We illustrate three different patterns of genotype–environment interaction, all at ages 12–14, in our analyses in Figs 2–4. Fig. 2 depicts the interaction of GR-ExtD and alcohol availability. The maximal monthly intake of alcohol over this age period increased with increasing levels of genetic risk at all levels of alcohol availability. However, at low levels of availability, the increase was fairly modest whereas at high levels the increase was much stronger. Fig. 3 shows the interaction of GR-AUD and peer group deviance in the prediction of maximal alcohol consumption. At low levels of peer deviance, genetic risk had no effective impact on the level of alcohol consumption. By contrast, at high levels of peer deviance, levels of alcohol consumption were strongly related to level of genetic risk. Fig. 4 depicts the results for the interaction of GR-ExtD and prosocial behaviors. At low levels of genetic risk, alcohol consumption was low and unrelated to level of prosocial behaviors. However, as the level of genetic risk for externalizing disorders increased, there was a greater effect of involvement in prosocial behavior.
