Nutritional genomics

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Nutritional genomics, also known as nutrigenomics, is a science studying the relationship between human genome, nutrition and health. People in the field work toward developing an understanding of how the whole body responds to a food via systems biology, as well as single gene/single food compound relationships.[1][2]

Background and preventive health[edit]

Nutritional science originally emerged as a field that studied individuals lacking certain nutrients and the subsequent effects,[1] such as the disease scurvy which results from a lack of vitamin C. As other diseases closely related to diet (but not deficiency), such as obesity, became more prevalent, nutritional science expanded to cover these topics as well.[1] Nutritional research typically focuses on preventative measure, trying to identify what nutrients or foods will raise or lower risks of diseases and damage to the human body.

For example, Prader–Willi syndrome, a disease whose most distinguishing factor is insatiable appetite, has been specifically linked to an epigenetic pattern in which the paternal copy in the chromosomal region is erroneously deleted, and the maternal loci is inactivated by over methylation.[3] Yet, although certain disorders may be linked to certain single-nucleotide polymorphisms (SNPs) or other localized patterns, variation within a population may yield many more polymorphisms.[4]


Obesity is one of the most widely studied topics in nutritional genomics. Due to genetic variations among individuals, each person could respond to diet differently. By exploring the interaction between dietary pattern and genetic factors, the field aims to suggest dietary changes that could prevent or reduce obesity.[5]

There appear to be some SNPs that make it more likely that a person will gain weight from a high fat diet; for people with AA genotype in the FTO gene showed a higher BMI compared those with TT genotype when having high fat or low carbohydrate dietary intake.[5] The APO B SNP rs512535 is another diet-related variation; the A/G heterozygous genotype was found to have association with obesity (in terms of BMI and waist circumference) and for individuals with habitual high fat diet (>35% of energy intake), while individuals with GG homozygotes genotype are likely to have a higher BMI compared to AA allele carriers. However, this difference is not found in low fat consuming group (<35% of energy intake).[5]

See also[edit]


  1. ^ a b c Neeha, V. S.; Kinth, P. (2013). "Nutrigenomics research: a review". Journal of Food Science and Technology. 50 (3): 415–428. doi:10.1007/s13197-012-0775-z. PMC 3602567. PMID 24425937.
  2. ^ Fenech, Michael; El-Sohemy, Ahmed; Cahill, Leah; Ferguson, Lynnette R.; French, Tapaeru-Ariki C.; Tai, E. Shyong; Milner, John; Koh, Woon-Puay; Xie, Lin; Zucker, Michelle; Buckley, Michael; Cosgrove, Leah; Lockett, Trevor; Fung, Kim Y.C.; Head, Richard (2011). "Nutrigenetics and Nutrigenomics: Viewpoints on the Current Status and Applications in Nutrition Research and Practice". Journal of Nutrigenetics and Nutrigenomics. 4 (2): 69–89. doi:10.1159/000327772. ISSN 1661-6758. PMC 3121546. PMID 21625170.
  3. ^ Xia, Q; Grant, SF (2013). "The genetics of human obesity". Ann N Y Acad Sci. 1281: 178–90. doi:10.1111/nyas.12020. PMC 3717174. PMID 23360386.
  4. ^ Bisen, Prakash A.; Debnath, Mousumi; Prasad, Godavarthi B.K.S. (2010). Molecular Dianostics: Promises and Possibilities. Springer Science & Business Media. p. 26.ISBN 9048132614.
  5. ^ a b c Doo, Miae; Kim, Yangha (2015-03-01). "Obesity: interactions of genome and nutrients intake". Preventive Nutrition and Food Science. 20 (1): 1–7. doi:10.3746/pnf.2015.20.1.1. ISSN 2287-1098. PMC 4391534. PMID 25866743.