For the INT− (Figure 3A), three results are highlighted. First, higher OXTR methylation at birth was prospectively associated with higher CU at age 13, and this association was stronger for INT− vs INT+ (Δχ2[1] = 4.78, p = .03). Higher OXTR methylation at birth also associated with lower risk exposure during early childhood (birth – age 7) – specifically direct victimization (e.g., bullying by peers, physical harm by adults) – and this association was stronger for INT− vs INT+ (3 Δχ2[1] = 7.11, p = .01). In other words, for INT−, higher OXTR methylation at birth associated with both (i) higher CU and (ii) less subsequent victimization, suggestive of what we refer to as an ‘evocative epigenetic-environment correlation’. Second, although no effect of overall prenatal environmental risk on OXTR methylation at birth was observed, one specific risk domain, prenatal parental risks, was found to be significantly associated with OXTR methylation levels at birth. This association was stronger for INT− vs INT+ (Δχ2[1] = 4.07, p = .04). Third, temporal stability between birth and age 9 was greater in magnitude for the INT− vs. INT+ (Δχ2[2] = 12.00, p = .001).
