Increased maternal age at reproduction is often associated with decreased offspring performance in numerous species of plants and animals (including humans). Current evolutionary theory considers such maternal effect senescence as part of a unified process of reproductive senescence, which is under identical age-specific selective pressures to fertility. We offer a novel theoretical perspective by combining William Hamilton's evolutionary model for aging with a quantitative genetic model of indirect genetic effects. We demonstrate that fertility and maternal effect senescence are likely to experience different patterns of age-specific selection and thus can evolve to take divergent forms. Applied to neonatal survival, we find that selection for maternal effects is the product of age-specific fertility and Hamilton's age-specific force of selection for fertility. Population genetic models show that senescence for these maternal effects can evolve in the absence of reproductive or actuarial senescence; this implies that maternal effect aging is a fundamentally distinct demographic manifestation of the evolution of aging. However, brief periods of increasingly beneficial maternal effects can evolve when fertility increases with age faster than cumulative survival declines. This is most likely to occur early in life. Our integration of theory provides a general framework with which to model, measure, and compare the evolutionary determinants of the social manifestations of aging. Extension of our maternal effects model to other ecological and social contexts could provide important insights into the drivers of the astonishing diversity of lifespans and aging patterns observed among species.S enescence is the age-related deterioration of organismal function and fitness. Evolutionary theory explains its pervasiveness as the result of age-related declines in the strength of natural selection to preserve survival and reproduction (1). Genes deleterious to survival or fertility in late life can persist or even come to fixation as a result of this weakening of selection in old age (2-4). To date, most theoretical and empirical research into the evolution of senescence has focused on age-specific survival and fertility (vital rates), as these rates are most proximate to fitness. Both age-related declines in survival (actuarial senescence) and fertility (reproductive senescence) can evolve independently from initially nonsenescent life histories (1).These vital rates are a product of complex interactions among different physiological systems, phenotypic traits, and their environment. One important source of environmental contributions involves social interactions. The influence of other individuals in the environment on a particular phenotype can itself be heritable, and the importance of these so-called "indirect genetic effects" (IGEs) is now established within evolutionary biology (5-7). IGEs are known to readily alter the evolutionary predictions of standard quantitative genetic models incorporating only direct genetic ...