Department of Nutrition, Harvard School of Public Health, Boston, MA 02115, USA.
N Engl J Med. 2012 Oct 11;367(15):1387-96. doi: 10.1056/NEJMoa1203039. Epub 2012 Sep 21.
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.
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.
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).
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.).
含糖饮料消费的增加与肥胖症的流行呈平行关系,但这种饮料的摄入是否与肥胖的遗传易感性相互作用尚不清楚。
我们分析了遗传易感性与含糖饮料摄入之间的相互作用与护士健康研究(NHS)中的 6934 名女性和健康专业人员随访研究(HPFS)中的 4423 名男性以及女性基因组健康研究(WGHS)中的 21740 名女性的复制队列中 BMI(体重公斤数除以身高米数的平方)和肥胖风险之间的关系。基于 32 个与 BMI 相关的基因座计算了遗传易感性评分。含糖饮料的摄入量与 BMI 进行前瞻性检查。
在 NHS 和 HPFS 队列中,与 BMI 的遗传相关性在摄入较高含糖饮料的参与者中强于摄入较低含糖饮料的参与者。在合并队列中,每增加 10 个风险等位基因,BMI 增加 1.00,每月摄入少于 1 份,1.12 份,每月 1 至 4 份,每周 2 至 6 份,每天 1 份或更多份(交互作用 P<0.001)。对于相同的摄入量类别,每增加 10 个风险等位基因,肥胖的相对风险为 1.19(95%置信区间 [CI],0.90 至 1.59),1.67(95% CI,1.28 至 2.16),1.58(95% CI,1.01 至 2.47)和 5.06(95% CI,1.66 至 15.5)(交互作用 P=0.02)。在 WGHS 队列中,每增加 10 个风险等位基因,BMI 增加 1.39、1.64、1.90 和 2.53,在四个摄入量类别中(交互作用 P=0.001);肥胖的相对风险为 1.40(95% CI,1.19 至 1.64),1.50(95% CI,1.16 至 1.93),1.54(95% CI,1.21 至 1.94)和 3.16(95% CI,2.03 至 4.92)(交互作用 P=0.007)。
与肥胖的遗传相关性似乎与含糖饮料的摄入增加更为明显。(由美国国立卫生研究院和其他机构资助)。