induced brain lesions through injection or force-feeding methods in rodents. In one study, Olney subcutaneously injected neonatal mice, ages 2 to 9 days old, with single dosages of MSG. The amount of MSG injected varied from 0.5 mg/g to even larger dosages of 4 mg/g of the neonate's body weight, inducing brain lesions and a variety of other physiological effects in the rodents. (19)
However, the dosages of MSG used in these studies were extremely high and the methods of injection, as well as force-feeding, do not accurately represent the way humans consume MSG. Interestingly, Olney's results could not be duplicated when large amounts were administered in the diet.
Indeed, studies evaluating the normal dietary ingestion of MSG in food, including amounts exceeding 40 g/kg body weight (5,000 times higher than normal amounts ingested), found no harmful effects on the brain. (1)
BOUND GLUTAMATE FREE GLUTAMATE MILK/MILK PRODUCTS Cow 819 2 Human 229 22 Parmesan Cheese 9,847 1200 POULTRY PRODUCTS Eggs 1,583 23 Chicken 3,309 44 Duck 3,636 69 MEAT Beef 2,846 33 Pork 2,325 23 Fish Cod 2,101 9 Mackerel 2,382 36 Salmon 2,216 20 VEGATABLES Peas 5,583 200 Corn 1,765 130 Beets 256 30 Carrots 218 33 Onions 208 18 Spinach 289 39 Tomatoes 238 140 Green Peppers 120 32 Source: Institute of Food Technologies (1)
Following Olney's observations, early research conducted by Bazzano, D'Elia and Olson compared large amounts of glutamate fed to adult humans and gerbils. The study involved 11 human adult males who consumed diets containing MSG dosages up to 147 g per day for a maximum of 42 days (200 times higher than normal consumption). During that time, researchers did not observe any sign of adverse reactions to the dosage and concluded that very high oral doses of glutamate are tolerated, with no neurological changes by adult gerbils as well as humans. (20)
Takasaki et al noted in their findings that when mice were given MSG orally with food, plasma glutamate rose significantly less than after injections of similar doses.
The researchers observed that pregnant, weanling and lactating mice fed large amounts of MSG in the diet at up to 14, 42 and 42.8 g/kg body weight respectively, did not develop brain lesions. Furthermore, plasma glutamate levels in mice that were fed large amounts of MSG in the diet were much lower than those required to induce brain damage. Takasaki et al concluded that MSG in the diet does not cause any acute or long-range adverse effect on the brain. (21, 22)
William Pardridge, M.D., further illustrated that dietary glutamate does not enter the brain because the blood-brain barrier maintains a transport system for acidic amino acids, such as glutamate, to effectively exclude circulating glutamate from the brain. Pardridge also showed that the levels of brain glutamate do not rise or fall with changes in plasma glutamate levels. (23)
Substantiating Pardridge's observations, Brian Meldrum, M.D., of the London Institute of Psychology, reported on amino acids' role as dietary excitotoxins that may contribute to neurodegenerative disorders. After reviewing numerous studies of various fields, he concluded that "the dietary consumption of glutamate has not been shown to cause neuropathology in man."
Meldrum also affirmed that the blood-brain barrier and the very powerful glial and neuronal uptake systems for glutamate help keep the extracellular concentration of glutamate low in the brain. (24)
In January 1994, John Fernstrom, Ph.D., professor of psychiatry, pharmacology and behavioral neuroscience at the University of Pittsburgh, reviewed literature examining the influence of food intake and ingestion of acidic amino acids, such as glutamate, on the formation of neurotransmitters and any possible repercussions on brain function.
Fernstrom pointed out that while glutamate is a neurotransmitter, it does not have ready access to the brain from the circulation system or the diet. After reviewing over 20 published studies, Fernstrom stated that the abundance of scientific evidence indicates that dietary glutamate does not present a risk to normal brain function. (25)
The weight of scientific evidence has shown that MSG as consumed in food does not impair brain function or pose risk to public health. As further concluded in WHO's Food Additive Series, scientific examinations have shown a lack of MSG mutagenicity, teratogenicity or carcinogenicity. (14)
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Allergic reactions to environmental agents, such as pollen, are typical, whereas the occurrence of an allergic reaction to foods or food ingredients is rare. In fact, recent research has indicated that nearly 30 percent of adults believe they have a food allergy, when in reality less than two percent of the adult population is sensitive to foods or food additives. (26)
Physicians have documented many psychological factors that play a role in perception of food allergy or food sensitivity. (27, 28) Likewise, Parker et al reported in January 1993 that individuals with unconfirmed reactions to foods were influenced by popular news media. (29) However, many questions still persist about MSG's role in food hypersensitivity.
