The association between maternal diabetes and the risk of epilepsy in offspring: a systematic review and meta-analysis

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Background Epilepsy is among the most prevalent neurological disorders in children, with nearly half of all cases remaining idiopathic. The global prevalence of maternal diabetes—encompassing both pregestational types (type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM)) and gestational diabetes mellitus (GDM)—has been steadily increasing, raising growing concerns regarding its impact on offspring neurodevelopment. While accumulating evidence suggests that maternal diabetes is associated with an elevated risk of various neurodevelopmental disorders in children, its specific relationship with the risk of epilepsy remains unclear, with available data being both limited and conflicting. To address this gap, we conducted a meta-analysis to comprehensively evaluate the association between distinct types of maternal diabetes (pregestational and gestational) and the subsequent risk of epilepsy in offspring. Methods We systematically searched the PubMed, Embase, Web of Science, and the Cochrane Library for observational studies examining the association between maternal diabetes and offspring epilepsy risk, covering the period from database inception to July 2026. Two independent reviewers performed literature screening, data extraction, and risk-of-bias assessment. Statistical analyses were performed using Stata version 14.0. Results A total of three studies, encompassing 5,287,837 participants, met the inclusion criteria. Pregestational diabetes—both T1DM and T2DM—was significantly associated with an increased risk of epilepsy in offspring (T1DM: HR = 1.33, 95% CI [1.17, 1.52], P < 0.001; T2DM: HR = 1.38, 95% CI [1.25, 1.51], P < 0.001). Nevertheless, owing to the observational design of the included studies, these associations should not be interpreted as causal. Regarding GDM, the pooled estimate did not reach conventional statistical significance (HR = 1.04, 95% CI [0.93, 1.16], P = 0.469). Furthermore, sensitivity analyses revealed that this null finding lacked robustness, with the pooled estimate being substantially influenced by individual studies. Consequently, the current evidence is insufficient to either support or refute a conclusive association between GDM and offspring epilepsy, and any positive findings must be interpreted with considerable caution. Conclusions This meta-analysis suggests that pregestational T1DM and T2DM may increase the risk of epilepsy in offspring. In contrast, for GDM, the available analytical evidence remains inconclusive and displays notable between-study heterogeneity; although the summary effect was not statistically significant, it proved highly unstable under sensitivity testing. Given the limited number of included studies and the inability to fully exclude residual confounding, the above findings—particularly those pertaining to GDM—should be regarded as exploratory rather than definitive causal inferences. Interpretation of these results warrants prudence. Future large-scale, high-quality prospective cohort studies are urgently needed to validate these observations, with special emphasis on stringent glycemic management in pregnant women with diabetes and long-term neurodevelopmental surveillance of their offspring. Systematic review registration https://www.crd.york.ac.uk/PROSPERO/view/CRD420261465624 , identifier CRD420261465624.