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Why did they only study 350 out of the 20,000+ participants?

Lol, that has some funny implications: Ants have an expectation of death, but certain jellyfish and lobsters don’t. Dogs live shorter lives than us because they expect to die sooner. We should never tell anyone they have a terminal diagnosis because that might speed things up.

Ugh, I don’t believe she has a good understanding of LC or ME/CFS at all. It looks a lot like what I thought of both diagnoses after around one year, and I was wrong about pretty much everything. It seems to me like she’s had some kind of PVF based on how she says that she didn’t fit some of...

It looks like they might have only done a submaximal CPET: Current optimal treatment to avoid PEM in patients with long COVID includes avoiding overexertion, and as such, long COVID participants were instructed to avoid exercise above the heart rate at the first ventilatory threshold. This was...

They are essentially saying: We accepted the model as true without actually checking. We’ve now checked, and we concluded that it isn’t true. But we still want to use it. So they’ve essentially showed that they have no integrity at all.

It seems like they just put the set of genes into something calles ToppGene Suite and reported to result.

Tearing down societal barriers to being able to work is a good thing, but you have to be pretty tone deaf or ignorant if that’s what you propose as a solution for something like post covid ME/CFS.

Ah, Xitter always confuses me with their ordering. So we could be looking at a Rituximab style placebo? No way to tell, really

I wish he included an ‘this is obviously just an unblinded n=1’ disclaimer. And ‘chronic disease’ could mean anything.

I wonder how HRV would correlate with PEM if you never get close to your VT1, e.g. low intensity physical activities over a long period of time. Surely that could also trigger PEM?

I believe they did some live measurements of nerves and lots of probing and insertion of instruments. There are some diagrams in the figures.

I believe these are the questions of SSD-12. No wonder they correlate with anxiety etc. ————— Q1_I think my somatic symptoms are due to a serious illness Q2_I am very concerned about my health Q3_My health concerns hinder me in daily life Q4_I am convinced my symptoms are serious Q5_My...

Several criticisms of the BPS model can be distinguished: it is vague and not testable (5, 44–46); too general and eclectic (46, 47); a mere juxtaposition of causal factors without an integrative framework (48, 49); and not methodological and inapplicable in daily practice (22, 45, 50)...

THF-beta was mentioned here (I have no idea about the relevance): https://www.s4me.info/threads/tgf%CE%B2-links-ebv-to-multisystem-inflammatory-syndrome-in-children-2025-goetzke-et-al.43084/

They’ll just spin it as another win for the gut-brain-axis and neuroplasticity.

If we could get them to stop exploring disproven hypotheses it would be a good start. Putting more money into bad research will probably only do harm.

Risking harm from an infection in order to decrease the likelihood of harm from an infection seems kind of backwards to me.

It seems like they might be trying to gently shut down the lunacy of ‘immunity debt’.

Do they speculate about the reasons for the increase in severity?

Anything on what the clinic is supposed to do for the patients?