This is an actual problem, actually. The “media” thinks people with large Twitter accounts like Putrino, Iwasaki and Proal are the real experts because Twitter. So these folks get amplified by “the media” and in certain cases this coverage leads to them being funded at higher levels than people who have been working on MECFS for many years, which is bad, because the new folks are just wheel re-inventors.
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USA: Mount Sinai PACS clinic and Dr David Putrino
- Thread starter Kalliope
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This is an actual problem, actually. The “media” thinks people with large Twitter accounts like Putrino, Iwasaki and Proal are the real experts because Twitter. So these folks get amplified by “the media” and in certain cases this coverage leads to them being funded at higher levels than people who have been working on MECFS for many years, which is bad, because the new folks are just wheel re-inventors.
mango
Senior Member (Voting Rights)
Here's some more context from Putrino's thread:
"I don't like any confusion or lack of transparency about our thoughts'/approaches regarding our research strategy surrounding #LongCOVID, chronic #Lyme, #MECFS, vaccine injury and other complex chronic illnesses that we study, so I wanted to post an end of year thread to share 1/
where we are right at this moment. This thread is by no means our "end game" in terms of strategy, just where we are at right now and how we're thinking about things. This may certainly change as we learn more and, as always, viewpoints other than ours are valid. So, with that 2/
let's begin. We're interested in studying conditions that can be framed as post-acute infection (#LongCOVID, chronic #Lyme, #MECFS triggered by infection) OR exposure (vax injury, ME/CFS triggered by mold exposure, trauma, etc) syndromes. When an infection or exposure event 3/
triggers a disease state such as #LongCOVID, chronic #Lyme, #MECFS or other infection/exposure-associated complex chronic illness, we believe it is due to 1 of 2 root causes: 1. the initial pathogen is persisting in the body and causing ongoing illness, 2. the body's immune 4/
system has been locked into a state of overactivity since the initial triggering event and this prolonged immune reaction is now causing damage to the body. Since nothing is ever simple, we also need to make room for 3: some people will have both - viral persistence PLUS a 5/
prolonged, overactive immune response. This year has seen multiple review and original research pubs showing that there is ample, direct evidence for both of these mechanisms, but when it comes to translating this research to clinical practice, we have a problem: most of 6/
our lab tests don't adequately test for viral persistence: they test for the antibodies your immune system is producing to fight pathogens. This could be happening because you either have the pathogen or your overactive immune system is producing antibodies for everything as 7/
though you have the pathogen. This can also be true for those whose illness was triggered by non-infectious causes: when your immune system has been overactive for a long period, it can lead to T-cell exhaustion and an exhausted immune system can then result in reactivation 8/
of viruses that were previously latent like EBV, HHV and other common pathogens. What will we be putting research effort into in 2024 and beyond? Creating tests for persisting pathogens that go beyond simply looking for antibodies and look for proteins produced by active 9/
pathogens or evidence of the pathogens themselves. Our hope is that this will lead to better testing procedures that allow us to understand who has pathogens, who has an overactive immune system and who has both. Making these distinctions regarding root causes of complex 10/
illness is crucial. You've all probably read the same case series' that we have of people experiencing complete remission from #LongCOVID, #MECFS or chronic #Lyme from application of different antibiotics, antivirals, monoclonals (addressing persistent pathogens) or IVIG, JAK 11/
inhibitors or other immunotherapies (addressing immune overactivity). Many pw complex chronic illness read these articles and react the same way: I tried these drugs and they didn't help me (or they made me worse!). This, of course, makes sense since clinicians can't tell for 12/
sure if you're experiencing these illnesses because of persistent pathogens or immune overactivity. If you give someone whose immune system is highly active due to persistent pathogens a drug that suppresses the necessary response their immune system is having, they will get 13/
sicker. If you give someone with no persisting pathogens, but an overactive immune system that is producing antibodies for a particular virus, an antiviral that boosts immune function, they will get sicker because the last thing they need is more immune activity. So a major 14/
gap here is that even if you find a clinician who is willing to try some of these drugs, they don't have adequate tests that allow them to identify "who is who" when it comes to prescribing these meds. We need guidelines and for that we need research. Therefore, in addition 15/
