appearing in progress against human mortality at older ages in developed societies. The climate of biological opinion made it natural for demographers to see the plateau as a long-term phenomenon. Diminishing returns at older ages fitted into the broad-brush theoretical picture and made it reasonable to discount the likelihood of that resumption of progress that did, as it turned out, actually occur.

Evolution coddles you when young and forsakes you when old. This central idea can be traced back more than a century to Alfred Russel Wallace (Rose, 1991:4); the evolutionary theory of senescence that has grown from it is described by Shripad Tuljapurkar, Linda Partridge, and Michael Rose in Chapters 4, 5, and 6, respectively. Natural selection clears away genes that compromise reproduction or survival to and through the ages of reproduction. Natural selection leaves to their own devices genes with bad effects at ages that no longer matter as far as the propagation of progeny is concerned. In most mathematical implementations of this kind of theory, ''ages that no longer matter" have been equated to postreproductive ages of zero fertility; the efficacy of natural selection on mortality as a function of age has been taken to decline smoothly throughout the reproductive period, reaching zero at its end. These ideas have ramified into two intertwining but distinguishable theories, the "mutation-accumulation theory" and "antagonistic pleiotropy."

The mutation-accumulation theory recognizes that most mutations are unfavorable. Some portion of mutations elude repair. Suppose there are genes that specifically impair survival at some range of older ages without substantially reducing net reproduction. Suppose that the structures affected by the genes and the environmental preconditions for their actions have been in place for a very long time and that what is bad for survival stays bad in the face of surrounding change. Then mutations deleterious to survival at older, postreproductive or postnurturant ages should accumulate over eons, since selection is not clearing them away. Genes predisposing to cancers are often adduced as examples. In its simple forms, this mutation-accumulation theory predicts sharply rising hazard functions beyond some threshold age.

Antagonistic pleiotropy, as it pertains to senescence, occurs if there are genes that have positive effects on net reproduction and negative effects on postreproductive survival. If such genes exist, then organisms would be making a tradeoff between investments in younger-age reproductive fitness, which matters to natural selection, and older-age viability, which does not matter to natural selection. Kirkwood's (1977) "disposable soma theory" sees tradeoffs of this kind as a general phenomenon arising as organisms allocate limited energy between functions of reproduction and functions of somatic—bodily—maintenance. Like mutation accumulation, antagonistic pleiotropy and the tradeoffs posited by the disposable soma theory are reasons for hazard rates to rise with age.

Sustaining these considerations is the timeless observation that life in the wild is, as Hobbes put it, "nasty, brutish, and short"—in the wild few creatures survive to old age, so genes governing late-age processes have had little opportu-



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