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Causal relationship between cigarette smoking behaviors and the risk of hernias: a Mendelian randomization study

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Abstract

Purpose

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.

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Data availability

The outcome data used to conduct the analyses in the present study were obtained from FinnGen study https://www.finngen.fi/en (accessed on 11 September 2023). The exposure data used to conduct the analyses in the present study were obtained from GWAS and Sequencing Consortium of Alcohol and Nicotine Use https://conservancy.umn.edu/handle/11299/201564 (accessed on 11 September 2023). The data used to screen out SNPs were accessed from the human genotype–phenotype association database, PhenoScanner http://www.phenoscanner.medschl.cam.ac.uk (accessed on 11 September 2023).

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Acknowledgements

We want to acknowledge the participants and investigators of the FinnGen Study and GWAS and Sequencing Consortium of Alcohol and Nicotine Use for providing the data publicly.

Funding

The present study received no funding.

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Conceptualization, QW and YG; formal analysis and investigation, QW and WD; writing—original draft preparation: QW, writing—review and editing: ZS and JY; resources: DY; supervision: YG, All the authors have read and agreed to the published version of the manuscript.

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Correspondence to Y. Gu.

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Wu, Q., Yang, D., Dong, W. et al. Causal relationship between cigarette smoking behaviors and the risk of hernias: a Mendelian randomization study. Hernia 28, 435–446 (2024). https://doi.org/10.1007/s10029-023-02925-6

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