Nutrigenetics, Nutrigenomics and the Global Obesity Crisis

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The new USDA My Food Pyramid is a first step to a personalized diet. Image courtesy of the US Department of Agriculture

Nutrigenetics and Obesity

Nutrigenetics focuses on genes and genetic variants of dietary requirements, many of which also are also biomarkers for chronic diseases. Science has found these genetic differences, referred to as single nucleotide polymorphisms (SNP’s), among ethnic groups and populations, as well as within individuals. Nutrigenetics seeks to match the diet to a person’s or a population group’s genetic makeup.

Even prior to the study of nutrigenetics, common sense dictated that nutritional requirements vary by age and sex. Dietary guidelines, or Recommended Daily Allowances (RDA’s), were developed based on the most recent scientific knowledge. However, the obesity epidemic brings their validity into question.

Significant progress has been made by the “Mypyramid” program, in which the individual inputs additional data, such as activity levels, to determine his or her own optimal diet.

Nutrigenetics Can Clarify Conflicting Information on Diet

There is no question that nutrigenetics has the potential to send your RDA a massive step forward. Variations in genetic composition of individuals may account for the plethora of conflicting studies on specific nutrients that confuse the public. For example:

  • Is moderate alcohol consumption good for you or bad for you?
  • Is milk good for you or bad for you?
  • Is a vegetarian diet good for you or bad for you?

Nutrigenetics in Epidemiological Studies

Recently, Michael Fenech discussed the benefits of epidemiological studies including genetic variations in his article, “Nutrigenetics and Nutrigenomics: Viewpoints on the Current Status and Applications in Nutrition Research and Practice,” published in the Journal of Nutrigenetics and Nutrigenomics in July 2011. He explains that studies that do not take genetic variation into consideration may have conclusive results, only to be confounded later by conflicting evidence. Coffee is a good example. Fenech also states:

Caffeinated-coffee was found to increase the risk of a heart attack among individuals who carry a version of a gene that makes them ‘slow’ caffeine metabolisers, but has no effect among individuals who are ‘fast’ caffeine metabolisers.”

Obesity Studies and the Nutrigenetic Diet

As of 2007, six hundred genes, chromosomes and genetic markers were identified as being linked to obesity or were found to be biomarkers for disease, and the number has continued to increase. This research offers fertile ground for nutrigenetic studies on obesity. Fenech’s 2011 review provides examples of two recent studies in obesity:

  • A personalized, calorie-based diet was developed that considered 24 variants in 19 genes that control metabolism. One-half of participants were given a calorie-restricted diet that took into account the genetic differences in each individual. The second group was given the same diet for all participants.
  • The group with the genetically-tailored diet lost more weight than the second group and had greater success in maintaining weight loss.

A second study mentioned by Fenech focused on the gene variant FTO (fat mass and obesity-related gene), which is a fairly common SNP. Children with the variant show greater propensity for obesity and type 2 diabetes. In this study, when presented with unlimited access to food, children with the FTO variant consumed more calories. Interestingly, increased physical activity counteracted the effect.

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