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.

Personalized weight loss strategies—the role of macronutrient distribution

“…Opportunities for providing personalized nutritional advice are increasing along with the availability of low-cost, highthroughput analysis of genomic information. 118 This situation is opening the door for development of commercial, direct-to-consumer genetic testing, but uncertainties in the processing and interpretation of genetic data, as well as concerns about the ethical implications. await the development of suitable policies.…”

Abnormal Folate Metabolism and Maternal Risk for Down Syndrome

“…The conflicting results shown by literature have raised the suggestion that the presence of individual polymorphisms in genes involved in folate metabolism might not increase the risk of having a child with DS, although the effect of combined risk genotypes might modify their individual effect and increase DS risk (J.M., Biselli et al, 2008a;Brandalize et al, 2010;Coppedè et al, 2006;Coppedè et al, 2009;da Silva et al, 2005;Martínez-Frías, et al, 2006;Scala et al, 2006;Wang et al, 2008). Moreover, there is evidence that the significance of genetic polymorphisms seems to depend on interactions with nutritional factors (Papoutsakis et al, 2010;Stover & Caudill, 2008).…”

“…On these terms, two premises are important: (a) inappropriate nutrient supply can cause considerable levels of genome mutation and alter the expression of genes required for genome maintenance, and (b) common genetic polymorphisms may alter the activity of genes that affect the bioavailability of micronutrients and/or the affinity for micronutrient cofactors in key enzymes involved in DNA metabolism or repair, resulting in a lower or higher reaction rate (Bull & Fenech, 2008;Fenech, 2005). As mentioned before, the folate-dependent biosynthesis of nucleotide precursors for DNA synthesis and genome methylation is dependent on the availability of many vitamins, including B 12 , B 6 , niacin, riboflavin, and minerals (zinc, cobalt), and is subject to regulation by other nutrients, such as iron and vitamin A, not directly involved in DNA or SAM biosynthesis (Stover, & Caudill 2008). Therefore, impairments in one-carbon metabolism, and the SAM cycle in particular, induced by nutritional deficiencies and/or genetic polymorphisms that encode folate-dependent enzymes, alter genome methylation patterns and gene expression levels (Stover, 2004;Stover, & Caudill 2008).…”

“…As mentioned before, the folate-dependent biosynthesis of nucleotide precursors for DNA synthesis and genome methylation is dependent on the availability of many vitamins, including B 12 , B 6 , niacin, riboflavin, and minerals (zinc, cobalt), and is subject to regulation by other nutrients, such as iron and vitamin A, not directly involved in DNA or SAM biosynthesis (Stover, & Caudill 2008). Therefore, impairments in one-carbon metabolism, and the SAM cycle in particular, induced by nutritional deficiencies and/or genetic polymorphisms that encode folate-dependent enzymes, alter genome methylation patterns and gene expression levels (Stover, 2004;Stover, & Caudill 2008). Since 1992, supplementation with 0.4 mg/daily of folic acid is recommended for women of childbearing age for the prevention of neural tube defects (Centers for Disease Control, 1992).…”

Women’s Diet During Pregravid Preparation, Pregnancy and Lactation

“…Новое направление в науке -нутритивная эпиге-нетика -дает возможное объяснение тому, как питание человека на любой стадии онтогенеза может оказывать влияние на развитие многих распространенных заболева-ний путем изменения экспрессии генов (без повреждения самой генной последовательности) с краткосрочными или отдаленными последствиями для организма [3][4][5]. В свою очередь, повреждения в эпигенетической регуляции генов могут приводить к глубоким изменениям в фенотипе [6,7]. …”