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抑郁症状与吸烟量之间的基因-环境相互作用

Gene-Environment Interactions Between Depressive Symptoms and Smoking Quantity.

作者信息

Keskitalo-Vuokko Kaisu, Korhonen Tellervo, Kaprio Jaakko

机构信息

Department of Public Health,University of Helsinki,Helsinki,Finland.

出版信息

Twin Res Hum Genet. 2016 Aug;19(4):322-9. doi: 10.1017/thg.2016.36. Epub 2016 May 10.

Abstract

We investigated genetic and environmental correlations and gene by environment interactions (GxE) between depressive symptoms measured by the Beck Depression Inventory (BDI) and quantity smoked measured by number of cigarettes smoked per day (CPD) using quantitative genetic modeling. The population-based sample consisted of 12,063 twin individuals from the Finnish Twin Cohort Study. Bivariate Cholesky decomposition revealed that the phenotypic correlation (r = 0.09) between BDI and CPD was explained by shared genetic (r g = 0.18) and environmental (r e = 0.08) factors. GxE models incorporating moderator effects were built by using CPD as trait and BDI as moderator and vice versa. The importance of the genetic variance component increased with increasing moderator value in both models. Thus, the influence of genetic effects on variance of smoking quantity was enhanced in individuals with elevated depression score and vice versa; the genetic effects on depression variance were potentiated among heavy smokers. In conclusion, shared genetic and environmental factors as well as GxE underlie the association of smoking with depression.

摘要

我们采用定量遗传模型,研究了通过贝克抑郁量表(BDI)测量的抑郁症状与通过每日吸烟量(CPD)测量的吸烟量之间的遗传和环境相关性以及基因与环境的相互作用(GxE)。基于人群的样本包括来自芬兰双胞胎队列研究的12,063名双胞胎个体。双变量Cholesky分解显示,BDI与CPD之间的表型相关性(r = 0.09)由共同的遗传因素(r g = 0.18)和环境因素(r e = 0.08)解释。通过使用CPD作为特质,BDI作为调节变量,反之亦然,构建了纳入调节效应的GxE模型。在两个模型中,遗传方差成分的重要性随着调节变量值的增加而增加。因此,在抑郁评分升高的个体中,遗传效应对吸烟量方差的影响增强,反之亦然;在重度吸烟者中,遗传效应对抑郁方差的影响增强。总之,共同的遗传和环境因素以及GxE是吸烟与抑郁关联的基础。

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