Three years after the pandemic had destroyed any attempt to get back to the East Coast and Washington, DC, I was back in Avindra Nath’s office at the NIH’s huge Clinical Center.
Avindra Nath led the 5-year intensive ME/CFS study at the NIH. The results are expected soon.
The world’s largest hospital that’s devoted entirely to clinical research, the Clinical Center generally has 1,500 researchers packed away working on research projects – and it showed. I quickly got lost in the seemingly endless maze of offices and was beginning to panic (not late again!), but someone took pity on me and walked me down to Nath’s office.
At 11:03 AM, apologizing for being late – he’s clearly committed to being on time – Nath popped in and we sat down in a nearby conference room. Other than the fact that I was masked and he was masked – and I wasn’t late and soaked this time – everything seemed pretty normal.
The Chronic Fatigue Syndrome (ME/CFS) Intramural Study
Nath has been the Clinical Director of the work the National Institute for Neurological Diseases and Stroke (NINDS) does at the Clinical Center for over ten years.
The study was truncated by the pandemic, but Nath said the results of the study – to identify abnormalities the NIH could further study – had been achieved.
He’s been running the massive NIH-funded intramural ME/CFS study. The study, which painstakingly assessed its participants to ensure they had an infection-triggered case of chronic fatigue syndrome (ME/CFS), involved two week-long stays at the hospital.
While the study didn’t have all that many participants, its scope – using exercise studies to assess the immune system, brain, autonomic nervous system functioning, and many others – was large, indeed. The intense initial examination – which took up a week at the facility – was designed to ensure that only people with a post-infectious onset of ME/CFS were in the study. Another week of testing followed later. That, in itself, made it a unique study in the annals of ME/CFS research.
So did its goal. The intramural study – created entirely by and within the NIH – was produced with the implicit promise that if the study found something, the NIH would pursue it. That promise made it potentially the most important study in the history of ME/CFS.
As it did with so many things, the coronavirus pandemic upended the study. It put an abrupt end to the ME/CFS study, but what it took away on one hand, it gave with another as it also fostered a similar long-COVID study. Since long COVID appears to closely resemble ME/CFS, the study, in a sense, went on – just with another facet of ME/CFS – the long-COVID facet.
Still, it’s ME/CFS at this point that needs the funding, and the early ending of an already small study was concerning. I asked Nath how the early end of the ME/CFS study had affected it?
Nath replied that the sample size was smaller than what he would have wanted but that they’d studied everyone extensively and collected a lot of data on them. The studies were probably going to get critiqued in the journals because of their small sample size, but the goal of the project – to find further avenues for research – was accomplished. Nath said, “While we may not be able to make conclusive statements, we can certainly say that these are very important things to pursue in other studies.”
That was huge. As Nath said, the study was never designed to solve ME/CFS – it was designed to set a framework for future funding, and that was accomplished.
This was a big project that ended up requiring many different disciplines which had never worked together to work together. Ultimately, Nath created five different research groups to analyze the data.
As the data came in, he brought the groups together to take a crack at it. As each group interrogated their data in relation to the other groups’ data, new questions came up. Should we dig deeper into this? Should we analyze these samples differently? This kind of iterative multidisciplinary process basically mimicked what goes on in the body as different systems interact with each other. It made total sense and one wishes more projects like it were underway.
It sounded like such a complex process that I asked him if he’d ever done anything like this before? He laughed and said no. It was a lot of fun, and a lot of learning took place, but it also took quite a while.
The Papers
The multi-dimensional project – which exposed different research groups to each other for the first time – elicited new questions and approaches.
Each group has written up its own section which is being amalgamated into a big paper that is pretty close to being submitted. There won’t be just one manuscript, though. Some of the researchers got excited enough about their findings to write papers on their own. Those smaller papers are being held back until the main one is published.
I remarked that it sounded like the project has triggered quite a bit of interest (???). Nath said it’s triggered “a lot of interest”, that he expects many papers to come out of the study, and thinks the results are going to be “fascinating”.
The long-COVID study that’s underway is similar to the ME/CFS study: the huge questionnaires, the intense screening process, and the several weeks stay at the hospital – they were all retained in the new study. So, by the way, are the research teams that are now comfortable working together in this new multidisciplinary environment.
A few things will be different – a more intense focus is being given to coagulation and the metabolic chamber is probably going by the wayside. It was so difficult to get access to the metabolic chamber that it considerably slowed the study down and wasn’t revealing enough in itself to justify the wait.
Always hoping for good news, I asked (fingers crossed) if, in his experience, long COVID had sparked more interest in ME/CFS. He said it had sparked “huge interest…Everybody knows somebody who has had long COVID and is asking “What can I do to make a difference? The self-motivation factor is extremely high and everyone understands there is overlap with ME/CFS. If you study one, you’re going to benefit the other.”
