The RECOVER Initiative needed a helping hand – and got one.
Recovering RECOVER?
They had to do something. With the money running out next year, the NIH and its RECOVER Initiative were looking at pulling the plug on over 80 clinics and kissing the $1.15 billion Congress had invested in the program goodbye – all the while hardly making a splash in the research arena. Lacking more funding, it looked like the RECOVER Initiative was about to go down as one of the biggest white elephants in the history of medical research.
A recent webinar on RECOVER’s observational studies was not promising. While the presenters were clearly sincere about their efforts and the condition in general, their outlook for the rest of the year was focused on things like characterizing symptoms, finding subsets, understanding demographics, and the like. No promises regarding getting at the roots of the illness were made.
Even the publications the Initiative pointed to as signs of success – that severe cases of COVID can turn off genes; that people with HIV and long COVID are worse off; that the virus can persist in the tissues for many months; that there may be changes in the immune system – only illuminated how far the RECOVER Initiative is at this point from being a leader in the field.
In a kind of, “Give us a break guys, this is really difficult stuff!”, in its report about the new monies, the NIH referenced how difficult infection-associated chronic conditions such as ME/CFS and Post-Treatment Lyme Disease Syndrome have been to understand. In a statement that will only gall people with ME/CFS, the NIH stated, “Despite years of research, the underlying biological mechanisms for …ME/CFS… have not been identified. Using ME/CFS with its $13 million/year NIH funding to explain why the NIH’s $1.15 billion RECOVER Initiative had produced little thus far seemed more like an act of desperation than anything else. (And yes, NIH funding for ME/CFS fell about 20% last year…)
Before anyone gets too excited about the NIH suddenly turning a new leaf and funding long-COVID research, the money is not coming from the NIH. It’s being taken from the Public Health and Social Services Emergency Fund, which received huge infusions of cash from Covid-19 relief legislation, and was given to the NIH’s RECOVER project by the Biden administration. It appears, in other words, that the RECOVER Initiative lucked out. That money will not be available in the future.
Success the Only Option?
500 million dollars will go to the RECOVER Initiative through 2028.
Despite its failings thus far, and its weird and late-to-the-party treatment trials (only 4 of which are underway), it’s seemingly ultraconservative approach, the RECOVER Initiative is still an impressive program that everyone with long COVID or ME/CFS or other post-infectious diseases should desperately want to succeed.
RECOVER is an effort by the largest medical funder in the world – the National Institutes of Health – to do it right the first time. Every time I look at a Systematic Review of a drug or a disease, I see the same words again and again – small sample sizes, lack of standardization, etc., that preclude the authors (even after 20 or 30, or more, studies) from drawing a solid conclusion. That’s what the NIH is trying to prevent happening with long COVID. Since this has never been done before, it’s perhaps not surprising that the early going has been so rough.
If the RECOVER Initiative succeeds, it will illuminate clear pathways of pathology that provide biological targets for treatments – pathways and treatments that can then be assessed in other post-infectious diseases. In other words, it’s a once-in-a-lifetime opportunity for diseases like ME/CFS. Whatever stumbles the RECOVER Initiative has had, it still, more than any other effort (and it’s not even close), holds the potential key to solving ME/CFS and similar diseases. If it fails, people with ME/CFS fail too – it’s as simple as that. RECOVER surely needs to be tweaked in some ways, but most of all it just needs to keep going.
Ditching RECOVER at this point would throw a dark cloud over long-COVID research, provide fertile ground for naysayers who believe long COVID is made up, and destroy the effort before it really got started. Given that, it’s very good news that the Biden administration gave it a substantial infusion of funds. This is the first time, after all, that an administration has pledged significant monies for post-infectious disease research.
