Abstract
OBJECTIVE: This study aimed to investigate the influence of lung function on the relationship between allergies and hypertension, thereby elucidating significant potential mechanisms from a genetic standpoint. We investigated the causal relationship between childhood allergies (age <16 years) and essential hypertension and identified and quantified the role of lung function (forced vital capacity [FVC] and forced expiratory volume in the first second/forced vital capacity [FEV1/FVC]) as potential mediators. METHODS: Using data from a genome-wide association study and the Fenn Genn consortium, a two-sample Mendelian randomization (MR) analysis of genetically predicted childhood allergies (7128 cases and 211,703 controls) and essential hypertension (116,714 cases and 1,032,659 controls) was performed. Furthermore, we used two-step MR to quantify the effect of lung function-mediated childhood allergies on essential hypertension. The FVC and FEV1/FV sample size was 371,898. RESULTS: Childhood allergies were associated with increased odds of developing essential hypertension (odds ratio [OR] = 1.0900, 95% confidence interval [CI] = 1.0034-1.1842, P = 0.0414). No strong evidence that genetically predicted essential hypertension affected childhood allergy risk was identified (OR = 1.0631, 95% CI = 0.9829-1.1498, P = 0.1264). The proportion of genetically predicted childhood allergies mediated only by FVC was 5.67% (95% CI, 5.13%-5.73%). CONCLUSION: A causal relationship between childhood allergies and essential hypertension was identified, with a proportion of the effect mediated by FVC. Therefore, implementing early interventions in children with allergies is imperative to mitigate the long-term risk of developing hypertension. Further research is required to identify additional risk factors as potential mediators.