Our large sample of ES females with disruptive behavior disorders has provided an opportunity to pursue novel hypotheses concerning gender-specific risks. For example, Burt et al. (2006) showed that the heritability of CD varies as a function of age of menarche, with heritability being greatest when menarche occurs at a normative age rather than early age. This result is consistent with the notion that CD in early maturing girls reflects psychosocial environmental mediation. Puberty may also be important to understanding the etiology of eating disorders, which we have shown to predict increases in externalizing behavior during adolescence (Marmorstein et al., 2007). In a research program that has been extended by the use of ES twins as a replication sample, researchers (Culbert et al., in press; Klump et al., 2007) have shown that the heritability of disordered eating increases as girls enter puberty. This finding supports the possibility that the increase in ovarian hormones at puberty in girls activates or moderates genetic effects on disordered eating. These results are also consistent with a possible role for active genotype-environment correlation leading to an increase in genetic effects after pubertal onset.
