Deep phenotyping of post-infectious myalgic encephalomyelitis/chronic fatigue syndrome, 2024, Walitt et al

I wonder if we are using language differently.
The paper says that there were 484 inquiries for participation. 267 of those were screened out in initial screening. 217 of those 267 had medical record reviews and a phone interview. 146 of those 217 were excluded after review. 44 people did not complete the review process before COVID shut the study down.

NIIH wanted 40 PwME for the study but couldn't get enough people who met the necessary criteria and didn't have exclusionary factors.
For me, that's different than not be enough people coming forward for the study.

 

If long COVID is like ME/CFS, you will learn nothing until you get to placebo controlled trials, because there's a lot of spontaneous fluctuation up and down. Given that people have had long COVID for max 4 years, there will, again if it's like ME/CFS, be plenty of spontaneous recovery and spontaneous substantial remission. You really won't know until all of that is controlled in a well-run trial.

 

in all honesty im not sure if there is much spontaneous ME remission, and im certainly not holding out for it
there ARE very good placebo trails ongoing thats what im saying, just not by the NIH lol

 

I'm not sure that it's about using language differently.
Brian was concerned about 200 patients who had made contact and got through initial screening who then disappeared and did not return follow up calls. A small proportion of those getting involved would have brought them up to 40. So enough people had come forward and got through first screening.

There was a lot of concern in ME Advocacy groups around 2016 about Walitt's background and somatoform beliefs. Did this affect recruitment? I think it possible indeed likely.

 

FWIW - I am one of the one who was very concerned about Walitt (and Saligan and.....)

 

Me too!

 

While on the ski slope yesterday, I was thinking about the finding that the catechol level correlating the symptom severity. Even though there is no such correlation in HV, it could mean that high dopamine/norepinephrine level can provide some protection against MECFS. i.e., high dopamine/norepinephrine individuals are less likely to develop MECFS, and less severe when they do. That seems to be consistent with the finding that the history of depressive disorder being a predisposing factor for Long COVID. It could also explain why I, a recovered patient, get under the weather after a heavy exercise (post-exercise depression) and become vulnerable to PEM.

 

Astonishing. Again: why does this not happen in every other limiting illness? And ME-like syndrome would be the norm if this were true.

More pertinently, they collected no evidence that allowed them to plausibly speculate along these lines. What they could easily have done is asked their participants if disability or deconditioning inactivity came first as some kind of sensible check - since the patients were there to see the sequence. But they chose not to. this is not science, it's bar room opining.

 

Do we know who from the NIH that was involved in the ME/CFS study will be involved in the LC effort besides Nath and Walitt?

I worry about a research template of sorts being passed down. There is also the Lyme group. And isn't there a new overarching group that looks at several diseases in tandem?

 

Interesting that muscles are considered to be deconditioned when that's the explanation being offered for a person's disabled state, but the same muscles are considered to be working normally when we're talking about "effort preference" and "mismatch between what someone thinks they can achieve and what their bodies perform”?

 

Lots of findings have been critiqued or dismissed on this thread, but I'm interested to know which findings are, well, interesting.

The results below are beyond my powers, but I would really appreciate others' views on them:

 

Just wanting to re-emphasise this because i'm not sure Elanor's mic drop was loud enough

!!!! very interesting indeed...

 

... and it's not going to take him (Rob Wust) anything like 8 years either! ... not if this is anything to go by:

https://twitter.com/user/status/1760992978623959089

 

hahaha this hadn't even occurred to me, but yea. wow. well spotted. jesus!
I know there are so many other concerning issues with this paper which people have already spotted, but does this thing @Eleanor has spotted not expose the Walitt analysis (maybe not the raw data) as completely ridiculous?
Maybe I'm missing some nuance but it seems like he really is attempting to claim that the data shows the study participants had muscle de-conditioning but also simultaneously didn't have muscle de-conditioning. I mean I know that's what @Eleanor has just said.. but yea.. I'm struggling to get my head around someone actually publishing that.. I must be missing something.

 

When you think about it, it is really insane the NIH can publish a study where they say the functional disability is caused by deconditioning, yet at the same time claim exercise wouldn't help.

Even without knowing anything about the history or context of ME, how could anyone approve this paper?

 

Sharing in here if not already shared.

Live Science: '''It took the rug right out from under my life': Milestone ME/CFS study begins to explain disease, but will it lead to treatments?’'

NPR: 'Clues to a better understanding of chronic fatigue syndrome emerge from a major study'

MedPage Today: "Brain Dysfunction, Immune Abnormalities Seen in Post-Infectious Chronic Fatigue — Deep phenotyping study provides new clues about ME/CFS"

 

My guess is that the lack of coherence is due to different authors having different opinions.

 

similar study --- as in an fMRI---Long Covid study?
At the very least the study should be conducted in a way which tests whether the fMRI signal is just an artifact e.g. by including people with other diseases (rather than just healthy controls) --- larger umbers ---. But yes, the illogical way this study has been promoted as finding that it's "effort preference", rather than aberrant signalling, doesn't inspire confidence.