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How do we know MSG causes unwanted observable reactions?
Studies completed in the 1970's demonstrated that
at least 25% of the population react to monosodium glutamate in processed
food at that time(1-4).
Today, we recognize that there are at least
40 additional ingredients that contain the same manufactured amino acid that
causes the adverse reactions caused by monosodium glutamate. The
reactions to this processed (manufactured) free glutamic acid (MSG) range from
mild and transitory to debilitating and/or life threatening, and include skin
rash, simple headache, nausea/vomiting, asthma-like symptoms, migraine
headache, tachycardia, panic attack, anaphylactic shock, seizures, depression,
and more. See the list of the adverse reactions
compiled by the Truth in Labeling Campaign.
The first published report of an
adverse reaction to monosodium glutamate appeared in 1968 in a letter published
in The New England Journal of Medicine(175). Dr. Robert Ho Man Kwok,
senior research investigator at the National Biomedical Research Foundation in
Silver Spring, Maryland, told his colleagues that for several years, since he
had been in the United States, he had experienced a strange syndrome whenever
he ate in a restaurant serving Northern Chinese food--an experience he had
never experienced in his native land. He reported that 15 or 20 minutes after
beginning to eat, he experienced "...numbness at the back of the neck,
gradually radiating to both arms and the back, general weakness and
palpitation." The syndromes lasted about two hours. He had never heard of
such a syndrome until he received complaints of the same symptoms from both
medical and nonmedical friends. Through The New England Journal of Medicine,
he asked his colleagues in the medical field if they might be interested in
seeking more information about this "rather peculiar" phenomenon
which someone at the journal dubbed, "Chinese Restaurant Syndrome."
Ten people responded almost immediately. Eight had
experienced similar, but not necessarily identical reactions when dining in certain
Chinese restaurants(179-186) and, as in Kwok's case,
had no clear cut notion of what the causative factor might be; and two had
experienced similar reactions which they traced to probable muscarine
poisoning (187) or to the potent nonprotein neurotoxin,
tetrodotoxin found in the puffer fish(188).
While Kwok offered that the syndrome might be
attributable to the ingestion of monosodium glutamate, a subsequent issue of
the New England Journal of Medicine carried letters from both Schaumburg
and Byck(189)
and a group of New York University pharmacology students who had studied the
condition for an elective project(190) who stated, unequivocally, that the
syndrome which Kwok and his friends had experienced was a reaction to ingesting
monosodium glutamate.
Schaumburg and Byck(189) pointed out that
the reaction being discussed was well known to experienced allergists and
Chinese-restaurant owners; and they offered preliminary hypotheses pertaining
to the nature of the reaction. Ambos et al.(190) added
that although the reaction had not been cited in the literature, it had been
clearly recognized by "...certain persons and within some families."
There was general agreement that monosodium glutamate caused a reaction in
sensitive individuals which most often consisted of the reactions mentioned by
Kwok. Schaumburg and Byck mentioned that syncope,
tachycardia, lacrimation, fasciculation and nausea
were noticed among the people they had found to be monosodium glutamate
sensitive but at the time, they were attributed to causes other than monosodium
glutamate. (At the time, no one dreamed that monosodium glutamate could be a
neurotoxin.) Onset time for the adverse
reactions being considered as possible reactions to monosodium glutamate was 10
to 25 minutes with a duration of 45 minutes to 2 hours. Schaumburg mentioned
that 5 grams of monosodium glutamate would produce a reaction in a sensitive
individual. Ambos et al.(190) indicated that 2
teaspoons per 6 ounce glass of tomato juice was needed to provoke a reaction in
females, while 4 teaspoons per 6 ounce glass was needed to provoke a reaction
in males.
In 1969, Schaumburg et al.(191)
reported results of studies they had undertaken. This time, both headache and
chest pain were added to the symptom list, and a point was made of the fact
that there is considerable variability in threshold dose among individuals.
Experiments were done with a wide range of test materials and a variety of
experimental conditions. Schaumburg et al. concluded, "We now have shown
that [monosodium glutamate] can produce undesirable effects in the amounts used
in the preparation of widely consumed foods"(191).
Additional case reports presented themselves from
time to time. In 1972, Upton and Barrows (192) warned that, based on their
observations of an epileptic woman, it would seem reasonable to advise patients
on diphenylhydantoin to avoid foods rich in
monosodium glutamate.
