As discussed earlier, childhood trauma, particularly in the first few years of life, is associated with psychopathology including early onset of problem drinking in adolescence and AUD and DUD in early adulthood.16 The risk-resilience balance for addiction may in part be due to the interaction between environment stressors and variation in stress and anxiety related genes (G × E). The X linked MAOA gene has a repeat promoter polymorphism (MAOA-LPR) that influences gene activity. This gene encodes the MAOA enzyme that plays an important role in the metabolism of the stress-related neurotransmitters norepinephrine and serotonin. There is an extensive literature, starting with Caspi et al, 200261 showing a G × E effect between MAOA-LPR and childhood trauma on antisocial behaviors, particularly in males.62 There is one published G × E study in AI, specifically Southwestern American Indian women, that investigated the interaction between CSA and MAOA-LPR . This study showed that the MAOA-LPR low activity allele was associated with AUD, particularly antisocial alcoholism, but only in women exposed to CSA.63 Thus women who were carriers of the genetic risk allele but had been spared CSA were resilient to the development of AUD.
