As a risk factor, FHD captures a combination of biological (genetic) and psychosocial/environmental factors. The genetics of alcohol consumption has garnered interest (e.g., previous studies 69 , 70 ), yet binge and high‐intensity phenotypes are relatively unexplored. Use of the AUDIT consumption subscale 71 has been productive, 72 , 73 , 74 but this measure does not specifically capture the high‐intensity drinking phenotype and may reflect non‐problematic alcohol usage. 74 Further, some work suggests the prediction of clinical phenotypes based on AUDIT consumption‐based polygenic risk scores may be sample‐dependent. 75 Maxdrinks, which, at higher ranges, is more specific to Binge and High‐Intensity Drinking, has proven a valuable phenotype in genetic studies. 14 , 76 , 77 Consequently, our laboratory finding of an association between FHD and drinking intensity group is congruent with the literature and significantly strengthened by replication in the much larger COGA sample. In fact, supplementary COGA analyses showed that drinking intensity accounted for more variability in the alcohol screening measures than FHD (See Supporting Information), highlighting the importance of collecting information on drinking patterns within and across events.
