The exact cause of FM is unclear but both genetics and environment appear to play a role in the development of this condition.
Support of genetic association comes from several studies that show first degree relatives of FM patients are 9 times more likely to get the disorder as compared to general population. In addition, genetic studies reveal an association with dysfunction in the serotonergic, dopaminergic, and catecholaminergic pathways involved in pain transmission and modulation. Catecholaminergic pathways include neurotransmitters dopamine, epinephrine and norepinephrine. Dopamine and serotonin are neurotransmitters that affect the way the body interprets pain.
Gene association studies found single nucleotide polymorphism in three genes: gamma-aminobutyric acid receptor subunit-β3 (GABRB3), trace amine receptors (TAAR1) and guanylate binding protein 1 (GBP1) that differed in FM patients and healthy controls.
Environmental factors and infection
These factors may include stress, trauma, and certain infections like Epstein Barr virus and Lyme disease. Studies have also implicated early sexual abuse in development of FM. Evidence suggests the role of cytokines, which are linked to the immune inflammatory process, in the pathogenesis of FM. Pro-inflammatory cytokine such as IL-1RA, IL-6, and IL-8 have been found to be increased in FM patients.