Genes influence every aspect of human physiology, development, and adaptation. Obesity is no exception. Yet relatively little is known regarding the specific genes that contribute to obesity and the scale of so-called “genetic environment interactions” the complex interplay between our genetic makeup and our life experiences.
In the 21st century, obesity is a health problem affecting rich and poor, educated and uneducated, Westernized and non-Westernized societies. Body fat level varies from person to person, however, and some people have always tended to carry a bit more body fat than others. Evidence from animal models, human linkage studies, twin studies, and association studies of large populations suggests that this variation in our susceptibility to obesity has a genetic component. But rather than being controlled by a single gene, susceptibility to common obesity is thought to be affected by many genes.
In 2007, researchers using genome-wide association studies identified the first obesity related gene variants in the so-called “fat mass and obesity-associated” (FTO) gene on chromosome 16. (1,2) These gene variants are fairly common, and people who carry one have a 20 to 30 percent higher risk of obesity than people who do not.
A 2014 study found that consumption of fried food could interact with genes related to obesity, underscoring the importance of reducing fried food consumption in individuals genetically predisposed to obesity. (3)
To date, genome-wide association studies have identified more than 30 candidate genes on 12 chromosomes that are associated with body mass index. (4-6)
Although most people probably have some genetic predisposition to obesity, depending on their family history and ethnicity, it’s important to remember that overall, the contribution of genes to obesity risk is small. Moving from genetic predisposition to obesity itself generally requires some change in diet, lifestyle, or other environmental factors.
In August, we will focus on one of the most important environmental factors affecting our diet and waistline, stress. Harvard researchers have reported that stress from work and other sorts of problems correlates with weight gain, but only in those who were overweight at the beginning of the study period. One theory is that overweight people have elevated insulin levels, and stress-related weight gain is more likely to occur in the presence of high insulin.
Excerpt from Obesity Prevention Source; Harvard T.H. Chan School of Public Health.
References
- Dina C, Meyre D, Gallina S, et al. Variation in FTO contributes to childhood obesity and severe adult obesity. Nat Genet. 2007; 39:724-6.
- Frayling TM, Timpson NJ, Weedon MN, et al. A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity. Science. 2007; 316:889-94.
- Qi, Q, Chu, AY, Kang, JH, Huang, J, Rose, LM, Jensen, MK, Liang, L, Curhan, GC, Pasquale, LR, Wiggs, JL, De Vivo, I, Chan, AT, Choi, HK, Tamimi, RM, Ridker, PM, Hunter, DJ, Willett, WC, Rimm, EB, Chasman, DI, Hu, FB, Qi, L. (2014). Fried food consumption, genetic risk, and body mass index: gene-diet interaction analysis in three US cohort studies. BMJ 19;348:g1610.
- O’Rahilly S. Human genetics illuminates the paths to metabolic disease. Nature. 2009; 462:307-14.
- Speliotes EK, Willer CJ, Berndt SI, et al. Association analyses of 249,796 individuals reveal eighteen new loci associated with body mass index. Nat Genet. 2010; 42:937-48.
- Heid IM, Jackson AU, Randall JC. Meta-analysis identies 13 novel loci associated with waist-hip ratio and reveals sexual dimorphism in the genetic basis of fat distribution. Nat Genet. 2010; 42:949-60.