to studying better ways to test, we're also going to explore some of these antiviral and immunotherapies in the next few years alongside deep immune profiling so we can understand the immune characteristics of responders and non-responders to these medications. We think combo 16/
therapies will also hold great merit, but it is very difficult for us to get ethical approval to test combination therapies in clinical trials without first having done monotherapy trials, especially when we're repurposing existing drugs. Therefore, our pipeline over the next 17/
couple of years will be to first understand what some of these promising drugs do for these patients and then move into more complicated clinical trial designs that combine medications. Finally, I want to end this thread with acknowledgement of dysautonomia, MCAS, endothelial 18/
dysfunction (platelet hyperactivation and microclots), neuropathic pain, gut dysbiosis, small intestinal bacterial overgrowth, mitochondrial dysfunction and many other issues we see emerging in folks with #LongCOVID, #MECFS, chronic #Lyme and other complex chronic illnesses. 19/
Our clinic tests for all of these issues and we treat using existing guidelines (and in 2024 we will be releasing free educational content addressing these topics), but we consider them to be downstream of the root causes that this thread has addressed. There have been some 20/
great publications showing how immune overactivity and persisting pathogens can cause all of these issues. To be clear: it is still CRUCIAL that these issues are addressed - if I could snap my fingers and resolve immune overactivity or persistent infection, if those issues 21/
have already triggered POTS/dysautonomia or MCAS, you aren't going to feel better until we resolve these issues as well. In addition to sharing our assessment and interventional guidelines for these conditions, we're also investigating novel therapies for these commonly 22/
co-occurring conditions. Anyway, I'll leave it here and I hope that this provides some clarity for how I'm thinking about these issues and how we're developing our research strategy for the future. We will make some specific announcements about the drugs and therapies we're 23/
testing in 2024 as soon as we're able to do so. As always, I'd like to express my gratitude to some of the phenomenal researchers and clinicians who educate my uninformed ass regularly like @VirusesImmunity
, @microbeminded2
, @hmkyale
, @resiapretorius
and @doctorasadkhan
as 24/
well as all of the people living with these conditions who so freely give their time and their energy to work collaboratively with us so that we can develop research strategies like this one here. Hope this has been helpful. Wishing everyone a safe holiday period/end"
[Carole Bruce asked] Thank you. How much of your research applies to severe, bedbound cases of MECFS and LongCovid. There always seems to be a gap here.
[Putrino Lab replied] "Thank you for asking. We have worked this into our protocols so that we can include severe individuals as well by doing home visits."
Code:
https://twitter.com/PutrinoLab/status/1740356301115580871
Jonathan Edwards
Senior Member (Voting Rights)
Yes.
That's Iwasaki, Proal, Pretorius, and Khan and maybe someone else at Yale.
Edit: Harlan Krumholz at Yale - does a lot of Tik Tok work it seems.
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Sid
Senior Member (Voting Rights)
There is literally zero evidence for this word salad. As far as I can tell based on the totality of published literature, the immune system is functioning normally in ME/CFS.
Sid
Senior Member (Voting Rights)
Haha, I didn't know that. That makes all this even funnier. It reminds me of a recent remark by a doctor on twitter remarking that they get the likes of physios coming in to inform them that POTS is actually FND.
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RaviHVJ
Senior Member (Voting Rights)
He’s definitely more than a physiotherapist - he has a PhD in neuroscience and has done some really interesting work at Mt Sinai, which Cort Johnson discusses here: https://www.healthrising.org/blog/2023/12/17/long-covid-treatment-polybio/
RaviHVJ
Senior Member (Voting Rights)
To be fair, I think those three are indeed experts and do deserve substantial media attention. Putrino’s spent three years treating Long Covid patients, and alongside Iwasaki, published that big Nature paper alongside several other studies. He’s also worked with David Tuller several times to push back against BPS figures, and has several other studies on the go looking at microclots, viral persistence in the gut, VNS, and replicating the Nature paper in ME/CFS patients. Iwasaki is an enormously impressive scientist - exactly the kind of person we want in this field. Proal has been instrumental is pushing forward the Long Covid Research Collaborative, and even if she’s a bit evangelical about viral persistence, clearly that’s a hugely important hypothesis to explore. Alongside Putrino and Iwasaki she published that recent Nature literature review on viral persistence - and my understanding is that prior to the pandemic, incredibly few if any ME/CFS papers made it into the top journals (which isn't an indictment of the top ME/CFS researchers, but is an indication that things are changing for the better).
