Abstract
Today, dietary recommendations are based on recommended daily intake for the general population, and only a few subgroups are considered for additional dietary advice. Nutrigenetics aim to optimize health and prevent disease. Particularly for lifestyle disease, such as obesity, which has increased
epidemically worldwide, the investigation of genetic predisposition might help to prevent and treat obesity. Predisposition to obesity includes syndromes, such as Prader-Willi Syndrome (PWS), severe early-onset obesity, such as mutations
in the melanocortin 4 receptor (MC4R), and common forms of obesity, such as genetic variation in the fat mass and obesity associated gene (FTO). Several studies have explored gene-diet interactions in obesity, weight loss, and regain, but there is a lack of consistency in the identified interactions. This inconsistency
is most probably due to a low-moderate effect size of these interactions, which results in the need for large cohorts or replication between several cohorts. However, with large studies the accuracy of phenotypic characterization also might suffer. Currently, consistent results on nutrigenetics in obesity are
limited but investigations of rare mutations, copy number variation, and epigenetics might identify additional genetic contributions to obesity, and the use of omics data with integration of nutrigenetics and nutrigenomics will identify genetic subgroups who will benefit from specific dietary advice to optimize health and prevent disease.
Keywords: Diet . Mutation . Obesity . Single nucleotide polymorphism (SNP) . Gene-diet interaction . Weight loss . Weight regain
epidemically worldwide, the investigation of genetic predisposition might help to prevent and treat obesity. Predisposition to obesity includes syndromes, such as Prader-Willi Syndrome (PWS), severe early-onset obesity, such as mutations
in the melanocortin 4 receptor (MC4R), and common forms of obesity, such as genetic variation in the fat mass and obesity associated gene (FTO). Several studies have explored gene-diet interactions in obesity, weight loss, and regain, but there is a lack of consistency in the identified interactions. This inconsistency
is most probably due to a low-moderate effect size of these interactions, which results in the need for large cohorts or replication between several cohorts. However, with large studies the accuracy of phenotypic characterization also might suffer. Currently, consistent results on nutrigenetics in obesity are
limited but investigations of rare mutations, copy number variation, and epigenetics might identify additional genetic contributions to obesity, and the use of omics data with integration of nutrigenetics and nutrigenomics will identify genetic subgroups who will benefit from specific dietary advice to optimize health and prevent disease.
Keywords: Diet . Mutation . Obesity . Single nucleotide polymorphism (SNP) . Gene-diet interaction . Weight loss . Weight regain
| Original language | English |
|---|---|
| Journal | Current Nutrition Reports |
| Volume | 2 |
| Issue number | 3 |
| Pages (from-to) | 159-166 |
| Number of pages | 8 |
| ISSN | 2161-3311 |
| DOIs | |
| Publication status | Published - 2013 |
