The worldwide obesity epidemic has been largely attributed to marked changes in diet and lifestyle in the last 3 decades. Strong evidence from numerous studies supports a positive association between increased consumption of sugar-sweetened beverages and the risk of obesity. It is unclear whether increased intake of such beverages is associated with a genetic predisposition to adiposity. Large-scale genome-wide association studies have identified 32 loci within the genome associated with the body mass index (BMI).
This longitudinal cohort study was designed to test the hypothesis that high intake of sugar-sweetened beverages is associated with a genetic predisposition for obesity.
Prospective data were obtained for 6934 women enrolled in the Nurses’ Health Study (NHS) and for 4423 men from the Health Professionals Follow-up Study (HPFS), and also for 21,740 women enrolled in a replication cohort, the Women’s Genome Health Study (WGHS). The interaction between the intake of sugar-sweetened beverages and BMI was analyzed. The genetic predisposition score was calculated on the basis of the 32 loci previously shown to have an established association with BMI. The difference in BMI for each increment of 10 risk alleles was stratified according to 4 categories of beverage intake (<1 serving per month, 1–4 servings per month, 2–6 servings per week, and ≥1 servings per day).
The genetic association with BMI in the NHS and HPFS cohorts was stronger in participants with a higher intake of sugar-sweetened beverages than in those with a lower intake. The pooled data in the 2 cohorts showed that the relative risk (RR) of genetic predisposition according to increased BMI for an increment of 10 risk alleles was 1.00 for an intake of less than 1 serving per month, 1.20 for 1 to 4 servings per month, 1.37 for 2 to 6 servings per week, and 1.85 for 1 or more servings per day (P < 0.001 for interaction). Using the same categories of beverage intake, the RR of incident obesity per increment of 10 risk alleles was 1.19 (95% confidence interval [CI], 0.90–1.59), 1.67 (95% CI, 1.28–2.16), 1.58 (95% CI, 1.01–2.47), and 5.06 (95% CI, 1.66–15.5) (P = 0.02 for interaction). Similar results were found in the WGHS cohort. In that cohort, the RR of incident obesity per increment of 10 risk alleles was 1.40 (95% CI, 1.19–1.64), 1.50 (95% CI, 1.16–1.93), 1.54 (95% CI, 1.21–1.94), and 3.16 (95% CI, 2.03–4.92) (P = 0.007 for interaction).
These findings suggest that greater intake of sugar-sweetened beverages is associated with a more pronounced genetic predisposition to elevated BMI and obesity risk.