Advocates say more is needed. The Long COVID Moonshot is asking for a billion dollars a year in funding. MEAction reported that the recent Congressional HELP committee hearing on long COVID was packed and it wasn’t just about long COVID. Dr. ZIad Al Alyly gave an impassioned presentation about the need to create an NIH Institute to study long COVID, ME/CFS, and other post-infectious diseases. In a similar vein, Michael Peluso told Stat News, “even more funding would be needed to meet the scope and scale of long Covid and related illnesses”. This new commitment can only support our efforts to build a post-infectious disease Institute at the NIH.
RECOVER may be focused on long COVID, but in the end, it’s really about all of us.
Hey Cort
In addition to the recent Swiss study showing complement activation in long covid, another study showing the same thing is in pre-print. I provide the link below. With two good studies, this is sounding quite compelling, and as I mentioned elsewhere complement activation disturbs a whole range of things proven to be out of whack in ME/CFS. So I feel there could really be something in this! Given this, it could be great if there was an article. And promisingly, there are existing drugs that tone down complement activation.
https://www.medrxiv.org/content/10.1101/2023.10.26.23297597v1
Thanks! The first complement study was by RECOVER I think – that was the kind of study we’ve been looking for. Looking forward to checking the other one out. I love the title to it: “Complement dysregulation is a predictive and therapeutically amenable feature of long COVID” 🙂
Mathias, what are those things that you think compliment activation disturbs in MECFS?
TK a few things, including mitochondria and energy production. Also evidence that it increases allergic responses.
I like this article on the link between complement and mitochondria:
https://bpspubs.onlinelibrary.wiley.com/doi/10.1111/bph.15238
Thanks for the info, Mathias.
I am going to try a couple of natural products that have inhibitory actions on complement activation – artemisin, fucoidan.
Interesting – maybe you can update here about results
For sure. I need to decide which one to start with. I might also try on my 16 year old daughter who has long covid ( luckily more at the mild end of the spectrum, but still….).
Give me a couple of weeks
Best wishes!
Matthias, would you like to say a few sentences for the addled brain what complement system is about? (Is it part of the immune system, staying switched on when it shouldn’t?)
Hi JR
Good ‘ole Wikipedia summarises it nicely (edited by me below):
The complement system is a part of the immune system that enhances the ability of the immune system to clear infections and promote inflammation.
So…. An activated complement system means activated immunity.
So yes, exactly, if complement remains activated the immune system has remained ‘switched on’.
Some people will argue that is a result of a persistent viral trigger. I think it’s more likely that it was activated by a virus but is not perpetuated by one.
Ie the switch was not turned off
By the way, exercise further activates complement, so that’s a potential link in terms of PEM.
Matthias, thank you :-)!
Though Scheibenbogen as far as I know does not research the complement system, it mirrors the simplified explanation she gives on TV about the immune system remaining activitated in ME/CFS.
As there’s been discussion between you and TK about onset triggers: My best guess is that as due to similar set of symptoms in all ME/CFS patients (as TK writes), the same central process is off-kilter in all ME/CFS patients, but initial onset triggers can differ. In my opinion what all known ME/CFS triggers have in common is an immune system connection, probably an immune activiation event (like infections, vaccinations, operations, chemical poisoning, even stress, due to the close connection between stress system and immune system, and because stress is also a known epigenetic modulator). These may be triggers, or co-triggers in conjunction with viral activity in the background (for example herpes viruses, endogenous viruses).
To me, ME/CFS looks more and more like a complex systemic cascade dysregulation failure, probably with the same central process determining PEM, but different initial onset triggers and possibly different perpetuating factors.
Looking at lists of onset factors for autoimmune disease, the same autoimmune disease can also have a list of different onset factors and risk factors, which may overlap with factors known for ME/CFS. Also, for many diseases today the onset model is as far as I known believe a model of (slumbering) genetic predisposition versus actual onset via epigenetic changes triggered by environmental (onset/risk) factors. Also, a probable viral component has been shown for other systemic disease (If I remember correctly, there was this much reported study which, based on a large set of veterans’ data, showed EBV infection was a prerequisite for developing MS).
