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I don't believe the Nutt study amounted to anything.

Garner's not going to be able to contain himself reading this

This is ambiguous to say the least. The Facebook post says nothing about long covid, but the poster says participants must be diagnosed with "ME/CFS to CCC/ICC and long covid."

Yes, I remember now. OI comon in ME/CFS but it's not always PoTS.

This survey estimated 27%: https://meassociation.org.uk/2023/11/the-me-association-postural-orthostatic-tachycardia-syndrome-survey-results/

Ok, but that means you have to measure blood pressure, which it sounds like they didn't do for half the test. Active stand rather than TTT will likely explain the low POTS rates. I don't trust anyting from Knoop + co having looked into some of his work.

Yep. We are perfectly capable of reconditioning ourselves — if only our bodies would allow that.

I think they are seeing things through the lens of exercise science, because most of them are exericse scientists. The focus on physical exercise and rehab is party, I think, because many still think PEM is just about exercise intolerance — this is something I tried to convey in my response. So...

Ah ok. Yes, these are not blanket statements — they are refering to the individual patient, but perhaps that's not clear. "if there is no evidence of deconditioning in a patient" night have been better.

The crux is what is driving these abnormalities. You could get similar results, for example in CPET, from very different mechanisms, which is sort of what Charlton et al are arguing. I don't intend to argue that deconditioning isn't present in some patients, only that we should challenge the...

I have just subitted the following rapid response. Not sure how often this journal publishes RRs, and this might be too off-topic for a sports medicine journal, so I'm posting here. It was helpful to get my thoughts in order, but now I need a break. -- Post-exertional malaise cannot be reduced...

That is more in line with most estimates, but the range is huge.

For me, the issue is the simplisitic cause–effect language that is used to describe exertion and PEM. It's just not that simple in reality. There seems to be an element of randomness and it's very easy for patients to fall into the trap of over-attributing PEM and crashes to exertion/activity...

Do the findings of the recent Ryback et al. paper refute these results?

Thread here about a FOI request by @Lucibee showing pitiful numbers of NHS staff taking the ME/CFS Delivery Plan e-learning courses. https://skyview.social/?url=https%3A%2F%2Fbsky.app%2Fprofile%2Flucibee.bsky.social%2Fpost%2F3megstha5j22m&viewtype=tree Twitter link here:

Highlights • Semaglutide alleviates OA in a weight loss-independent manner • Semaglutide shifts chondrocyte metabolism from glycolysis to oxidative phosphorylation • Semaglutide exerts its chondroprotective effect via the “GLP-1R-AMPK-PFKFB3” axis • Semaglutide could serve as an effective drug...

I don't have phobias but I do have OCD and I was in my 30s before I realised that OCD was a form and manifestation of anxiety. It had never really clicked before. It certainly makes sense to me that phobias are included under the banner of anxiety. Like OCD, phobias are essentially underpinned...

What a bizzare trial design, which has made it harder to test whether the intervention has benefit.

What comprises the 'blurb' here? And what's wrong with it? (I am interested in the lack of fatigue research, given it is a core feature of so many different diseases and illnesses.)

Recording here: