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      Genetic correlations between pain phenotypes and depression and neuroticism

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          Abstract

          Correlations between pain phenotypes and psychiatric traits such as depression and the personality trait of neuroticism are not fully understood. In this study, we estimated the genetic correlations of eight pain phenotypes (defined by the UK Biobank, n = 151,922 to 226,683) with depressive symptoms, major depressive disorders and neuroticism using the the cross-trait linkage disequilibrium score regression (LDSC) method integrated in the LD Hub. We also used the LDSC software to calculate the genetic correlations among pain phenotypes. All pain phenotypes, except hip pain and knee pain, had significant and positive genetic correlations with depressive symptoms, major depressive disorders and neuroticism. All pain phenotypes were heritable, with pain all over the body showing the highest heritability ( h 2 =0.31, standard error=0.072). Many pain phenotypes had positive and significant genetic correlations with each other indicating shared genetic mechanisms. Our results suggest that pain, neuroticism and depression share partially overlapping genetic risk factors.

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          Shape shifting pain: chronification of back pain shifts brain representation from nociceptive to emotional circuits.

          Javeria A Hashmi, Marwan N Baliki, Lejian Huang … (2013)
          Chronic pain conditions are associated with abnormalities in brain structure and function. Moreover, some studies indicate that brain activity related to the subjective perception of chronic pain may be distinct from activity for acute pain. However, the latter are based on observations from cross-sectional studies. How brain activity reorganizes with transition from acute to chronic pain has remained unexplored. Here we study this transition by examining brain activity for rating fluctuations of back pain magnitude. First we compared back pain-related brain activity between subjects who have had the condition for ∼2 months with no prior history of back pain for 1 year (early, acute/subacute back pain group, n = 94), to subjects who have lived with back pain for >10 years (chronic back pain group, n = 59). In a subset of subacute back pain patients, we followed brain activity for back pain longitudinally over a 1-year period, and compared brain activity between those who recover (recovered acute/sub-acute back pain group, n = 19) and those in which the back pain persists (persistent acute/sub-acute back pain group, n = 20; based on a 20% decrease in intensity of back pain in 1 year). We report results in relation to meta-analytic probabilistic maps related to the terms pain, emotion, and reward (each map is based on >200 brain imaging studies, derived from neurosynth.org). We observed that brain activity for back pain in the early, acute/subacute back pain group is limited to regions involved in acute pain, whereas in the chronic back pain group, activity is confined to emotion-related circuitry. Reward circuitry was equally represented in both groups. In the recovered acute/subacute back pain group, brain activity diminished in time, whereas in the persistent acute/subacute back pain group, activity diminished in acute pain regions, increased in emotion-related circuitry, and remained unchanged in reward circuitry. The results demonstrate that brain representation for a constant percept, back pain, can undergo large-scale shifts in brain activity with the transition to chronic pain. These observations challenge long-standing theoretical concepts regarding brain and mind relationships, as well as provide important novel insights regarding definitions and mechanisms of chronic pain.
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            Neuroticism and common mental disorders: meaning and utility of a complex relationship.

            Johan Ormel, Bertus Jeronimus, Roman Kotov … (2013)
            Neuroticism's prospective association with common mental disorders (CMDs) has fueled the assumption that neuroticism is an independent etiologically informative risk factor. This vulnerability model postulates that neuroticism sets in motion processes that lead to CMDs. However, four other models seek to explain the association, including the spectrum model (manifestations of the same process), common cause model (shared determinants), state and scar models (CMD episode adds temporary/permanent neuroticism). To examine their validity we reviewed literature on confounding, operational overlap, stability and change, determinants, and treatment effects. None of the models is able to account for (virtually) all findings. The state and scar model cannot explain the prospective association. The spectrum model has some relevance, especially for internalizing disorders. Common causes are most important but the vulnerability model cannot be excluded although confounding of the prospective association by baseline symptoms and psychiatric history is substantial. In fact, some of the findings, such as interactions with stress and the small decay of neuroticism's effect over time, are consistent with the vulnerability model. We describe research designs that discriminate the remaining models and plea for deconstruction of neuroticism. Neuroticism is etiologically not informative yet but useful as an efficient marker of non-specified general risk.
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              Unpacking the burden: understanding the relationships between chronic pain and comorbidity in the general population.

