Male and female 10-12 year old children of men with Alcohol Use Disorder (AUD) (high risk) and control fathers (low risk) will be studied at baseline and on two follow-ups (ages 12-14 and 16) to developmentally clarify liability for an Alcohol Use Disorder. In addition to obtaining behavioral measures, the project will measure cognitive, electrophysiological and eye movement processes using a multitrait multimethod (MTMM) paradigm. High risk subjects (N=400) are hypothesized to perform deficiently compared to low risk subjects (N=400) on measures that differentially reflect prefrontal cortex functioning and to be comparable on non-prefrontal measures. Within the developmental framework encompassing transition from late childhood to mid-adolescence, it is hypothesized that the manifest behavioral dysregulation (due to prefrontal cortex impairment) is associated with disruptive parent-child interactions and affiliation with deviant peers. The resulting maladjustment, namely, an externalizing disposition, predisposes to precocious alcohol exposure, early age intoxication and, by mid-adolescence, heavier alcohol involvement. In effect, individual liability (dysregulation explicable by prefrontal cortex dysfunction), via interaction with the family and peer environments, biases the developmental trajectory toward an externalizing adjustment style (proximal outcome) and problem alcohol consumption (distal outcome). Confirmation of the individual basis of AUD liability would point to innovative approaches to prevention by identifying the specific components of risk which are subsumed within well-known functional neuroanatomical systems. Furthermore, this project will afford the opportunity to elucidate AUD etiology as the culmination of person- environment interactions.
