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BackgroundExtensive observational evidence suggests an association between psychiatric disorders (PDs) and obstructive sleep apnea (OSA), but their causal relationship remains unexplored. The objective of this study was to examine the causal relationship between PDs and OSA.MethodsMendelian randomization (MR) analysis was conducted with summary genetic data from the FinnGen and Psychiatric Genomics Consortium (PGC). Inverse-variance weighted (IVW), MR-Egger, weighted median, and weighted mode methods were employed to ascertain causal influence. Sensitivity analysis employing various methodologies assessed the robustness of the findings. Furthermore, multivariable Mendelian randomization (MVMR) was used to clarify if the exposures independently caused OSA.ResultsMR analysis showed that genetically determined major depressive disorder (MDD) increased the risk of OSA (IVW odds ratio [OR]: 1.377, 95% confidence interval [CI]: 1.242–1.526, P = 1.05×10-9). Sensitivity analysis showed no evidence of pleiotropy and heterogeneity. In MVMR, the significant association persisted after adjusting for BMI, smoking, and alcohol consumption. No conclusive evidence indicated the causal impact of other psychological characteristics on OSA. In the reverse MR analyses, there was no causal effect of OSA on PDs.ConclusionThis study suggests a causal effect of MDD on OSA risk. Further research is needed to confirm these findings and understand how MDD contributes to OSA development, potentially aiding in reducing OSA incidence.

BackgroundPrevious observational studies have provided cumulative data linking gut microbiota to myasthenia gravis (MG). However, the causal link between the two remains unexplored. Hence, the current study was performed to explore the causal link between them.MethodsMendelian randomization (MR) analysis was conducted using the summary statistics of 211 gut microbiota taxa and the largest genome-wide association studies (GWAS) for MG currently available. The inverse variance-weighted (IVW), MR-Egger, weighted median, and weighted mode methods were employed to ascertain the causal influence. Sensitivity studies utilizing several methodologies were then used to assess the robustness of the findings. Lastly, to evaluate reverse causality, a reverse MR analysis was performed.ResultsSeven suggestive causal associations between the gastrointestinal microbiota and MG were identified based on the outcomes of the MR analysis. Specifically, phylum Actinobacteria (OR: 0.602, 95% CI: 0.405–0.896, p = 0.012), class Gammaproteobacteria (OR: 0.587, 95% CI: 0.357–0.968, p = 0.037), and families Defluviitaleaceae (OR: 0.695, 95% CI: 0.485–0.996, p = 0.047), Family XIII (OR: 0.614, 95% CI: 0.412–0.916, p = 0.017), and Peptococcaceae (OR: 0.698, 95% CI: 0.505–0.964, p = 0.029) had suggestive protective effects on MG, while order Mollicutes RF9 (OR: 1.424, 95% CI: 1.015–1.998, p = 0.041) and genus Faecalibacterium (OR: 1.763, 95% CI: 1.220–2.547, p = 0.003) were suggestive risk factors for MG. The outcomes indicate that neither heterogeneity nor horizontal pleiotropy had any discernible impact. Nevertheless, this reverse analysis did not reveal any apparent effect of MG on the gut microbiota composition.ConclusionThe MR investigation has substantiated the suggestive causal connection between gut microbiota and MG, which may provide helpful insights for innovative therapeutic and preventative approaches for MG. Further randomized controlled trials are needed to elucidate the gut microbiota’s precise role and therapeutic potential in the pathogenesis of MG.