Evidence map›Paper›PMID 27454463›Full record

ArticlePain2016

Genome-wide association analysis of pain severity in dysmenorrhea identifies association at chromosome 1p13.2, near the nerve growth factor locus.

Amy V Jones, James R F Hockley, Craig Hyde, Donal Gorman, Ana Sredic-Rhodes, James Bilsland, Gordon McMurray, Nicholas A Furlotte, Youna Hu, David A Hinds and 2 more

Abstract read
In one paragraph

Article in Pain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 4 pooled it
3.6field-weighted citation impact, top 7% of its field
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

26 citing papers in PubMed, 4 syntheses or guidelines pooled it, 56 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Article
  7. Dysmenorrhea and Adolescent Mental Health: A School-Based Cross-Sectional Study.BJOG : an international journal of obstetrics and gynaecology · 2025
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  15. Disease Burden of Dysmenorrhea: Impact on Life Course Potential.International journal of women's health · 2023
    Review
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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

12 authors at 3 institutions in 2 countries.

Amy V JonesHuman Genetics and Computational Biomedicine, Pfizer WRD, Cambridge, United Kingdom.
James R F HockleyNeuroscience and Pain Research Unit, Pfizer Ltd, Cambridge, United Kingdom.
Craig HydeResearch Statistics, Pfizer WRD, Groton, CT, USA.
Donal GormanResearch Statistics, Pfizer WRD, Pfizer Ltd, Cambridge, United Kingdom.
Ana Sredic-RhodesHuman Genetics and Computational Biomedicine, Pfizer WRD, Cambridge, United Kingdom.
James BilslandNeuroscience and Pain Research Unit, Pfizer Ltd, Cambridge, United Kingdom.
Gordon McMurrayNeuroscience and Pain Research Unit, Pfizer Ltd, Cambridge, United Kingdom.
Nicholas A Furlotte23andMe, Inc, Mountain View, CA, USA.
Youna Hu23andMe, Inc, Mountain View, CA, USA.
David A Hinds23andMe, Inc, Mountain View, CA, USA.
Peter J CoxNeuroscience and Pain Research Unit, Pfizer Ltd, Cambridge, United Kingdom.
Serena ScollenHuman Genetics and Computational Biomedicine, Pfizer WRD, Cambridge, United Kingdom.
Pfizer (United Kingdom) · GB23andMe (United States) · USPfizer (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysmenorrhea is a common chronic pelvic pain syndrome affecting women of childbearing potential. Family studies suggest that genetic background influences the severity of dysmenorrhea, but genetic predisposition and molecular mechanisms underlying dysmenorrhea are not understood. In this study, we conduct the first genome-wide association study to identify genetic factors associated with dysmenorrhea pain severity. A cohort of females of European descent (n = 11,891) aged 18 to 45 years rated their average dysmenorrhea pain severity. We used a linear regression model adjusting for age and body mass index, identifying one genome-wide significant (P < 5 × 10) association (rs7523086, P = 4.1 × 10, effect size 0.1 [95% confidence interval, 0.074-0.126]). This single nucleotide polymorphism is colocalising with NGF, encoding nerve growth factor. The presence of one risk allele corresponds to a predicted 0.1-point increase in pain intensity on a 4-point ordinal pain scale. The putative effects on NGF function and/or expression remain unknown. However, genetic variation colocalises with active epigenetic marks in fat and ovary tissues, and expression levels in aorta tissue of a noncoding RNA flanking NGF correlate. Participants reporting extreme dysmenorrhea pain were more likely to report being positive for endometriosis, polycystic ovarian syndrome, depression, and other psychiatric disorders. Our results indicate that dysmenorrhea pain severity is partly genetically determined. NGF already has an established role in chronic pain disorders, and our findings suggest that NGF may be an important mediator for gynaecological/pelvic pain in the viscera.

Indexed as

AdolescentAdultAge FactorsChromosomes, Human, Pair 1Cohort StudiesDysmenorrheaFemaleGenome-Wide Association StudyHumansMiddle AgedNerve Growth FactorPain MeasurementPolymorphism, Single NucleotideYoung AdultNerve Growth FactorNGF protein, human

Identifiers

PMID27454463
PMCPMC5436737
OpenAlexW2477401472

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.