Genetic Factors Explain the Association Between Pain Catastrophizing and Chronic Widespread Pain - 30/08/17
Abstract |
Abstract |
This study aimed to clarify whether there are shared genetic and/or environmental factors explaining the strong link between pain catastrophizing (PC) and chronic widespread pain (CWP). Data were available for N = 1,109 female twins from TwinsUK. Information on self-reported CWP and PC was subject to variance component twin analysis. Heritabilities were 40% for PC and 77% for CWP. The genetic correlation between PC and CWP was .40%, whereas no evidence of an environmental correlation could be detected (.0). According to the best-fitting additive genetic, non-shared environmental (AE) Cholesky model, an additive genetic factor loading on PC as well as CWP, as well as an additive genetic factor loading on CWP alone was found. In terms of environmental influences, 2 individual environmental factors could be identified, loading separately on PC and CWP. Overall, the results add to the knowledge on the nature of CWP and the basis of its close relationship with PC by suggesting a shared genetic etiological structure. The findings highlight a potential avenue for future research and may provide useful insight for the clinical management of pain and pain coping.
Perspective |
Results suggest a shared genetic etiological structure between CWP and PC with no shared influence of environmental factors. Clinicians should be aware of this biological link within the context of clinical management of pain and pain coping.
Le texte complet de cet article est disponible en PDF.Highlights |
• | Genes explain approximately 40% of the variance in pain catastrophizing (PC). |
• | The correlation between PC and chronic widespread pain (CWP) was .14. |
• | PC and CWP share a genetic etiology. |
• | The environmental factors influencing PC and CWP are distinct. |
Key words : Pain catastrophizing, chronic widespread pain, twins, genetics, etiology
Plan
| F. Williams is supported by the EU FP7 project Pain_OMICS and has grant support from Arthritis Research UK (grant number 20682) and the Chronic Disease Research Foundation. TwinsUK is supported by the Wellcome Trust; European Community's Seventh Framework Programme (FP7/2007-2013). The study also receives support from the National Institute for Health Research-funded BioResource, Clinical Research Facility, and Biomedical Research Centre based at Guy's and St Thomas' NHS Foundation Trust in partnership with King's College London. S. Ogata is supported by JSPS KAKENHI grant 15J03698. |
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| The authors have no conflicts of interest to declare. |
Vol 18 - N° 9
P. 1111-1116 - septembre 2017 Retour au numéro
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