Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet and Centre for Epidemiology and Community Medicine, Stockholm County Council, Stockholm, Sweden.
Int J Epidemiol. 2019 Jun 1;48(3):926-933. doi: 10.1093/ije/dyz002.
Smoking and use of Swedish smokeless tobacco (snus) are associated with increased risk of type 2 diabetes (T2D). Our aim was to estimate the unique and shared genetic components of these traits and to what extent the association is explained by shared genetic factors.
We used twins of the Swedish Twin Registry who responded to a questionnaire between 1998 and 2006 (n = 40 247) and were followed until 2015 in the National Prescription and Patient Registries. We estimated hazard ratios (HRs) and odds ratios (ORs) for the association between smoking/snus use and T2D (n = 2130) and used structural equation models to estimate genetic and environmental variance components and genetic correlations.
Current smokers [HR 1.69, 95% confidence interval (CI), 1.49-1.92] and snus users (HR 1.19, 95% CI 1.01-1.41) had an increased risk of T2D. In within-pair analyses of monozygotic twins, corresponding ORs were 1.36, 95% CI 0.75-2.46 (smoking) and 1.54, 95% CI 0.80-2.99 (snus). Heritability was 43% (95% CI 36-51) for ever smoking, 58% (95% CI 44- 70) for ever snus use and 66% (95% CI 59-72) for T2D. The genetic correlation with T2D was 18% (95% CI 1-35) for smoking and -6% (95% CI -24 to 4) for snus use, indicating that only a small fraction of the genetic influence is shared.
We could confirm that consumers of snus and cigarettes are at increased risk of T2D. Both snus use and smoking have strong genetic components, which appears to be attributable primarily to genes that are distinct from those promoting T2D.
吸烟和使用瑞典无烟烟草（鼻烟）与 2 型糖尿病（T2D）风险增加有关。我们的目的是估计这些特征的独特和共同遗传成分，以及共同遗传因素在多大程度上解释了这种关联。
我们使用了瑞典双胞胎登记处的双胞胎，他们在 1998 年至 2006 年期间对问卷做出了回应（n=40247），并在国家处方和患者登记处跟踪至 2015 年。我们估计了吸烟/鼻烟使用与 T2D（n=2130）之间的关联的风险比（HR）和优势比（OR），并使用结构方程模型估计遗传和环境方差分量和遗传相关。
当前吸烟者（HR 1.69，95%置信区间[CI]，1.49-1.92）和鼻烟使用者（HR 1.19，95%CI 1.01-1.41）T2D 的风险增加。在同卵双胞胎的配对内分析中，相应的 OR 分别为 1.36，95%CI 0.75-2.46（吸烟）和 1.54，95%CI 0.80-2.99（鼻烟）。吸烟的遗传率为 43%（95%CI 36-51），使用鼻烟的遗传率为 58%（95%CI 44-70），T2D 的遗传率为 66%（95%CI 59-72）。与 T2D 的遗传相关性吸烟为 18%（95%CI 1-35），使用鼻烟为-6%（95%CI-24 至 4），表明只有一小部分遗传影响是共同的。
我们可以证实，鼻烟和香烟的消费者患 T2D 的风险增加。鼻烟使用和吸烟都有强烈的遗传成分，这似乎主要归因于与促进 T2D 的基因不同的基因。
