Body mass index and the risk of abdominal hernia: a Mendelian randomization study

Abdominal hernia (AH) is one of the most common clinical diseases. A large number of observational studies have found that obesity is an important risk factor for AH. However, the causal relationship between obesity and AH cannot be determined because of the clinical studies on AH induced by obesity are relatively few and only have some small- or medium-scale observational studies. Observational studies have so many confounding factors and reverse causality due to their shortcomings. From an evidence-based medicine perspective, they are not sufficiently convincing. Therefore, there is still a lack of high-quality, evidence-based medical evidence supporting a causal relationship between obesity and AH. A causal relationship between obesity and AH is also almost impossible to confirm by randomized controlled trials (RCTs). Our study based on Mendelian randomization (MR) may provide a higher level of evidence-based medical support for the relationship between obesity and AH. Body mass index (BMI) is the most common measure used for defining obesity. Finally, we employed two-sample Mendelian randomization (TSMR) to explore the causal relationship between BMI and AH.

AH-related single nucleotide polymorphisms (SNPs) data were obtained from the FinnGen Biobank (FB), and BMI-related single nucleotide polymorphisms (SNPs) data were obtained from the UK Biobank (UKB). Genetic loci are used as instrumental variables (IVs), methods such as inverse variance weighted (IVW) were used for two-sample Mendelian randomization analysis, and the odds ratio (OR) value was used to evaluate the causal relationship between BMI and AH.

The results of the horizontal pleiotropy test were calculated by Egger-intercept method: p = 0.34 > 0.05. The Cochran Q test of MR-Egger method and IVW method showed heterogeneity P = 0.03 < 0.05, so the IVW random effect model was used as the gold standard. We found a genetically determined 1-standard deviation (SD) increment of BMI causally increased a 66.0% risk of AH (N = 371 SNPs, OR = 1.66, 95% CI 1.46–1.89, p = 1.55E–14) based on the IVW random effect model which was almost consistent with the results of other seven methods.

Our MR found genetic evidence for BMI and AH. The risk of developing AH increases with the number of BMI. This finding provides further evidence that maintaining a healthy BMI can prevent the development of AH. In addition, clinicians may need to focus on the potential risk of AH on some high-BMI patients.