We also considered GWAS-positive loci for Alzheimer’s disease26 (AD, N=49), Parkinson’s disease27 (PD, N=29), and type 2 diabetes28 (T2D, N=40) to determine the specificity of our results. Among the CNS disorders, there was no enrichment overall (p > 0.3), with only perhaps marginal enrichment among CpGs that were more highly methylated in fetal life among AD GWAS loci (OR = 1.23, p=0.03), suggesting some specificity to schizophrenia. Interestingly, while we found significant enrichment among the T2D GWAS loci among all birth-associated CpGs (OR=1.19, p=6.56×10−3), this association was driven by CpGs more highly methylated in postnatal life (OR=1.41, p=5.4×10−4) with no association among the CpGs more highly methylated in prenatal life (OR=1.01, p=0.92). This finding may reflect adult lifestyle influences on epigenetic states that are associated with risk for T2D, including diet, body weight and exercise.
