Environmental epigenomics and the human imprintome

Genomic imprinting is a phenomenon in which one parental allele is silenced epigenetically. My research has focused on the role of epigenetics in human health and disease since 1995 when we identified the first tumor suppressor gene that is also imprinted, the <i>IGF2R</i>. Subsequently, by using the agouti viable yellow (A^vy) mouse model, we demonstrated that increased maternal dietary exposure to methyl donors <i>in utero</i> altered offspring phenotype in adulthood by modifying the epigenome, providing a plausible mechanism for the developmental origins of health and disease (DOHaD). Consequently, the field of epigenetics can be thought of as the "science of hope," since personal changes in diet and physical activity can potentially alter the epigenome to prevent chronic disease formation, and potentially, even ameliorate the negative effects of environmental exposures to chemical and physical toxicants. In this perspectives article, I address a series of questions posed about the field of environmental epigenetics, and discuss the role that the environmentally labile <i>cis</i>-acting, imprint regulatory elements in the human genome (i.e. the human imprintome) and the correlated regions of systemic interindividual variation (CoRSIVs) play in disease formation and behavioral development.