later ages. This does not mean that the genes should be expressed at these ages. For instance, genes active during development could affect the durability of the soma, while genes affecting levels of activity and reproduction could determine the levels of damage that are incurred. The mutation-accumulation theory does not, therefore, rest on the implausible assumption that the late-life decline in state relies on gene expression of an increasing number of deleterious mutations. Rather, effects of variation between alleles and their patterns of expression at all ages become apparent in the phenotypes of old age.

How Can the Rate of Aging Be Measured?

What do these evolutionary theories allow us to predict about age-related changes in death rate in the later part of life in any population, including human populations? This question raises an important empirical issue, which is how the intrinsic deterioration that causes death rate to increase and fertility to decline at later ages can be detected and compared between different populations. There is considerable current interest in measuring the rate of aging in different natural populations, and in using such measures to deduce the evolutionary mechanisms at work (e.g., Nesse, 1988; Abrams, 1991; Promislow, 1991; Gaillard et al., 1994; Carey et al., 1992; Curtsinger et al., 1992; Abrams and Ludwig, 1995), which has led to lively debate about exactly how aging can be detected and its rate measured.

Most measures of the aging rate used thus far have focused on death rates. If intrinsic deterioration is occurring and death rate alone is used as a measure, then death rate clearly must change with age. Two populations that differ from each another in death rates that remain constant with age within each population do not, by this criterion, differ in their rate of aging (Medawar, 1952; Tatar et al., 1993; Blarer et al., 1995). Various measures of the rate at which death rate increases with age have therefore been proposed (Finch, 1990; Finch et al., 1990; Promislow, 1991; Carey et al., 1992) and have been used, for instance, to examine the occurrence of aging in natural populations (Promislow, 1991; Gaillard et al., 1994), to document the rate of change in death rate with age in humans (Finch et al., 1990), or to show an apparent slowing down in the rate of aging at later ages in insects (Carey et al., 1992; Curtsinger et al., 1992), nematodes (Brooks et al., 1994), and in humans (Vaupel, in this volume). An increase in age-specific death rates in theoretical models has been used to claim that spurious evidence for aging can be found in the absence of any intrinsic decline in the organism (Blarer et al., 1995) or that aging can occur as a direct result of an intrinsic improvement in state (McNamara and Houston, 1996). Superficially, some of these findings might be at variance with evolutionary theories of aging. However, they rest, in part, on the use of an inappropriate measure of aging from the evolutionary point of view, based solely on the way that death rates change with age.



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