Sugar-sweetened beverages and genetic risk of obesity
- PMID: 22998338
- PMCID: PMC3518794
- DOI: 10.1056/NEJMoa1203039
Sugar-sweetened beverages and genetic risk of obesity
Abstract
Background: Temporal increases in the consumption of sugar-sweetened beverages have paralleled the rise in obesity prevalence, but whether the intake of such beverages interacts with the genetic predisposition to adiposity is unknown.
Methods: We analyzed the interaction between genetic predisposition and the intake of sugar-sweetened beverages in relation to body-mass index (BMI; the weight in kilograms divided by the square of the height in meters) and obesity risk in 6934 women from the Nurses' Health Study (NHS) and in 4423 men from the Health Professionals Follow-up Study (HPFS) and also in a replication cohort of 21,740 women from the Women's Genome Health Study (WGHS). The genetic-predisposition score was calculated on the basis of 32 BMI-associated loci. The intake of sugar-sweetened beverages was examined prospectively in relation to BMI.
Results: In the NHS and HPFS cohorts, the genetic association with BMI was stronger among participants with higher intake of sugar-sweetened beverages than among those with lower intake. In the combined cohorts, the increases in BMI per increment of 10 risk alleles were 1.00 for an intake of less than one serving per month, 1.12 for one to four servings per month, 1.38 for two to six servings per week, and 1.78 for one or more servings per day (P<0.001 for interaction). For the same categories of intake, the relative risks of incident obesity per increment of 10 risk alleles were 1.19 (95% confidence interval [CI], 0.90 to 1.59), 1.67 (95% CI, 1.28 to 2.16), 1.58 (95% CI, 1.01 to 2.47), and 5.06 (95% CI, 1.66 to 15.5) (P=0.02 for interaction). In the WGHS cohort, the increases in BMI per increment of 10 risk alleles were 1.39, 1.64, 1.90, and 2.53 across the four categories of intake (P=0.001 for interaction); the relative risks for incident obesity were 1.40 (95% CI, 1.19 to 1.64), 1.50 (95% CI, 1.16 to 1.93), 1.54 (95% CI, 1.21 to 1.94), and 3.16 (95% CI, 2.03 to 4.92), respectively (P=0.007 for interaction).
Conclusions: The genetic association with adiposity appeared to be more pronounced with greater intake of sugar-sweetened beverages. (Funded by the National Institutes of Health and others.).
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Comment in
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Calories from soft drinks--do they matter?N Engl J Med. 2012 Oct 11;367(15):1462-3. doi: 10.1056/NEJMe1209884. Epub 2012 Sep 21. N Engl J Med. 2012. PMID: 22998341 No abstract available.
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Sugar-sweetened beverages, genetic risk, and obesity.N Engl J Med. 2013 Jan 17;368(3):286-7. doi: 10.1056/NEJMc1213563. N Engl J Med. 2013. PMID: 23323907 No abstract available.
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Sugar-sweetened beverages, genetic risk, and obesity.N Engl J Med. 2013 Jan 17;368(3):285. doi: 10.1056/NEJMc1213563. N Engl J Med. 2013. PMID: 23323908 No abstract available.
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[Sugar-sweetened beverages and genetic risk of obesity].Rev Clin Esp (Barc). 2013 Apr;213(3):163. doi: 10.1016/j.rce.2012.12.001. Rev Clin Esp (Barc). 2013. PMID: 23700594 Spanish. No abstract available.
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References
-
- McCarthy MI. Genomics, type 2 diabetes, and obesity. N Engl J Med. 2010;363:2339–50. - PubMed
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