Abstract
Striking familial aggregation is found in fibromyalgia (FM) as well as in other chronic pain conditions, leading to the assumption that a genetic component plays an important role in the pathogenesis of this condition. However, as in other complex conditions involving the central nervous system, a polygenic background is most likely. Studies into the genetics of FM initially focused on candidate genes, thus identifying some important markers including genes related to the autonomic nervous system and to neurotransmitters involved in pain processing. Subsequent progress in genetic technology such as the application of genome-wide association studies (GWAS) has added additional insight into the complex genetics of FM. Notably, FM appears to be ultimately the result of an interaction between a genetic predisposition and the deleterious effects of various life triggers, e.g., stress, trauma, and infection. Thus, the novel field of epigenetics is particularly relevant in order to understand the road to transition from health toward the heightened processing of pain which is the hallmark of FM. In this chapter, we will review salient points in the genetics as well as the epigenetics of FM.
Original language | English |
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Title of host publication | Fibromyalgia Syndrome |
Publisher | Springer International Publishing |
Pages | 109-118 |
Number of pages | 10 |
ISBN (Electronic) | 9783030786380 |
ISBN (Print) | 9783030786373 |
DOIs | |
State | Published - 1 Jan 2021 |
Externally published | Yes |
Keywords
- Catechol-O-methyl transferase (COMT)
- Chronic pain
- Epigenetics
- Fibromyalgia
- Genetics
- Genome-wide association studies (GWAS)
- Serotonin transporter gene (SLC6A4)
- Transient receptor and the vanilloid channel 2 gene (TRPV2)