Brunkwall Louise, Chen Yan, Hindy George, Rukh Gull, Ericson Ulrika, Barroso Inês, Johansson Ingegerd, Franks Paul W, Orho-Melander Marju, Renström Frida
Diabetes and Cardiovascular Disease-Genetic Epidemiology and.
Genetic and Molecular Epidemiology Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden;
Am J Clin Nutr. 2016 Sep;104(3):809-15. doi: 10.3945/ajcn.115.126052. Epub 2016 Jul 27.
The consumption of sugar-sweetened beverages (SSBs), which has increased substantially during the last decades, has been associated with obesity and weight gain.
Common genetic susceptibility to obesity has been shown to modify the association between SSB intake and obesity risk in 3 prospective cohorts from the United States. We aimed to replicate these findings in 2 large Swedish cohorts.
Data were available for 21,824 healthy participants from the Malmö Diet and Cancer study and 4902 healthy participants from the Gene-Lifestyle Interactions and Complex Traits Involved in Elevated Disease Risk Study. Self-reported SSB intake was categorized into 4 levels (seldom, low, medium, and high). Unweighted and weighted genetic risk scores (GRSs) were constructed based on 30 body mass index [(BMI) in kg/m(2)]-associated loci, and effect modification was assessed in linear regression equations by modeling the product and marginal effects of the GRS and SSB intake adjusted for age-, sex-, and cohort-specific covariates, with BMI as the outcome. In a secondary analysis, models were additionally adjusted for putative confounders (total energy intake, alcohol consumption, smoking status, and physical activity).
In an inverse variance-weighted fixed-effects meta-analysis, each SSB intake category increment was associated with a 0.18 higher BMI (SE = 0.02; P = 1.7 × 10(-20); n = 26,726). In the fully adjusted model, a nominal significant interaction between SSB intake category and the unweighted GRS was observed (P-interaction = 0.03). Comparing the participants within the top and bottom quartiles of the GRS to each increment in SSB intake was associated with 0.24 (SE = 0.04; P = 2.9 × 10(-8); n = 6766) and 0.15 (SE = 0.04; P = 1.3 × 10(-4); n = 6835) higher BMIs, respectively.
The interaction observed in the Swedish cohorts is similar in magnitude to the previous analysis in US cohorts and indicates that the relation of SSB intake and BMI is stronger in people genetically predisposed to obesity.
在过去几十年中,含糖饮料(SSB)的消费量大幅增加,这与肥胖和体重增加有关。
在美国的3个前瞻性队列研究中,已证明肥胖的常见遗传易感性会改变SSB摄入量与肥胖风险之间的关联。我们旨在在2个瑞典大型队列中重复这些发现。
马尔默饮食与癌症研究中有21824名健康参与者以及基因-生活方式相互作用与疾病风险升高相关复杂性状研究中有4902名健康参与者的数据可用。自我报告的SSB摄入量分为4个水平(很少、低、中、高)。基于30个与体重指数[(BMI),单位为kg/m²]相关的基因座构建了未加权和加权遗传风险评分(GRS),并通过对GRS和SSB摄入量的乘积及边际效应进行建模,在年龄、性别和队列特异性协变量校正后的线性回归方程中评估效应修饰,以BMI作为结果。在一项次要分析中,模型还对假定的混杂因素(总能量摄入、饮酒、吸烟状况和身体活动)进行了校正。
在逆方差加权固定效应荟萃分析中,每个SSB摄入量类别增加与BMI升高0.18相关(标准误=0.02;P=1.7×10⁻²⁰;n=26726)。在完全校正模型中,观察到SSB摄入量类别与未加权GRS之间存在名义上的显著交互作用(交互作用P值=0.03)。将GRS最高和最低四分位数内的参与者与SSB摄入量的每次增加进行比较,分别与BMI升高0.24(标准误=0.04;P=2.9×10⁻⁸;n=6766)和0.15(标准误=0.04;P=1.3×10⁻⁴;n=6835)相关。
在瑞典队列中观察到的交互作用在程度上与之前在美国队列中的分析相似,表明在遗传上易患肥胖的人群中,SSB摄入量与BMI之间的关系更强。