Trial reportAlcohol, clinical & experimental research2025
Moderation of treatment outcomes by polygenic risk for alcohol-related traits in placebo-controlled trials of topiramate.
Trial report in Alcohol, clinical & experimental research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Moderation of treatment outcomes by polygenic risk for alcohol-related traits in placebo-controlled trials of topiramate.Alcohol, clinical & experimental research · 2025Trial
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9 authors.
Funding
Abstract
backgroundIn two 12-week, randomized, placebo-controlled trials (RCTs) in individuals with alcohol use disorder (AUD), topiramate significantly reduced heavy drinking days (HDDs), and alcohol-related problems. In a secondary analysis of those findings, we examined four broad measures of genetic risk-polygenic scores (PGS)-of problematic alcohol use (PAU), drinks per week (DPW), and time to relapse to any drinking (TR) and heavy drinking (THR) as moderators of topiramate's effect on HDDs and alcohol-related problems.
methodsWe analyzed data from 285 individuals with AUD (65.6% male) of European-like ancestry, who were treated with either topiramate (49.1%) or placebo (50.9%). All patients underwent genome-wide array genotyping, and PGS were calculated using summary statistics from genome-wide association studies of PAU, DPW, and TR and THR (two time-to-event outcomes among patients treated in AUD pharmacotherapy trials). We hypothesized an interaction effect in which greater genetic risk-particularly for PAU-would be associated with a greater therapeutic response to topiramate than placebo.
resultsAs shown previously, topiramate significantly reduced both HDDs (odds ratio [OR] = 0.50, p < 0.001) and Short Index of Problems (SIP) scores (b = -3.04, p < 0.001) more than placebo. There were nonsignificant associations of higher PGS with more HDDs (OR = 1.17, 95% CI = 0.98-1.41, p = 0.091) and a greater reduction in HDDs in the topiramate group (OR = 0.80, 95% CI = 0.62-1.03, p = 0.089). There were also significant interaction effects with treatment on SIP score by PGS for PAU (b = -1.64, SE = 0.78, p = 0.033), TR (b = -2.16, SE = 0.72, p = 0.003), and TRH (b = -2.17, SE = 0.72, p = 0.003).
conclusionsThese findings provide proof of principle for the use of alcohol-related PGS as moderators of the effects of topiramate for treating AUD. Larger RCTs of topiramate are needed to provide adequate statistical power to validate this pharmacogenetic approach to precision AUD treatment.
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