There is prior evidence linking genetic variation in the serotonin transporter to differential susceptibility in response to the SAAF prevention program (Brody, et al., 2009), and Beach et al. (2014) found that the “s” allele also was associated with differential impact of SES related risk factors on methylation, suggesting that biological embedding may be influenced by presence of the “s” allele. Accordingly, we anticipated a similar pattern of genetic moderation for the effect of SAAF on methylation at OXTR. Further supporting the expectation of moderated effects of SAAF on methylation of OXTR, low serotonin is implicated in disruptions of social behavior among primates and humans (Raleigh, McGuire, Brammer & Yuwiler, 1984), suggesting that “s” allele carriers may be more vulnerable to social disruption and so more likely to experience benefits in response to SAAF, increasing effects on OXTR methylation.
