Symptoms of depression in chronic pain: prevalence in UK Biobank and shared genetic factors
Casey, H.; Adams, M. J.; McIntosh, A. M.; Fallon, M. T.; Smith, D. J.; Strawbridge, R. J.; Whalley, H. C.
Show abstract
Background Chronic pain and depression are leading causes of disability and frequently co-occur. Depression presents with diverse symptoms, but despite this variability, the prevalence of individual depressive symptoms in chronic pain and the genetic and causal associations linking these traits remain poorly characterised. Methods Using data from 142,688 age- and sex-matched UK Biobank participants, we compared depressive symptom severity levels and item-level Patient Health Questionnaire-9 (PHQ-9) prevalences, spanning affective, cognitive and somatic domains, between participants with and without chronic pain. Using genome-wide association study (GWAS) summary statistics of multisite chronic pain (MCP), major depressive disorder (MDD), and individual symptoms of depression, genetic correlations and bidirectional causal effects between MCP and depressive phenotypes (MDD and individual symptoms) were estimated via linkage disequilibrium score regression (LDSC) and two-sample Mendelian randomisation (MR), respectively. Results Depression (at every severity level) was more common in the chronic pain group compared to controls, with the largest between-group difference for severe symptoms (7.50-fold increase). All individual depressive symptoms were at least 2.79 times as prevalent in chronic pain. Additionally, chronic pain had a significant and positive genetic correlation with MDD (rg = 0.59) and all depressive symptoms (rg = [0.24, 0.55]). MR supported a bidirectional causal association between MCP and MDD (MCP[->]MDD: OR = 1.85, pFDR < 0.001, MDD[->]MCP: {beta} = 0.17, pFDR < 0.001). At the symptom level, MR indicated bidirectional effects between MCP and anhedonia (MCP[->]anhedonia: OR = 1.60, pFDR < 0.001, anhedonia[->]MCP: {beta} = 0.08, pFDR = 0.005), and unidirectional effects of MCP on appetite/weight gain (OR = 1.90, pFDR = 0.022) and appetite/weight loss (OR = 1.63, pFDR = 0.005), concentration problems (OR = 1.63, pFDR = 0.044), and suicidal thoughts (OR = 1.46, pFDR = 0.021). Additionally, genetic liability to concentration problems was associated with a lower risk of MCP ({beta} = -0.04, pFDR = 0.022). Conclusion Chronic pain is associated with a marked depressive burden spanning all symptom domains. Shared genetic architecture and symptom-specific causal pathways, particularly involving anhedonia, highlight potential targets for improved treatment of comorbid chronic pain and depression.
Matching journals
The top 6 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- Stress, Epigenetic Remodeling and FKBP51: Pathways to Chronic Pain Vulnerability 92%
- Polygenic risk for immuno-metabolic markers and specific depressive symptoms: A multi-sample network analysis study 92%
- Blood Immuno-metabolic Biomarker Signatures of Depression and Affective Symptoms in Young Adults 92%
Similar papers in this journal
- Endogenous modulation of pain relief: evidence for dopaminergic but not opioidergic involvement 93%
- Protective role of neuronal and lymphoid cannabinoid CB2 receptors in neuropathic pain 93%
- Instructions and experiential learning have similar impacts on pain and pain-related brain responses but produce dissociations in value-based reversal learning 92%
Similar papers in this journal
- Integrating HiTOP and RDoC Frameworks Part II: Shared and Distinct Biological Mechanisms of Externalizing and Internalizing Psychopathology 93%
- A computational approach to understanding effort-based decision-making in depression 90%
- A Multivariate Genome-Wide Association Study Reveals Neural Correlates and Common Biological Mechanisms of Psychopathology Spectra 90%
Similar papers in this journal
- Adolescents with non-suicidal self-injury exhibit increased pain empathic neural reactivity and personal distress to physical but not affective pain 91%
- Glycoprotein Acetyls and Depression: testing for directionality and potential causality using longitudinal data and Mendelian randomization analyses 91%
- Genomics-based identification of a potential causal role for acylcarnitine metabolism in depression 89%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.