Nutrition, epigenetics, and developmental plasticity: implications for understanding human disease.
There is considerable evidence for induction of differential risk of noncommunicable diseases in humans by variation in the quality of the early life environment. Studies in animal models show that induction and stability of induced changes in the phenotype of the offspring involve altered epigenetic regulation by DNA methylation and covalent modifications of histones. These findings indicate that such epigenetic changes are highly gene specific and function at the level of individual CpG dinucleotides. Interventions using supplementation with folic acid or methyl 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.
Burdge
Graham C
GC
Institute of Human Nutrition, University of Southampton School of Medicine, Southampton, SO16 6YD, United Kingdom. g.c.burdge@southampton.ac.uk
Lillycrop
Karen A
KA
D000222:Adaptation, Physiological; D044127:Epigenesis, Genetic / Q000235:genetics; D005260:Female; D047109:Fetal Development / Q000235:genetics; D018507:Gene Expression Regulation, Developmental / Q000235:genetics*; D006801:Humans; D039382:Maternal Nutritional Physiological Phenomena / Q000235:genetics / Q000502:physiology*; D008659:Metabolic Diseases / Q000196:embryology / Q000235:genetics; D009747:Nutritional Physiological Phenomena / Q000502:physiology*; D010641:Phenotype; D011247:Pregnancy; D039401:Prenatal Nutritional Physiological Phenomena / Q000235:genetics / Q000502:physiology