              Clare H Dominick, Fiona M Blyth, Michael K. Nicholas (2012)
              We investigated the association of chronic pain with physical and mental comorbidity in the New Zealand population by measuring chronic pain status separate from comorbid conditions. Models of allostatic load provided a conceptual basis for considering multi-morbidity as accumulated comorbid load and for using both discrete conditions and cumulative measures in analyses. The nationally representative cross-sectional survey data included self-reported doctor-diagnosed chronic physical and mental health conditions, Kessler 10-item scale scores, an independent measure of chronic pain, and sociodemographic characteristics. The population prevalence of chronic pain is 16.9%, and a quarter (26%) of the population report 2 or more comorbid physical conditions statistically associated with chronic pain (unadjusted P<0.01). Results indicate that accumulated comorbid load is independently associated with chronic pain. Six physical conditions independently associated with chronic pain (adjusted odds range from 1.4 to 3.9) increase the risk of chronic pain in an additive manner, and residual accumulated load further increases risk for 2 or more conditions (adjusted odds 1.6). Anxiety/depression interacts synergistically with arthritis and neck/back disorders to increase the odds of reporting chronic pain beyond an additive model. This synergistic effect is not apparent for other conditions or for additional comorbid load. Results imply that measurement of chronic pain independent of comorbid conditions and adjustment for comorbid conditions is important for more accurate prevalence estimates and understanding relationships between conditions. Future epidemiological research might usefully incorporate independent measurement of chronic pain alongside adjustment for specific physical and mental health conditions as well as accumulated comorbid load. Copyright © 2011 International Association for the Study of Pain. All rights reserved.
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                Author and article information

                Journal
                Journal ID (nlm-journal-id): 9302235
                Journal ID (nlm-ta): Eur J Hum Genet
                Journal ID (iso-abbrev): Eur. J. Hum. Genet.
                Title: European journal of human genetics : EJHG
                ISSN (Print): 1018-4813
                ISSN (Electronic): 1476-5438
                Publication date Nihms-submitted: 28 September 2019
                Publication date (Electronic): 29 October 2019
                Publication date (Print): March 2020
                Publication date PMC-release: 20 February 2020
                Volume: 28
                Issue: 3
                Pages: 358-366
                Affiliations
                [1 ]Division of Population Health and Genomics, School of Medicine, University of Dundee, Dundee, UK, DD2 4BF
                [2 ]Division of Psychiatry, Edinburgh Medical School, University of Edinburgh, Edinburgh, UK, EH10 5HF
                [3 ]Centre for Cognitive Ageing and Cognitive Epidemiology, Department of Psychology, University of Edinburgh, Edinburgh, UK, EH8 9JZ
                Author notes
                [* ]Corresponding author: Weihua Meng w.meng@ 123456dundee.ac.uk , Address: Division of Population Health and Genomics, School of Medicine, University of Dundee, Dundee, UK, DD2 4BF. Tel.: +44 1382383419; fax: +44 1382383802
                Article
                Manuscript ID: EMS84501
                DOI: 10.1038/s41431-019-0530-2
                PMC ID: 7028719
                PubMed ID: 31659249
                SO-VID: 606998ba-b296-4c3d-bf7e-01609225e158
                License:

                Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms

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                Subject: Article

                ScienceOpen disciplines: Genetics
                Keywords: genetic correlation,pain,genome-wide association study,uk biobank,depression,neuroticism
                Data availability:
                ScienceOpen disciplines: Genetics
                Keywords: genetic correlation, pain, genome-wide association study, uk biobank, depression, neuroticism

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