In 1968, Robert Ho Man Kwok, M.D. described a collection of symptoms he allegedly experienced after eating Chinese food. He coined the phrase "Chinese Restaurant Syndrome" (CRS) to describe these symptoms, which included numbness at the back of the neck and a feeling of pressure in the face and upper chest muscles. (30)
As a consequence of Kwok's account, Kerr et al developed a subjective questionnaire to assess the prevalence of CRS in the population. The survey employed listed 18 adverse symptoms related to food, of which three were related to CRS. Of the 3,222 general households that responded to the survey, 43 percent reported food-related adverse reactions, but only 1.8 percent reported possible CRS symptoms. (31)
Adding to this, data from the Centers for Disease Control in Atlanta showed that reported reactions to MSG accounted for less than one percent of food related complaints between 1975 and 1987. (32, 33)
After anecdotal reports of MSG inducing CRS, Morselli and Garattini examined 17 males and seven females, between 18-34 years old in a double-blind, crossover challenge. The researchers administered 3 g doses of MSG in 150 ml of beef broth and evaluated the subjects every 20 minutes for a three-hour period. The participants were divided into two groups, one group which received the MSG broth the first day and the other group received the MSG broth on the following day.
Upon examination, no difference in subjective symptoms were observed between the MSG group and the control group. These symptoms included tightness in the chest, flushing and headache. However, no participant in either group experienced the burning sensation which is typical of CRS.
There was also no significant difference in the number of times each single symptom occurred nor how many participants experienced symptoms. Based on these observations, the researchers concluded that there is no evidence that CRS is associated with the ingestion of MSG. (34)
Richard Kenney, M.D., of George Washington University tested over 200 individuals from 1972 through 1980. In his studies, Kenney found that sensations reported after MSG administration were seen at high concentrations of MSG and were not reproducible from day to day. He also found no correlation with blood glutamate levels or blood chemistry measurements, and that they were not correlated with any objective measurements.
He further tested 60 subjects with orange juice, spiced tomato juice, black coffee, flavored milk and a two percent MSG solution. Upon examining reactions, Kenney found that six subjects responded to coffee, six to spiced tomato juice and only two to the MSG solution, indicating that MSG was not unique in producing symptoms typical of CRS. (35, 36)
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Considered the "gold standard" for testing potential adverse reactions to a substance, double-blind placebo-controlled studies provide dependable findings that are free of bias introduced by either the patient or the researcher.
In this type of study, neither the subject nor the researcher conducting the study knows whether the test substance or a placebo has been administered. For the results to be valid and to ensure the subject cannot violate the "blindness", the placebo and the test substance must look, smell and taste similar, if not identical.
The "blindness" of the study is crucial. It eliminates the possibility of a participant's personal beliefs to undermine the study's validity, as well as the researcher's expectations to influence the test results.
In 1986, Kenney conducted a double-blind placebo controlled investigation of subjects who believed they adversely reacted to MSG. Subjects were given a soft drink solution for four days, and on two of the days the solution contained 6 g of MSG. Two of the six subjects reacted to both solutions and the other subjects reacted to neither solution. Kenney further noted that while a reaction may occur to an extremely large ingestion of MSG, the reaction is usually transient and benign. (37)
Additionally, Jonathan Wilkin, M.D., of the Medical College of Virginia, studied 24 individuals, 18 of whom described a history of flushing upon ingesting MSG. After failing to provoke flushing when using 3 g or 5 g of MSG, Wilkin determined that MSG-provoked flushing is rare. (38)
In December 1993, Tarasoff and Kelly published a study examining the sensory side effects possibly caused by ingesting MSG. Using a randomized double-blind cross-over study, seventy-one healthy participants were administered five different treatments, which included two placebos and three different doses of MSG (1.5, 3 and 3.15 g) In a random order, neither the researchers nor the subjects knew which or how much of the test material was being consumed.