Therefore, based on the similar main symptom of PEM, my “best bet” 🙂 as of today is on a central ME/CFS specific disease process with various initial onset triggers/co-triggers, and possibly a viral background component interfering at the cellular level.
Nice JR. I generally agree. Not convinced on the viral background component but it’s certainly possible.
Ampligen ?
The long COVID Ampligen study did not apparently meet its endpoints but there were some positive findings. I’m trying to learn more.
No
Ampligen never was and never will be the answer.
Is there anything patients in the US can do to encourage development of a post-infectious disease Institute at the NIH and to get it the billion dollar funding I expect?
Yes there is and its coming up – stay tuned!
👏🏻👏🏻👏🏻
About the only thing hopeful from this HUGE expenditure of cash is the belief I have that if there had been something easy or obvious to blame for losing my entire life to this disease (okay, only 34 years out of 74), and almost my entire research career as a plasma physicist at Princeton, they probably would have found SOMETHING by now.
And we are, BY DEFINITION, closer to the solution (if there is one). While I still hope the answers might apply to decades-old cases of ME/CFS, etc., rather than, “Sorry, folks. If you didn’t get the cure within six months of getting the post-infectious sequelae, it’s too late to benefit – because the damage to your body and brain are irreversible.” Even AIDS is something people can live with.
At least, once we have it, future cases may survive. And that will be our gift to future generations.
Yes, if it was easy I think we probably would have found something. The fact that long COVID – which was triggered by a clear pathogen – is so darn difficult to understand does say something doesn’t it?
It might be worse if they had found something easily – and we had missed it all these decades.
I just don’t know why I had to go catch the most difficult disease in two centuries. Which is true of all the LC people, as well as us.
Even EBOLA is under control! And malaria! Not perfectly, but there is stuff, and their mechanisms of action are known.
Wish I could build more empathy by getting more readers for the books I’m writing with an ME/CFS main character – but I’m so darned slow, and marketing takes so much energy. It would be kind of cool to be the Anna Sewell or Harriet Beecher Stowe of my generation. I’ve invested over twenty-three sick years already.
Well, scientist still don’t know what causes MS … but they have been more successful in finding signs of disease detectable by existing examining proceedings, MR and samples of spinal fluids. And that goes for many diseases.
And for long covid, we know the virus, but it impacts in so many ways it seems. And every little thing can take a lifetime to research.
But I do hope that treatment is easier 😉 Like for other mysteries like MS, migraines etc.
I’ll bet treatments will come first. Researchers will and are identifying things and smart minds will and are jumping on them. Oxaloacetate showed up in a ME/CFS metabolomics study and Kaufman jumped on it – and now we’re exploring that.
We’d be closer to solution if we ever find the solution. I’m not that hopeful with DISCOVER.
PASC is not same as MECFS; their definitions are entirely different. MECFS also includes multiple non-viral triggers. Will they get to the solution by chasing only the viral/post-viral cause? Possibly. But I think it’s more likely that they’ll end up like a blind man calling an elephant a snake. The biggest failure with MECFS has been its singular focus on viral/post-viral cause and DISCOVER is only perpetuating that. It is mostly repeating what’s been going on for the past 40 years with MECFS — antivirals, exercise, muscle biopsy, viral reactivation, immune dysregulation, and all kinds of viral damages — which have proved futile. Which is what you expected when you start with “clean slate” rather than building on what’s been learned in MECFS.
Good points all.
There may be subgroups (since we don’t even have a diagnostic yet, anything could happen) in the ME/CFS bunch.
For me, however, it may work to depend on the virus idea – I’m pretty sure I had an acute viral onset in 1989. Many of us don’t have that certainty – I had the flaming high-temperature sore-throat experience. Possible it’s not viral, highly probable it is. So LC remedies MIGHT help me, unless they only work BEFORE all the long term damage.
Well, yeah, if you believe in subgroups. But it’s hard to imagine multiple diseases (different causes/treatment) with the same set of symptoms. No doubt though, the majority of MECFS cases are post-viral.
