Abstract
Late life is a distinct phase of life that occurs after the aging period and is now known to be general among aging organisms. While aging is characterized by a deterioration in survivorship and fertility, late life is characterized by the cessation of such age-related deterioration. Thus, late life presents a new and interesting area of research not only for evolutionary biology but also for physiology. In this article, we present the theoretical and experimental background to late life, as developed by evolutionary biologists and demographers. We discuss the discovery of late life and the two main theories developed to explain this phase of life: lifelong demographic heterogeneity theory and evolutionary theory based on the force of natural selection. Finally, we suggest topics for future physiological research on late life.
Highlights
It might be thought that adaptation and aging exhaust the contexts in which particular physiological mechanisms evolve
In the first type of research, natural selection acts intensely, producing a fine-tuned physiology that can be studied much as a car company’s engineers might dismantle a sedan produced by a competitor that makes more reliable vehicles, say, Lexus or Honda
With the second type of physiological research, on aging, natural selection is waning in influence
Summary
It might seem paradoxical for very late ages to be characterized by a cessation of aging, when the continued acceleration of physiological impairment might seem inevitable This pattern of nonaging is well known from research on fissile species. Both Bell (1984) and Martınez (1998) have shown that increasing death rates do not arise in symmetrically fissile aquatic invertebrates. This pattern conforms to evolutionary expectations: if there is no differentiation of parent and offspring during fission, there is an absence of the kind of age structure that is expected to lead to the evolution of aging (Charlesworth 1980, 1994). Rose (1991, p. 171) offers a typical evolutionary explanation of the connection between s(x) and the Gompertz equation: “the ‘Gompertz’ form of mortality among iteroparous species may be due to a broad conformity of mortality under good conditions to the intensity of natural selection on age-specific mortality rates.” patterns of pleiotropy connecting mortality and fecundity at different ages are expected to quantitatively obscure such patterns, making age-specific mortality conform to the waning force of natural selection only crudely
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