Two hours after ingestion, each subject was interviewed and half reported they experienced more than one symptom regardless of MSG content. While the most common reaction was none at all, the next significant symptom reported was tingling and thirst, which was experienced by the subgroup of strong reactors. Thus, similar to Kenney, Tarasoff and Kelly found that the small number of effects seen were statistically insignificant and that MSG in food had no discernible effect for healthy individuals. (39)
Interestingly, Chin et al explained that histamine toxicity produces symptoms individuals may interpret as being CRS related. Therefore, Chin et al surmised that the histamine levels in some foods may be the cause for the adverse reactions consumers associate with restaurant meals. (40)
Though numerous studies have evaluated MSG's possible causative role in food hypersensitivity, a majority of scientific challenges have failed to reproduce the adverse reactions many individuals associate with ingestion of MSG. (41) Studies measuring objective responses such as blood pressure, heart rate, skin temperature and muscle tone have been unable to detect differences between persons fed MSG and placebo.
Nonetheless, anecdotal reports may suggest that a small percentage of the population may be sensitive to MSG. However, these reactions are mild and transitory. (42)
Hydrolyzed proteins used for flavor-related purposes are prepared by using food grade acid or enzymes to chemically digest proteins from soy meal, wheat gluten, corn gluten, edible strains of yeast, or other food sources.
This process, known as hydrolysis, breaks proteins down into their component amino acids. Glutamate is predominantly naturally occurring in these protein sources, and when proteins are broken down, glutamate is converted into glutamic acid. The level of free glutamate varies from product to product and is very minute. (48)
In 1991 Scopp alleged that MSG and hydrolyzed proteins triggered headaches in sensitive individuals. The study was based on a MSG elimination diet and relied on patient recorded symptoms rather than a double-blind challenge. (49) Furthermore, because free glutamate is in virtually all foods, it seems questionable that the study's subjects were successful in eliminating all sources of free glutamate from their diet. (48)
Some scientists believe that persons who report a sensitivity to hydrolyzed proteins may be sensitive to the soy, wheat or other protein source used to produce the hydrolysate, rather than to glutamate itself. These sources are well-known to be involved in IgE-mediated food allergies and other adverse reactions including celiac disease. Thus, reactions could be due to ingestion of soy, wheat or other proteins that are not completely hydrolyzed. (26, 48)
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Earlier studies have also suggested that MSG might induce, as well as exacerbate, asthma. (43) However, follow-up double-blind challenges have not replicated those results.
Researchers at the Harvard Medical School measured the pulmonary reactions of asthmatic participants in a double-blind, randomized cross-over study. Participants received either a placebo or MSG in a dose of 25 mg/kg of body weight.
After comparing reactions on placebo day and MSG day, as well as those reactions of three subjects who reported a history of food sensitivity, researchers saw no difference in pulmonary reactions. Thus they concluded that MSG does not induce asthma and it is unnecessary to advise asthmatics to avoid MSG. (44, 45)
Moreover, in 1991 and 1993, researchers from the National Institutes of Health's Allergy and Infectious Diseases Institute presented data analyzing the possible association of MSG to asthma. (46, 47) In one study, they challenged 13 non-asthmatics and 30 asthmatics with a total dose of 7.6 g of MSG administered through a single-blind oral challenge. Upon observation, none of the non-asthmatics experienced any change in pulmonary reactions and only one asthmatic participant experienced some discomfort.
However, when the asthmatic patient was challenged through double-blind placebo controlled effort, no effect was seen. Thus, researchers concluded that "7.6 g of MSG ingested over two-hours posed no respiratory hazard to normal subjects and to the asthmatic population in the study." (46)
It is apparent that there is no shortage of research conducted on this ubiquitous ingredient and its potential health effects. Because MSG is one of the most intensely studied food ingredients in the food supply and has been found safe, the Joint Expert Committee on Food Additives of the United Nations Food and Agricultural Organization and WHO placed it in the safest category for food additives. (14)
Subsequently, in 1991 the European Community's Scientific Committee for Food confirmed the safety of MSG. Based on the extensive scientific data, and in view of large normal dietary intake of glutamates, the committee determined that specification of an Acceptable Daily Intake (ADI) was unnecessary. (50)
Finally, the American Medical Association's Council on Scientific Affairs, the National Academy of Sciences, as well as the FDA, have all determined that MSG, at current consumption levels, is safe. (8, 51, 52)
(1) Institute of Food Technologists'
Expert Panel on Food Safety and Nutrition.
