Abstract：
OBJECTIVE: As the global population continues to age, there is a noticeable yearly rise in the incidence of hernias. Simultaneously, smoking, a widespread addictive behavior and a significant contributor to mortality, has evolved into a pervasive public health concern. Existing literature has already established a connection between smoking and an increased risk of postoperative recurrence and postoperative infections following hernia surgery. However, there remains a dearth of research exploring the association between smoking and hernia morbidity. In this study, our objective is to systematically evaluate the causal relationship between cigarette smoking behaviors and hernia morbidity using a Mendelian randomization (MR) approach.
METHODS: Hernia-related data were sourced from the FinnGen Biobank database, while cigarette smoking behavior data were gathered from the GWAS and Sequencing Consortium of Alcohol and Nicotine Use. To assess the causal relationship, we employed five methods: the weighted median, the weighted mode the inverse variance weighted (IVW), MR-Egger, and the simple mode. Sensitivity analysis was conducted, incorporating Cochran\'s Q test, the MR-Egger intercept test, leave-one-out analysis, and funnel plot. The presentation of the causal relationship is expressed as an odds ratio (OR) along with their corresponding 95% confidence intervals (CI).
RESULTS: Employing the IVW method as the reference standard, we found that smoking intensity is associated with an increased risk of diaphragmatic hernia (OR = 1.21, 95% CI 1.00-1.46, P = 0.047). These consistent findings were further corroborated by the weighted median and weighted mode methods (OR = 1.26, 95% CI 1.03-1.54, P = 0.026; OR = 1.25, 95% CI 1.02-1.52, P = 0.045). Conversely, when applying the IVW method, we identified no statistically significant causal relationship between smoking age, smoking initiation status, smoking cessation status, and the incidence of hernia.
CONCLUSIONS: Our MR study has uncovered genetic evidence linking smoking intensity and the occurrence of diaphragmatic hernia. The risk of developing diaphragmatic hernia rises in tandem with the intensity of smoking. This emphasizes the crucial role of regularly advising patients to cease smoking in clinical settings.
METHODS: Hernia-related data were sourced from the FinnGen Biobank database, while cigarette smoking behavior data were gathered from the GWAS and Sequencing Consortium of Alcohol and Nicotine Use. To assess the causal relationship, we employed five methods: the weighted median, the weighted mode the inverse variance weighted (IVW), MR-Egger, and the simple mode. Sensitivity analysis was conducted, incorporating Cochran\'s Q test, the MR-Egger intercept test, leave-one-out analysis, and funnel plot. The presentation of the causal relationship is expressed as an odds ratio (OR) along with their corresponding 95% confidence intervals (CI).
RESULTS: Employing the IVW method as the reference standard, we found that smoking intensity is associated with an increased risk of diaphragmatic hernia (OR = 1.21, 95% CI 1.00-1.46, P = 0.047). These consistent findings were further corroborated by the weighted median and weighted mode methods (OR = 1.26, 95% CI 1.03-1.54, P = 0.026; OR = 1.25, 95% CI 1.02-1.52, P = 0.045). Conversely, when applying the IVW method, we identified no statistically significant causal relationship between smoking age, smoking initiation status, smoking cessation status, and the incidence of hernia.
CONCLUSIONS: Our MR study has uncovered genetic evidence linking smoking intensity and the occurrence of diaphragmatic hernia. The risk of developing diaphragmatic hernia rises in tandem with the intensity of smoking. This emphasizes the crucial role of regularly advising patients to cease smoking in clinical settings.
摘要：
目标：随着全球人口的老龄化，疝气的发病率每年明显上升。同时,吸烟,广泛的成瘾行为和死亡率的重要因素，已经演变成一个普遍的公共卫生问题。现有文献已经建立了吸烟与疝气手术后术后复发和术后感染风险增加之间的联系。然而,关于吸烟与疝气发病率之间关系的研究仍然缺乏。在这项研究中,我们的目标是使用孟德尔随机化(MR)方法系统评估吸烟行为与疝气发病率之间的因果关系.
方法：与疝相关的数据来自FinnGenBiobank数据库，而吸烟行为数据来自GWAS和酒精和尼古丁使用测序联盟。为了评估因果关系，我们采用了五种方法：加权中位数，加权模式为逆方差加权(IVW)，MR-Egger,和简单的模式。进行了敏感性分析，结合Cochran的Q测试，MR-Egger截距测试,遗漏分析，和漏斗图。因果关系的表示表示为比值比（OR）及其相应的95％置信区间（CI）。
结果：采用IVW方法作为参考标准，我们发现吸烟强度与膈疝风险增加相关(OR=1.21,95%CI1.00-1.46,P=0.047).加权中位数和加权模式方法进一步证实了这些一致的发现（OR=1.26，95％CI1.03-1.54，P=0.026；OR=1.25，95％CI1.02-1.52，P=0.045）。相反，当应用IVW方法时，我们发现吸烟年龄之间没有统计学上显著的因果关系，吸烟起始状态，戒烟状况,和疝气的发病率。
结论：我们的MR研究发现了吸烟强度与膈疝发生有关的遗传证据。发生膈疝的风险随着吸烟强度的增加而增加。这强调了在临床环境中定期建议患者戒烟的关键作用。
方法：与疝相关的数据来自FinnGenBiobank数据库，而吸烟行为数据来自GWAS和酒精和尼古丁使用测序联盟。为了评估因果关系，我们采用了五种方法：加权中位数，加权模式为逆方差加权(IVW)，MR-Egger,和简单的模式。进行了敏感性分析，结合Cochran的Q测试，MR-Egger截距测试,遗漏分析，和漏斗图。因果关系的表示表示为比值比（OR）及其相应的95％置信区间（CI）。
结果：采用IVW方法作为参考标准，我们发现吸烟强度与膈疝风险增加相关(OR=1.21,95%CI1.00-1.46,P=0.047).加权中位数和加权模式方法进一步证实了这些一致的发现（OR=1.26，95％CI1.03-1.54，P=0.026；OR=1.25，95％CI1.02-1.52，P=0.045）。相反，当应用IVW方法时，我们发现吸烟年龄之间没有统计学上显著的因果关系，吸烟起始状态，戒烟状况,和疝气的发病率。
结论：我们的MR研究发现了吸烟强度与膈疝发生有关的遗传证据。发生膈疝的风险随着吸烟强度的增加而增加。这强调了在临床环境中定期建议患者戒烟的关键作用。
