The FTO gene or ‘fat mass and obesity-associated gene’ is associated with increased obesity in animals and humans. A 2007 study of 38,759 Europeans examined how variants of the FTO gene affects human obesity. It showed that  carriers of one variation of the gene weighed an average of 2.6 pounds more than those with no variants of the gene. Another 16% of the study subjects carried two variants of the FTO gene, and they weighed 6.6 pounds more than those with no FTO gene variants and also showed a 1.67-times higher rate of obesity. 

In humans, it’s common to have slight changes in genes that produce large health effects that will determine the extent to which they can affect physiology. These variants are known as single nucleotide polymorphisms or SNPs. An example of this are the SNPs that exist in those who live to over age 100.  

Certain genes in these people, such as those that control blood lipids such as cholesterol, have SNPs that produce beneficial effects. They also show SNPs in genes related to cellular repair, such as repair of DNA.  

This allows for enhanced cellular repair mechanisms – autophagt and largely explains why these people live longer than others 

Getting back to SNPsin the FTO gene are strongly related to obesity.  

A recent study showed that carriers of the FTO gene showed significantly higher body fat mass and a higher body fat percentage compared to those lacking this gene variant, even though they were all athletes. No other body composition measurements, such as lean mass, bone mass, and others differed between the groups. One difference, however, was that those who lacked the gene variant showed significantly higher resting cortisol levels. Excess cortisol, an adrenal steroid hormone, is associated with catabolic or breakdown effects in muscle, as well as increased body fat in the central or trunk area of the body.  

The highest expression of the FTO gene exists in the hypothalamus in the brain, which also happens to be the main site of appetite control. Having a particular SNP in the FTO gene will result in a greater appetite and a higher propensity for getting fat. This raises the question of whether exercise and diet can modify the effect of FTO SNPs on body composition, or does having this particular gene configuration make losing body fat an uphill battle? 

What this study shows is that those who possess a SNP in the FTO gene tend to have higher body fat levels that are not related to having higher cortisol levels. What this means in a practical sense is that if you have this particular gene configuration, it will be more difficult for you to lose body fat even with stringent dieting and exercise. What it means it that you will have to be stricter in your dieting and exercise practices in order to maintain lower body fat levels 


You think you’re fit, but your genes say you’re fat: a polymorphism in the fat mass and obesity-associated (FTO) gene predicts body fat in well-trained athletes, J Int Soc Sports Nutrion 2018;15:A3  

Vegan diets, Jerry Brainum; Applied Metabolics, 2018