Due to the substantial effects that prenatal alcohol exposure has on brain development (reviewed by Spadoni et al. 2007), as well as the chronic effects of alcohol consumption on brain structure and function (reviewed by Oscar-Berman and Marinkovic 2007; Sullivan and Pfefferbaum 2005), it has been a challenge to delineate the neurobiological risk for AUD from the consequences of alcohol on brain systems. Therefore, it is useful to focus on studies of high risk individuals with minimal alcohol exposure to identify possible etiologic mechanisms for the development of AUD. Neurobiological factors that have been documented prior to alcohol exposure in the offspring of alcoholics and the offspring from families with multiplex alcohol dependence are more likely to be causally related to risk for AUD.
