American Journal of Clinical Nutrition, Vol 26, 803-813, Copyright © 1973 by The American Society for Clinical Nutrition, Inc.

Effects of dietary supplementation of monosodium glutamate on infant monkeys, weanling rats, and suckling mice

¹ From the Department of Nutrition, Harvard School of Public Health, 665 Huntington Avenue, Boston, Massachusetts 02115

The effects of large dietary supplements of MSG were studied in infant monkeys, weanling rats, and preweanling mice for varying periods of time. Ten infant squirrel monkeys were fed either a 0, 4.8, 9.1, or 16.7%-MSG formula diet for 9 weeks and evaluated clinically and histopathologically. None developed hypothalamic or retinal lesions. Three of the ten squirrel monkeys receiving MSG died, although two deaths appeared unrelated to treatment. The growth of the surviving monkey receiving the largest supplement of MSG was retarded, but a battery of clinical examinations was unremarkable in any of the surviving monkeys. Feeding the 9.1% MSG formula for 1 year to an infant cynomolgus and another infant bushbaby monkey had no effect when compared with two control monkeys. The intramuscular injection of 2.7 mg MSG/g body wt into a 3-week-old cynomolgus monkey produced marked elevation in circulating glutamate and vomiting but has had no demonstrable deleterious effect during the subsequent 2.5 years.

Groups of weanling rats were fed high levels of MSG or isocaloric, isonitrogenous, or isonatrogenous control diets. The growth depression observed in rats fed MSG diets appeared to reflect sodium intake more than glutamic acid consumption. Dietary sodium content was also a factor in kidney size, water consumption, urinary pH, and plasma glutamate concentration. No conclusive endocrine effect was found.

Infant mice dosed with varying levels of MSG from 6 through 10 days of age did not have hypothalamic lesions when killed on the 11th day. In a similar experiment in which the mice were allowed to live, approximately one-third died within 30 days. The high mortality was thought to be a function of the sodium content or osmolarity of the MSG administered. The surviving mice were raised for 1 year without developing hyperphagia, obesity, or hyperactivity.

The relative lack of toxicity of MSG in these studies when compared with previous reports is believed to be related to the route of administration, as MSG was neither injected nor force-fed to fasted animals but offered as a supplement to an otherwise normal diet.