Chunk #37 — HOW DO NEURAL SIGNATURES ASSOCIATED WITH AUD HELP ELUCIDATE THE ROLE OF BRAIN FUNCTION IN THE RISK AND CONSEQUENCES OF ALCOHOL USE AND AUD ACROSS THE LIFESPAN? — How does the social–environmental context (and interaction with genetic risk factors) impact brain functioning and ultimately impact risk for AUD?
Social–environmental experiences throughout the life course, such as interpersonal influences (parenting, peers, romantic relationships) and traumatic stress, may alter neurophysiological and behavioral development, thereby increasing risk for AUD and related psychopathology over and above the contributions of genetics and neurophysiology. 133 , 134 COGA has examined the influence of social‐environmental context on neurocognitive function and AUD as well as how genetic risk may moderate these associations. For example, COGA examined the association of childhood traumatic experiences with developmental trajectories of brain function during response inhibition. 66 Data were drawn from the COGA prospective cohort, comprising offspring from high‐risk and comparison families who were aged 12–22 at enrollment, with follow ups at two‐year intervals since 2004 (see 2. Sample and Clinical Data). Individuals exposed to sexual assaultive trauma prior to age 10 had slower rates of change in developmental trajectories of frontal theta during response inhibition. Importantly, these effects remained significant after accounting for other traumatic exposures, parental history of AUD and participants' substance use, but not measures of impulsivity. Lagged frontal neurophysiological development during response inhibition may reflect delays in
