Research

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.

GoodSupportsHIGH confidence
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)
Joshua Reitz et al. · Molecular Psychiatry · 2025

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

cohort · n=1812013Cited 8×
Read the paper
DOI resolved against Crossref · corpus check 2026-06-10

This is one finding among thousands. Every one is graded and traced to its source, so you can see what the evidence actually supports. Browse the research →