& McCartney, 1983), in which individuals seek out environments (e.g., substance-using peers) that facilitate expression of this vulnerability. Furthermore, gene-environment interaction may influence risk for substance misuse, such that heritable influences on adolescent involvement are increased in more “facilitative” environments (for instance, those characterized by low parental monitoring; Dick, 2011). Finally, our finding of significant unique environmental overlap across initiation and disorder suggests a potentially causal relation between these outcomes, indicating that delaying early substance initiation may help directly reduce risk for disorder.