I asked how close the two diseases were. Thus far, Nath has found that they’re mostly the same but not entirely. Besides the fact that some people with long COVID have organ damage, there appears to be more microvascular disease, blood clots, and blood vessel problems in long COVID. There also appears to be less PEM.
I asked him if anything had surprised him about ME/CFS? He said different groups in the study would probably tell you they were quite surprised to find what they did. From an immunological point of view, he found immune activation. How and why it’s present is unclear, though.
Immune activation can be present without being the culprit in a disease. Nath noted that a subset of individuals with ALS, for instance, have immune activation, but halting it doesn’t stop the progression of the disease. It’s a secondary effect of the disease and something else is driving it. The immune activation he’s found could be driving ME/CFS, could be a secondary effect of the disease, or it could even be protective.
Neurological Issues
Nath noted how important central nervous system problems are in long COVID and ME/CFS. While the early symptoms like food and smell problems get a lot of press, the long-term consequences, the ones that are disabling, the ones that allow you to function in society – are mostly neurological.
(A recent study found that a COVID-19 infection is increasing the risk of a vast array of neurological disorders, including ischemic and hemorrhagic stroke, cognition and memory disorders, peripheral nervous system disorders, episodic disorders (e.g. migraine and seizures), movement disorders, mental health disorders, musculoskeletal disorders, sensory disorders, Guillain–Barré syndrome, and encephalitis or encephalopathy.)
In fact, Nath is now engaged in a two-part neurological study of long COVID, the second part of which involves a clinical trial in which high-dose steroids, IVIG, or placebo will be given to see how these different immune factors affect the immune system.
Nath’s done two brain autopsy papers of COVID-19 patients. The second brain autopsy paper found blood vessel damage, protein leakage into the brain, immune complex formation, microglial activation (neuroinflammation), and activation of the classical complement pathway.
Nath believed that antibody attacks on the endothelial cells lining the blood vessels were probably the inciting trigger. Next came platelet activation and leaky blood vessels. Those macrophages, though, were a problem. If they enter the brain, they are like unwanted guests – they never leave. If they remain activated, they can damage the myelin covering the neurons for a long time.
(Jarred Younger is studying immune cell infiltration into the brain in ME/CFS. Nath wondered whether something similar could be happening in long COVID and ME/CFS, and noted that new and better radioligands that can more definitively determine if activated microglia are present have recently been developed (the older ones are not very effective). He was “very eager” to use them in long COVID and was talking to people at Johns Hopkins to get that done.
Immune Therapies?
That brought up what to do if immune activation is driving these diseases. Nath noted that researchers at long-COVID conferences are already talking about trying immunotherapies. (Dr. Klimas is a bit ahead of the game here – she’s has been wanting to use immunotherapies in ME/CFS for at least a decade.) They’re tricky, though, and Nath warned that they have to be done in the context of clinical trials – doctors should not be trying them as they can do more harm than good if you’re not careful.
The Gist
- Three years after the pandemic interrupted any attempts to get back to DC and see Avindra Nath, I was back. (This time I was on time. (lol)).
- Nath is finishing up the 5-year (but interrupted) NIH Intramural ME/CFS study, which included two week-long stays at the facility, exercise testing, immune testing, brain imaging, etc.
- The study was truncated by the pandemic, but Nath said mounds of data were gathered and the goal of the study – to uncover areas for the NIH to study – was met.
- The study was so wide-ranging the five different research teams participated and ultimately collaborated with each. One large paper is almost done, and Nath expects many smaller papers to come out of it. He said the study had sparked “huge interest” and called the results “fascinating”.
- Nath, an immunologist, said he found evidence of immune activation but could not say whether it was driving the disease, was an add-on effect, or if it might be protective.
- His COVID-19 brain autopsy work, though, suggested that antibodies were attracting immune cells and platelets to the endothelial cells lining the blood vessels and causing blood vessel leaks which were being mopped up by macrophages.
- The trouble is that macrophages are not supposed to be in the brain, and once they’re there, they behave like unwanted guests: i.e. they stick around.
- If macrophages are the issue – and some other studies suggest they might be – Nath noted that a variety of immunotherapies (IVIG; anti-TNF-a, IL-1, IL-6, or JakStat inhibitors) could be helpful. These types of drugs are already being discussed with regard to long COVID in conferences.
- Recent strains of the virus are less virulent, but more immune evasive and stick around longer in the body. In the long term, it’s possible they cause more damage including things like long COVID.
- Nath called diseases like ME/CFS, long COVID, fibromyalgia, POTS, post-Lyme Syndrome, Gulf War Illness, and Sick Building Syndrome the “mysteries of medicine” and believes that “if you solve one – you’ll solve them all.”
- He proposed that “the best way to get at any one of them is to pick one and throw everything at it and solve it. Don’t jump around studying a little bit of this one and a little bit of that one – pick one and dig into it. You’ll probably find that what you found there is applicable to all these other diseases.”
