USA: Mount Sinai PACS clinic and Dr David Putrino

More Putrino controversies about exercise/GET. Thread.



This is an issue that has been coming up today from various folks and I want to address it. As I said when we launched the manual, this is the beginning of a conversation, not the "final word". I also want to say that reading it with 20/20 hindsight, I understand why this
 
Putrino's statement courtesy of Nitter for those wanting to read w/o a Twitter account:

@PutrinoLabs
This is an issue that has been coming up today from various folks and I want to address it. As I said when we launched the manual, this is the beginning of a conversation, not the "final word". I also want to say that reading it with 20/20 hindsight, I understand why this 1/

language has been inflammatory to members of the community, because it the feedback I have received is that it "feels like we're trying to say that exercise is curative even with PEM, without saying the word exercise". I regret that this was the impression that our wording 2/

gave. In previous communication and education we have been quite clear that IF rehabilitation protocols are being attempted (and not all of our patients with PEM are considered suitable for rehabilitation), then PEM is the factor that governs all aspects of care delivery, from 3/

rehab choices even out to location of care (home-based care versus location-based care). In addition, when we talk about symptom-titrated rehab or symptom-titrated movement, we are NOT talking about exercise and we are not trying to "dog whistle" about exercise. Our position 4/

on exercise (physical activity with the intention of increasing cardiovascular fitness) and PEM is clear: exercise is not a treatment for PEM. However, when we're talking about symptom-titrated rehabilitation, we're talking about things like breathwork, gentle calf pumps to 5/

prevent DVT and autonomic rehabilitation in people who are eligible and able. We introduced "symptom-titrated" to these activities because we wanted to honor the fact that even things that might be considered by a clinician as non-exertional like breathwork can, in fact, 6/

trigger PEM in folks with severe PEM or who are in a crash. Similarly, when we're talking about "symptom-titrated movement" we are also talking about things like passive movements to prevent contractures in the bed bound population, gentle rolls to prevent skin breakdown: what 7/

we view to be crucial rehabilitative activities *if* they can be tolerated. The final thing I want to touch on is the wording around "exercise intolerance" - we try to clinically differentiate exercise intolerance from PEM because exercise intolerance is immediate: you're 8/

exercising and you physically have to stop because you can't continue (for various reasons), versus PEM which usually presents more insidiously: you can do the thing asked of you, but then you pay for it afterwards. Understanding that these are two different things and should 9/

be assessed and managed differently is important, we think.
Ok. Back to start - I hope that this has been at least a little clarifying for the spirit of what we had hoped to communicate and we're actively working with our lived experience community and clinicians to reword 10/

this section. I apologize if this caused hurt or upset, that absolutely was not our intention, but I also want to reiterate that this is intended as a living document: the idea is that we continue to work together to clarify these points as much as we can. This manual is not 11/

likely ever going to stop being reworked, and if members of the community engage us for edits, we will listen and work to make your voices heard through this work. Finding the balance of honoring and communicating the lived experience and the published science of such a 12/

diverse community is challenging, but not impossible if we all work together. I hope that this message has helped and we will be working on edits.Thank you all./end
 
Nobody should be suprised if people who don't care about actual evidence make statements not based on any evidence.
While this is certainly true, may I ask whether your comment is in response to the recent statement concerning PEM and "symptom titrated" activities, to the lactic acid slide pictured above, or to something else?
 
Putrino on Twitter responding to Todd Davenport.



Davenport:

Today’s unpopular opinion is that we’ve put too many resources toward studies looking into treating viral persistence, even though it seems to follow but does not lead in the pathophysiological process of Long Covid. These are studies on “pacing using meds” for the immune system.

Putrino responds with Long Thread

I was asked to respond to this. Honestly I don't pay too much attention to this account because I prefer to spend energy on people and things that build community in #LongCOVID and IACI rather than curating divisiveness, but this shouldn't go without rebuttal so here we go.

Anyone can post the whole thread?
 
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He cites e.g. this paper for evidence of viral persistence
Meanwhile, Peluso et al were not just showing persistent spike, they were finding double-stranded RNA in folks with LC - the implication here is that you can't get this flavor of RNA in your body unless there is live, replicating virus somewhere in your body.

And this review:
 
I’m not abled enough or knowledgeable enough to be able to judge the “evidence” behind Viral Persistence.

But from what I can tell it doesn't seem particularly strong, like it doesn’t seem particularly linked or causal to PCC.
 
Full on “BioBS” territory.

Annoys me how much reach and legitimacy Putrino has. Guess I’d rather him then Wessely but pwME deserve so much better vis à vis scientific standards.
For those reading in the future, and who, like me, may be wondering about the term "BioBS", its origins appear to be in the following thread (though please correct me if I am wrong, Jaybee00):

https://www.s4me.info/threads/bio-bs-is-worse-than-bps-change-my-mind-prove-me-wrong.41459/

As for this particular bit of "BioBS", while I have certainly picked up on a fair degree of animus toward Putrino on this board, I did not realize that the possibility of different approaches being required for different subgroups of pwME was understood to be unworthy of consideration. May I ask why? Happy to make another thread if this isn't the place for it.

Edit: By way of clarification, my "why" question was in reference to the dismissal of multiple "drivers", rather than the distaste for Putrino.
 
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For those reading in the future, and who, like me, may be wondering about the term "BioBS", it's origins appear to be in the following thread (though please correct me if I am wrong, Jaybee00):

Guilty as charged.
 
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I have no idea where the claim about dsRNA is coming from. The cited paper uses RNAscope which is an in-situ hybridization method. By definition it binds to single-stranded RNA. Am I missing something?

The study also says that they failed to find any signal for nucleocapsid or envelope viral RNA, which makes me suspicious that the findings are off-target binding of the spike RNA probe (RNAscope is supposed to be a lot better than other methods in terms of target sequence specificity but it’s still not perfect). Or even that this signal somehow came from the mRNA vaccines.

I’m not abled enough or knowledgeable enough to be able to judge the “evidence” behind Viral Persistence.

But from what I can tell it doesn't seem particularly strong, like it doesn’t seem particularly linked or causal to PCC.
The gold standard for viral persistence is a quantitative viral outgrowth assay (qVOA), where you basically take infected cells, expose them to uninfected cultured cells, and quantify the increase in viral titres over time. If this team had a background in HIV I’m guessing that’s the first thing they would have tried (though I’m not an expert in this so maybe there’s some technical reason why it couldn’t be done here).

It’s a hard assay to do if you have a very small amount of infected cells to begin with, but it’s the gold standard because it’s the only one that conclusively proves the presence of replication-competent virus. But yes, even if they did have proof of viral persistence, I agree that it doesn’t seem to be particularly correlated with post-COVID symptoms.
 
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