Decades of twin, family, and adoption research have established that genetic influences underlie substance use disorders (SUDs; e.g alcohol, nicotine, and drug use/dependence) (Goldman, Oroszi, & Ducci, 2005). Elucidating the genetic etiology of SUDs would help to inform intervention and treatment strategies, greatly easing the public health impact of these disorders (Merikangas & Risch, 2003). SUDs, however, rarely occur in isolation; disorders that commonly occur comorbidly with SUDs include a spectrum of disorders characterized by behavioral disinhibition, e.g. conduct disorder and antisocial behavior. Large-scale epidemiological studies with twins have shown that the common comorbidity among these disorders can be accounted for by an underlying externalizing (EXT) factor that is highly heritable (Kendler, Prescott, Myers, & Neale, 2003; Krueger et al., 2002; Young, Stallings, Corley, Krauter, & Hewitt, 2000), and that the source of the comorbidity in these externalizing disorders can be largely attributed to common genetic factors (Hicks, Krueger, Iacono, McGue, & Patrick, 2004; Kendler et al., 2003). The high heritability and common genetic influence across these disorders suggest that a behavioral/clinical phenotype based on this EXT factor may be
