outside these loci (5.4%, OR = 1.06, p=0.32). However, we note that stratifying by directionality resulted in significant enrichment among schizophrenia GWAS loci here among a minority of CpGs (N=144) more highly methylated in adolescence than later adulthood (OR=1.42, p=3.38×10−5). Interestingly, these CpGs also tended to be more highly methylated in fetal than postnatal life (80.6%), consistent with the general trend in GWAS positive loci being associated with CpGs relatively hypermethylated in fetal compared with postnatal life. Overall, these data suggest that epigenetic changes around the age of onset of schizophrenia do not in general reflect genetic risk mechanisms, in contrast to the associations contrasting fetal to postnatal life, but they may contain a subset of risk loci relatively hypermethylated in late postnatal epigenetic regulation.
