ArticlemedRxiv : the preprint server for health sciences2026
Genome-wide association meta-analyses over one million individuals identify 54 loci associated with urinary incontinence and its subtypes.
Article in medRxiv : the preprint server for health sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors.
Funding
Abstract
Urinary incontinence (UI) markedly reduces quality of life, and its genetic basis remains to be elucidated. Here, we performed GWAS meta-analyses of four UI phenotypes, using hospital-based data from 1,045,436 individuals from the Trøndelag Health Study (HUNT), UK Biobank, FinnGen, and the Michigan Genomics Initiative, and self-reported UI from 56,957 females from HUNT and the Nurses' Health Study. We identified 54 (52 novels) genetic loci associated with at least one UI phenotype. Analyses revealed tissue-specific involvement, with connective and muscular tissues for stress UI, and neural tissues for urge UI, and supported key roles of SUI-prioritized genes in the extracellular matrix organization and muscle function. Further, genetic variations contributes to UI through inflammation, immune, and aging pathways. We identified smoking, higher BMI, higher parity, and pelvic organ prolapse as causal risk factors for UI in females, and benign prostatic hyperplasia in males. Our findings identify key genetic factors, tissues, pathways, and causal underlying UI.
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.