the complex longitudinal models tested. Consequently, the present findings should be interpreted as well-grounded hypotheses for further examination in larger longitudinal studies. The use of larger studies may help to clarify the present findings, including (i) which aspects of prenatal parental risks associate with OXTR methylation at birth (e.g. parental criminality vs substance use) in INT− youth; (ii) what biological mechanisms mediate the effect of prenatal environmental risk exposure on CU for INT+ youth; and (iii) why we find a negative association between postnatal environmental risks and CU traits in the INT+ group. Third, the current study was based on a community sample of youth with relatively low rates of internalizing problems. This resulted in the classification of groups based on a median split. In future, it will be important to replicate developmental pathways to CU in high-risk youth who show more severe internalizing problems (e.g. young offenders, psychiatric inpatients). Finally, although the current study did not find that DNA sequence-based variation in OXTR influenced DNA methylation or CU levels, analyses were limited to four SNPs. In future, it will be necessary to examine additional local (cis) and distant (trans) SNPs to better establish the relationship between genetic variation across
