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nity to matter. The higher the background frequency of deaths from predators or accidents, the more this should be so. Evolutionary theory successfully predicts an association between greater vulnerability and more rapidly rising age-specific mortality. Small insects are an example. Small, exposed, ground-dwelling mammals are another example, contrasting with safer, tree-dwelling mammals and birds (see Charlesworth, 1994:247-248). Finch (1990:22-25 and throughout) sets out an impressive array of evidence from modest samples from many species displaying rising and often accelerating hazard rates with age. Ever-accelerating hazard rates with age imply de facto limits on later life expectancy, and if the observed accelerations with age do share a common general evolutionary origin, that would be a rationale for expecting genetically preprogrammed limits to longevity.
Alongside these ideas from evolutionary biology, there is the mystique of the "Hayflick limit" from cell biology (see Hayflick, 1994:111-136). Certain types of mammalian cells transplanted to cultures only divide up to a limited number of times. The limits correlate roughly with the typical life spans of the organisms from which the cells come. The cells that have stopped dividing often continue to survive in less-than-prime condition. While this process may be implicated in some localized phenomena of aging, any pervasive role for the Hayflick limit on cells in determining the senescent mortality of organisms remains uncertain, as Caleb Finch discusses in the concluding chapter. Nonetheless, as the most frequently cited result in all of gerontology, the Hayflick limit has contributed powerfully to a general sense that the study of longevity is a study of limits, tradeoffs, and diminishing returns.
The ideas that lead to the theories of mutation accumulation and antagonistic pleiotropy are very general principles of evolution. They serve as a paradigm for thinking more broadly—transcending specific reference to genes—about the investments reflected in the ways we and other creatures are designed. Nature puts a premium on solving problems of the kind that show up early in the life course. Organ systems need not be constructed to implement repairs or withstand cumulating challenges late in life.
Out of this essentially pessimistic view, however, has come a simile with an optimistic turn. In this volume, James Vaupel develops it in Chapter 2. The body is likened to a planetary space probe like the Pioneer mission to Mars. The Pioneer's engineers worked through all the problems and built in all the safeguards needed to be sure that the Pioneer probe would reach Mars and complete its mission. Just so, the body must be engineered to complete its evolutionary mission—produce and nurture its young and pass on its genes. After its mission is accomplished, it is disposable. No special provisions for longer operation or late-stage repair are advantageous. But the Pioneer space probe was still functioning as it left the Solar System. The same mechanisms built in to guarantee fail-safe completion of the mission may endow the body, as they did the Pioneer, with residual post-completion life.