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Peer-reviewedCC BYIBRO neuroscience reports

The causal relationship between diabetes mellitus and meningioma: Insights from the genetic perspective.

  • Qi Sun1
  • Lin Chen2
  • Donghai Ren2
  • Chen Chai3
  1. 1Department of Emergency Medicine, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310016, China.
  2. 2Emergency Center, The First People's Hospital of Xiantao, Affiliated Hospital of Hubei University of Science and Technology, XianTao, China.
  3. 3Emergency Center, Zhongnan Hospital of Wuhan University, Hubei Provincial Clinical Research Center for Emergency and Resuscitation, WuHan, China.
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Abstract

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. 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. 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. 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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Cite

BibTeXRIS
BibTeX
@article{sun2026causal,
  title = {{The causal relationship between diabetes mellitus and meningioma: Insights from the genetic perspective.}},
  author = {Qi Sun and Lin Chen and Donghai Ren and Chen Chai},
  journal = {IBRO neuroscience reports},
  year = {2026},
  month = oct,
  doi = {10.1016/j.ibneur.2026.10.012},
  url = {https://europepmc.org/article/MED/42999564},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - The causal relationship between diabetes mellitus and meningioma: Insights from the genetic perspective.
AU  - Qi Sun
AU  - Lin Chen
AU  - Donghai Ren
AU  - Chen Chai
PY  - 2026
DA  - 2026/10/17
JO  - IBRO neuroscience reports
DO  - 10.1016/j.ibneur.2026.10.012
UR  - https://europepmc.org/article/MED/42999564
AB  - 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. 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. 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. 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.
SN  - 2667-2421
ER  -