Our goal was to examine whether aetiological pathways to CU differed for INT − vs INT + youth, using repeated measures of environmental risk exposure and OXTR methylation. Consistent with our hypothesis, INT− and INT+ did not differ in CU levels, but INT-experienced lower risk exposure than INT+. Our integrative developmental model showed that, for INT− youth: (i) OXTR methylation at birth associated with higher CU (age 13), as well as decreased experience of victimization during childhood (birth – age 7); (ii) higher prenatal parental risks (e.g. maternal psychopathology, criminal behavior, substance use) associated with higher OXTR methylation at birth; and (iii) temporal stability of OXTR methylation was greater (birth – age 9) than for INT+. In contrast, for INT+ youth, OXTR methylation did not associate with CU. Rather, prenatal risks of an interpersonal nature (e.g., intimate partner violence and family conflict) associated with higher CU levels. Findings support the existence of distinct pathways to CU.
