Epidemiologic studies have identified specific childhood environmental exposures as substantial risk factors for subsequent behavioral disorders. Epigenetic processes mediate the impact of environmental influences (e.g., life experiences) on risk of illness through regulation of gene expression and function. The role of stressors in epigenetic variation in animal models is well established but extant human epigenetic studies are relatively small and typically rely on simple phenotypes (Tsankova, Renthal, Kumar, & Nestler, 2007). However, preliminary studies reporting associations between methylation and aspects of addiction (Hopf & Bonci, 2010), prenatal stress (Oberlander et al., 2008), childhood abuse (McGowan et al., 2009), PTSD (Uddin et al., 2010), and depression (Uddin et al., 2011) provide motivation for the inclusion of epigenetic measures in exploration of the relationship between intervention and later behavioral outcomes. Although acquired adverse epigenetic changes were once thought to be permanent, new evidence suggests they are plastic and potentially reversible (Kelly, De Carvalho, & Jones, 2010), opening the possibility for the impact of targeted interventions.
