First, we built upon recent investigations of the genetic etiology of AUDs and related traits by analyzing each of the ten unique items that comprise AUDIT. At this higher resolution, we were able to identify sources of genetic heterogeneity among the items, such as the consistently weaker genetic correlations between frequency of alcohol consumption (item 1) and other drinking patterns (items 2–3) and AUD symptoms (items 4–10). Our item-level approach also allowed us to empirically model the genetic relationships between AUDIT items, providing the first empirical evidence of a correlated, two-factor structure for AUD symptoms at the genetic level. In doing so, we also generated empirically-derived weights to determine how individual items contribute to aggregate measures of alcohol consumption and problematic use. This is an important advance from most quantitative or dimensional genetic studies of AUDs (and other forms of psychopathology), which often use composite score measures that lack statistical justification.
