into adulthood. Others might harbor multiple risk variants that underlie only the adolescent-limited genetic factor, leading to temporally limited genetic risk to excessive consumption. Still others could carry genetic risk primarily from variants underlying the adult-onset factor, thus leading to a relatively late onset of high consumption. Similar genetic and/or environmental liabilities could account for the phenotypic subtypes of antisocial behavior described by Moffitt (1993). One study of persistent antisocial behavior in a prospectively assessed twin sample reported support for Moffitt’s theory from a genetic perspective: a common latent factor, largely genetic in nature, accounted for continuity of antisocial behavior from mid-childhood through to early adulthood (Tuvblad et al. 2011). This persistent latent liability was supplemented by significant time-specific genetic influences at ages 8–9 years (in both genders) and 13–14 years (females only), indicating that even individuals who were not genetically liable to persistent antisocial behavior might still be genetically liable to such behavior at early ages. Those findings and the current results are complementary to the concept of ‘heterotypic continuity ’: rather than a single latent liability manifesting differently across development, we observe here a consistent phenotype (alcohol consumption) that is influenced by distinct latent liabilities during different developmental
