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 increasing the age at 1st drink would have an impact on the likelihood of developing AD via causal pathways or via reduction of those environmental exposures (e.g. childhood traumas) that jointly increase the likelihood of early drinking and AD.
