According to this hypothesis, the relationship between age at 1st drink and AD symptomatology extends beyond shared predispositions. The most stringent form of this hypothesis posits that early age at 1st drink leads to onset of AD symptomatology. Less stringent forms suggest that even after accounting for common predispositions (or common vulnerabilities), age at 1st drink exerts a causal influences on AD symptoms. Discordant twin studies (Grant et al., 2005; Prescott and Kendler, 1999) have been widely used to test this hypothesis. By selecting pairs of twins who are discordant for early onset drinking and examining their corresponding risk for AD symptoms, these studies show that even in genetically matched individuals, those who start drinking at an early age are at increased risk for developing AD. This study design has also demonstrated that this increased risk, which may be construed as causal, is in part accounted for by the individual-specific environmental milieu in which age at 1st drink and subsequent AD develop. We do not test for this hypothesis, but if this hypothesis were supported, then prevention efforts targeted at
