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

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.

 

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.

 

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.

 

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.

 

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.

 

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.

 

I don't really see the relevance of this to the paper. It is abut a speculative immunological model. I have no evidence on which to base any advice to patients as to what they should do.

 

Thanks again to everyone for the comments. I plan to make some edits but am waiting to see if comments are posted on Qeios. If anyone here with an institution address cares to comment please do. Anyone is allowed to be an expert on Qeios.

 

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]

 

Can people who don't have an institution address post a comment on Qeios?

 

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.

 

I don't know but when people have reviewed my papers they have talked about registering and that may need an institution address.

 

When I tried to sign up it asks for an Orcid ID or «work email address».

 

I just tried registering with my Gmail address. This is the first screen



This is the draft email that following the Click Here link generates:



So it seems not.

 

One doesn't need to be at an institution or anything else to get an Orcid ID. So that way could work.

 

This is what they say on their about page:

Although this random FAQ elsewhere indicates that anyone can sign up:

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:

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?

 

My crystal ball is a bit smudgy.

 

What happens in RA, for example? Are people on rituximab constantly? (Or is RA not a good comparison?)