***in August 2021, Goebel after a mouse-study said fibromyalgia is (only) autoimmune, so some of us hawked that. But Martínez-Lavín commented: perhaps partly.That is what I also think, feeling the mitochondrial/ATP-hypothesis explains my symptoms better than the CSS-hypothesis one, but that all three may be relevant to explain the wide variance in FM, also the 5 other hypotheses and the 6 biomarkers I’ve listed on my cause/trigger list to date and more.
As already ‘hidden’ in my cause/trigger references since it was published and interviews were given in August 2021, Goebel et al published a study this summer with findings that mice with human fibromyalgia-immunoglobulines got a few fibromyalgia-like symptoms and Goebel then championed FM to therefore ’be’ autoimmune. The study found that IgG from a few fibromites causes “sensitivity to pressure and cold” and reduces “movement grip strength” in mice, and autoimmune-treatment helped.
In August, so shortly after Goebel’s results were published, Martínez-Lavín commented “Is fibromyalgia (primarily) an autoimmune illness?” “perhaps sort of”: “Goebel et al.’s provocative study supports our reiterated proposal of DRG [dorsal root ganglia] as the key neural hub where different fibromyalgia-inducing stressors, including autoimmune illnesses, are converted into neuropathic pain”. “More research is needed to define if fibromyalgia is a localized autoimmune illness.” And ends nicely “We are transiting from an era of misogynistic disbelief of fibromyalgia structural underpinning to a time of innovative research based on well-structured scientific evidence.”
Researchers see their’s more than the whole picture of our variety. They haven’t really got any other chance to find a starting point. But any hopes that their ideas are anywhere close to helping us much will be disappointed. I prefer not to put my hopes there, instead in that they are doing their best, that a lot of them are working on it, and in my own ‘treatment trials’.