This chapter began by arguing that an evolutionary perspective directs us to consider the fertility behavior of men because selective forces on males, as the sex with less direct energetic parental investment, may be particularly strong. Yet at the same time human males clearly do invest in offspring postnatally, adding an additional level of complexity to the way in which selection has shaped the reproductive biology and behavior of human males from that of our primate ancestors.

My description of reproductive maturation in humans as stretching from adrenarche to young adulthood suggests a distinct human version of male reproductive maturation. Changes in behavior needed for successful reproduction span this entire period, beginning with changes in cognition and social relationships during the prepubertal period, continuing with reproductive maturation during adolescence and the onset of sexual behavior, and ending in the onset of reproduction and parenting during the young adult phase.

This extended definition of reproductive maturation in human males highlights the role of both the testicular and adrenal axis in male reproductive behavior. Sufficient evidence exists to argue that pubertal maturation in males is part of individual variation in the reproductive axis that persists into adulthood and underlies individual continuity in sexual behavior. In the same way, cortisol is a marker of the adrenal axis, which underlies individual continuity in social behavior. However, the role of adrenal hormones in the onset of sexual behavior is only beginning to receive attention. While the association of cortisol and risk taking suggests a role for cortisol in the expression of sexual behavior, at this point only the slimmest of data substantiate the link.

There is even less empirical evidence demonstrating that DHEA/S is related to variation in adolescent sexual behavior, yet DHEA/S potentially is involved in a variety of mechanisms that may affect sexual behavior. On the one hand, conversion of DHEA/S to testosterone means that it may augment the essential role of gonadally produced testosterone in the maturation of the reproductive system, including promoting libido and somatic growth, both of which have been related to adolescent sexual behavior. In addition, DHEA/S and testosterone have been shown to have similar effects on gene expression in immune cells (Maurer et al., 2001). On the other hand, conversion of DHEA/S to estrogen means that it may play a suppressive effect in reproductive maturation but promote aspects of cognitive function related to the forebrain (Keenan et al., 2001).

In addition to its potential role as an androgen or estrogen, DHEA/S may play a role in adolescent behavior through more direct mechanisms. These include its role in stimulating GABA(A) neurons, with effects on

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