Ericson Ulrika, Hindy George, Drake Isabel, Schulz Christina-Alexandra, Brunkwall Louise, Hellstrand Sophie, Almgren Peter, Orho-Melander Marju
1Diabetes and Cardiovascular Disease, Genetic Epidemiology, Department of Clinical Sciences, Malmö, Lund University, Malmö, Sweden.
Clinical Research Centre, Building 60, floor 13, SUS in Malmö, entrance 72, Jan Waldenströms gata 35, SE-205 02 Malmö, Sweden.
Genes Nutr. 2018 May 16;13:13. doi: 10.1186/s12263-018-0599-1. eCollection 2018.
Both lifestyle and genetic predisposition determine the development of type 2 diabetes (T2D), and studies have indicated interactions between specific dietary components and individual genetic variants. However, it is unclear whether the importance of overall dietary habits, including T2D-related food intakes, differs depending on genetic predisposition to T2D. We examined interaction between a genetic risk score for T2D, constructed from 48 single nucleotide polymorphisms identified in genome-wide association studies, and a diet risk score of four foods consistently associated with T2D in epidemiological studies (processed meat, sugar-sweetened beverages, whole grain and coffee). In total, 25,069 individuals aged 45-74 years with genotype information and without prevalent diabetes from the Malmö Diet and Cancer cohort (1991-1996) were included. Diet data were collected with a modified diet history method.
During 17-year follow-up, 3588 incident T2D cases were identified. Both the diet risk score (HR in the highest risk category 1.40; 95% CI 1.26, 1.58; trend = 6 × 10) and the genetic risk score (HR in the highest tertile of the genetic risk score 1.67; 95% CI 1.54, 1.81; trend = 7 × 10) were associated with increased incidence of T2D. No significant interaction between the genetic risk score and the diet risk score ( = 0.83) or its food components was observed. The highest risk was seen among the 6% of the individuals with both high genetic and dietary risk scores (HR 2.49; 95% CI 2.06, 3.01).
The findings thus show that both genetic heredity and dietary habits previously associated with T2D add to the risk of T2D, but they seem to act in an independent fashion, with the consequence that all individuals, whether at high or low genetic risk, would benefit from favourable food choices.
生活方式和遗传易感性都决定了2型糖尿病(T2D)的发生发展,且研究表明特定饮食成分与个体基因变异之间存在相互作用。然而,尚不清楚包括与T2D相关的食物摄入量在内的总体饮食习惯的重要性是否因T2D的遗传易感性而异。我们研究了由全基因组关联研究中鉴定出的48个单核苷酸多态性构建的T2D遗传风险评分与在流行病学研究中一直与T2D相关的四种食物(加工肉类、含糖饮料、全谷物和咖啡)的饮食风险评分之间的相互作用。总共纳入了来自马尔默饮食与癌症队列(1991 - 1996年)的25069名年龄在45 - 74岁之间、有基因型信息且无糖尿病病史的个体。饮食数据采用改良饮食史方法收集。
在17年的随访期间,共识别出3588例T2D新发病例。饮食风险评分(最高风险类别中的风险比为1.40;95%置信区间为1.26, 1.58;趋势 = 6×10)和遗传风险评分(遗传风险评分最高三分位数中的风险比为1.67;95%置信区间为1.54, 1.81;趋势 = 7×10)均与T2D发病率增加相关。未观察到遗传风险评分与饮食风险评分(P = 0.83)或其食物成分之间存在显著相互作用。在遗传和饮食风险评分均高的个体中,6%的个体风险最高(风险比为2.49;95%置信区间为2.06, 3.01)。
因此,研究结果表明,先前与T2D相关的遗传因素和饮食习惯都会增加T2D的风险,但它们似乎以独立的方式起作用,结果是所有个体,无论遗传风险高低,都会从良好的食物选择中受益。