From time to time, case reports have been
published describing instances of adverse reactions associated with ingestion of
monosodium glutamate. There have been reports of tachycardia(213),
hyperactive or hysterical activity in children(214-215), paraesthesiae
of hands and feet(216), severe "burning" headache(217), severe upper
abdominal pain and pressure accompanied by diaphoresis and a burning sensation
in the chest(217), angio-oedema(218), and a
hypertensive reaction(219) in the form of vascular headache, typical of those
seen in patients taking monoamine oxidase inhibitors.
Ratner et al.(217) report that the initial diagnoses
in seven patients whose complaints were eventually resolved as monosodium
glutamate sensitivity, were migraine (twice), myocardial infarction, brain
tumor, neurosis, functional colitis, and depression.
In 1975 Reif-Lehrer
wrote to The New England Journal of Medicine, reporting that children
react to ingestion of monosodium glutamate, and describing symptoms similar to
adults with almost the same degree of prevalence. She presented three
cases and discussed the relation between shudder in children, epileptic
"seizures", "[monosodium glutamate] shivers", and the fact
the glutamic acid has been reported to cause convulsive disorders in animals(220). Subsequently, Andermann,
et al., commented on a possible relationship between glutamic acid and essential
tremor(221).
During the next two years, Reif-Lehrer
published 1) an additional report of children's apparent adverse reactions to
monosodium glutamate(222); 2) results of a
questionnaire study establishing that 25% of those responding to the
questionnaire and 30% of the persons reporting that they had been exposed to
Chinese restaurant food reported adverse reactions(223); and 3) a lengthy
review and report on the possible significance of adverse reactions to
monosodium glutamate in humans(224).
Colman(225) wrote to The New England of Medicine in 1978,
reporting two cases of psychiatric reactions to monosodium glutamate.
Comments and observations also have been
published. Neumann(226) reported having seen reactions
involving frequent ventricular premature beats. He cautioned that,
"Because sensitivity to [monosodium glutamate] is not rare and because of
the unpredictable consequences given a damaged, vulnerable, or irritable
myocardium, patients with a tendency to rhythm disturbances should be made wary
of prefabricated soups, and meat 'tenderizers,' in addition to the fare of
Chinese restaurants. Incidentally, the term 'Chinese
restaurant syndrome,' while picturesque, is too narrow considering the tons of
monosodium glutamate used in less exotic foods. The syndrome should
really be termed what it is, an [monosodium glutamate] atopy.
And the cardiovascular system is its chief target"(226).
Gore and Salmon(227)
observed 55 subjects given randomized monosodium glutamate and placebo trials,
and noted that although the reactions to monosodium glutamate were significant,
the symptoms recorded were not those of the CRS. They questioned the meaning of
reaction to symptoms which were not CRS (Chinese Restaurant
Syndrome). Sauber(228) pointed out that the meaning was perfectly clear --
that the symptoms which Gore and Salmon found to be most prevalent, were,
indeed, the most prevalent visible effects of monosodium glutamate.
Asthma has been studied extensively by Allen(229-230). He explored and discussed the possible
relation of monosodium glutamate to asthma, questioning the possible links, and
exploring possible mechanisms for a relationship. In a single blind study(230)
using 32 subjects with asthma, some of whom had histories of severe asthma
after Chinese restaurant or similar meals, he found a dose dependent reaction
which in some cases was delayed up to 12 hours.
Moneret-Vautrin(231)
reported finding a "...very small subset of patients with intrinsic
asthma..." with an intolerance to high doses (2.5g) of monosodium
glutamate.
Fibromyalgia is a common rheumatologic disorder
that is often difficult to treat effectively. Smith et al. reported on
four patients diagnosed with fibromyalgia syndrome for two to 17 years, all of
whom had undergone multiple treatment modalities with limited success.
All had completed, or nearly completed, resolution of their symptoms within
months after eliminating monosodium glutamate or monosodium glutamate plus
aspartame from their diets. All had recurrence of symptoms whenever monosodium
glutamate was ingested(232).
The relationship between processed (manufactured)
free glutamic acid (MSG) and migraine headache was explored by Alfred Scopp who, in 1991, published a study entitled "MSG
and hydrolyzed vegetable protein induced headache: review and case
studies"(233). In 1993, Martinez et al.(234)
measured glutamic and aspartic acid levels in plasma and cerebrospinal fluid
(CSF) of patients with common and classic migraine during attacks, making
comparisons with controls suffering from stress. Plasma levels of amino acids
in migraine patients were lower than in controls, while CSF concentrations of
glutamic acid were higher in migraineurs than in
controls. The authors concluded that "... results suggest an excess of
neuroexcitatory amino acids in the [central nervous system] of migraine
patients during attacks, possibly favoring a state of neuronal hyperexcitability." Martinez et al. had found a
relationship between glutamate levels in the CSF of the central nervous system
and migraine headache.
