Proximate Determinants of Sexual Differences in Adult Body Size

In many animal species, males and females attain different adult body sizes. The processes underlying such sexual differences are undoubtedly complex and may involve an interplay between adaptive, exaptive, and nonadaptive genetic influences on the one hand and environmental variables on the other. For example, large body size may be shown by males because genes for that character confer a selective advantage in that sex (see, e.g., Darwin 1871; Trivers 1972), because such genes have been inherited from an ancestral form (see, e.g., Cheverud et al. 1985), or because local environmental conditions happen to be particularly favorable for the survival and growth of males (see, e.g., Howard 1981; Woolbright 1983, 1989; Halliday and VerrellI986). The relative importance of such alternative factors is difficult to assess but may be clarified by considering the proximate determinants of sexual differences in body size (hereafter, "sexual size dimorphism," or SSD). Alternative hypotheses about the causation of SSD make different assumptions and predictions about the stage in ontogeny at which sexual dimorphism in mean adult body size is determined. There are two main possibilities for ontogenetic determination of sexual differences in mean adult body size. (1) This dimorphism is determined mainly by the direction and degree of SSD present at the attainment of sexual maturity. Under this hypothesis, sexual differences in mean adult size are determined by processes operating on juveniles: sex differences either in growth rate or in the age at maturation. (2) Mean adult SSD is determined mainly by sex differences in growth or survival rates during adult life. Under this hypothesis, differences in adult size between the sexes result because adults of one sex grow faster or survive better than adults of the other sex. The first of these alternatives-SSD at maturation is the prime determinant of dimorphism in mean adult body size-is consistent with a wide range of hypotheses that explain SSD as an adaptation or as a result of phylogenetic conservatism. Even if mean adult SSD is the actual target of selection, this may well be achieved evolutionarily by a modification of the genes that control SSD at maturation. Local environmental conditions as well as genotypic factors may influence the SSD at maturity (Gibbons et al. 1981; Stearns and Koella 1986). The hypothesis that processes operating during adult life (i.e., after maturation) are the primary determinants of mean adult SSD is also consistent with a wide variety of evolutionary and ecological ideas. For example, such differences in growth or survival rates between the sexes could be influenced by sex-specific adaptations of physiology, morphology, or behavior, in which case the resulting