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(5) Schiffman, S.S. Taste and smell perception in elderly persons. In J.E. Fielding & H.I. Frier (eds.), Nutritional Needs of the Elderly. New York: Raven Press, pp. 61-73, 1991.
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(8) National Academy of Sciences National Research Council. The 1977 Survey of the Industry on the Use of Food Additives: Estimates of Daily Intake. Vol. 3, Washington, D.C.: National Academy Press, 1979.
(9) Giacometti, T. Free and bound glutamate in natural products. In L.J. Filer, Garattini, S., Kare, M.R. et al. (eds.), Glutamic Acid: Advances in Biochemistry and Physiology. New York: Raven Press, pp. 25-34, 1979.
(10) U.S. Department of Health and Human Services. Subpart A - General Provisions Substances that are general recognized as safe. Code of Federal Regulations: Food and Drugs. Vol. 21, No. 182.1(a), revised April 1990.
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(13) Anantharaman, K. In utero and dietary administration of monosodium L-glutamate in mice: reproductive performance and development in a multigeneration study. In L.J. Filer, Garattini, S., Kare, M.R. et al. (eds.), Glutamic Acid: Advances in Biochemistry and Physiology. New York: Raven Press, pp. 231-253, 1979.
(14) Joint FAO/WHO Expert Committee on Food Additives. L-Glutamic acid and its ammonium, calcium monosodium and potassium salts. In Toxicological Evaluation of Certain Food Additives and Contaminants, WHO Food Additives Series No. 22, New York: Cambridge University Press, pp. 97-161, 1988.
(15) Baker, G.L., Filer, L.J., &Stegink, L.D. Factors influencing dicarboxylic amino acid content of human milk. In L.J. Filer, Garattini, S., Kare, M.R. et al. (eds.), Glutamic Acid: Advances in Biochemistry and Physiology. New York: Raven Press, pp. 111-124, 1979.
(16) American Academy of Pediatrics' Committee on Drugs. The transfer of drugs and other chemicals into human milk. Pediatrics, 93:137-150, 1994.
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(18) SCOGS (Select Committee on GRAS Substances). Evaluation of the Health Aspects of Certain Glutamates as a Food Ingredient (SCOGS-37a.-Suppl.). Paper presented to U.S. Food and Drug Administration, 1980.
(19) Olney, J.W. Brain lesions, obesity and other disturbances in mice treated with monosodium glutamate. Science, 164:719-721, 1969.
(20) Bazzano, G., D'Elia, J.A., & Olson, R.E. Monosodium glutamate: Feeding of large amounts in man and gerbils. Science, 169:1208-1209, 1970.
(21) Takasaki, Y. Studies on brain lesions after administration of monosodium L-glutamate to mice. II. Absence of brain damage following administration of monosodium L-glutamate in the diet. Toxicology, 9:307-318, 1978.
(22) Takasaki, Y., Matsuzawa, Y., Iwata, S. et al. Toxicological studies of monosodium L-glutamate in rodents: relationship between routes of administration and neurotoxicity. In L.J. Filer, Garattini, S., Kare, M.R. et al. (eds.), Glutamic Acid: Advances in Biochemistry and Physiology. New York: Raven Press, pp. 255-275, 1979.
(23) Pardridge, W.M. Regulation of amino acid availability to brain: selective control mechanisms for glutamate. In L.J. Filer, Garattini, S., Kare, M.R. et al. (eds.), Glutamic Acid: Advances in Biochemistry and Physiology. New York: Raven Press, pp. 125-137, 1979.
(24) Meldrum, B. Amino acids as dietary excitotoxins: a contribution to understanding neurodegenerative disorders. Brain Research Reviews, 18:293-314, 1993
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(30) Kwok, R.H.M. Chinese restaurant syndrome. New England Journal of Medicine, 17:796, 1968.
