BIOLOGICAL ASPECTS OF SENESCENCE

Summary 1. Senescence is treated as a generic term for the processes in certain organisms which lead to a decreasing power of homoeostasis with increasing age. 2. The presence of these processes in a species can be inferred from life‐tables prepared and interpreted with suitable precautions. It cannot be inferred from the desultory examination of anatomical changes in species of unknown life cycle. Secondary criteria of senescence, e.g. decline of reproductive capacity are of value in judging the degree of age change in individuals of well‐studied species. 3. Decreasing homoeostasis with increasing age is known to arise from different causes in different phyla. No single general or ‘inherent’ process can be invoked to explain all types of senescence. 4. Senescence occurs only rarely in the wild state, and except in large or social animals regularly occurring senescence is a feature of domestication. 5. Susceptibility to senescence is apparently not universal in Metazoa, and may not be so in vertebrates. Probable exceptions to its occurrence are among forms where somatic cells are continually replaced, where there is no limiting size, or where virtual attainment of a limiting size is accompanied by a persisting capacity for growth. 6. The ‘senescence’ of asexually reproducing protozoan stocks is not a phenomenon directly analogous to metazoan senescence. 7. The specific age of invertebrates and of mammals can be modified by factors modifying the rate of development. The evidence in mammals indicates that senescence results from the attainment of a developmental stage, or from the exhaustion of developmental ‘programme’ not from the cessation of growth per se . 8. The specific age varies widely between inbred stocks. Longevity is most readily produced by heterosis, and is probably a correlate of heterozygosity. 9. The role of postponed lethal genetic effects, and of the reduction of the selection value of the individual with increasing age, in the evolution of senescence is discussed. The materials for this article were collected during the tenure of a personal grant from the Nuffield Foundation for study and research on the biology of senescence. I am also very grateful to many colleagues who have furnished me with facts and criticisms, without bearing any responsibility for the uses to which I have put them, and to Miss Rosemary Birbeck, for her work in preparing the manuscript.