SynthesisPLoS genetics2023
Genome wide association joint analysis reveals 99 risk loci for pain susceptibility and pleiotropic relationships with psychiatric, metabolic, and immunological traits.
Synthesis in PLoS genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it.
- A multi-ancestry genetic study of pain intensity in 598,339 veterans.Nature medicine · 2024Pooled it
- Review
- Associations ofPharmaceuticals (Basel, Switzerland) · 2026Article
- GWAS of extended prescription analgesic use identifies genetic loci in chronic pain.Nature communications · 2026Article
- Review
- Causal evidence linking chronic pain genetics to late-onset asthma via the nervous system.British journal of anaesthesia · 2026Article
- The cell-type-specific genetic architecture of chronic pain in brain and dorsal root ganglia.The Journal of clinical investigation · 2025Article
- Genetic variants associated with chronic postsurgical pain: evidence from the China Surgery and Anaesthesia Cohort study.British journal of anaesthesia · 2025Observational
- Modeling Pain Without Injury: Inherited Rodent Models as Mechanistic Windows into Chronic Pain.Function (Oxford, England) · 2025Review
- The genetic architecture of fibromyalgia across 2.5 million individuals.medRxiv : the preprint server for health sciences · 2025Article
- Etiological basis for chronic pain genetic variation in brain and dorsal root ganglia cell types.medRxiv : the preprint server for health sciences · 2025Article
- Gene discovery and pleiotropic architecture of chronic pain in a genome-wide association study of >1.2 million individuals.Research square · 2025Article
- Gene discovery and pleiotropic architecture of Chronic Pain in a Genome-wide Association Study of >1.2 million Individuals.medRxiv : the preprint server for health sciences · 2025Article
- A genome-wide association study of European advanced cancer patients treated with opioids identifies regulatory variants on chromosome 20 associated with pain intensity.European journal of pain (London, England) · 2025Article
- Deciphering the genetic architecture of pain intensity.Nature medicine · 2024Article
- Genome-wide association study identifies novel genetic variants associated with widespread pain in the UK Biobank (Molecular painArticle
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Chronic pain is at epidemic proportions in the United States, represents a significant burden on our public health system, and is coincident with a growing opioid crisis. While numerous genome-wide association studies have been reported for specific pain-related traits, many of these studies were underpowered, and the genetic relationship among these traits remains poorly understood. Here, we conducted a joint analysis of genome-wide association study summary statistics from seventeen pain susceptibility traits in the UK Biobank. This analysis revealed 99 genome-wide significant risk loci, 65 of which overlap loci identified in earlier studies. The remaining 34 loci are novel. We applied leave-one-trait-out meta-analyses to evaluate the influence of each trait on the joint analysis, which suggested that loci fall into four categories: loci associated with nearly all pain-related traits; loci primarily associated with a single trait; loci associated with multiple forms of skeletomuscular pain; and loci associated with headache-related pain. Overall, 664 genes were mapped to the 99 loci by genomic proximity, eQTLs, and chromatin interaction and ~15% of these genes showed differential expression in individuals with acute or chronic pain compared to healthy controls. Risk loci were enriched for genes involved in neurological and inflammatory pathways. Genetic correlation and two-sample Mendelian randomization indicated that psychiatric, metabolic, and immunological traits mediate some of these effects.
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Registered trials
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