I agree, my personal guess is the same central disease process (related to PEM) in all ME/CFS patients, but different initial triggers/co-triggers (all of them possibly related to immune activation like infection, operation, vaccination, stress…) and possibly different perpetuating factors. Possibly a viral background component active regardless of initial trigger (e.g. herpes viruses messing at the cellular level). ME/CFS likely a systemic cascade regulation failure in my opinion. I elaborated a bit more in the reply above to Matthias.
I mentioned subgroups only because a number of people I know claim ‘slow onset’ for their ME/CFS, and can’t point to an obvious viral infection that started their disease, but believe they have the same symptoms now.
This will possibly be easier to determine once there is a test, but the test will have the problem of determining if the slow onset people have the same disease as the post-viral folk.
In addition there are the ‘ME purists’ who claim the CFS people are muddying the water, and don’t have ME – another thing we can’t know without a diagnostic. Some of those may also fight believing whether the test measures what THEY have.
I have no idea how it’s going to play out unless they have some easy objective measurements.
My ‘diagnosis’ – and I didn’t realize there was no diagnostic – was the insurance company physician who, back in the early 1990s told me he was sorry, but that I had CFS, and whom I never saw again. Based on symptoms, and he saying I had CFS, my long term disability insurance kicked in from Princeton U., and supported me until SS granted disability insurance a number of years later when I got my own lawyer for the 2nd appeal, after being turned down by SS twice.
No knowledge then – it was considered a ‘diagnosis by exclusion’ – and I was obviously both sick and not getting better AND incapable of doing the physics position I had at PPPL. After ten years of doing that job.
Well, people can say/believe whatever they want. But the MECFS definition doesn’t say anything about subtypes or “pure ME”, so there is only one MECFS, at least till the definition changes.
Anyway, I’m glad it all worked out for you. (Financially, I mean.) I can’t imagine having this disease and having to worry about making living or fight SSA. Let’s hope that all changed with Long COVID.
Do remember that ‘disability income’ NEVER replaces income – only a part of it, and that disability brings needs and challenges and expenses not part of the normal course of events (for example, an assistant for me several times a week for several hours, is not cheap). I found out that they also didn’t increase the payout for inflation, and of course they wouldn’t cover any raises I might have earned as a working person over a period of decades. It is not a panacea, even when you manage to get it.
Private disability companies then keep trying to dump the responsibility for your income, as much as possible, onto the public SS system (you are required to reapply every couple of years, and then have to repay the private company any lump sums you get from SS). I would never describe that as ‘worked out for me’ – only as a barely adequate system for a no-frills lifestyle, which doesn’t cover increased needs.
I’m pretty sure others feel the same way, especially when it extends for decades, years when they would have been progressing through a career and earning significantly more.
Barely adequate/better than nothing is more like it.
Well said TK. I am very much on the same page. A virus is not the singular cause of ME/CFS, although it can obviously be a common triggering factor. And a virus does not perpetuate it.
Sorry I meant JR 😀
Btw I have been a bit obsessed for a while about CCL2/MCP-1. It has strong links to fatigue, neuroinflammation, and sickness behaviour. There was some interesting research from Canada 10-15 years ago on this, they showed if you blocked CCL2 you got rid of fatigue (in mice). Also in Canada, an interesting study was done that showed that in MS nicotine could block CCL2, reducing the invasion of immune cells into the brain. For me this is a more compelling explanation of why nicotine can really help some people with ME/CFS and long covid ( it has really helped me and my daughter) than the hypothesis that has been put forward to date.
And now I am interested in the link between complement and CCL2, and the idea of reducing activation of both 😀 sorry for the digressive rant.
I sympathize with ranting :-)! Nicotine makes me kind of a lose canon with regard to overexertion/crashing, so it’s not the best medication in my case.
