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  1. Simon M

    How should biological researchers present their results about ME/CFS to the media - discussion thread.

    I agree, and that's why I was joining the discussion GWAS are good at providing causal evidence. If there is a link to anxiety-related genes, or other relevant jeans – even if subthreshold in. DecodeME – that coup support the BPS claim to a degree. They've always accepted that they are...
  2. Simon M

    How should biological researchers present their results about ME/CFS to the media - discussion thread.

    Sorry, I see what you mean. I'm not sure what case BPS proponents would make, so this feels like shadow boxing. And I don't think we can award the non-BPS view a knockout win without knowing BPS arguments. I expect that, at least, they would argue for the 'success' of CBT (which takes us back to...
  3. Simon M

    How should biological researchers present their results about ME/CFS to the media - discussion thread.

    ? I'm not sure what you said, I was responding to Robert.. But is surely depends on the results. If anxiety-related genes show up in DecodeME, or at least are prominent if not significant at the threshold, wouldn't that make it hard to rule out a role for them? (I don't know what the results...
  4. Simon M

    How should biological researchers present their results about ME/CFS to the media - discussion thread.

    I think it might be quite difficult to prove that there isn't a substantial role for the mind. My reading of CBT in particular is that it's built on the idea of anxiety about symptoms. So you might expect to see anxiety-related genes in a GWAS. Possibly, you would expect to see such things as...
  5. Simon M

    How should biological researchers present their results about ME/CFS to the media - discussion thread.

    I think that's the most important point. Based on the discussion here, it's still not clear what the best way is to respond , or how best to present an argument. I am very wary of the risk going down mind/body rabbit holes. I think we can be sure that those wedded to a psychosocial...
  6. Simon M

    Who is Simon Wessely?

    I'm sure that's the journal, so that must be it, thanks.
  7. Simon M

    Who is Simon Wessely?

    I suspect this has been covered before, but I'm looking for a paper/journal piece penned by SW, possibly in 1999 (maybe later). In it, IIRC, he reflects on how the BPS model has held up and concludes, 'pretty well', though he concedes that his original suggestion that CFS was a form of...
  8. Simon M

    Neurodevelopment Genes Encoding Olduvai Domains Link Myalgic Encephalomyelitis to Neuropsychiatric Disorders, 2025, Lidbury et al

    Abstract: >We applied this method to a very homogeneous sample of patients belonging to a unique and clinically well-characterized multigenerational pedigree with one of the most severe forms of early onset AD, carrying the PSEN1 p.Glu280Ala mutation (often referred to as E280A mutation), which...
  9. Simon M

    Neurodevelopment Genes Encoding Olduvai Domains Link Myalgic Encephalomyelitis to Neuropsychiatric Disorders, 2025, Lidbury et al

    I will be interested to see how this holds up in DecodeME. With only 77 cases, the WES looks underpowered to me.
  10. Simon M

    Unwilling or unable? Interpreting effort task performance in myalgic encephalomyelitis/chronic fatigue syndrome, 2025, Kirvin-Quamme et al

    An SF 36 physical function of under 30 is lower than usual in clinical cohorts, I think. IIRC, the pace trial was mid 30s. Similarly, 97.5 is above average for the population. Maybe that's because it's specifically healthy controls, but it looks like there's been no attempt to control for...
  11. Simon M

    Preprint Indistinguishable mitochondrial phenotypes after exposure of healthy myoblasts to myalgic encephalomyelitis or control serum, 2025, Ryback et al

    I think that's the key point: we need replication. These are all interesting findings. But there are hundreds, if not thousands, of interesting findings out there. Almost none of them have been replicated, so we can't rely on them. What we need are more independent replications, like this...
  12. Simon M

    Webinar 2pm today (Friday 6 June 2025): Genetics Centre of Excellence (Edinburgh Ponting lab): update on recent research

    Maybe it's that, I think I've seen a presentation suggesting the trials would be underway by now. I thought I'd also read that they had sorted the genetic test they need to identify sub groups protesting. But I haven't seen any confirmation that those trials are in progress – that was an...
  13. Simon M

    Webinar 2pm today (Friday 6 June 2025): Genetics Centre of Excellence (Edinburgh Ponting lab): update on recent research

    I find that surprising, even though the combinatorial method, in theory, is able to find true results from much smaller samples. The big problem I see in saying that a gene or genes explains the symptom of any subgroup is that these are SNPs. Snips are common variants , which indicates they...
  14. Simon M

    Preprint Indistinguishable mitochondrial phenotypes after exposure of healthy myoblasts to myalgic encephalomyelitis or control serum, 2025, Ryback et al

    I don't know how significant this is. I quite often don't have symptoms at rest, but I always have the problem of minimal exertion exhausting me. In other words, if the problem was that something in my blood was stopping my mitochondria working properly, I would've expected that something in the...
  15. Simon M

    Webinar 2pm today (Friday 6 June 2025): Genetics Centre of Excellence (Edinburgh Ponting lab): update on recent research

    I didn't hear the talk, but understand that she and @chillier attempted to replicate the most robust/replicable 'something in the blood' finding, and could not Negative replication results are so important because they stop the field from having endless possible theories. Culling things that...
  16. Simon M

    National patterns of age of ME/CFS onset

    As we have year of onset, we could look at 2009/10 in isolation.
  17. Simon M

    Preprint A Proposed Mechanism for ME/CFS Invoking Macrophage Fc-gamma-RI and Interferon Gamma, 2025, Edwards, Cambridge and Cliff

    Thanks for bearing with me, @Jonathan Edwards. My brain is in slightly bit of shape this evening, so I’ll try one more post. my brain is doing better this evening, so I’ll try again in response to your points. First of all, it would be wonderful if everything amounts to signalling issues –...
  18. Simon M

    Preprint A Proposed Mechanism for ME/CFS Invoking Macrophage Fc-gamma-RI and Interferon Gamma, 2025, Edwards, Cambridge and Cliff

    Yes and no - for me at least pain and fatigue and not the only thing that limit our ability. This goes to the heart of psychosocial and biopsychosocial views of the world and what we need to do to recover, at least as I understand them. I hope I make more sense below: Pain and fatigue exist...
  19. Simon M

    National patterns of age of ME/CFS onset

    Thanks. That’s possible, though the participation rate was lower than for the Nordic countries, and my understanding is that The survey was promoted by the main ME organisation. I’m guessing If this happened, we might see it in the age survey, Which we will look at, as above.
  20. Simon M

    National patterns of age of ME/CFS onset

    Good question – we have the information and will check ( from memory, countries were pretty similar, but my memory isn’t so good).
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