have some small deleterious effect earlier in life (Partridge and Barton, 1993a). The evolutionary theories do predict a monotonic decline to zero in reproductive value at some point in the life history. Re-examination of the reported anomalous cases in which "aging" (measured as mortality rate) appeared in theoretical models where there was either no change (Blarer et al., 1995) or a positive change (McNamara and Houston, 1996) in intrinsic state also shows that use of reproductive value as a measure of aging would have removed the anomaly.
To advance this issue will require the production of explicit theoretical models of the mutation-accumulation and pleiotropy theories that examine outcomes for age-related patterns of mortality in not only the reproductive but also the postreproductive period. Two recent studies (Abrams and Ludwig, 1995; Rose, in this volume) are promising starts in this direction. We also need more data. There is at present a paucity of information about the degree and pattern of age-specificity of fitness effects of new mutations, and of the relevant mutation rates. The timing of the effects of costs of reproduction or of investment in repair processes on future fertility and survival is also poorly known (Partridge and Sibly, 1991). These data are not easy to collect and are a challenge for future work. To understand how postreproductive survival evolves, we need to understand its genetic correlations with survival and mortality patterns during the reproductive period.
What can evolutionary theories of aging predict about its rate in different populations? One of the broadest predictions is that there will be a relationship between the impact of external factors on the survival and fertility of the population, on one hand, and the intrinsic rate of aging that it is expected to evolve, on the other (Medawar, 1952; Williams, 1957; Hamilton, 1966; Charlesworth, 1980 and 1994; Tuljapurkar, Rose, in this volume). For instance, higher externally imposed death rates of adults are expected to cause evolution of higher rates of aging for both survival and fertility. However, the precise nature of this prediction and the nature of the measurements necessary to test it have been the subject of some discussion (Abrams, 1993; Promislow, 1991; Blarer et al., 1995).
Population dynamics are one important consideration. If one vital rate is changed by a change in, for instance, the size-specificity of predators, then for the population to remain regulated in numbers, it must compensate in some way. For an alteration in externally imposed factors to impose a permanent change in selection on the life history, the population must not respond by restoring a pattern of age-specific vital rates that leaves the pattern of selection unaltered (Abrams, 1993). The first thing that must be established, therefore, is that a difference in the impact of external factors results in an altered pattern of age-specific vital rates. This external impact must be separated from any intrinsic