*Corresponding author:Joseph Curtis, Cascade Biotherapeutics, Inc, 4938 Hampden Ln, Bethesda, MD 20814, USA
Received: June 27, 2017 Published: July 06, 2017
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This review presents an omics systems perspective that presents an integrated approach to understanding the contribution of the genetic, epigenetic, metabolomic, and proteomic interactions under the influence of a dynamic nutritional environment. The review takes into account the application of genomic and post-genomic era methodologies being used to study the impact of inter-individual phenotypic differences and disease susceptibility to current and future generations. Every individual alive today is a combination of the heliotypes inherited from their parents, and the results of genetic-epigenetic interaction influencing the fetal epigenome during pre-natal development and post-natal life. Epigenetic marks imprinted in-utero are attributed to deficits in the maternal contribution to the fetal nutritional environment. Integral to this discussion is the concept of developmental plasticity, which presents itself as an unfolding narrative in the “developmental origins of health and disease” (DOHaD) hypothesis, and the ‘predictive adaptive response (PAR)’ concept. When taken together, these concepts present the case for an adaptive response to developmental programming that canpredispose an individual to future diseaseor confers an advantage. Nutriepgenomics is the study of how nutrients affect human health through epigenetic modifications. Recent advances investigating how the nutritional environment during embryonic development influences the establishment of metabolic phenotypes that can contribute to the emergence of disease are discussed. Several encouraging trials suggest that prevention and therapy of age- and lifestyle-related diseases by individualized tailoring to optimal epigenetic diets including combinations of natural products, polyphenols or drugs are conceivable.
Keywords: Developmental; Diabetes; Genome; Macronutrients; Micronutrients; Metabolic; Nutriepigenomics; Nutirgenomics; Obesity; Personalized; Phenotype; Polyphenols
Abbreviations: CGD: Cytosines-Guanine Dinucleotides; DOHaD: Developmental Origins of Health and Disease; EWAS: Epigenome-Wide Association Studies; FOCM: Folate One-Carbon Metabolism; GWAS: Genome-Wide Association Studies; Hap-ASM: Haplotype-Dependent Allele- Specific Methylation; IUGR: Intrauterine Growth Restriction; LD: Linkage Disequilibrium; MQTL: Methylation Quantitative Trait Loci; miRNA: microRNA; PAR: Predictive Adaptive Response; PPL: Postprandial Lipemia; SNPs: Single Nucleotide Polymorphisms