I wish researchers who had significant pre-pandemic ME/CFS experience played a greater role in setting the Long Covid and post-viral research agenda, but these newer figures have undoubtedly done very good work, and also because the field was so starved of funding, there were just a handful of pre-pandemic ME/CFS researchers.
I can see why these figures would be frustrating, particularly given recent statements about the relationship between ME/CFS and Long Covid, but this is exactly what the field has always needed - high profile researchers thoroughly dedicated to patients pushing research forwards.
I just think, in big picture terms, it’s a huge net positive that the figure leading post-viral research and getting the most funding are Iwasaki, Putrino, Proal et al vs Michael Sharpe, Esther Crawley, Peter White ten years ago. Still a huge way to go - above all in terms of ME/CFS research funding, but a radically better situation.
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The problem I have with all of this is it sounds too grand, too sweeping.
If you only dealt with one third of the proposed triumvirate it would represent an enormous undertaking. Huge. We're talking proving or disproving persistence. If successful, it would be virtually unprecedented as a game changer.
But this is taking three tigers by the tail, and two of those - ME/CFS and Lyme - have nasty histories of mauling researchers.
This isn't just science at work. There are politics involved.
If you only dealt with one third of the proposed triumvirate it would represent an enormous undertaking. Huge. We're talking proving or disproving persistence. If successful, it would be virtually unprecedented as a game changer.
But this is taking three tigers by the tail, and two of those - ME/CFS and Lyme - have nasty histories of mauling researchers.
This isn't just science at work. There are politics involved.
Jonathan Edwards
Senior Member (Voting Rights)
I agree that there are signs that things are improving, but to be honest I would not include any of this stuff. There is difference between real innovative science and stuff that just sounds like it. Putrino's Twitter thread is empty waffle I am afraid.
RaviHVJ
Senior Member (Voting Rights)
Agreed about Putrino’s thread. Even if those three aren’t necessarily doing innovative science, they’re helping establish these illnesses as an important and legitimate field of study, and that innovative science can’t really happen at any serious scale before the field has been established. It’s frustratingly a process that will inevitably involve treading ground already covered by ME/CFS researchers.
Mij
Senior Member (Voting Rights)
Yes, reactivated theories of viruses that are recycled every 5 yrs or so.
Binkie4
Senior Member (Voting Rights)
Somewhere on the forum there is a tweet from Putrino's lab asking for people with a pre Covid ME diagnosis to give blood samples. When I had plans to be in NYC last autumn, I offered a blood sample. (2008 diagnosis, 1986 infection) and was asked to get in touch when my dates were known, but then my plans changed.
I went by ship and only stayed for 3 days and was too depleted. I regret I didn't push myself now especially since they are offering to come and collect blood samples. Mon and Tues morning were their collection times. They are doing a lot right.
I went by ship and only stayed for 3 days and was too depleted. I regret I didn't push myself now especially since they are offering to come and collect blood samples. Mon and Tues morning were their collection times. They are doing a lot right.
I have seen so many failed attempts. I've also seen a few successes that didn't stick. I'd want real granular specifics before I'd participate.
So I respectfully disagree with this. To me, the “scientific” flim-flam is more pernicious than the BPS flim flam.
To almost all patients the BPS stuff is obvious BS. By contrast, many patients are big supporters of this Proal viral persistence stuff and really believe that their disease is caused by persistent viruses, where there is no evidence for this. Because there is a lot of patient buy-in, it is easier for these researchers to secure funding for research that I believe is a dead end.
ETA
Having said that, I do think Putrino has been helpful in supporting MECFS LC patients generally by believing them and highlighting their plight.
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The perniciousness I’m referring to has more to do with the LC researcher’s ability to burn through a lot of funding without gaining much useful knowledge in return. The BPS people are useless/harmful whatever but they are funded (at least since Pace) at much lower levels.
If you don’t view LC MECFS funding as a zero sum game then it’s all good. If you do think it’s zero sum, then funding less promising research is problematic.
If you don’t view LC MECFS funding as a zero sum game then it’s all good. If you do think it’s zero sum, then funding less promising research is problematic.
Sid
Senior Member (Voting Rights)
This is a serious and ongoing problem in our patient community. The pushback against psychobabble is robust but hardly anyone outside of S4 criticises biobabble studies. As a result, I go to other websites and see people who think their symptoms are caused by an enteroviral infection they caught in 1980, a broken spine etc.