-Caveat Lector-
Source: Journal of the American Dietetic Association, July 1997 v97n7
p793(2).
Title: 'We think your son has Lennox-Gastaut syndrome'- a case study of
monosodium glutamate's effect on a child.
Author: Anne Shovic, Robert D. Bart and Apryll M. Stalcup
Abstract: A two-year-old boy presented with signs and symptoms of
uncontrollable seizures of multiple types mimicking that of Lennox-Gestaut
syndrome. It was later diagnosed as monosodium glutamate (MSG) related
seizures following a comparison with a similarly related case wherein
withdrawal from monosodium glutamate intake resulted to resumption of
normal functions. A component of MSG known as aspartame acting as
proconvulsant was believed to be the etiologic factor. Control of dietary
MSG is the
effective prevention of a more drastic intervention.
Subjects: Glutamates - Health aspects
Monosodium glutamate - Health aspects
Chemicals - Adverse and side effects
Electronic Collection: A19792007
RN: A19792007
Full Text COPYRIGHT 1997 American Dietetic Association
Glutamate is a naturally occurring nonessential amino acid that serves as one
of the body's excitatory neurotransmitters (1). It occurs in food as
either a free amino acid or bound as a constituent in proteins. Although foods
high in protein (eg, meat and dairy products) may have fairly high levels of
bound glutamate, free glutamate in foods is thought to be more closely
associated with adverse effects (1). Monosodium glutamate (MSG), which is used
extensively as a flavor enhancer, can be a major source of free glutamate (2).
A US Food and Drug Administration (FDA) panel has declared MSG safe,
Stating that MSG poses little health risk (3). However, Daniel Raitin, PhD,
who
prepared the MSG report for the FDA stated, "Individual sensitivity to
food is just beginning to be explored and there is no reason to believe people
exquisitely sensitive to MSG are not out there" (4). In a report
prepared by the Life Sciences Research Office, Federation of American
Societies for
Experimental Biology (1), the ad hoc expert panel acknowledged that
preexisting conditions (eg, genetic predisposition, endogenous
anomalies in glutamate metabolism, impaired vitamin B-6 metabolism or
deficiency)
might predispose persons to reactions from MSG. They concluded that it
appeared that oral ingestion of MSG had the potential to provoke a response in
some
persons with severe unstable asthma. In addition, the panel validated some of
the work by Olney (5) that implicates MSG in the formation of lesions in
certain
regions of the brain that are not protected by the blood-brain barrier.
The Institute of Food Technologists has also declared MSG to be safe for
human consumption (6). Any concern that is mentioned appears to apply only to
a small number of adult subjects who consumed large amounts of MSG. Very
little information is available on the effects of MSG in
sensitivity-heightened
children. The following case study illustrates these effects and the unique
process that was taken by a mother and health professionals to deal
with the situation.
CASE STUDY
In the fall of 1991, the mother of D.S., a 2.5-year-old boy, noticed
that her normally healthy son was experiencing "head dropping" incidents. She
later recalled that D.S.'s head would drop suddenly, as if he had sneezed but
without the exhalation of air. Although D.S. did not seem to be affected by
the episodes, his mother noted that he began stuttering and having unexplained
tantrums. By the end of February 1992, the head-dropping episodes were
occurring almost every night and with greater intensity. D.S. was brought
to a pediatrician after head-dropping episodes two nights in a row in which
he hit his head on a cup hard enough to leave a mark on his forehead. He was
examined on March 3, 1992, but because he seemed so healthy, the pediatrician
delayed obtaining an electro-encephalogram (EEG) or blood samples.
On the evening of March 5, 1992, D.S. experienced 10 to 12 seizures
that appeared to come in waves. His mother reported that D.S. had an initial
seizure that seemed to involve more than just his head and seemed to be
triggered by eating. That seizure was followed by 2 or 3 more seizures
within 5 minutes. An emergency EEG was performed the next day and shortly
after, a computerized axial tomography scan and spinal tap were done.
According to the neurologist, D.S.'s EEG had the generalized spike and
slow wave pattern that is characteristic of Lennox-Gastaut syndrome. Lennox-
Gastaut syndrome is a rare form of epilepsy (about 1% of childhood epilepsies)
characterized by multiple seizure types that cannot be controlled with
currently available antiseizure medications (7,8). Most children with
this form of epilepsy develop progressive mental retardation and very few
adult patients are able to live independently.
Klonopin (Roche Laboratories, Nutley, NJ), an anticonvulsant
medication, was prescribed to D.S. Possible side effects include drowsiness,
ataxia,
behavioral disturbances, hyperactivity in children, dizziness,
headaches, blurred vision, confusion, congestion, anorexia, edema, and rash (9).
D.S.'s major symptoms while on the medication were hyperactivity, clumsiness,
and anorexia. The hyperactivity and clumsiness subsided when the dosage was
reduced.