About viral persistence: In my opinion, it’s a no about ongoing classic “lytic” (replicating, in the bloodstream) infection (though it could be one perpetuating factor in some cases, like flare-ups related to overall state of system being off-balance, and there are people who were helped a bit by antivirals – I guess an antiviral like Aciclovir targets the replication phase?). But a possible yes to viruses actively interfering at cellular level in insiduous and much more stealthy ways without even needing to enter the replication phase (with only few infected cells needed to influence many cells), like Prusty showed for HHV6. Which is also why I think research on tissue specific persistence has only just started (like Prusty showing active HHV6 in brain cells in autopsy study, or Ann1 posting link to Coronavirus persisting in bone marrow), and why I do not yet exclude the possibility of “backgound viral activity” being involved in ME/CFS.
Fair points and well articulated!
If correct, is there any foreseeable way such stealthy viruses could be targeted ?
Hi Matthias, apologies for the late reply, had to look up some links from my favorites for this. What I wrote above are some general takeaways I remember from Prusty’s research on HHV6 and ME/CFS. Though I don’t know how concrete a link he has been able to establish between his findings and ME/CFS or if it is still at the hypothesis stage, I do think that the recent scientific findings that viruses do not just have the 2 states “replicating” or “dormant”, but that there’s a world of in-between where viruses – as permanent inhabitants of a cell – interact with and influence cells, are so new (and challenge what was probably a medical dogma of “there’s no such thing as subclinical infection/smoldering infection”) that I would not be surprised at all if relevant answers were to come from that direction.
About your question, could therapeutics target stealthy viruses?, here’s a link to a press release about Prusty’s nature paper (https://www.nature.com/articles/s41586-022-04667-4): https://www.uni-wuerzburg.de/en/news-and-events/news/detail/news/herpesviruses-awaken/ , https://www.ukw.de/aktuelle-meldungen/detail/news/wie-herpesviren-aufwachen/. It explains how Herpes viruses send out a microRNA (an epigenetic communication tool) that does not only reactivate other herpes viruses but also fragments mitochondria and thereby sabotages their immune function. It says that as a therapeutic, complementary artificial RNAs could be bioengineered that neutralise the virus microRNAs and stop Herpes reactivation.
Here’s also the link to Prusty’s autopsy paper on HHV6 and EBV in brain cells https://www.frontiersin.org/articles/10.3389/fmolb.2022.1044964/full,
plus two general articles on how viruses affect cells via epigenetic mechanisms: https://www.news-medical.net/news/20200825/Advances-in-Virus-Epigenetics.aspx https://www.meresearch.org.uk/research/activated-hervs-and-immune-response/.
Looking back on bits and pieces I’ve seen about viral persistence, there seem to be quite different aspects of it, like:
– persistence of active virus in true hidden reservoirs that replicates from time to time (as I think is discussed for Covid), and also what this might mean for the immune system in general for example will this keep it in a change of constant activation,
– then the fact that certain viral proteins or even viral debris (be it from repeated activation, or remaining after the initial infection) may provoke unwanted reactions in the body, for example confuse the immune system into autoimmunity particularly when virus material looks similar to something native to the body, or spike protein possibly contributing to clotting),
– then the interaction of viruses with cells that I’ve written about above, where viruses install themselves as permanent inhabitants of cells (like e.g. Herpes viruses or endogenous retroviruses) and can influence cell function and metabolism, and where reactivation may not need necessarily mean replication.
The viral focus has been fascinating and I would say it’s actually been underexplored in ME/CFS. Researchers are now looking deep into the tissues for viral reservoirs and trying monoclonal antibodies and new antivirals. With viruses its really a new world.
Researchers are also using tools that have never been used before. The muscle biopsy stuff for instance is going way beyond stuff that’s been done before.
Well, I’m afraid I don’t share your optimism there. Tissues and viruses are low hanging fruits that’s been picked over and over and they don’t easily explain PEM/brain fog/etc. Maybe they are unto something real this time, but I don’t think I’ll hold my breath…
Agree. Definitely don’t buy the theories around viral persistence, anywhere in our bodies.
