Mendelian randomization highlights insomnia as a risk factor for pain diagnoses
| Autor: | Martin Broberg, Hanna Ollila, FinnGen, Juha Karjalainen |
|---|---|
| Přispěvatelé: | Institute for Molecular Medicine Finland, Helsinki Institute of Life Science HiLIFE, HUS Helsinki and Uusimaa Hospital District |
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
insomnia
Genome-wide association study DETERMINANTS 3124 Neurology and psychiatry 0302 clinical medicine Risk Factors Sleep Initiation and Maintenance Disorders Insomnia GWAS genetics pain MUSCULOSKELETAL PAIN 0303 health sciences AcademicSubjects/SCI01870 LONGITUDINAL DATA Chronic pain Mendelian Randomization Analysis ASSOCIATION 3. Good health PREVALENCE sleep disorders medicine.symptom SENSITIVITY AcademicSubjects/MED00370 medicine.medical_specialty Polymorphism Single Nucleotide 03 medical and health sciences Physiology (medical) Internal medicine Mendelian randomization mental disorders medicine Humans Risk factor AcademicSubjects/MED00385 030304 developmental biology COMPLEX business.industry 3112 Neurosciences HUNT Odds ratio medicine.disease SLEEP Confidence interval Insomnia and Psychiatric Disorders Neurology (clinical) business 030217 neurology & neurosurgery Genome-Wide Association Study |
| Zdroj: | Sleep |
| Popis: | Study Objective Insomnia has been linked to acute and chronic pain conditions; however, it is unclear whether such relationships are causal. Recently, a large number of genetic variants have been discovered for both insomnia and pain through genome-wide association studies (GWASs) providing a unique opportunity to examine the evidence for causal relationships through the use of the Mendelian randomization paradigm. Methods To elucidate the causality between insomnia and pain, we performed bidirectional Mendelian randomization analysis in FinnGen, where clinically diagnosed ICD-10 categories of pain had been evaluated. In addition, we used measures of self-reported insomnia symptoms. We used endpoints for pain in the FinnGen Release 5 (R5) (N = 218,379), and a non-overlapping sample for insomnia (UK Biobank (UKBB) and 23andMe, N = 1,331,010 or UKBB alone N = 453,379). We assessed the robustness of results through conventional Mendelian randomization sensitivity analyses. Results Genetic liability to insomnia symptoms increased the odds of reporting pain (odds ratio (OR) [95% confidence interval (CI)] = 1.47 [1.38–1.58], p = 4.12 × 10−28). Manifested pain had a small effect on increased risk for insomnia (OR [95% CI] = 1.04 [1.01–1.07], p < 0.05). Results were consistent in sensitivity analyses. Conclusions Our findings support a bidirectional causal relationship between insomnia and pain. These data support a further clinical investigation into the utility of insomnia treatment as a strategy for pain management and vice versa. |
| Databáze: | OpenAIRE |
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