The role of methylation as a relatively stable marker of promoter-mediated regulation of gene expression makes it a logical target for understanding the mechanisms of environmental exposure. Moreover, methylation is known to vary both between and within individuals assessed at multiple time-points (Langevin et al., 2011). Evidence suggests several important driving forces behind differential methylation including, underlying genetic variation (meQTLs) (Smith et al., 2014), life experiences, differential tissue and cell-types, and chronological age (Horvath, 2013). Variation in DNA methylation has been investigated as a mediator of the physiologic responses to acute and chronic exposures, including environmental adversity or response to intervention/prevention. Longitudinal data allows for the examination of change in epigenetic profiles potentially reflecting response to an intervention which potentially confer liability to outcome phenotypes. Identification of these mechanisms will inform prevention strategies at the most critical point(s) in the developmental risk trajectory.
