Evidence map›Paper›PMID 42209495›Full record

ArticleNature communications2026

GWAS of extended prescription analgesic use identifies genetic loci in chronic pain.

Charli E Harlow, Emeka Uzochukwu, Hazel A Fernando, Charles E Mordaunt, Jordan M Hughey, John D Eicher, Lara Robinson, Nicholas Bowker, Laurence Howe, Jimmy Liu and 11 more

Abstract read
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

21 authors.

Charli E HarlowGSK, Gunnels Wood Road, Stevenage, UK. charli.e.harlow@gsk.com.
Emeka UzochukwuUK Dementia Research Institute, Department of Psychological Medicine and Clinical Neuroscience, University of Cardiff, Cardiff, UK.
Hazel A FernandoGSK, Gunnels Wood Road, Stevenage, UK.
Charles E MordauntGSK, Upper Providence, PA, USA.ORCID http://orcid.org/0000-0002-3820-3298
Jordan M HugheyGSK, Upper Providence, PA, USA.
John D EicherGSK, Cambridge, MA, USA.
Lara RobinsonNuffield Department of Clinical Neuroscience, Kavli Institute for Nanoscience Discovery, Dorothy Crowfoot Hodgkin Building, Sherrington Road, University of Oxford, Oxford, UK.ORCID http://orcid.org/0009-0001-7675-6029
Nicholas BowkerGSK, Gunnels Wood Road, Stevenage, UK.
Laurence HoweGSK, Gunnels Wood Road, Stevenage, UK.
Jimmy LiuGSK, Upper Providence, PA, USA.ORCID http://orcid.org/0000-0002-8379-5480
Adrian CortesGSK, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-3490-007X
Paul WilsonGSK, Gunnels Wood Road, Stevenage, UK.ORCID http://orcid.org/0000-0003-4151-1846
Usha GungabissoonGSK, Oxford Street, London, UK.
Victoria S BensonGSK, Gunnels Wood Road, Stevenage, UK.
Anthony NashNuffield Department of Clinical Neuroscience, Kavli Institute for Nanoscience Discovery, Dorothy Crowfoot Hodgkin Building, Sherrington Road, University of Oxford, Oxford, UK.
Gareth YoungGSK, Upper Providence, PA, USA.
Laura AddisGSK, Gunnels Wood Road, Stevenage, UK.ORCID http://orcid.org/0000-0001-8455-4278
Chun-Fang XuGSK, Gunnels Wood Road, Stevenage, UK.
Caleb WebberUK Dementia Research Institute, Department of Psychological Medicine and Clinical Neuroscience, University of Cardiff, Cardiff, UK.ORCID http://orcid.org/0000-0001-8063-7674
Jonathan Davitte *GSK, Upper Providence, PA, USA. jonathan.m.davitte@gsk.com.
M Zameel Cader *Nuffield Department of Clinical Neuroscience, Kavli Institute for Nanoscience Discovery, Dorothy Crowfoot Hodgkin Building, Sherrington Road, University of Oxford, Oxford, UK. zameel.cader@ndcn.ox.ac.uk.ORCID http://orcid.org/0000-0002-6952-406X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pain-related conditions are the leading cause of disability worldwide. Existing GWAS for chronic pain have mainly focused on individual pain-related disorders, which may not optimally capture the phenotype. Here, we define chronic pain based on prescription analgesic use ( ≥ 90 days) in two large biobanks (UK Biobank and FinnGen). GWAS meta-analyses of 11 prescription-based pain phenotypes identify 140 associations with chronic pain, including 78 novel (e.g. ARPP21, CNTNAP2) and 62 previously reported (e.g. SLC39A8, DCC, TRPM8) associations. Integrating these genetic associations with functional data including transcriptome-wide association studies, cell-type and pathway enrichment, and gene enrichment in mouse phenotypes identifies potential mechanisms involved in chronic pain, implicating oligodendrocyte differentiation, neuronal guidance, endolysosomal function and post-synaptic endosome recycling. Our study showcases how the use of prescription data to identify and characterize pain can provide insights into pain genetics and its underlying biology.

Indexed as

AnalgesicsChronic PainGenetic LociGenome-Wide Association StudyAnimalsGenetic Predisposition to DiseaseHumansMicePhenotypePolymorphism, Single NucleotideAnalgesics

Identifiers

PMID42209495
PMCPMC13402304

What OpenQuestion holds

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Registered trials

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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 OpenQuestion graph.