The early life environment and the epigenome.
Several lines of evidence point to the early origin of adult onset disease. A key question is: what are the mechanisms that mediate the effects of the early environment on our health? Another important question is: what is the impact of the environment during adulthood and how reversible are the effects of early life later in life? The genome is programmed by the epigenome, which is comprised of chromatin, a covalent modification of DNA by methylation and noncoding RNAs. The epigenome is sculpted during gestation, resulting in the diversity of gene expression programs in the distinct cell types of the organism. Recent data suggest that epigenetic programming of gene expression profiles is sensitive to the early-life environment and that both the chemical and social environment early in life could affect the manner by which the genome is programmed by the epigenome. We propose that epigenetic alterations early in life can have a life-long lasting impact on gene expression and thus on the phenotype, including susceptibility to disease. We will discuss data from animal models as well as recent data from human studies supporting the hypothesis that early life social-adversity leaves its marks on our epigenome and affects stress responsivity, health, and mental health later in life.
Szyf
Moshe
M
Department of Pharmacology and Therapeutics, McGill University, Montreal, Quebec, Canada. moshe.szyf@mcgill.ca
D000818:Animals; D002843:Chromatin / Q000737:chemistry; D019175:DNA Methylation; D004777:Environment; D044127:Epigenesis, Genetic; D005838:Genotype; D006657:Histones / Q000378:metabolism; D006801:Humans; D008425:Maternal Behavior; D010641:Phenotype; D011401:Promoter Regions, Genetic; D012335:RNA, Ribosomal / Q000235:genetics; D011965:Receptors, Glucocorticoid / Q000235:genetics; D015398:Signal Transduction
D002843:Chromatin; D006657:Histones; D012335:RNA, Ribosomal; D011965:Receptors, Glucocorticoid