Could how much and often people eat depend on their genes?

Thanks to the Human Genome Project, we humans now know that we are all really very much the same at the level of our DNA. Our genomes are 99.9 percent identical, leaving really only 0.1 percent responsible for giving each of us what we would consider our differences or unique qualities. It's within this 0.1 percent that may also explain why some of us may be more likely to be overweight, obese, or susceptible to a disease such as type 2 diabetes.

One of the most promising developments in nutrition research are the insights provided by studies on how dietary components interact with genes. The knowledge gleaned could one day be used for reducing risk of disease and staying healthier, longer. This area of research is nutritional genomics, or nutrigenomics for short. Eventually understanding more about nutrigenomics could lead to our ability to better personalize our diet plans and make better food choices based on our genetic code.

Interestingly, however, new research suggests that it may be genes themselves that are guiding how much we eat as well as our food choices. The Genetic Subgroup of Look AHEAD and the Look AHEAD Research Group have recently reported findings in the American Journal of Clinical Nutrition that obesity-related gene sequences (loci) may affect how overweight or obese with type 2 diabetes consume food.

Their study found that a group of obesity-risk alleles, FTO, significantly predicted eating and snacking more frequently. Another, BDNF, was significantly associated with eating more servings of protein-rich dairy, meat, eggs, nuts and beans. SH2B1 was associated with eating more servings of dairy (perhaps due to changes in leptin signaling). On the other hand, TNN13K, was significantly associated with lower percent of protein energy in the diet and higher intake of fats, oils, and sweets energy.  

Obvious limitations to these genetic associations are that -- although there were 2,075 participants in the study from an ethnically diverse sample including men and women -- the conclusions were based a cohort of only overweight or obese people with type 2 diabetes. Additionally, the study measured dietary intake through food frequency questionnaires, which are often limited in accuracy because of over- or under-reporting. Lastly, other factors like physical activity would probably affect any of the correlations.

Despite limitations, the researchers report the results suggest that markers within FTO, BDNF, TNN13K, and SH2B1 could be used to predict a predisposition to overweight or obesity perhaps because of the way the genes may affect eating patterns and frequency.

And, if replicated, the researchers report, could lead to new discoveries on mechanisms by which these genes affect eating.  

Reference

McCaffery JM, Papandonatos GD, Peter I, Huggins GS, Raynor HA, Delahanty LM, Cheskin LJ, Balasubramanyam A, Wagenknecht LE, Wing RR. Obesity susceptibility loci and dietary intake in the Look AHEAD Trial. American Journal of Clinical Nutrition. doi: 10.3945/ajcn.111.026955.