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  1. Jonathan Edwards

    If you have one autoimmune disease (or immune mediated disease) is it more or less likely that you will have another one?

    Sort of. One autoantibody loop could explain all three probably. But always nice to see my treatment in the news. ;)
  2. Jonathan Edwards

    [IgG] Complexes from infectious ME/CFS, including post-COVID ME/CFS Disrupt Cellular Energetics and Alter Inflammatory Marker Secretion, 2026, Prusty+

    Was that actually shown? It is a highly implausible claim. A small proportion of IgG gets into cells. Endothelial cells can internalise IgG using Fc receptors if I remember rightly.
  3. Jonathan Edwards

    ME/CFS Atlas site

    I wish I knew but I have a rough idea of what sort of thing it might be. The link to viral infection suggests to me that immune signals such as cytokines are being generated as part of an immune response and that for some reason these persist. My work in the past was on autoimmune diseases and...
  4. Jonathan Edwards

    Epigenetics, Telomeres and ME/CFS

    Epigenetics is just the study of changes in DNA that do not involve changes in the nucleotide base sequence of the genes as such. Changes of this sort are going on all the time every day, in responses to food, temperature, exercise and in cell maturation from stem cells and all sorts of other...
  5. Jonathan Edwards

    Problems arising for pwME from additional diagnoses of MCAS, hEDS and POTS. Advocacy discussion.

    But we are not talking about information from NHS or NIH. The NHS view is biopsychosocial and so is NIH. There is also widespread access to poor quality research - which is the problem here. Stuff put out by advocacy organisations that are happy to promote nonsense offered by fringe clinicians -...
  6. Jonathan Edwards

    ME/CFS Atlas site

    Norway has actually produced much of the best innovative science in ME/CFS - epidemiology and Fluge and Mella's work. The Norway Health Institute is 'behind' the UK NICE guidelines maybe but our College of Physicians takes much the same view as the Norway Institution under Signe Flottorp. So the...
  7. Jonathan Edwards

    Hypothesis A hypothesis connecting dysgeusia due to defects in ATP-P2X3 signaling and fatigue in [ME/CFS]: lessons learned from long-COVID,2026, Srinivasan et al

    As far as I can see type II taste receptors are true taste buds - mediating salt an umami etc. In Covid I understood that the problem was with olfactory receptors. Most loss of taste called 'dysgeusia' is based on olfactory problems. I cannot see it likely that type II receptors are a problem...
  8. Jonathan Edwards

    ME/CFS Atlas site

    I agree that it is not a reason to reject your material. And you have made an impressive response to the S4ME fusillade! I learnt about ME/CFSS for the first time in around 2015 as well but had the advantage of having been an academic physician working on chronic disabling disease for a...
  9. Jonathan Edwards

    ME/CFS Atlas site

    The objectives are worthy. My first concern is that we do not who is writing this (I don't think). The more I am involved with advocacy the more I think we should all say who we are. The text i have looked at does not stand up to the standards aimed at. The pieces on What is ME/CFS?, PEM and...
  10. Jonathan Edwards

    Preprint Initial findings from the DecodeME genome-wide association study of myalgic encephalomyelitis/chronic fatigue syndrome, 2025, DecodeMe Collaboration

    My limited unserstanding is that DecodeME will have only produced a signal for these genes if there are relatively common SNP variants that alter function. If deficient function is only associated with rather rare variants then that would be missed I think. It raises th point that maybe has not...
  11. Jonathan Edwards

    Anidulafungin (IV antifungal)

    Yes, or at least be overt enough to be readily identified.
  12. Jonathan Edwards

    Anidulafungin (IV antifungal)

    Fungal infections in the immunodeficient tend to be life threatening and either progress to fatality or are successfully eradicated. I don't see the relevance to ME/CFS really.
  13. Jonathan Edwards

    Preprint Identification of Novel Reproducible Combinatorial Genetic Risk Factors for [ME] in [DecodeME Cohort] and Commonalities with [LC], 2025, Sardell+

    There isn't really anything to test. For each gene there were some people in DecodeME with one variant and others without. The proportions were statistically skewed a bit for a few. But there is no way of knowing in someone with a variant that cropped up more in DecodeME whether it had anything...
  14. Jonathan Edwards

    Anidulafungin (IV antifungal)

    Not really. If fungi were responsible they would have shown themselves in at one of tens of thousands of people with ME/CFS who has had medical attention. Just now and again at least they would have got out of hand enough to show. I actually think you can discount this.
  15. Jonathan Edwards

    Serum BAFF and APRIL Levels, T-Lymphocyte Subsets, and Immunoglobulins after B-Cell Depletion Using Rituximab in MECFS 2016 Lunde Fluge

    That preprint looks a confused muddle to me. I wouldn't take it as evidence of BAFF being worth blocking in ME/CFS.
  16. Jonathan Edwards

    Serum BAFF and APRIL Levels, T-Lymphocyte Subsets, and Immunoglobulins after B-Cell Depletion Using Rituximab in MECFS 2016 Lunde Fluge

    I think this is just a reflection of the pharmacodynamics of rituximab (which didn't work). I don't see any reason to follow up. I isn't telling us anything about ME/CFS.
  17. Jonathan Edwards

    Anidulafungin (IV antifungal)

    Only to the extent that it is conceivable that the editor of the Guardian is a Moldovan spy, I think. You can conceive it, but we don't have any reason to ponder it very long! Infections do not cause autoimmunity, generally speaking.
  18. Jonathan Edwards

    Review Mechanisms of action of therapeutic exercise for knee and hip OA remain a black box phenomenon: an (IPD) mediation study..., 2023, Runhaar et al

    A useful analysis. I can now point out that not only is the claim that exercise works for OA likely due to bias but that even if it helps it doesn't do anything to strength and control (which are the explanations always given).
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