Today, virtually every headache clinic in the
United States acknowledges that "processed free glutamic acid"
(popularly referred to as MSG) is one of the triggers of migraine headache.
According to Scopp (who, at the time, was at the
Northern California Headache Clinic), at least 33 per cent of migraine patients
have some migraine headaches triggered by MSG(235).
There are only a few reports of adverse reactions
associated with monosodium glutamate in the published literature, and most of
those are reports of badly flawed research pretending to have found no
relationship between monosodium glutamate and any sort of adverse reaction to
it, all funded, at least in part, by Ajinomoto's International Glutamate
Technical Committee and/or others in the glutamate industry. Those
industry-sponsored reports that claim to have demonstrated that monosodium
glutamate is "safe" far outnumber studies reported by independent
researchers. The reason for the discrepancy is simple. Those who generate
studies that pretend to find that monosodium glutamate is "safe" are
invariably paid to do so, directly or indirectly, by the glutamate industry.
But no food or drug company or the U.S. Food and Drug
Administration (FDA), is funding research designed to explore the potential
toxicity of a food additive. Moreover,
people who do studies that displease the industrial giants have been
known to be both smeared and harassed. The few published reports of observed
adverse reactions to food additives come primarily in the form of letters to
the editor, relating clinical observations.
The FDA, both in its Adverse Reactions Monitoring
System (ARMS) and elsewhere, has in its files numbers of letters from people
reporting their sensitivities to monosodium glutamate and/or the other
ingredients that contained processed free glutamic acid (MSG). In a Memorandum
to the Health Hazards Evaluation Board of the FDA dated October 6, 1989 and
June 8, 1990, entitled, "Adverse reactions associated with [monosodium
glutamate] ingestion," Linda Tollefson detailed the symptoms that had been
reported to ARMS as of each date. The lists included headache, vomiting and
nausea, diarrhea, change in heart rate, change in mood quality or level,
abdominal pain and cramps, dizziness or problems with balance, localized pain
and tenderness, sleep problems, change in vision, fatigue, weakness, change in
body temperature, difficulty breathing, local swelling, joint and bone pain,
chest pain, change in sensation (numbness, tingling) change in activity level,
blood pressure changes, difficulty swallowing, and more.
(In must be noted that Tollefson concluded, after
considering all of the material available to her, that, "...there was
nothing...submitted...to suggest that MSG is a human health hazard." The
fact that Tollefson chose to regard all of the cases presented as
non-indicative of sensitivity to MSG says nothing about the facts.)
Additional reports of
adverse reactions have been shared with the Truth in Labeling Campaign. Examples will be found at Consumers Tell Us That…
REFERENCES
1. Reif-Lehrer, L. A questionnaire study of the prevalence of Chinese restaurant
syndrome. Federation Proceedings 36:1617-1623,1977.
2. Kenney, RA and Tidball,
CS Human susceptibility to oral monosodium L-glutamate. Am
J Clin Nutr.
25:140-146,1972.
3. Kerr, G.R., Wu-Lee, M., El-Lozy,
M., McGandy, R., and Stare, F. Food-symptomatology questionnaires: risks of demand-bias questions
and population-biased surveys. In: Glutamic Acid: Advances in Biochemistry
and Physiology Filer, L. J., et al., Eds. New York: Raven Press, 1979.
4. Schaumburg, H.H., Byck,
R, Gerstl, R, and Mashman,
J.H. Monosodium L-glutamate: its pharmacology and role in the Chinese
restaurant syndrome. Science 163:826-828,1969.
175. Kwok, R.H.M. The Chinese
restaurant syndrome. Letter to the editor. N
Engl J Med 278: 796, 1968.
179. Schaumburg, H. Chinese-restaurant Syndrome. N
Engl J Med 278: 1122, 1968.
180. McCaghren, T.J.
Chinese-restaurant syndrome. N Engl J Med 278:
1123, 1968.
181. Menken, M. Chinese-restaurant syndrome. N Engl J Med 278, 1123, 1968.
182. Migden, W.
Chinese-restaurant syndrome. N Engl J Med 278:
1123, 1968.
183. Rath, J. Chinese-restaurant
syndrome. N Engl J Med 278: 1123, 1968.
184. Beron, E.L.
Chinese-restaurant syndrome. N Engl J Med 278:
1123, 1968.
185. Kandall, S.R.
Chinese-restaurant syndrome. N Engl J Med 278:
1123, 1968.
