The gifts reserved for age.

Many disciplines from the biological and social sciences are relevant to the study of human ageing. The unique contribution of epidemiology lies in defining the phenomenon of ageing and identifying the influences that determine its manifestations. With sadness we recognise, wherever we look in the world, that these influences include privilege, prejudice, and politics. Ageing, in the sense of senescence, is characterized by progressive loss of adaptability of individual organisms as time passes. Such loss of adaptability is revealed by a rise of age-specific mortality rates. In the human being, mortality rates fall from infancy to a nadir at the age of ten or eleven. Thereafter with minor perturbations in early adult life due to deaths from accident and violence, senescence is manifest as a steady and approximately exponential rise in mortality rates for the rest of the lifespan. Perhaps more importantly, loss of adaptability is also declared in the prevalence of disability, which rises exponentially throughout adult life. 1 Most ageing individuals fear disability, and the loss of independence and autonomy it may bring, more than death. Age-associated loss of adaptability comes about through interactions of extrinsic factors in lifestyle and environment with intrinsic, genetically determined susceptibilities. Some interactions are specific; in genetically susceptible organisms a high dietary sodium intake will raise blood pressure. Genetically determined metabolic pathways may turn cigarette smoke into carcinogens. Some of the age-associated syndromes produced by such interactions are dignified with the name of diseases, usually because they have a characteristic pathology or because they can be benefited by treatment. Both in a public health and a biological context, however, attempts to draw some fundamental distinction between disease and 'normal ageing' are likely to hinder rather than help. Extrinsic factors also modify the trajectory of human ageing through cohort and secular effects. The work of Barker and colleagues 2 suggests that a powerful form of cohort effect may be generated during life in utero where the metabolism of the fetus adjusts to cues indicative of the sort of environment it is likely to be born into. This form of plasticity can be seen as one example of metabolic switches that may be available to organisms, of some species at least, in other contexts. 3 Examples include the well known life prolongation effects of caloric restriction in rodents 4 which may also prove to exist in primates 5 and in the amenorrhoea precipitated by anorexia …