Long-standing beliefs about the ill-effects of mild to moderate obesity have been called into question by recent epidemiological studies and by critical review of older studies. A review of these studies reveals that the effects of obesity on health and longevity is more complex than we had realized. An attempt is made to throw light on this relationship by reviewing the large number of laboratory studies on nutrition, aging and obesity. The first series of such studies showed that restriction of food intake, beginning early in life, greatly increased longevity.
Four classes of etiologic agents that cause human illness have been discovered. Sometimes members of two or more classes of agents cooperate to cause illness. Knowledge of etiology is necessary if a disease is to be eradicated. The leading causes of death in the United States have changed dramatically in the last century. Infection has been replaced by chronic illnesses of obscure etiology. Ischemic heart disease is the leading cause of death in middle age and is the major obstacle to becoming old.
The publication of two books on the relationship between dietary restriction and aging has been taken as an opportunity to write a critical review on this field. The content of the two books is summarized and the implications of the major conclusions reached by the authors are appraised. It is concluded that dietary restriction should be more widely studied by gerontologists because of the light it throws on 'clocks' of aging, error detection and repair systems, and the possibilities of devising pharmacological control of these systems.
Certain guidelines may exist for selecting and using rodent models for aging research. These are based, however, on only operational criteria because we presently lack good biomarkers for (or even a suitable definition of) normal aging. Longevity and disease characteristics of the experimental population are the most important of the operational criteria for choosing a particular rodent model. These factors, in turn, are influenced by genetics and by environmental factors, including diet, housing, and physical activity.
The insulin-sensitizing drug phenformin, in addition to its clinical utility in type II diabetes, has been reported to lower blood lipids, reduce body fat, enhance cellular immunity, and--in rodents--to increase mean lifespan and retard the development of growth of cancer. Initial studies with the insulin-sensitizing nutrient chromium picolinate indicate that it aids glucose tolerance in type II diabetes, lowers elevated LDL cholesterol, reduces body fat while increasing lean mass, and--in rats--increases median lifespan.