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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.

Genetic and epigenetic epidemiology of chronic widespread pain