that a child’s genetic characteristics can influence his or her environment (40–43). Importantly, this finding may lend insight into how INT− youth experience less victimization than INT+ youth (6, 7). In light of prior evidence showing that (i) higher OXTR methylation is associated with lower circulating levels of oxytocin (10) and (ii) lower levels of oxytocin are associated with deficits in prosocial and affiliative behaviours (12, 13), it is possible that INT− youth develop socio-emotional characteristics that actively discourage victimizing behaviour from others (e.g. showing lower empathy and trust), and potentially fit more of a ‘bullying-only’ profile (44, 45).Moreover, it is possible that higher OXTR methylation ‘protects’ INT− youth from developing internalizing problems, which act as both an antecedent and maintaining factor for victimization (46). More generally, this effect may lend support to the notion that epigenetic mechanisms can prepare children to cope with forthcoming environmental challenges (47). The second finding is that one specific domain of environmental risk, prenatal parental risks, are associated with higher OXTR methylation at birth. It is unclear whether this association is causal (e.g., a direct impact of parental risks on fetal development) or correlational (e.g., reflecting genetic confounding; 48, 49). Third, OXTR methylation in
