indicators of deviance and/or poor ECF. Nevertheless, before we can reject a mediating role of selectivity it will be critical to determine whether the rare low-risk sample members who initiated drinking before age 18 were characterized by AUD risk factors beyond the typical indicators of deviancy. Potential candidates might include early-onset mood and anxiety disorders, positive expectancies related to the effects of alcohol, peer alcohol use, parental approval of drinking, and so forth. Pending additional investigation, it would be premature to rule out either selectivity, habituation of heavy drinking or direct neurotoxic effects of adolescent drinking as causal mechanisms mediating the association between early AFD and risk of adult-onset AUD, although it might be argued that the persistence of increased AUD risk over the lifespan, as indicated by the lack of interactions between AFD and age at interview, are more supportive of underlying vulnerabilities than of direct effects.
