期刊
AMERICAN JOURNAL OF CLINICAL NUTRITION
卷 104, 期 3, 页码 809-815出版社
OXFORD UNIV PRESS
DOI: 10.3945/ajcn.115.126052
关键词
sugar-sweetened beverage; genetic risk score; BMI; gene-lifestyle interaction; Sweden
资金
- Swedish Research Council
- Swedish Heart and Lung Foundation
- Novo Nordisk Foundation
- Swedish Diabetes Foundation
- Pahlsson Foundation
- Knut and Alice Wallenberg Foundation
- Region Skane
- Skane University Hospital
- Linneus Foundation
- Swedish Diabetes Association
- Pahlsson's Foundation
- Umea Medical Research Foundation
- Novo Nordisk
- Heart Foundation of Northern Sweden
- Wellcome Trust
- Novo Nordisk Fonden [NNF14OC0011049, NNF14OC0011039, NNF15OC0016320, NNF11OC1014855, NNF13OC0005781, NNF16OC0021370, NNF12OC1016167] Funding Source: researchfish
Background: The consumption of sugar-sweetened beverages (SSBs), which has increased substantially during the last decades, has been associated with obesity and weight gain. Objective: 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. Design: Data were available for 21,824 healthy participants from the Malmo 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). Results: 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 X 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 X 10(-8); n = 6766) and 0.15 (SE = 0.04; P = 1.3 X 10(-4); n = 6835) higher BMIs, respectively. Conclusions: 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.
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