吸烟、饮酒与动脉硬化风险:双样本孟德尔随机研究

Yingzhen Gu, Zuozhi Li, Xiaorong Han, Jinxing Liu, Yifan Li, Wei Zhang, Na-qiang Lv, Aimin Dang
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引用次数: 0

摘要

背景:尽管观察性研究已证明吸烟、饮酒和动脉僵化之间存在联系,但由于潜在的混杂因素,要建立因果关系却很困难。为了解决这个问题,我们采用了双样本孟德尔随机方法。方法:我们从涵盖 3,383,199 人的全基因组关联研究中选取了这些风险因素的遗传工具,并达到了全基因组显著性水平(p < 5 × 10 - 9)。动脉僵化数据来自英国生物库,其中包括 127 121 名参与者。我们的主要分析采用了反方差加权法来探讨因果关系。为了确认结果的稳健性,我们使用埃格回归法、加权中位法和孟德尔随机多向性RESidual Sum and Outlier(MR-PRESSO)进行了敏感性分析。结果:我们的分析表明,开始吸烟的遗传倾向与动脉僵化指数增加之间存在显著关联(β = 0.11;95% 置信区间[CI],0.06 至 0.16;P = 1.95 × 10 - 5)。此外,遗传预测的每天吸烟次数与动脉僵化指数之间也存在提示性联系 ( β = 0.05; 95% CI, 5.25 × 10 - 4 to 0.10; p = 4.75 × 10 - 2 )。根据基因预测的开始吸烟、戒烟或饮酒年龄与动脉僵化指数风险之间没有因果关系。结论 :这项孟德尔随机研究表明,开始吸烟可能是动脉僵化的一个致病风险因素。然而,要确定每天吸烟的数量是否直接导致动脉僵化的发生,还需要进一步的研究。至于饮酒量、开始吸烟的年龄和戒烟情况,目前还没有足够的证据来确定其因果关系。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Smoking, Alcohol Consumption, and Risk of Arterial Stiffness: A Two-Sample Mendelian Randomization Study
Background : While observational studies have demonstrated connections between cigarette smoking, alcohol consumption, and arterial stiffness, establishing a causal relationship has proven challenging because of potential confounding factors. To address this problem, we employed a two-sample Mendelian randomization approach. Methods : We selected genetic instruments for these risk factors from genome-wide association studies encompassing 3,383,199 individuals at the genome-wide significance level ( p < 5 × 10 − 9 ). Arterial stiffness data were acquired from the UK Biobank, which included 127,121 participants. Our primary analysis utilized the inverse variance-weighted method to explore causality. To confirm our results’ robustness, we conducted sensitivity analyses using Egger regression, the weighted median method, and Mendelian Randomization Pleiotropy RESidual Sum and Outlier (MR-PRESSO). Results : Our analysis revealed a significant association between genetic inclination to smoking initiation and an increase in the arterial stiffness index ( β = 0.11; 95% confidence interval [CI], 0.06 to 0.16; p = 1.95 × 10 − 5 ). Additionally, there was a suggestive connection between genetically predicted number of cigarettes per day and the arterial stiffness index ( β = 0.05; 95% CI, 5.25 × 10 − 4 to 0.10; p = 4.75 × 10 − 2 ). No causal relationships were observed between the genetically predicted age of smoking initiation, smoking cessation, or alcohol consumption and the risk of arterial stiffness index. Conclusions : This Mendelian randomization study indicates that smoking initiation is likely a causative risk factor for arterial stiffness. However, further research is needed to determine if the quantity of daily cigarettes directly contributes to arterial stiffness development. Regarding alcohol consumption, age of smoking initiation, and smoking cessation, there was insufficient evidence to establish causality.
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