Gene identification studies, however, typically focus on a snapshot of behavior at a single timepoint, such as a composite measure of current consumption quantity, past-year alcohol problems, or lifetime AUD diagnoses (4, 5, 25). This approach, while aiming to maximize statistical power, risks missing out on differences critical to the etiology of AUBs such as longitudinal variation or changes in the relative importance of broad versus specific risk processes across time. Existing evidence indicates that the genetic influences on AUBs are not homogeneous, but can be separated into distinct factors related to consumption, problems, and patterns of AUBs and beverage preferences (26–28), as well as effects that are shared with EXT or are specific to alcohol use (8). EXT-related genes are correlated with early initiation of substance use, while alcohol-specific genes are more relevant for increasing alcohol use/problems over time (8, 29). The precedence of different neurobiological systems at different stages of the addiction cycle (19) also suggests that different sets of genes may be important for initiation, acceleration, and/or persistence of alcohol use. Such different sets of genes have