Virus often initiates (or co-initiates), but does not perpetuate the disease.
I think viruses are clung to because it’s a simple thing to latch on to ‘virus causes and perpetuates illness, smash the virus and the illness is resolved / treated’
I am moderately optimistic, but not on theories (and potential treatments) re: viral persistence as being central to ME/CFS.
Hey happy to eat my hat though if someone proves this soon, with a treatment avenue 😀
I always had a lot of time for Dr Andrew Lloyd who was a big ‘Virus in ME/ CFS’ skeptic. From what I recall I think he thought a virus initiated ME/CFS but did not perpetuate. Rather there was ‘hit and run’ damage to the brain.
I don’t think he got a lot of love from the patient community with that view….
I think the idea is that viral reservoirs maintain some sort of immune response (and potentially trigger an autoimmune response), which leads to metabolic disfunction, which causes fatigue and brain fog. There are lots of compelling hypotheses about the way in which the immune system disrupts ATP production. Supposing the viral persistence hypothesis is true, it is still not clear to me in advance why some populations (such as women or those with EDS) are more likely to get me/cfs or long covid.
Yeah, the predisposing factors, like sex-bias and allergies, are abound and virus hypothesis explains none of them. At least not in a straightforward way. Same thing goes for PEM, the supposed hallmark symptom. If the hypothesis is that metabolic dysfunction is causing PEM, that would be easy to test: put metabolic disease patients on stationary bike, subject them to 2-day CPET test and see if their VO2MAX drops like MECFS patients.
I think the innovative research on viral interference with cell function without even needing to replicate (which Prusty showed for HHV6 in the last 2 years) is a possibly relevant topic of vital perdistence, which is only starting to be researched. Also there’s EBV molecular mimikry aspects relating to autoimmunity…I’m not writing off a viral interaction component to this disease yet.
Amen !!!
My thoughts exactly.to me this illness is more about metabolism thrown out of whack, organs not functioning correctly, and so on. I’ve been focusing more on getting the dead cells and debris out of my body lately. While oim not cured, I can tell you I’ve made more leaps and bounds than ever before.
That’s great, best wishes! I wonder, how does one do that to detox the body from dead cells – I could only think of drinking lots of fluids, but I suppose that’s not what you’re doing?:-)
Fasting .. , resveratrol, herbs,etc …go to flccc website….they have protocols on their website.very good Dr’s. That actually care about human beings
……..and getting heavy metals out
Thank you for taking the time to reply! I will check it out.
You’re welcome…you may also want to check out the perrin technique. Dr raymond perrin
I really hope whomever is running RECOVER takes the critiques to heart when deciding how to spend the next half a billion. It also feels as though there is no real effort to build off of the foundation of what has been learned to date about ME/CFS. That seems like a giant missed opportunity. Lastly, I’ll say that because of how poorly run much of RECOVER has been (speaking somewhat from experience here trying to get into the Mount Sinai study) and how underwhelming the findings have been to date, I’d put my (disability) money on PolyBio or Yale LISTEN before I’d put it on any RECOVER sites. I’d love to be wrong about this. We’ll see.
Yes, Polybio – which is doing fantastic work – has taken a very different approach. They are funding studies. RECOVER, on the other hand, decided to spend a ton of money building out an immense infrastructure that should serve as the basis for their studies – but thus far we’ve seen few studies.
RECOVER could have spent its money funding hundreds of large studies and not building out its infrastructure but it chose not to. Time will tell if their approach eventually pays off.
Immune Exhaustion – The Common Denominator with all these autoimmune disorders.
Help strengthen the immune system and the immune system itself will keep these viruses and infections under control.
Hi Cort,
Thanks for the article. Could you comment on the “immense infrastructure” and roughly what percent of the money was spent on it?I just hope it was not a case of opportunistic lobbying vendors that got their products sold. Big companies steering solutions that profit them the most….
