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The causal relationship between gut microbiota and cerebral cortex development remains unclear. We aimed to scrutinize the plausible causal impact of gut microbiota on cortical thickness via Mendelian randomization (MR) study. Genome-wide association study (GWAS) data for 196 gut microbiota phenotypes (N = 18,340) were obtained as exposures, and GWAS data for cortical thickness-related traits (N = 51,665) were selected as outcomes. Inverse variance weighted was used as the main estimate method. A series of sensitivity analyses was used to test the robustness of the estimates including Cochran's Q test, MR-Egger intercept analysis, Steiger filtering, scatter plot funnel plot and leave-one-out analysis. Genetic prediction of high Bacillales (β = 0.005, P = 0.032) and Lactobacillales (β = 0.010, P = 0.012) abundance was associated with a potential increase in global cortical thickness. For specific functional brain subdivisions, genetically predicted order Lactobacillales would potentially increase the thickness of the fusiform (β = 0.014, P = 0.016) and supramarginal (β = 0.017, P = 0.003). Meanwhile, order Bacillales would increase the thickness of fusiform (β = 0.007, P = 0.039), insula (β = 0.011, P = 0.003), rostralanteriorcingulate (β = 0.014, P = 0.002) and supramarginal (β = 0.006, P = 0.043). No significant estimates of heterogeneity or pleiotropy were found. Through MR studies, we discovered genetic prediction of the Lactobacillales and Bacillales orders potentially linked to cortical thickness, affirming gut microbiota may enhance brain structure. Genetically predicted supramarginal and fusiform may be potential targets. • Our study demonstrated the causal associations between gut microbiota and cortical thickness. • A systematic investigation between gut microbiota and cortical thickness was carried out. • We discovered genetic prediction of the Lactobacillales and Bacillales orders may potentially enhance brain structure. • Our research suggested fusiform and supramarginal as possible brain regions for investigating the microbiota-gut-brain axis. [ABSTRACT FROM AUTHOR]

Background: The incidence of gastroesophageal reflux disease (GERD) has been shown to be elevated in individuals with epilepsy. Traditional observational studies have led to a limited understanding of the effects of GERD and BE on epilepsy due to the interference of reverse causation and potential confounders. Methods: We conducted a bidirectional two‐sample Mendelian randomization (MR) analysis to determine whether GERD and BE can increase the risk of epilepsy. Genome‐wide association study data on epilepsy and its subgroups were obtained from the International League Against Epilepsy consortium for primary analysis using three MR approaches and the FinnGen consortium for replication and meta‑analysis. We calculated causal estimates between the two esophageal diseases and epilepsy using the inverse‐variance weighted method. Sensitivity analysis was conducted to detect heterogeneity and pleiotropy. Results: We found a potential effect of genetically predicted GERD on the risk of epilepsy (odds ratio [OR] = 1.078; 95% confidence interval [CI], 1.014–1.146, p =.016). Specifically, GERD showed an effect on the risk of generalized epilepsy (OR = 1.163; 95% CI, 1.048–1.290, p =.004) but not focal epilepsy (OR = 1.059, 95% CI, 0.992–1.131, p =.084). Notably, BE did not show a significant causal relationship with the risks of generalized and focal epilepsy. Conclusions: Under MR assumptions, our findings suggest a potential risk‐increasing effect of GERD on epilepsy, especially generalized epilepsy. Considering the exploratory nature of our study, the association between GERD and epilepsy needs to be confirmed by future prospective studies. [ABSTRACT FROM AUTHOR]