(31) Kerr, G.R., Wu-Lee, M., El-Lozy, M. et al. Prevalence of the Chinese restaurant syndrome. Journal of The American Dietetic Association, 75:29-33, 1979.
(32) Centers for Disease Control. Report on foodborne disease, 1975-1981. CDC Surveillance Annual Summary, April 1981.
(33) Centers for Disease Control. Foodborne disease outbreaks, 5-year summary, 1983-1987. CDC Surveillance Summaries, Vol. 39, No. SS-1, pp. 15-59, March 1990.
(34) Morselli, P.L. & Garattini, S. Monosodium glutamate and the Chinese restaurant syndrome. Nature, 227:611-612, 1970.
(35) Kenney, R.A. & Tidball, C.S. Human susceptibility to oral monosodium L-glutamate. The American Journal of Clinical Nutrition, 25:140-146, 1972.
(36) Kenney, R.A. Chinese restaurant syndrome. The Lancet, 8163:311-312, 1980.
(37) Kenney, R.A. The Chinese restaurant syndrome: an anecdote revisited. Food and Chemical Toxicology, 24(4):351-354, 1986.
(38) Wilkin, J.K. Does monosodium glutamate cause flushing (or merely "glutamania")? Journal of the American Academy of Dermatology, 15:225-230, 1986.
(39) Tarasoff, L. & Kelly, M.F. Monosodium L-glutamate: a double-blind study and review. Food and Chemical Toxicology, 31:1019-1035, 1993.
(40) Chin, K.W., Garriga, M.M. & Metcalfe, D.D. The histamine content of oriental foods. Food and Chemical Toxicology, 27:283-287, 1989.
(41) Pulce, C., Vial, T, Verdier, F., et al. The Chinese restaurant syndrome: a reappraisal of monosodium glutamate's causative role. Adverse Drug Reaction Toxicology Review. pp. 19-39, 1992.
(42) Beaudette, T. Adverse Reactions to Food. Chicago: The American Dietetic Association, pp. 27-32, 1991.
(43) Allen, D.H., Delohery, J., & Baker, G. Monosodium L-glutamate induced asthma. Journal of Allergy & Clinical Immunology, 80:530-537, 1987.
(44) Schwartzstein, R.M., Kelleher, M., Weinberger, S.E. et al. Airways effects of monosodium glutamate in subjects with chronic stable asthma. Journal of Asthma, 24:167-172, 1987.
(45) Schwartzstein, R.M. Pulmonary reactions to monosodium glutamate. Pediatric Allergy and Immunology, 3:228-232, 1992.
(46) Germano, P., Cohen, S.G., Hahn, B. & Metcalfe, D.D. An evaluation of clinical reactions to monosodium glutamate (MSG) in asthmatics using a blinded, placebo-controlled challenge. Journal of Allergy and Clinical Immunology, 87:(Suppl., Abstract), 1991.
(47) Germano, P., Cohen, S.G., Hibbard, V. & Metcalfe, D.D. Assessment of bronchial hyperreactivity by methacholine challenge (MTC) administration. Journal of Allergy and Clinical Immunology, 91:(Suppl., Abstract), 1993.
(48) Taylor, S.L. Possible Adverse Reactions to Hydrolyzed Vegetable Protein. Paper submitted to the Federation of American Societies for Experimental Biology review panel, April 1993.
(49) Scopp, A.L. MSG and hydrolyzed vegetable protein induced headache: review and case studies. Headache, 31:107-110, 1991.
(50) Commission of the European Communities. L-glutamic acid and its salts. Report of the Scientific Committee for Food: 25th Series, No. EUR 13416, 1991.
(51) American Medical Association's Council on Scientific Affairs. Report D of the Council on Scientific Affairs on Food and Drug Administration Regulations regarding the inclusion of added L-glutamic acid content on food labels. Report adopted at proceedings of the American Medical Association's House of Delegates Meeting. June 1992.
(52) U.S. Food and Drug Administration. Monosodium Glutamate. FDA Backgrounder, BG-91-7.1, October 1991.
Prepared Summer 1997 by Bernadene Magnuson, Ph.D.
University of Idaho, Dept. of Food Science and Toxicology - EXTOXNET FAQ Team.