When the government has a lot of money to spend, it can happen.
The number I heard was $300 million spent creating the plan and building out the infrastructure. One reason it was so high was that it had to be done so quickly I was told.
The girl at polybio,(don’t recall her name) is said to have cured her own me/cfs
With some sort of a drug or treatment. I don’t understand why we never here about these people that are lucky enough to be able to pull out of this horrible illnesses.seems it’s top secret, how they are able to access these treatments while others suffer. Same with the German treatment bc007…..pulls people out of heart failure but nobody gets to use it. The reason we all continue to suffer is, for the most part, is roadblocks
Are you referring to Amy Proal? (who is a woman, not a girl; sorry, but we never refer to adult men, especially scientists, as boys).
Check out Raelan Agle’s YouTube channel if you haven’t already. Loads of recovery videos there. The only thing that seems apparent to me is that no treatment seems to work for everyone. But I agree with you that we should at least have the option to try things off-label.
Haha…yeah, I just wasn’t thinking at the time. I suppose because I’ve been ill for so long, I recall her when she was very young, perhaps 20 years ago.
Yes, I’ve followed raelen for a long time.
I say we stop waiting for science and dig deep into each of our own history.
I find there are just sooo many different subsets of this illness that it will take a very long time to sort all this out.
The reason most of us are chronic is due to us being outright lied to and gaslit.i know I was for decades.there should be a full inquiry into all this gas lighting. If we could have got the correct help early on, the outcome may have been so different.many illnesses ,if caught early can be reversed. Early on, I had a complete reversal.many of us have gone into remission.
The absolutely biggest contributin RECOVER achieves is a huge cohort. Science does not only take money – it takes time. And even if we have several small studies that confirm each others results, they are still small studies. We need to learn from ie the Retuximab study. Good results in a small cohort, not as good with a larger cohort. And if for instance if we had had subgroups of ME defined, it might had come out differently.
Yes I am disgustingly positive, I know. But finally we have large cohorts in long covid and also there is building up of cohorts in ME too. Even buildning and defining a cohort may take years. It is annoying, but that is what science is.
All the small studies though , I think, contributes in the knowledge that has come out from long covid research. Excactly as “our” ME researchers has applied already existing ideas to their research. And I am trying to finding research that is applicable to ME in other research like research in fatigue, MS, reactivation of viruses like varicella, EBV in MS etc.
There is a need of cooperation between diciplines and that has been made obvious by covid-19. And I want that to stay that way. Imperative.
NIH should set aside some of the money to help fund independent researchers that are already working on treatments based on science. Researchers like Wirth, Pridgen and others could benefit from the infusion of cash. The goal should be on finding solutions from a variety of researchers instead of trying to produce the most lucrative patent.
They spent about $40 million dollars on outside projects I believe – far below what I thought they should actually!
They could have used some of that previous money to fit out a couple of very nice autonomic research labs for in empty office buildings …
Pouring more money into a failed initiative will not fix anything. They should replace RECOVER with “Researching MECFS to Enhance Recovery” first and then fund another billion. That will do a whole lot more good for Long COVID patients.
Nice idea but it would never happen. ME/CFS is not going to go from $13 million to 250 million a year! I think we’re stuck with either having RECOVER or having nothing.
Yep, I agree REMOVER would never happen and that’s the unfortunate thing. Because that means we’ll be stuck with viral/post-viral/anti-viral focus for another 40 years with the solution nowhere in sight. RECOVER happened only because of the enormity of Long COVID, but Long COVID will get classified as MECFS and then the whole thing will blow over.
ME advocacy for the non covid community seem to have ceased. EG last ME awareness day joined with long covid and It got all the media. It’s time to start emphasizing that the NIH ME position, of essentially shelving research on ME subgroups, stages and severity, is unacceptable to the non Covid community. There’s no reason , as Maureen Hanson said, why ME funding couldn’t jump up , if there was enough pressure exerted on them to do so.
