From its inception, COGA has focused on the importance of brain function as it relates to the risk and consequences of alcohol use and AUD, through the examination of noninvasively recorded brain electrical activity and neuropsychological tests. A landmark study in 1984 from Begleiter and Porjesz reported that sons of fathers affected with AUD displayed neurophysiological differences even before they ever consumed alcohol. 9 These findings, which were replicated in both males and females by several independent research groups throughout the world and within both male and female offspring of the original COGA participants, 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 changed the field's thinking from an assumption that all neural anomalies were a result of prolonged alcohol consumption to the hypothesis that neural differences before onset of use may also contribute to risk for AUD. Decades later, COGA's sophisticated neurophysiological and neuropsychological measures, together with the rich multi‐modal family and longitudinal data collection, have allowed us to disentangle brain‐related risk and resilience factors from the consequences of prolonged and heavy alcohol use in the context of genomic, psychosocial and environmental influences over the lifespan.
