Taken together, these findings indicate that phenotypic correlations among dimensions of child and adolescent psychopathology are primarily, but not entirely, due to correlated additive genetic influences. This does not rule out the possibility of gene-environment correlations and interactions as sources of shared etiologic influences. This is because gene-environment correlations and gene-environment interactions with C are folded into estimates of A in biometric models, whereas gene-environment interactions with E are included in estimates of E.37, 38 Nonetheless, the present findings on child and adolescent psychopathology are generally consistent with Plomin's “generalist genes, specialist environments” hypothesis for cognitive abilities.39, 40 That is, pleiotropic genetic factors tend to promote correlations among phenotypes, whereas environments tend to promote their differentiation.
