ArticleIBRO neuroscience reports2026
The causal relationship between diabetes mellitus and meningioma: Insights from the genetic perspective.
Article in IBRO neuroscience reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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4 authors.
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Abstract
Background: Epidemiological evidence reports the inconsistent association between diabetes mellitus and meningioma risk. We conducted a Mendelian randomization (MR) analysis to evaluate the causality between diabetes-related phenotypes and meningioma. Methods: Genome-wide association study summary statistics for type 1 diabetes (T1D, N = 590,946), type 2 diabetes (T2D, N = 468,298), hemoglobin A1c (HbA1c, N = 146,806), fasting glucose (FG, N = 129,665), and 2-hour glucose post-oral challenge (2hGlu, N = 57,878) were obtained from the MRC-IEU OpenGWAS and MAGIC consortia. Meningioma data (1835 intracranial cases vs. 377,674 controls; 339 spinal cases vs. 500,009 controls) were derived from FinnGen R12. Genetic variants significantly associated with each exposure were selected as instrumental variables. Inverse-variance weighted regression served as the primary analysis, supplemented by MR-Egger, weighted median, and maximum likelihood methods. Sensitivity analyses evaluated heterogeneity, pleiotropy, outliers, and influential variants.Multiple comparisons were corrected using the Benjamini-Hochberg false discovery rate (FDR) procedure. Results: Genetically predicted liability to T2D was nominally associated with a lower risk of intracranial meningioma (IVW: OR = 0.07, 95% CI: 0.01-0.97, P = 0.047); however, this association did not remain significant after Benjamini-Hochberg FDR correction (FDR-adjusted P = 0.41). No significant associations were found for T1D (P = 0.334), HbA1c (P = 0.082), FG (P = 0.919), 2hGlu (P = 0.955), or spinal meningioma (all P > 0.05). Sensitivity analyses were reported individually for each exposure-outcome pair. Reverse MR provided no evidence supporting a causal effect of intracranial meningioma on T1D, T2D, or HbA1c. Conclusion: This MR study provides suggestive, but not definitive, evidence for a potential inverse association between genetically predicted T2D liability and intracranial meningioma risk. After FDR correction, this association did not remain significant, and no significant associations were observed for T1D or other diabetes-related traits.
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