Discriminating Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and comorbid conditions using metabolomics in UK Biobank, 2024, Huang et al

Can @melb and/or @DMissa comment a bit more on how the findings of Huang et al. 2024 link in with those of Missailidis, Armstrong et al. 2026 in simple terms please? (I'm aware team members overlap!)

I see these mentions of Huang 2024 in Missailidis 2026:


I'd like to hear more, in layman's words, of what you think of the Huang 2024 findings in light of Missailidis 2026?
The broad strokes that align are mentioned briefly in the paper but are left there. Didn't want to harp on about it too much because it would just be supposition. Can't make any confident or specific comment without more data. If we have primary cell data linked with biofluid data, collected together from the same people, it may be more possible to draw meaningful relationships between the studies. As it stands, what we have in one study is biofluid data, and in the other study transformed cell lines from a different cohort of people. Much too hard to dig into relationships between them in detail.

We have a couple of collaborative projects that may shed light here. Including a component of Chris's recent big grant :D
 
We absolutely don't want fast track to false positives. But I'd probably prefer an err on side of the earlier recommendation of pacing management. Yes you may get some people being told to pace that don't need to.

Do you think that is a problematic point of view?

I don't find that problematic, I think it's eminently sensible when ME/CFS is suspected.

Thing is, people who're finding activity makes them feel ill will already (consciously or not) have started pacing to some extent. To have a physician endorse that as a reasonable course of action, at least whilst we see what's going on, would be really valuable.

What I'm not sure about is whether we need a test to endorse it as a reasonable course of action for physicians. If a patient's feeling ill and exhausted, advice to avoid overdoing it is just common sense.

Interesting debate, though!
 
The broad strokes that align are mentioned briefly in the paper but are left there. Didn't want to harp on about it too much because it would just be supposition. Can't make any confident or specific comment without more data. If we have primary cell data linked with biofluid data, collected together from the same people, it may be more possible to draw meaningful relationships between the studies. As it stands, what we have in one study is biofluid data, and in the other study transformed cell lines from a different cohort of people. Much too hard to dig into relationships between them in detail.

We have a couple of collaborative projects that may shed light here. Including a component of Chris's recent big grant :D
Well that's good news!

Thank you for not speculating, and for explaining what data you would need to comment.
 
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