This has been a farcical waste by every possible metric except the NIHs own bullshit ones.

Wallitt sounds zealous and preposterous, but the explanation was that Nath came to depend on him for the organising. I vaguely recall this was on the RECOVER budget. I got the creeps in view of Wallit demonstrating a lady with fibromyalgia to prove some point she did not seem aware of. It was obscure, He has some wild ideas he is accustomed to "exploring" out loud. He sticks out.

I am surprised at the large number of various operations being networked by the budget. I could do with more local news from a lot of them. There must be some ingenious, independent-minded people in there.
 
The RECOVER Initiative recognizes International Long COVID Awareness Day on March 15—a day established by the Long COVID community to increase visibility of the condition, share resources, and educate the public.
Are they going to do that with medical professionals and their institutions? Because no one needs to hear and do more than them. The general public doesn't have to hear more about it, it won't ever change anything until health care systems actually do something about it.
 
Update from the NIH:

RECOVER-AUTONOMIC clinical trial results shared at 2026 ACC Conference

Ivabradine, an oral medication that lowers heart rate and is used to treat people who have chronic heart failure and an elevated heart rate, does not have a significant impact on Long COVID symptoms, according to results from the clinical trial RECOVER-AUTONOMIC (Ivabradine). These findings were shared by researchers of the NIH-funded RECOVER Initiative at the American College of Cardiology (ACC) Annual Conference on March 28, 2026.
Participant surveys showed that treatment with ivabradine did not significantly improve POTS symptoms in adults with Long COVID POTS. Ivabradine did produce a significant reduction in heart rate compared to placebo, but the lower heart rate did not improve POTS symptoms. Participants who received coordinated care in addition to ivabradine did report an improvement in their symptoms compared to those who received ivabradine and usual care.

More details about these results will be shared in an upcoming journal article.
 
"Ivabradine did produce a significant reduction in heart rate compared to placebo, but the lower heart rate did not improve POTS symptoms."

This is interesting because I've argued this for quite a while, and it fits my experience with propranolol. It lowers HR but really doesn't do much else of use and in the absense of really high HRs and symptoms caused by that, I do wonder if these drugs are actually helpful.
 
"Ivabradine did produce a significant reduction in heart rate compared to placebo, but the lower heart rate did not improve POTS symptoms."

This is interesting because I've argued this for quite a while, and it fits my experience with propranolol. It lowers HR but really doesn't do much else of use and in the absense of really high HRs and symptoms caused by that, I do wonder if these drugs are actually helpful.
That's been my experience with all POTS medications I've tried.
 
"Ivabradine did produce a significant reduction in heart rate compared to placebo, but the lower heart rate did not improve POTS symptoms."

This is interesting because I've argued this for quite a while, and it fits my experience with propranolol. It lowers HR but really doesn't do much else of use and in the absense of really high HRs and symptoms caused by that, I do wonder if these drugs are actually helpful.
I think sometimes the lowered HR can be a benefit in as much as preventing significant and extended periods of tachycardia can help to avoid a cascade of anxiety and discomfort which then becomes a problem of its own, one that can exacerbate and overlap with OI/POTS symptoms (as well as potentially producing PEM for pwME), but the effect on direct OI symptoms does not seem significant.

Edit to add: I suppose this is really just to say that drugs like propranolol may be useful for pwOI in pretty much the same way that they can be useful for otherwise healthy people with anxiety for various reasons, it's just that the same anxiety tends to impose an exaggerated and more complicated burden on pwOI & ME/CFS/LC/etc.
 
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I think sometimes the lowered HR can be a benefit in as much as preventing significant and extended periods of tachycardia can help to avoid a cascade of anxiety and discomfort which then becomes a problem of its own, one that can exacerbate and overlap with OI/POTS symptoms (as well as potentially producing PEM for pwME), but the effect on direct OI symptoms does not seem significant.
Yeah agree. I don't really fall into that category.
 
While we'll see how/if they spin things once the results are published, it's actually slightly heartening to see these negative results coming out. Perhaps some small amount of RECOVER work might not be a waste of time? I am sure it is too much to hope that it will actually have much of an impact with regard to the continued use of these drugs and the wasted research done in support of that use, but one can dream.
 
RECOVER does seem to have done well in showing that a lot of the trial studies on various drugs were just positivity bias and bad methods rather than genuine positive results. They also wasted a tonne of money attempting replication of drugs which even in the small studies didn't show a great deal of actual promise because the results were pretty lacklustre anyway. Its the waste of money on exercise that really irks me more than the others, that one especially its not like it hasn't had enormous funding already and shown nothing it doesn't require yet another study,
 
While we'll see how/if they spin things once the results are published, it's actually slightly heartening to see these negative results coming out. Perhaps some small amount of RECOVER work might not be a waste of time? I am sure it is too much to hope that it will actually have much of an impact with regard to the continued use of these drugs and the wasted research done in support of that use, but one can dream.
I haven't noticed the problems in drug trials that we see in 'pragmatic' trials, they almost always report honestly. Even when run by psychobehavioralists, though they are biased against them so I don't think it counts for much. If all clinical trials followed the same standards and had the same levels of bias, we wouldn't be in this mess. Drug trials are basically the real gold standard, the rest is basically fool's gold yee-hawing it. Well, aside from psychoactive drugs, now those are an unholy mess. Uh, there's some kind of pattern here.

Ivabradine is interesting, though, in that it definitely meets the threshold of 'benefits' we see in biopsychosocial/rehab trials, secondary improvements that ultimately don't make much difference. It really did make a difference for me, as reported, in terms of lowering my heart rate and reducing palpitations. But it probably didn't change much in terms of how long this returned to normal.

So this, by definition, meets the biopsychosocial Wessely "might be of help to some", but ultimately is of little value because it changes almost nothing. About on par with a weak painkiller, which is still valuable, but won't really fix the problem. The entire difference is in the fact that most physicians are biased towards taking as few drugs as necessary, whereas everything else is seen as ultimately so benign it doesn't matter, even if it ends up creating the endless, massive systemic nightmare they built for us.

Almost like they're not thinking 'holistically'.
 
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