Genetic and epigenetic contributions to human nutrition and health: managing genome-diet interactions

Abstract

The Institute of Medicine recently convened a workshop to review the state of the various domains of nutritional genomics research and policy and to provide guidance for further development and translation of this knowledge into nutrition practice and policy. Nutritional genomics holds the promise to revolutionize both clinical and public health nutrition practice and facilitate the establishment of (a) genome-informed nutrient and food-based dietary guidelines for disease prevention and healthful aging, (b) individualized medical nutrition therapy for disease management, and (c) better targeted public health nutrition interventions (including micronutrient fortification and supplementation) that maximize benefit and minimize adverse outcomes within genetically diverse human populations. As the field of nutritional genomics matures, which will include filling fundamental gaps in knowledge of nutrient-genome interactions in health and disease and demonstrating the potential benefits of customizing nutrition prescriptions based on genetics, registered dietitians will be faced with the opportunity of making genetically driven dietary recommendations aimed at improving human health.

Figure 1

Nutrient-genome interactions. Nutritional genomics encompasses both nutrigenetics, the influence of genetic variation on nutrient utilization/metabolism, food tolerances, and nutrient requirements; and nutrigenomics, the modulatory role of nutrients on genome evolution, mutation rate, in-utero viability, programming, and expression. In turn, several of the nutrigenomic outcomes (ie, genome evolution) contribute to the genetic variation observed within genetically diverse human populations. NOTE: This figure is available online at www.adajournal.org as part of a PowerPoint presentation.

Figure 2

The fetal origins of disease hypothesis. In utero environmental exposures, including nutrition, act early in life to program risk for adult health outcomes. ^aCVD=cardiovascular disease. NOTE: Information from this figure is available online at www.adajournal.org as part of a PowerPoint presentation.

Figure 3

Folate-mediated one-carbon metabolism is a conduit between the cellular nutrient environment and genome synthesis and methylation. ^aATP/ADP=adenosine triphosphate/adenosine diphosphate. ^bNADP⁺/NADPH=Nicotinamide adenine dinucleotide phosphate. NOTE: This figure is available online at www.adajournal.org as part of a PowerPoint presentation.

Figure 4

Possible genomic criteria for establishing dietary requirements. Estimated Average Requirement (EAR) represents the intake at which the risk of inadequacy is 0.5 (50%) to an individual in a population. Recommended Dietary Allowance (RDA) represents a level of nutrient intake at which the risk of inadequacy is less than 3%. Adequate Intake (AI) is not based on an EAR but is assumed to be near or above the RDA if one could be calculated. The Tolerable Upper Intake Level (UL) represents risk of excess that is set close to 0. NOTE: This figure is available online at www.adajournal.org as part of a PowerPoint presentation.