The physiological changes of adolescence may promote risk-taking behaviors, 
including binge drinking. Approximately 40% of alcoholics were already drinking 
heavily in late adolescence. Most cases of alcoholism are established by the age 
of 30 years with the peak prevalence at 18-23 years of age. Therefore the key 
time frame for the development, and prevention, of alcoholism lies in 
adolescence and young adulthood. Severe childhood stressors have 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-metabolizing genes, increased susceptibility to alcohol's 
sedative effects) and environmental (lack of alcohol availability, positive peer 
and parental support). Genetic vulnerability is likely to be conferred by 
multiple genes of small to modest effects, possibly only apparent in 
gene-environment interactions. For example, it has been shown that childhood 
maltreatment interacts with a monoamine oxidase A (MAOA) gene variant to predict 
antisocial behavior that is often associated with alcoholism, and an interaction 
between early life stress and a serotonin transporter promoter variant predicts 
alcohol abuse in nonhuman primates and depression in humans. In addition, a 
common Met158 variant in the catechol-O-methyltransferase (COMT) gene can confer 
both risk and resilience to alcoholism in different drinking environments. It is 
likely that a complex mix of gene(s)-environment(s) interactions underlie 
addiction vulnerability and development. Risk-resilience factors can best be 
determined in longitudinal studies, preferably starting during pregnancy. This 
kind of research is important for planning future measures to prevent harmful 
drinking in adolescence.