Saying it is psychological or not psychological missed the point (and shows a misunderstanding of both the illness, and the brain). Psychological factors *are* important in ME/CFS, but the symptoms are very physical.

The article links to a Gallup "Employee Burnout: Causes and Cures," study which reports that 76% of employees experience burnout on the job at least sometimes.

But his own bed rest study found no differences in mitochondria and muscles between lc and bed rest patients, and various lc studies have shown that exercise reduces pem in both lc and me patients. The question now is how to use exercise safely.

PS, "one paper" was incorrect of me to say, but it's not possible to edit tweets here.

The paper I mentioned above uses phrases directly from 13 items of the pain catastrophising scale, e.g. “It’s
terrible and I think it’s never going to get any better”, whereas the paper being discussed here only suggests fainting (which is not part of the PCS).

I think you need to look carefully at exactly replicating studies. In this case relevant factors are trait vs temporary catastrophising, and suggesting in increase in pain vs fainting. That would likely give more relevant info about catastrophising.

I do. Replication is everything. See my blog posts. My "view" is simply what has been properly replicated. You shouldn't dismiss science that you dislike.

I think pain catastrophising is pretty well established, and it's a bit strange that you feel the need to debunk it with one cherrypicked paper...

That's just one paper, and weirdly they used fainting rather than pain for the catastrophising. This paper did find that artificially increasing or decreasing catastrophing increased or decreased pain in both healthy volunteers and chronic pain patients. journals.lww.com/pain/abstrac...

It's a bit of a myth that only a small % recover. medium.com/@cfs_researc...

Also it generally depends on the intensity and duration. Most studies show that light exercise doesn't cause PEM whereas a 2-day CPET does. The main problem is that PEM itself is very vaguely defined.

Not for #MEcfs but for rheumatoid arthritis: Successful clinical trial of vagus nerve-mediated neuroimmune modulation: www.nature.com/articles/s41....
Question asked by Eric Topol and Kevin Tracey is: Can this be successfully applied to other diseases? bsky.app/profile/eric...

suggest statistical noise).

I'm a little confused, as it says AVR=CRAE/CRVE. CRVE was identical between all groups, so really it's just CRAE, which you can see above had a p=0.263. And yet the AVR has p=0.001. How is that possible? (I think it's likely due to CRVE differing between the ME and not ME PCS patients, which would

No differences at all between patients and never infected?

But, I don't think that is a useful term. Sure, if you also want to say depression is a biological neuroimmune condition (which is as true as it is saying that for ME). Where does that actually get us?

Yes, the DecodeME study also found gene enrichment mainly in the nervous system (including the brain), and the immune system. Similar findings are seen for depression, and there seems to be an overlap in the gene enrichment findings between ME and depression, according to unpublished data.

That's a study on 9 patients, which hasn't been replicated as far as I'm aware.