My research indicates that Fibromyalgia and may be caused by chronic infections and reactive oxygen damage. I will be posting links identifying silent systemic inflammation and detox pathway dysfunctions as a possible contributing risk factors in developing FM. Gastrointestinal Manifestations in Systemic Autoimmune Pathogenic monsters in Chronic Illnesses... Radio: FM cytokines connection? Increased levels of IL-8, 17 and interferon gamma in Fibromyalgia? Interleukin 8 may be a factor in the epithelial tissues damage. Please review these links below... "This analyses showed that fibromyalgia patients have increased levels of IL-17A. They also reveal that plasma concentrations of IL17A correlate with levels of IL-2, IL-4 and IL-10, TNF and IFNγ." CONCLUSIONS: "As far as we are aware, this is the first study to demonstrate increased levels of IL17A in fibromyalgia patients. The positive correlation between the levels of IL-17A and of other cytokines strengthens the hypothesis of the involvement of inflammatory mechanisms in the development of this syndrome. Pernambucomet al. Clin Ex Rheum. 2013 Nov-Dec;31 " Increased levels of IL-17A in patients with fibromyalgia. "Evidence of central inflammation in fibromyalgia-increased cerebrospinal fluid interleukin-8 levels." Abstract "Activation of glia cells resulting in intrathecal elevation of cytokines and chemokines has been hypothesized in chronic pain syndromes such as fibromyalgia. To our knowledge, this is the first study assessing intrathecal concentrations of pro-inflammatory substances in fibromyalgia. We report elevated cerebrospinal fluid and serum concentrations of interleukin-8, but not interleukin-1beta, in FM patients. This profile is in accordance with FM symptoms being mediated by sympathetic activity rather than dependent on prostaglandin associated mechanisms and supports the hypothesis of glia cell activation in response to pain mechanisms." See more here: Evidence of central inflammation in fibromyalgia-increased cerebrospinal fluid interleukin-8 levels.