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

Jonathan Edwards said:
The false argument is that false or exaggerated signals can be overcome by pushing through. You cannot do that for lupus or RA. It might seem you should be able to for ME/CFS but if there is a loop that amplifies the immune signal further every time you push then you cannot.
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This is the idea the BPS proponents have never understood.

Even when we had no idea at all what that signal might be, the basic concept was understood by patients.
 
Kitty said:
Even when we had no idea at all what that signal might be, the basic concept was understood by patients.
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And this is another reason I don’t think we should consider how some may interpret words or phrases used too much.
Those people who are set in their ways didn’t trust us as reliable witnesses to our own experiences then and likely won't now. It’s a waste of time trying. Focus on those who wll listen not those who won’t.
 
Jonathan Edwards said:
I think it would get too philosophical. My tactic is to introduce some specific negations of popular myths - that autoimmunity is triggered by infection or that ME/CFS involves inflammation. I think that is enough for this paper. People who do not understand the complexity of the puppetry will never understand I am afraid. They are in the majority in immunology and one just has to carry on without them. The sort of discussion we have here you cannot have in an immunology department. You have to have it in a back office with some bottles of wine. When you do a definitive experiment you do to expect most people to understand what it means but you have still made progress in solving the clinical problem.
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I've been thinking some more about this. I think an explanation would be useful for PwME, because the dominance of the BPS model - likely to continue for some time, especially if this is what your immunology colleagues think - mean that we'll need to defend ourselves against this kind of thinking. New PwME especially need to understand why they can't push through, when loads of health practitioners are saying or implying that they can.
 
Sasha said:
New PwME especially need to understand why they can't push through, when loads of health practitioners are saying or implying that they can.
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You don’t have to understand the physics behind a car crash to understand that going at higher speeds is dangerous. I think it’s enough to tell them that most people get worse from pushing through, and that you might get stuck down there.
 
Utsikt said:
You don’t have to understand the physics behind a car crash to understand that going at higher speeds is dangerous. I think it’s enough to tell them that most people get worse from pushing through, and that you might get stuck down there.
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People's mental models of what is going on can be very powerful, though. We read all the time about new PwME who didn't trust their own experience of decline and got repeatedly pushing into overdoing it.
 
Sasha said:
People's mental models of what is going on can be very powerful, though. We read all the time about new PwME who didn't trust their own experience of decline and got repeatedly pushing into overdoing it.
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Yes, but I don’t think complex hypothetical models of neuroimmune interactions are going to help that.

They need to learn to trust and listen to their bodies and symptoms, they are not going to be able to pace without it.

«When you do too much, you just get more symptoms. So if you goal is to be less sick, making yourself more sick isn’t going to help. You might need to cut back on activities and get help from others if you can. You need to adapt to avoid harming yourself.»

At least that’s a rough idea of the message I think needs to be conveyed.
 
Sasha said:
I've been thinking some more about this. I think an explanation would be useful for PwME, because the dominance of the BPS model - likely to continue for some time, especially if this is what your immunology colleagues think - mean that we'll need to defend ourselves against this kind of thinking. New PwME especially need to understand why they can't push through, when loads of health practitioners are saying or implying that they can.
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I think the message that there's no inflammation might be as useful as anything.

Perhaps not for new patients, but for those who've started reading content by researchers and clinicians. They may assume these people are knowledgeable simply because they're not following the BPS paradigm, and a lot of them push inflammation as part of the story.

This isn't to do with symptom management or understanding the research, it's about people not getting into unhelpful or antagonistic relationships with GPs or primary care physicians. Some of those doctors may know nothing much about ME/CFS yet still realise the inflammation angle sounds suspect.

It's a difficult area because patients do know more than their doctors about living with ME/CFS. They can be confident telling their own story about that, and insistent if they need to be. But taking the same approach based on iffy ideas of the biology is never going to wash.

If the research moves on quickly we're going to need those GPs/PCPs on our side.


[Minor edit to correct word order]
 
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I’ve missed if this had has come up in discussion, it’s not referenced in the paper but I came across it in some searches

ME/CFS patients exhibit altered T cell metabolism and cytokine associations (2019) Mandarano, Hanson et al

It’s perhaps less the cell metabolism part as cytokine associations and reduced mitochondrial membrane potential that got me wondering given some thoughts I had on the neurological angle. But I think I need to understand what the paper shows more and may be adding 1 and 2 and getting 5.
 
EndME said:
One doesn't need to be at an institution or anything else to get an Orcid ID. So that way could work.
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This is what they say on their about page:
The ORCID iD: a unique, persistent identifier free of charge to researchers
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Although this random FAQ elsewhere indicates that anyone can sign up:
Anyone can register for an ORCID iD. There is no set of requirements that you have to pass to be classified as a researcher and you do not need an official affiliation
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https://utsouthwestern.libguides.com/orcid/faqORCID Frequently Asked Questions - ORCID Guide - LibGuides at University of Texas Southwestern Medical Center
 
Thanks @Utsikt! I was just able to get an ORCID account and I do not have an instutional email address. I just used my Gmail account address. I just went to the ORCID homepage and followed the instructions. when they asked me my institution and institutional affiliation I put in my university I graduated from and my affiliation was alumni and this was accepted.
 
@Jonathan Edwards, you said on the pre-match thread, when I asked if all the likely treatment drugs would be horrible:

Jonathan Edwards said:
We have a short section on possible treatments but members here will probably be able to suggest a lot more. None of them are guaranteed to be from of horribility since most will suppress aspects of the immune response. But we have found drugs that do, that are safe enough to use routinely.
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You mentioned a while back that endemic Covid had changed the landscape of using (I think) the -mab drugs. Would that apply to the ones that you're thinking about, and that others are proposing? Would they be one-and-done treatments or would we be on them long-term, with our immune systems constantly squashed?
 
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