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Tell me about a recent study showing increased risk for dementia with gabapentin
Executive Summary
A cluster of recent observational studies and news reports identify an association between gabapentin use and higher rates of dementia or cognitive decline, particularly when prescriptions are repeated and in younger adults; the strongest signal arises from a July 2025 retrospective cohort using electronic-health records that found increased risks after six or more prescriptions [1] [2]. These findings are not uniform: earlier and some concurrent studies show smaller or no associations, and experts emphasize that association does not equal causation, so the evidence prompts caution and further research rather than definitive claims that gabapentin causes dementia [3] [4] [5].
1. A new alarm bell: What the 2025 cohort found and why it grabbed headlines
A July 2025 retrospective analysis using the TriNetX electronic‑health record network reported that adults with chronic low back pain who received six or more gabapentin prescriptions had a 29% higher relative risk of dementia and an 85% higher risk of mild cognitive impairment within ten years; the effect was strongest in non‑elderly adults (18–64), where the relative risk exceeded twofold [1] [2]. This study’s sample, methods, and stratified results were widely covered by trade press and medical news outlets because the magnitude of the association and apparent age gradient (younger adults showing larger relative increases) challenge prevailing expectations about dementia risk and prompt attention to prescribing practices for chronic pain [2] [6]. The paper and reports repeatedly emphasize that the analysis is observational and cannot establish causality.
2. Other population studies that support a link — and what they show about dose and age
Independent analyses using large administrative databases have reported similar patterns: a 2023 Taiwan National Health Insurance–based cohort pooling gabapentin or pregabalin exposures found a roughly 45% higher adjusted hazard of dementia, with risk rising at higher cumulative doses and particularly pronounced among those under 50 (HR ~3.16 for younger patients) [5]. A 2022 Frontiers analysis linked gabapentin initiation with subsequent neurocognitive and functional decline in older adults initially free of cognitive impairment, reinforcing that different datasets and methods have each produced signals between gabapentinoids and later cognitive problems [7]. These studies consistently point to dose/quantity relationships and stronger relative risks in younger subgroups, suggesting the association is not restricted to frail older populations.
3. Contradictions and null findings: studies that found no substantial risk
Not all analyses align. A 2024 nested case‑control study reported no significant association between gabapentin use and dementia in adults with chronic pain, with an adjusted odds ratio near 0.91 and no clear dose‑response across subgroups [3]. This null result underscores heterogeneity across datasets, choices about exposure windows and comparator groups, and the possibility that residual confounding, indication bias, or differences in coding and follow‑up can produce divergent estimates. News reports and commentators note these discrepancies and caution that single observational studies—whether showing risk or not—cannot settle causation without replication, mechanistic data, or randomized evidence [8] [4].
4. Limits of the evidence: why observational associations are fragile and what could bias them
All cited studies are observational and vary in design—retrospective cohorts, administrative claims analyses, and electronic health record studies—so confounding by indication, unmeasured comorbidities, and reverse causation (prodromal cognitive symptoms prompting gabapentin use for pain) are plausible explanations for associations [1] [5]. Exposure definitions differ (six or more prescriptions, cumulative defined daily doses, initiation vs ongoing use), follow‑up lengths vary, and some analyses pooled pregabalin with gabapentin, complicating attribution to a single drug class [5]. Authors and reporters consistently flag these methodological caveats and call for prospective studies, careful pharmacoepidemiologic replication, and investigation of biological plausibility to determine whether the signals reflect drug effects or confounding [4] [2].
5. Where this leaves clinicians, patients, and researchers right now
The balance of recent evidence justifies heightened pharmacovigilance rather than immediate prohibition: multiple large observational analyses show signals that merit conservative prescribing—especially limiting long‑term, high‑dose gabapentin in younger patients when alternatives exist—and active monitoring of cognition [1] [5]. At the same time, conflicting results and the inability of observational designs to prove causation mean regulatory bodies and clinicians will weigh these signals alongside gabapentin’s benefits for neuropathic pain and seizure control; researchers recommend targeted prospective studies and mechanistic work before changing broad clinical guidelines [3] [4].