Abstract
Genetic studies have shown that obesity risk is heritable and that, of the many common variants now associated with body mass index, those in an intron of the fat mass and obesity-associated (FTO) gene have the largest effect. The size of the UK Biobank, and its joint measurement of genetic, anthropometric and lifestyle variables, offers an unprecedented opportunity to assess gene-by-environment interactions in a way that accounts for the dependence between different factors. We jointly examine the evidence for interactions between FTO (rs1421085) and various lifestyle and environmental factors. We report interactions between the FTO variant and each of: frequency of alcohol consumption (P=3.0 × 10−4); deviations from mean sleep duration (P=8.0 × 10−4); overall diet (P=5.0 × 10−6), including added salt (P=1.2 × 10−3); and physical activity (P=3.1 × 10−4).
Highlights
The obesity epidemic is causing a growing burden on public health[1]
We found that the effect of fat mass and obesity-associated (FTO) on Body mass index (BMI) is diminished with more frequent consumption of alcohol ( À 0.24% [ À 0.37%, À 0.11%], P 1⁄4 3.0 Â 10 À 4)
We found that the effect of FTO on BMI is enhanced in individuals with a higher diet score (0.30% ([0.17%, 0.43%], P 1⁄4 5.0 Â 10 À 6), the strongest estimated FTO interaction effect in the joint model
Summary
The obesity epidemic is causing a growing burden on public health[1]. Body mass index (BMI), defined as weight divided by height squared, is the most commonly used measure of adiposity, with individuals exceeding a certain BMI threshold classed as obese[2]. In the Scores Model (Table 2), we estimate that each additional copy of the rs1421085 risk allele is associated with a BMI increase of 1.17% in the British Sample ([0.90%, 1.44%], P 1⁄4 1.0 Â 10 À 17) and 1.07% in the Diverse Sample ([0.58%, 1.57%], P 1⁄4 2.2 Â 10 À 5).
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