Hormonal
Genetically modeled dual GIPR/GLP1R agonism reduces binge drinking frequency and the risk of heavy drinking with psychiatric comorbidities.
Genetic evidence suggests that activating GLP-1 and GIP receptors (via drugs like semaglutide or tirzepatide) can reduce binge drinking and heavy drinking, especially in those with psychiatric comorbidities. This effect appears independent of general alcohol consumption (drinks per week), suggesting a specific impact on high-risk drinking patterns.
Genetic proxies for lowered BMI, modeling the appetite-suppressing and weight-reducing effects of variants in both the GIPR and GLP1R loci (“GIPR/GLP1R”), were linked with reduced binge drinking in the primary (β = −0.44, 95% CI [−0.72, −0.15], P = 2.42 × 10−3) and replication data (β = −0.13, [−0.22, −0.04], P = 0.0058). HbA1c lowering via GIPR/GLP1R variants was associated with reduced risk of heavy drinking with psychiatric comorbidities versus low-risk drinking (odds ratio [OR] = 0.62, [0.45, 0.85], P = 0.0031)
Why this rating
High-quality Mendelian Randomization with replication across independent cohorts and ancestry groups, though observational in nature.
Source
Genetically modeled GLP1R and GIPR agonism reduce binge drinking and alcohol-associated phenotypes: a multi-ancestry drug-target Mendelian randomization study
Joshua Reitz et al. · Molecular Psychiatry · 2025
DOI 10.1038/s41380-025-03199-3
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