Monosodium L-glutamate is metabolized in the same way as glutamic acid from any digested protein. After oral ingestion, glutamate is absorbed from the intestine by an active-transport system. During this process, a large portion is metabolized to alanine and a-ketoglutarate, which enters the tricarboxylic acid cycle. Glutamate is further metabolized in the liver to give glucose, lactate, glutamine, and other amino acids. Consequently, blood glutamate levels do not rise significantly unless very large doses are administered. Blood glutamate levels transiently rise when large doses are ingested on their own, but the coingestion of foods that contain metabolizable carbohydrate increases the metabolism of monosodium L-glutamate and eliminates or greatly attenuates this rise. Human infants, including premature infants, metabolize glutamate similar to adults (46,47).
The acute toxicity of MSG is low (48), the oral LD50 for humans, calculated on the basis of doses administered in different ways to various animals, would represent a single dose greater than 1 kg for a person weighing 70 kg. In contrast, the oral LD50 for sodium chloride in rats is 3.75 kg/kg body weight (49).
The main use of MSG is as a umami seasoning or a food ingredient, and so its safety when used in the diet is the most important aspect of its use. Both short-term and chronic toxicity studies on MSG in the diet of several species at doses of up to 4% (approximately 6 to 8 g/kg body weight/day) in the diet showed no specific toxic effects and no evidence for carcinogenicity or mutagenecity. Reproduction studies of up to three generations did not reveal any adverse effects of dietary MSG ingestion. Fertility, gestation, viability, and lactation indexes, or the pre- and post-weaning performance of offspring, were unaffected. In primates, it was found that the placenta serves as an effective barrier to the transfer of glutamate from the oral ingestion of large doses of MSG.
The concentration of glutamate is higher in the brain than in the blood. The demonstration that injected or force-fed neonatal rodents given extremely high doses of MSG showed evidence of brain leisons has led to much additional research to determine any possible link between neurotoxicity and human use of MSG (50). However, from animal tests on monkeys, guinea pigs, rat, and mice, glutamate levels in the brain remain unchanged after the administration of large oral doses of MSG (51). Numerous experiments on rodents, as well as dogs and monkeys, using dosage levels up to 43 g MSG/kg body weight have failed to show any link between dietary use of MSG and brain damage. In the case of dogs and monkeys, even experiments involving injection of MSG have not shown any effects on the brain.
An anecdotal report in 1968 triggered interest in Chinese restaurant syndrome (CRS), a reaction associated with transient subjective symptoms ofburning, numbness, and a tight sensation in the upper part of the body. Possible association with food ingredients such as MSG was suggested. No objective changes in skin temperature, heart rate, ECG, or tone were observed, and no correlation was seen between plasma glutamate levels and symptoms. In 1979 a questionnaire survey of more than 3,000 people in the United States was conducted for CRS. Only 1.8% of those surveyed acknowledged that they experienced possible CRS feelings (52), and 0.19% of those with symptoms attributed them to eating in Chinese restaurants. These feelings were also found to occur after consumption ofspicy tomato juice, orange juice, coffee, and tea. In 1986 self-identified MSG responders were challenged in a properly controlled double-blind study, and it was concluded that the link between MSG and CRS was not supportable (53). In 1987, the Joint FAO/WHO Expert Committee on Food Additives (JECFA), a scientific advisory body to the World Health Organization and Food and Agriculture Organization of the United Nations, concluded that properly conducted double-blind studies among individuals who claimed to suffer from the syndrome did not confirm MSG as the causal agent (54).
In 1981 Chinese restaurant asthma was reported following capsule administration of MSG to several asthmatics (55), but the researchers failed to account for other allergens to which the subjects could have been exposed and did not utilize the scientific practice of a "control" substance that would have helped to determine if glutamate triggered this response. In a double-blind crossover study in which chronic asthmatics were challenged with MSG or a placebo, no decrease in pulmonary function was observed (56).
JECFA reviewed the safety studies of glutamate and endorsed its safety by allocation of an acceptable daily intake (ADI) for L-glutamic acid and its monosodium salt, potassium salt, ammonium salt, calcium salt, and magnesium salt as being "not specified." This result is ascertained by the scientific committee for food of EC (57).
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