USA: National Institutes of Health (NIH) intramural ME/CFS study

Moved posts

I have had access to the NIH intramural study report but it is embargoed until next week. We can have a full discussion then.

I think it may be useful to examine their attempts to analyse brain activity and the role of sympathetic drive. I am not convinced so far that they are not looking at an artefact of being a test subject in a study. That could be overcome with studies of a range of other conditions.

Another thing that struck me, which might also be of relevance to DecodeME, is that they gathered quite a big cohort of people who had been told they had ME but did not fit criteria in the end. For the NIH study it was much bigger than the studied cohort. I think there would be very valuable information in studying these 'not quite ME' subjects to see to what extent they are different from ME subjects. In other words rather than simply bemoaning the inconsistency of diagnostic criteria for studies we should exploit the grey area to find out what is specific and what is not.

 

"For the NIH study it was much bigger than the studied cohort." --- NIH study?
EDIT - the Nath (NIH) study?

Thank you very much - I'll need to think about your reply (you're way ahead of me - great!). I think I noticed sleep studies - another option?

 

Thank you, @B_V

 

We will no doubt debate it at length next week!

 

Sounds like another nightmare about to hit us.

 

I wonder if Nath found cases where it looked like ME but was "X" and "X" is treatable?

 

It doesn't have to be. Stress is by definition a response to a threat. If the autonomic nervous system is screwed up by something like dysregulated cholinesterase (a bit like the screwed up AChR in myasthenia) then the effects could stop people in their tracks in the absence of any current threat. And lymphocytes have ACh receptors.

 

I suspect I have postexertional sympathetic overactivation. I think it's just a consequence of exertion being somehow physically more stressful than normal, so it triggers these threat responses. Prolonged upright posture also triggers it. Maybe that is an important clue: a manifestation of suboptimal perfusion?

The psychosomatic theorists are detached from reality and so full of their ideas that they can't listen and observe what is really happening in this illness.

 

Thank you very much for the insight.

OK my standard post (no need to reply!) would this be expected to have a genetic signature i.e. DecodeME or a rare genetic variant (whole genome sequence) study?

EDIT - "dysregulated cholinesterase" - "Gulf War" syndrome comes to mind!

Further EDIT(!) "lymphocytes" have they been shown to be relevant?

 

Don't know e.g. "dysregulated cholinesterase" (see Jonathan's comment) was raised re Gulf War syndrome ---

 

It's not clear from the comment if the NIH paper found anything in relation to cholinesterase or if this is just speculation based on the finding of sympathetic overactivation and what could be causing that.

 

I agree.
Interesting though (for me) that they struggled to find "true ME/CFS" i.e. many (/most?) didn't meet the criteria. I think Jonathan's comment, re this "grey" area being useful, is interesting.

 

Wasn't it. I'd assumed a good number of the exclusions could be due to comorbidities / medication / recent surgery / ongoing investigation / pregnancy or fertility treatment / etc, but it would be puzzling if that wasn't the case.

 

Interesting ---comorbidities --- cause or consequence or unrelated? If unrelated then presumably those with that [co-occurring] disease have the same incidence of ME/CFS as the rest of the population -- 0.4% or whatever?

I think the problem with PEM is that it's based on a questionnaire --- although maybe that's accurate?

 

Presume she means 5am Eastern so 10am GMT. https://twitter.com/user/status/1760022540037034066

 

People with co-morbidities might be excluded from some trials because they have diseases with overlapping symptoms, so it's not possible to say for certain which of them is causing Symptom X or Y. This could make the results of some studies unacceptably muddy.

I wasn't even sure I'd able to take part in DecodeME because I have psoriatic arthritis, which can cause severe fatigue during active phases. Also, my medication has side effects in some people that might be confused with ME symptoms. (In the end I was invited to submit a sample, but the disease might rule me out of some types of trial, specially if medication's involved.)

 

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