This is good but over four years?!? So $125 million per year
People have been talking about the absurd amount being spent on HIV yearly by the NIH so I looked it up, am I interpreting this right, It’s hard to believe when compared with what we get:
NIH HIV funding has increased by more than $200 million per year in the past few years from $3,090.0 million in FY 2021 to $3,294.0 million for FY 2023, and it looks like a permanent increase since it’s also $3,294.0 million for FY 2024 according to:
https://www.hiv.gov/federal-response/funding/budget/
Furthermore HIV is trying to squeeze the NIH to get well over $600 million more per year starting next year
https://oar.nih.gov/hiv-policy-and-research/budget/fiscal-year-2025-nih-hivaids-professional-judgment-budget-accelerating-progress
“The FY 2025 NIH HIV/AIDS Professional Judgment Budget identifies key scientific investment opportunities that will accelerate progress and promise in HIV research. OAR requests $3.953 billion for NIH HIV research—an increase of $659 million, or 20 percent, over the FY 2023 enacted budget of $3.294 billion.”
Wow. Amazing. 3+ Billion a year!
That tell us that science is expensive, and put the matter in different perspective. HIV have been researched for many years. Of course it is “easier” to fund because it is a lethal infection. ME or postviral syndromes are not as visable.
Perhaps the NIH need to perform all aready done research just to validate with larger cohort, proper diagnostic criterias etc?
Thank you Lane for the perspective!
It will be studying only those ambulant and ill <than 4 years, often one or two. Whilst this might have spin offs that benefit some with ME/CFS, it will fail the ME community with its peculiar subgroups, damage, stages and severity, not covered by long covid, to continue to act as if the ME community can just catch a ride with long covid and Divert all advocacy to that.
We need ME advocates , the ones that remain devoted to our community and all the decades of suffering and harm, to resume advocacy for fair funding for ME and reclaim ME awareness day for our own issues & dire neglect,whilst long covid enjoys its own day in March. Whilst collaborating is sometimes very Positive, Long covid advocates have a largely long-covid first Advocacy approach & ME advocates, In my view, need to recalibrate their efforts now to are focus on the non Covid ME community who the NIH are continuing to reprehensibly sideline as unimportant and undeserving.
There’s much more depth, complexity & difficulty studying infection-associated illness than is going to be represented by the long covid cohort , which is going to be early intervention and Covid-trigger focused ( and we know even without ME snowballing and causing damage it is complex). No one would agree to just the very early stages of multiple sclerosis being studied, when it, in some ways like ME, is an illness with a spectrum, that advances and changes And Sometimes progresses over time.
Has anyone ever donated their blood?
Seems to be helping me.
It seems absurd that Anthony Fauci ignore ME/CFS for decades. Then when Long Covid appeared he said several times how similar it was to ME/CFS. Yet Long Covid being one of the biggest mass disabling events in modern history, the NIH defund ME/CFS research by 20%
FAUCCI is ABSURD.He and Francis Collins have ignored us for decades…worse than ignored us.told us it was all in our heads.
Even if they do start helping us it’ll be just a bunch of drugs to make some shareholders wealthy.lots of people have their fingers in the drug profit pie.
I’ve been sick long enough to know what’s really going on.
This ongoing saga is just going to keep spending millions on useless “studies” so that the wrong scientists keep pumping out bull shit papers while the good meaning scientists get pennies.how many dead horses are they going to keep beating.reminds me much like the billions and billions spent on “runs for the cure” ,giving billions to cancer agencies so the people at the top of these agencies get paid huge astronomical sums of money to actually slow the progression of science.
I’ve been around long enough to follow these money trains.follow any money train….not just health, but any money train and you will soon find corruption….be it political,soccer,hockey…anywhere huge sums of money are involved
WAKE…UP…PEOPLE
Who’s studying the gut microbiome
NOBODY