Chronic Dietary Restriction and Longevity

Abstract

Life-span is a genetically controlled (1) characteristic of a species or strain. Longevity is, however, a result of delaying onset of the diseases to which the aged are especially prone. Almost all biomedical research has been aimed at enabling individuals to reach their species life-span by disease prevention or cure. The one method, however, that has been established for increasing longevity toward a maximum life-span is drastic food intake restriction (2). This has been demonstrated for all species studied. It has been found that disease-prone strains (e.g., of mice) show the most dramatic effect of food restriction on longevity (doubling or tripling and occasionally even quadrupling survival time). Animal strains which conform to established “normal’ life-spans do, however, also show impressive increases in longevity when subjected to similar drastic reduction in food intake, undernutrition without malnutrition, and it seems likely that the basic mechanism for the increased longevity in mice of short-and long-lived strains are the same.

The original observations of the effect of restricted food intake on longevity (delayed onset of aging diseases) were those of Moreschi in 1909 (3) and Rouse in 1914 (4), both dealing with mice carrying sarcomas. The results were dramatic. The work, however, which has stimulated the progressively increasing activity in this area is based on the reports of McCay et al. (5) from at Cornell University. Harper (1) points out the most serious problem of the original Cornell work. Half of the food intake-restricted rats died before 300 days of age, while all of the full-fed animals were alive and well. Thus, it was only the small and immature rats that showed extended longevity as a result of the food intake restriction. This problem can, however, be avoided by using 40% rather than 50% restriction of food intake.