Nutrition, epigenetics, and developmental plasticity: implications for understanding human disease

There is considerable evidence for induction of differential risk of noncommunicable diseases in human by variation in the quality of the early life environment. Studies in animal models show that induction andstability of induced changes in the phenotype of the offspring involve altered epigenetic regulation by DNAmethylation and covalentmodifications of histones. These findings indicate that such epigenetic changes are highly gene specific and function at the level of individualCpGdinucleotides. Interventions using supplementation with folic acid ormethyl donors during pregnancy, or folic acid after weaning, alter the phenotype and epigenotype induced by maternal dietary constraint during gestation. This suggests a possible means for reducing risk of induced noncommunicable disease, although the design and conduct of such interventions may require caution. The purpose of this review is to discuss recent advances in understanding the mechanism that underlies the early life origins of disease and to place these studies in a broader life-course context