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      Genetic and epigenetic epidemiology of chronic widespread pain

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          Abstract

          The etiology underlying chronic widespread pain (CWP) remains largely unknown. An integrative biopsychosocial model seems to yield the most promising explanations for the pathogenesis of the condition, with genetic factors also contributing to disease development and maintenance. Here, we conducted a search of studies investigating the genetic and epigenetic epidemiology of CWP through electronic databases including Web of Science, Medline, PubMed, EMBASE, and Google Scholar. Combinations of keywords including CWP, chronic pain, musculoskeletal pain, genetics, epigenetics, gene, twins, single-nucleotide polymorphism, genotype, and alleles were used. In the end, a total of 15 publications were considered relevant to be included in this review: eight were twin studies on CWP, six were molecular genetic studies on CWP, and one was an epigenetic study on CWP. The findings suggest genetic and unique environmental factors to contribute to CWP. Various candidates such as serotonin-related pathway genes were found to be associated with CWP and somatoform symptoms. However, studies show some limitations and need replication. The presented results for CWP could serve as a template for genetic studies on other chronic pain conditions. Ultimately, a more in-depth understanding of disease mechanisms will help with the development of more effective treatment, inform nosology, and reduce the stigma still lingering on this diagnosis.

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          Most cited references 45

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            Human genetics is now at a critical juncture. The molecular methods used successfully to identify the genes underlying rare mendelian syndromes are failing to find the numerous genes causing more common, familial, non-mendelian diseases. With the human genome sequence nearing completion, new opportunities are being presented for unravelling the complex genetic basis of non-mendelian disorders based on large-scale genome-wide studies. Considerable debate has arisen regarding the best approach to take. In this review I discuss these issues, together with suggestions for optimal post-genome strategies.
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              Environmental programming of stress responses through DNA methylation: life at the interface between a dynamic environment and a fixed genome

              Early experience permanently alters behavior and physiology. These effects are, in part, mediated by sustained alterations in gene expression in selected brain regions. The critical question concerns the mechanism of these environmental “programming” effects. We examine this issue with an animal model that studies the consequences of variations in mother-infant interactions on the development of individual differences in behavioral and endocrine responses to stress in adulthood. Increased levels of pup licking/grooming by rat mothers in the first week of life alter DNA structure at a glucocorticoid receptor gene promoter in the hippocampus of the offspring. Differences in the DNA methylation pattern between the offspring of high- and low-lickinglgrooming mothers emerge over the first week of life; they are reversed with cross-fostering; they persist into adulthood; and they are associated with altered histone acetylation and transcription factor (nerve growth factor-induced clone A [NGFIA]) binding to the glucocorticoid receptor promoter. DNA methylation alters glucocorticoid receptor expression through modifications of chromatin structure. Pharmacological reversal of the effects on chromatin structure completely eliminates the effects of maternal care on glucocorticoid receptor expression and hypothalamic-pituitary-adrenal (HPA) responses to stress, thus suggesting a causal relation between the maternally induced, epigenetic modification of the glucocorticoid receptor gene and the effects on stress responses in the offspring. These findings demonstrate that the structural modifications of the DNA can be established through environmental programming and that, in spite of the inherent stability of this epigenomic marker, it is dynamic and potentially reversible.
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                Author and article information

                Journal
                J Pain Res
                J Pain Res
                Journal of Pain Research
                Journal of Pain Research
                Dove Medical Press
                1178-7090
                2017
                24 August 2017
                : 10
                : 2021-2029
                Affiliations
                [1 ]Department of Psychology, University of Zurich, Zurich, Switzerland
                [2 ]Department of Physiotherapy, Health and Rehabilitation Research Institute, Auckland University of Technology
                [3 ]Waitemata Pain Service, Department of Anesthesia and Perioperative Medicine, North Shore Hospital, Auckland, New Zealand
                Author notes
                Correspondence: Andrea Burri, AUT University Health and Rehabilitation Research Institute, School of Clinical Sciences, North Shore Campus, 90 Akoranga Drive, Northcote, North Shore, Auckland 0627, New Zealand, Tel +64 9 921 9999, Email andrea.burri@ 123456aut.ac.nz
                Article
                jpr-10-2021
                10.2147/JPR.S143869
                5584918
                © 2017 Kerr and Burri. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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