186. Gordon, M.E., Chinese-restaurant syndrome. N
Engl J Med 278: 1123-1124, 1968.
187. Rose, E.K. Chinese-restaurant syndrome. N Engl J Med 278: 1123, 1968.
188. Davies, N.E. Chinese-restaurant syndrome. N
Engl J Med 278: 1124, 1968.
189. Schaumburg, H.H. and Byck,
R. Sin cib-syn: accent on glutamate. N Engl J Med 279: 105, 1968.
190. Ambos, M., Leavitt, N.R., Marmorek,
L., and Wolschina, S.B. Sin cib-syn:
accent on glutamate. N Engl J Med 279: 105,
1968.
191. Schaumburg, H.H., Byck,
R., Gerstl, R., and Mashman,
J.H. Monosodium L-glutamate: its pharmacology and role in the Chinese
restaurant syndrome. Science 163: 826-828, 1969.
192. Upton, A.R.M., and Barrows, H.S.
Chinese-restaurant syndrome recurrence. N Engl J
Med 286: 893-894, 1972
213. Gann, D. Ventricular tachycardia in a patient
with the "Chinese restaurant syndrome." Southern Medical J 70:
879-880, 1977.
214. Asnes, R.S. Chinese
restaurant syndrome in an infant. Clin Pediat 19: 705-706, 1980.
215. Cochran, J.W., and Cochran A.H. Monosodium glutamania: the Chinese restaurant syndrome revisited. JAMA 252: 899, 1984.
216. Freed, D.L.J. and Carter, R. Neuropathy due
to monosodium glutamate intolerance. Annals of Allergy 48: 96-97, 1982.
217. Ratner, D., Esmel, E., and Shoshani, E.
Adverse effects of monosodium glutamate: a diagnostic problem. Israel J Med Sci 20: 252-253, 1984.
218. Squire, E.N. Jr. Angio-oedema
and monosodium glutamate. Lancet 988, 1987.
219. Pohl, R., Balon,
R., and Berchou, R. Reaction t chicken nuggets in a
patient taking an MAOI. Am J Psychiatry
145: 651, 1988.
220. Reif-Lehrer, L. and
Stemmermann, M.B. Correspondence: Monosodium
glutamate intolerance in children. N Engl J Med
293: 1204-1205, 1975.
221. Andermann, F., Vanasse, M., and Wolfe, L.S. Correspondence: Shuddering
attacks in children: essential tremor and monosodium glutamate. N Engl J Med 295: 174, 1975.
222. Reif-Lehrer, L.
Letter: A search for children with possible MSG intolerance. Pediatrics
58: 771-772, 1976.
223. Reif-Lehrer, L. A
questionnaire study of the prevalence of chinese
restaurant syndrome. Fed Proc 36:1617-1623, 1977.
224. Reif-Lehrer, L.
Possible significance of adverse reactions to glutamate in humans. Federation
Proceedings 35: 2205-2211, 1976.
225. Colman, A.D. Possible psychiatric reactions
to monosodium glutamate. N Engl J Med 299: 902,
1978.
226. Neumann, H.H. Soup? It may be hazardous to
your health. Am Heart J 92:, 266, 1976.
227. Gore, M.E., and Salmon, P.R. Chinese
restaurant syndrome: fact or fiction. Lancet 1(8162): 251, 1980.
228. Sauber, W.J. What
is Chinese restaurant syndrome? Lancet 1(8170): 721-722, 1980.
229. Allen, D.J., and Baker, G.J.
Chinese-restaurant asthma. N Engl J Med 305:
1154-1155, 1981.
230. Allen, D.H., Delohery,
J., & Baker, G.J. Monosodium L-glutamate-induced asthma. Journal of
Allergy and ClinicalImmunology 80: No 4, 530-537,
1987.
231. Moneret-Vautrin,
D.A. Monosodium glutamate - induced asthma: Study of the potential risk in 30
asthmatics and review of the literature. Allergic et
Immunologie 19: No 1, 29-35, 1987.
232. Smith, J.D., Terpening,
C.M., Schmidt, S.O.F., and Gums, J.G. Relief of
fibromyalgia symptons followoing
discontinuation of dietary excitotoxins. The Annals
of Pharmacoltherapy. 35: (6) 702-706.
233. Scopp, A.L. MSG and
hydrolyzed vegetable protein induced headache: review and case studies. Headache. 31:107-110, 1991.
234. Martinez, F. et al. Neuroexcitatory amino
acid levels in plasma and cerebrospinal fluid during migraine attacks.Cephalalgia13:
89-93, 1993.
235. Scopp,
A. Personal communication. June 17, 2002.