Studies of inferred genetic risk indicate that G×E effects are indeed likely to underlie the risk of AUDs and DD. However, the challenge is to detect G×E effects in human studies using measured genotypes. The limited number of studies have so far largely focused on a range of alcohol consumption phenotypes in non-AUD/DD adolescents or young adults, whereas a better population to detect G×E effects might be treatment-seeking, severe alcoholics [6] or drug addicts, many of whom have a history of childhood maltreatment. Studies have included a range of stressors from childhood maltreatment to past year SLEs in adults. It has yet to be determined whether recent SLEs in adults without a history of childhood maltreatment are strong enough to unmask G×E effects. The neurobiological changes resulting from early-life stress may be influenced by genetic variation and may confer vulnerability to addiction. Whether the availability of alcohol/drug, particularly in adolescence, is sufficient to promote onset of disease or whether later stress exposure, perhaps resulting in drinking to cope, is a requirement remains to be determined. Clearly, it is important to
