genetics of obesity

Understanding the genetics of obesity and the gene-environment interactions that lead to obesity will lead to more tailored treatments. Heianza and Qi published a review of scientific findings on gene-environment interactions to date.


Obesity is a growing problem in the developed world and it is linked to increased rates of diabetes, stroke, high blood pressure, heart disease, sleep apnea, and other diseases. In the US, over one-third of adults are obese. Many have attributed the rise of obesity in the last several decades to increasingly sedentary lifestyles and unhealthy diets, as well as socioeconomic and demographic factors. However, some individuals may have a genetic predisposition to obesity that is exacerbated by this unhealthy environment. Understanding these gene-environment interactions will help us better target treatments through precision nutrition. In the International Journal of Molecular Sciences, Heianza and Qi published a review of recent findings about the genetics of obesity and gene-environment interactions that are likely linked to this condition.

Even individuals with healthy diets are more likely to get obesity given particular genetic variants. High-sugar diets are significantly linked to genetic risk scores in populations from Sweden and Costa Rica. In particular, among a population in Costa Rica, high-sugar diets are linked to increased heart attack risk via their interaction of a genetic variant on chromosome 9. Fried foods are also linked to genetic risk of obesity, particularly among individuals with the FTO genotype, as are fatty foods, which are associated with a high risk of obesity in individuals with a particular variant in the APOA2 gene.

Physical activity reduces the risk of obesity among individuals with the FTO genotype, while physical inactivity and a sedentary lifestyle increase it. This relationship is even stronger in individuals with poor sleep. Some variants of the FTO genotype are also linked to a high risk of childhood obesity, although a higher-protein diet or adequate vitamin D intake can reduce the risk.

Heianza and Qi also discuss a previous finding that the relative weight loss benefits of particular diets—like low-carbohydrate or low-fat diets—depend on the genetics of the individual. Low-fat diets are more effective in individuals with a particular variant of the IRS1 gene, for example, while low-carbohydrate diets may be more effective for individuals with a specific variant of the PPM1K gene. Similar effects could be at play for diseases associated with obesity, like diabetes.

The microbiome, the community of microorganisms that live in our bodies and help us function and digest food, has also been linked to obesity. Long-term diets can influence the microbiome, which may affect subsequent responses to diet and lifestyle. To some extent, genetic variants in humans can determine the composition of our microbiomes, and dietary intake of milk, for example, can lead to different outcomes in individuals with different gene variants and different microbiomes.

Although these findings present tantalizing evidence of gene-environment interactions and of ways in which we can use genetic data to better target treatment, more rigorous experimental work needs to be done to determine the links of particular diets to particular outcomes and genetic variants. Ultimately, understanding the genetics of obesity will allow us to tailor nutrition recommendations to individuals for optimal health.


Written By: C. I. Villamil

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