the new #fibromyalgia preprint is more interesting than many think, as it is relevant also for #longcovid #mecfs #MCAS narratives Long-standing claim I keep making: fibromyalgia is not “medically unexplained.” Rheumatology has been treating it the way neurology used to treat functional neurological disorder (FND) — as a diagnosis you reach only after everything else is ruled out, rather than a condition with its own mechanism. New preprint (Goebel/Marshall groups, bioRxiv) adds hard mechanistic evidence. IgG purified from FMS patients, transferred into mice, reproduces the core phenotype: mechanical and cold hypersensitivity, reduced locomotion, small-fiber pathology. This isn’t new on its own — what’s new is how. The IgG binds mast cells through the MRGPRX2 receptor, triggering degranulation and IL-6 release. Knock out that receptor, or deplete connective-tissue mast cells, and the FMS phenotype in mice disappears. It doesn’t disappear in a CRPS model treated the same way — so this isn’t a generic “any IgG causes pain” artifact, it’s FMS-specific. Skin biopsies from FMS patients independently showed elevated mast cell density and tryptase staining, consistent with the mouse data. This matters because it reframes FMS from “central sensitization, cause unknown” to “autoantibody-driven mast cell disease, mechanism identified.” That’s the same shift FND went through in neurology over the last 15 years — from “not neurological” to “a real, mechanistically distinct neurological condition” once imaging and physiology studies caught up. Rheumatology hasn’t made that shift yet for FMS, and patients pay the cost of that gap. Where I’ll be precise rather than overreach: this paper does not test an infectious trigger. It establishes the autoimmune/mast-cell mechanism, full stop. Whether that autoimmunity is commonly initiated by a prior infection — molecular mimicry, EBV reactivation, or another post-acute pathway — is a hypothesis that fits the broader post-acute infection syndrome (PAIS) framework, not a finding of this study. That distinction is exactly why we need dedicated centers for complex chronic conditions with a plausible post-infectious origin: to actually test that link prospectively, instead of leaving it as something clinicians argue about anecdotally for another decade.