For INT− youth, we highlight three main findings. First, we support Dadds et al’s (10) study showing an association between higher OXTR methylation and higher CU. Of interest, we show that this association is specific to INT− youth, and occurred at birth, whereas Dadds et al found an association in older youth. Together, these findings may suggest that there are multiple developmental periods of vulnerability for CU via OXTR methylation. In addition, it is worth noting that our methylation probes were different from Dadds et al’s, which raises the possibility that multiple sites across the CpG island mat be associated with CU. We also found that, in INT− youth, higher OXTR methylation at birth was associated with lower levels of direct victimization during childhood, suggestive of an ‘evocative epigenetic-environment correlation’. More specifically, this finding parallels evocative gene-environment correlation studies showing 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
