induces changes in brain chemistry, or 2) serves as a learning process for pleasurable effects of drugs. In fact, animal research has shown some support for changes in brain functioning as a result of substance exposures (Ellgren, Spano, & Hurd, 2007). Alternatively, the link between cannabis and other drug use and problems could stem from a general predisposition to drug use (or deviant behavior in general), such that the association is attributable to correlated vulnerabilities. Along this line, there is evidence, for both use and abuse/dependence, of moderate to substantial genetic overlap across illegal substances (Kendler et al., 2003, 2007; Tsuang et al., 1998). A third possibility is that both causal and correlated vulnerability mechanisms are involved in the association between cannabis use and other substance use/abuse/dependence. Agrawal et al. (2007) found support for the correlated vulnerabilities hypothesis, but could not rule out the possibility of causal influences as well. Our results are generally consistent with either: 1) a gateway model in which cannabis use, regardless of the age of initiation, increases risk, or 2) a correlated vulnerabilities model.
