Genetic and Environmental Influences on the Development of Alcoholism: Resilience vs. Risk

doi:10.1196/annals.1376.019

The physiological changes of adolescence may promote risk-takingbehaviors, including binge drinking. Approximately 40% of alcoholicswere already drinking heavily in late adolescence. Most casesof alcoholism are established by the age of 30 years with thepeak prevalence at 18–23 years of age. Therefore the keytime frame for the development, and prevention, of alcoholismlies in adolescence and young adulthood. Severe childhood stressorshave been associated with increased vulnerability to addiction,however, not all stress-exposed children go on to develop alcoholism.Origins of resilience can be both genetic (variation in alcohol-metabolizinggenes, increased susceptibility to alcohol's sedative effects)and environmental (lack of alcohol availability, positive peerand parental support). Genetic vulnerability is likely to beconferred by multiple genes of small to modest effects, possiblyonly apparent in gene–environment interactions. For example,it has been shown that childhood maltreatment interacts witha monoamine oxidase A (MAOA) gene variant to predict antisocialbehavior that is often associated with alcoholism, and an interactionbetween early life stress and a serotonin transporter promotervariant predicts alcohol abuse in nonhuman primates and depressionin humans. In addition, a common Met158 variant in the catechol-O-methyltransferase(COMT) gene can confer both risk and resilience to alcoholismin different drinking environments. It is likely that a complexmix of gene(s)—environment(s) interactions underlie addictionvulnerability and development. Risk–resilience factorscan best be determined in longitudinal studies, preferably startingduring pregnancy. This kind of research is important for planningfuture measures to prevent harmful drinking in adolescence.

Part II. Neurobiological Processes

Resilience vs. Risk