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.
 
Last edited:
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'.
 
I don't know if this limited Ivabradine-effect implies that the other postural and orthostatic problems are not autonomic.

RECOVER-AUTONOMIC (Ivabradine) is the name of the trial - I don't know how it got classifed as autonomic, and by who.

I don't know if everything labelled as an autonomic symptom is primarily or secondarily autonomic, or could be something else and not autonomic at all.

I don't know enough - and cannot now encompass enough - to clarify what Ivabradine does, and what it was expected to do but did not do.

It intervenes at some point in some process, reducing heart rate, which does not change the other symptoms.

I guess this could help make the systemic map.
 
Some "co-ordinated care" program actually worked a bit but this information is still withheld. Maybe its not profitable. Or it only makes jobs for specialist Long Covid nurses, and / or public health offices.

I don't know if the research program has specified the range of disability and exemption entailed by these problems, and so measured the effect of "co-ordinated care".

I would like to make sure that the program is comprehensively objective in its approach, not just selective.

And I wonder what happens to all that fuss on social media records about Paxlovid policy. I don't know if the Paxlovid results are conclusive.
 
I don't know if this limited Ivabradine-effect implies that the other postural and orthostatic problems are not autonomic.

RECOVER-AUTONOMIC (Ivabradine) is the name of the trial - I don't know how it got classifed as autonomic, and by who.

I don't know if everything labelled as an autonomic symptom is primarily or secondarily autonomic, or could be something else and not autonomic at all.

I don't know enough - and cannot now encompass enough - to clarify what Ivabradine does, and what it was expected to do but did not do.

It intervenes at some point in some process, reducing heart rate, which does not change the other symptoms.

I guess this could help make the systemic map.
I've been trying to get my head around it for the last day since reading the initial post about how it worked in reducing heart rate but not the symptoms

and of course I was a bit spooked out by the added 'the difference was between those who had it with 'co-ordinated care' alongside and those who just had normal care... as that understandably red flags me a bit until I know what was really in said 'co-ordinated care'.

I don't think I have POTS but I am debilitated by some form of OI and so for so so many years given POTS has been talked about in various places and you hear more of people who claimed to be fixed from that even wondered should I be looking into that etc. just in the hope that at such places someone might be interested and it might have been safe to talk about even when I was less ill always having to perch and find seats and by the end of the day eyeing up lying my head on things, but on bad days and most of the time now it's not just lying down, but more.

Hence that 'lie flat' thread was a godsend

Is this result just saying that POTS could in many be the case that the heart races as some compensatory mechanisms for OI and then for others there is less increased heart rate and they just feel awful like they will faint and/or desperate to get flat (how much of this lie flat and other phenomena is 'one thing' is another question)... in a different way because there isn't this attempt at compensation.

ie is it saying that they can reduce the heart rate but it doesn't take away the feeling awful in mostly the same circumstances. Which would just indicate the order of 'stream'/cause?

I guess the other interesting quesiton to me is whether there is a group of people with something called POTS but who don't have anythign else like ME/CFS .. or indeed anythign else at all - so it is 'only this', and does this sort of thing work for those ?

and then is what those who have something like POTS on top of an underlying condition like ME/CFS have that same thing they have being triggered or is it different etc - but I haven't formed my words to get that line exaclty right

But it feels like getting those phrases right might involve helping with narrowing down the understanding
 
April 1 update from the NIH:

RECOVER continues to focus on understanding symptoms that affect the brain

As RECOVER enters the next phase of its adult observational study, researchers will take a deeper look at how the brain interacts with the rest of the body—and how these connections may lead to symptoms like brain fog.

Cognitive symptoms (such as trouble thinking clearly, remembering things, and concentrating) are among the most common challenges reported by people with Long COVID. A 2024 RECOVER study found that 64% of people likely to have Long COVID reported these symptoms, often described by the term “brain fog.”

Despite how common they are, brain-related symptoms remain some of the most burdensome and least understood, said Jacqueline Becker, PhD, a RECOVER researcher, neurocognitive lead for the next phase of RECOVER’s adult observational study, and clinical neuropsychologist, who studies the brain and how it functions.

“These symptoms can affect nearly every part of daily life, from work to relationships. But we still don’t fully understand why they happen, which makes them difficult to treat,” said Dr. Becker.

RECOVER researchers have observed that cognitive symptoms rarely appear in isolation. Rather, they often appear alongside other symptoms, such as poor sleep, depression, post-exertional malaise (symptoms that get worse after physical, mental, or emotional activity), or cardiopulmonary issues (problems with the heart and lungs). This overlap makes it difficult to pinpoint what’s driving brain fog in any one person.

“’Brain fog’ is a catch-all term people use, but it likely reflects many different underlying problems,” Dr. Becker said. “In most cases, there isn’t one thing that causes brain fog, but rather a combination of factors.”
 
The April 1 NIH update also mentions an upcoming webinar:
In the next phase of RECOVER observational studies, researchers plan to “put brain health front and center” by collecting more detailed data on cognition and how it relates to other body systems. Dr. Becker will discuss key gaps in Long COVID neurocognitive research and how RECOVER plans to address them, at an upcoming R3 Seminar on April 14.

This webinar is scheduled for Tuesday, April 14, 9 am Pacific / 12 noon Eastern.

More webinar details here - Impact of Long COVID on Neurocognitive Function
 
Back
Top Bottom