Over the past three decades, there has been a global increase in the prevalence of obesity, which has been mainly driven by changes in lifestyle [1]. However, not everyone becomes obese in today’s obesogenic environment. In fact, twin studies suggest that changes in adiposity in response to environmental influences are genetically determined [2]–[6]. Until recently, there were no confirmed obesity-susceptibility loci that could be used to test whether the influence of genetic susceptibility on obesity risk is enhanced by an unhealthy lifestyle. However, in 2007, the intron 1 of the fat mass and obesity associated (FTO) gene was identified as the first robust obesity-susceptibility locus in genome-wide association studies [7],[8]. Each additional minor allele of the rs9939609 single nucleotide polymorphism (SNP) in FTO was found to be associated with a 20%–30% increase in the risk of obesity and a 1–1.5 kg increase in body weight [7],[8]. The risk-increasing allele of FTO is common, with 74% of individuals of European descent (HapMap CEU population), 76% of individuals of African-American descent (HapMap ASW population), and 28%–44% of individuals of Asian descent (HapMap CHB, CHD, GIH, and JPT populations) carrying at least one copy of the FTO risk allele.