DISCUSSION
Approximately 6 months later a literature search turned up a
20-year-old report in which a neurologist reported seizures in a very young
child
that were not controlled until MSG was removed from the diet (10). When the
neurologist was contacted, she indicated that the child in her study,
as well as other MSG-sensitive children, grew up to be cognitively normal and
apparently became desensitized to MSG around the time they entered
grade school. Given that D.S. had no clinical manifestations (eg,
developmental delay) of Lennox-Gastaut syndrome other than the seizures and the
appearance of the EEG, that D.S.'s seizures did not emerge until after he had
been
taken off baby food, and that many of the family meals tended to be
commercially prepared foods, a possible link between MSG and the seizures was
suspected.
The health care professionals treating D.S. recommended as an
intervention the elimination of MSG from the diet and continuation of
antiseizure
medication.
RESULTS
The seizures stopped. D.S.'s mother was skeptical of the role of MSG in
her son's seizures and, after several seizure-free months, allowed her son
to eat a hot dog at a birthday party. Later in the same week, D.S. and a
friend ate a large bag of snack chips (which listed MSG as an ingredient) when
his
mother was not watching. All that week, D.S.'s sleep patterns were disrupted
and his preschool teachers noted that he was clumsier than usual. He had
behavior problems (eg, was aggressive and difficult) and urinary incontinence,
sometimes several times a day. While attending another birthday party,
D.S. ate a slice of commercial pizza containing MSG. Three days later, after
again
exhibiting the same sleep pattern disruption and other symptoms, he had
another head-dropping incident.
These two incidents strongly suggested that MSG was a factor in D.S.'s
seizures, possibly by lowering his seizure threshold. This same effect
has been shown with aspartame (11). In one study, aspartame exacerbated EEG
spike-wave discharge in children with generalized absence epilepsy,
acting as a proconvulsant. Although most of the neurologic concerns associated
with aspartame have centered on phenylalanine, one of the amino acids that
comprise the dipeptide, it should be noted that aspartate, the other amino acid
in the dipeptide, and glutamate bind to many of the same receptor sites in
vivo, are subject to many of the same transport mechanisms, and undergo
interconversion via aspartate aminotransferase. It is also interesting to note
that the
incidence of febrile seizures in young children is almost five times higher in
Japan, where MSG is more commonly used as an additive, than it is in the United
States (12).
Currently, the FDA requires MSG to be listed on food labels as a food
additive. The agency will soon be proposing that foods containing notable
amounts of free glutamate be identified on the label. The amount considered
notable has yet to be determined (13).
Today, D.S. is a normal, healthy 7-year-old and has been completely off
antiseizure medication for more than a year. Caution is still being taken to
eliminate MSG from his diet.
A dietitian can be an important member of a health care team when working with
children with seizures like those described in this case study. Minimizing
dietary MSG is an easy, noninvasive approach to try first before
implementing a more drastic medical intervention.
References
1. Raiten DJ, Talbot JM, Fisher KD. Analysis of Adverse Reactions to
Monosodium Glutamate (MSG). Bethesda, Md: American Institute of
Nutrition; 1995.
2. IFIC [International Food Information Council] review on monosodium
glutamate: examining the
myths.http:/ificinfo.health.org/review/ir.msg.htm.
May 13, 1997.
3. MSG judged safe for most people. FDA Consumer. 1995;29(9):2.
4. Debate over MSG's safety reignited. Tufts University Diet &
Nutrition Letter. 1995;13(9):6-7.
5. Olney JW. Excitotoxic food additives: functional teratological
aspects. Prog Brain Res. 1988;73:283-294.
6. Monosodium glutamate. Food Technol. 1995; 49(10):28. 7. Dulac O,
Guyen TN.
The Lennox-Gastaut syndrome. Epilepsia. 1993;34(suppl 7):S7-S17.
8. Murphy JV, Dehkharghani F. Diagnosis of childhood seizure disorder.
Epilepsia. 1994;35(suppl 2):S7-S17.
9. Arky R. Physicians' Desk Reference. 48th ed. Montrale, NJ: Medical
Economics Data Production Company; 1994.
10. Rief-Lehrer L. Possible significance of adverse reactions to
glutamate in humans. Fed Proc. 1976;35:2205-2212.
11. Canfield PR, Canfield CS, Dooley JM, Gordon K, Jollymore S, Weaver
DF. Aspartame exacerbates EEG spike-wave discharge in children with
generalized absence epilepsy. A double-blind controlled study. Neurology.
1992;42:1000-1003.
12. Hauser WA. The prevalence and incidence of convulsive disorders in
children. Epilepsia. 1994;35(suppl 2):S1-S6.
13. Monosodium glutamate, a statement of the Institute of
Technologists. Nutr Today. 1996;31(3): 107.
A. Shovic is the Plan V director and R. D. Bart is a professor of Internal
Medicine and Pediatrics and the division chief of Neurology at the University
of Hawaii, Honolulu. A. M. Stalcup is an associate professor in the Department
of Chemistry at the University of Cincinnati, Cincinnati, Ohio. At the time of
the study she was with the Department of Chemistry, University of Hawaii,
Honolulu.
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