- Nath believes the long-COVID field is exploding and that over the next year we’re going to learn a lot.
- He’s not concerned about the ability of the ME/CFS field to integrate the findings that are sure to come from long COVID into it stating “It’s all going to get integrated….Even if you wanted to, you couldn’t separate them. There’s no reason to fear.”
After I asked whether different strains of the coronavirus might be producing different kinds of long COVID, Nath noted that recent strains of the virus are better able to evade the immune system, appear to be more persistent in the body, and may be less virulent but persist longer. This is actually a pretty common outcome of viruses as they learn to adapt to the body. It’s possible, though, that they may actually cause more long-term damage – something he wonders about with long COVID.
Then there’s the question of viral persistence. Could a persistent virus or part of a virus be driving long COVID or ME/CFS? Nath didn’t know but noted that we all have a lot of viruses in us (EBV, CMV, chickenpox, and others) which usually don’t cause any problems. If you become immune suppressed, on the other hand, they can cause bad things.
The Mysteries of Medicine… Solved?
Nath called diseases like ME/CFS, long COVID, fibromyalgia, POTS, post-Lyme Syndrome, Gulf War Illness, and Sick Building Syndrome the “mysteries of medicine” and believes there’s a huge overlap between all of them. His guess was “if you solve one – you’ll solve them all.”
He proposed that “the best way to get at any one of them is to pick one and throw everything at it and solve it. That’s the key thing. Don’t jump around studying a little bit of this one and a little bit of that one – pick one and dig into it. You’ll probably find that what you found there is applicable to all these other diseases.”
Let’s hope Nath is right – that’s precisely what’s happening with long COVID.
That’s why, he said, researchers sometimes study really rare diseases or rare forms of diseases. A single family with an unusual form of a disease could hold the key that unlocks the disease for everyone else.
For instance, there was a case report of a family whose members – except for one member – developed Alzheimer’s at a young age. A rare mutation was found in every member of the family – even the member who remained healthy – that turned on Alzheimer’s early. The healthy member, though, had a mutation that impeded the progress of Alzheimer’s – and that mutation presented a possible key to treating Alzheimer’s.
The Future
I asked him how much he thought we’ll know about long COVID in a year? He said:
“I think we’re going to know a lot. There are so many labs working simultaneously and the NIH is dumping a lot of money into the RECOVER Initiative, but they’re not the only source. There’s private money, philanthropy, industry – all kinds of ways people are doing things. It’s just exploding.”
The ME/CFS field is so small, though. Was he concerned about the ability of the ME/CFS field to integrate the long-COVID findings into it?
He wasn’t – stating, “It’s all going to get integrated….Even if you wanted to, you couldn’t separate them. There’s no reason to fear.”
That was good to hear, and that was a good note to end the interview on. It’s going to be fascinating to see what Nath and his multi-disciplinary team found. Plus, when his long-COVID project wraps up, Nath is also going to be able to give us the most detailed and wide-ranging comparison between ME/CFS and long COVID yet.
On our end, it will be critical to ensure that the NIH responds appropriately. Thus far, the NIH has been acting as if ME/CFS was somehow divorced from long COVID. No new funding opportunities have been announced and the NIH is sticking with the 3 rather meagerly funded NIH ME/CFS research centers.
Since the goal of the project is to uncover areas to concentrate on, that should change. The intramural ME/CFS study, though, was Francis Collins’s baby and he’s not there anymore. It was great to see Nath’s confidence that long-COVID results are going to filter down to ME/CFS and we are going to need to have the NIH honor its promise to us and devote significant new resources to ME/CFS.
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Exciting write up…any idea when we can expect the papers!?
It sounded like they would be submitted fairly shortly and then there’s the publication process which can take from several months to quite a bit more.
Will they publish a preprint?
I am not so sure about that. Pretty much everything that he mentions in this article has been mentioned over many years. Nothing novel stood out for me, but I will reserve full judgement till I see the papers.
It was good for me to hear that a) the project was a success – I know that’s not news but it was good to hear nevertheless (lol), and that there’s tremendous interest across all levels – academic, government, private industry – in long COVID that he believes is translating to a big boost in interest in ME/CFS (again, not really news – but good to be reaffirmed from a senior researcher) – and lastly that he thinks that the long COVID findings will quickly make their way to ME/CFS (that last one was news).
As to the actual findings – I, too, am itching to find out. I don’t have a clue what they are but it was encouraging that he said the some of the researchers were surprised and excited about what they found.
Still, the papers will tell the tale. We shall see!
I think Nath refers to looking for rare variants – genes which will result in you getting ME/CFS/greatly increase your risk – these studies require whole genome sequences about $1K/person – suggestion on Science 4 ME* you need 1000 – about $1 million.
What about also running Gene Wide Association Studies – GWAS – Chris Ponting’s currently running ME/CFS GWAS in the UK – about $4 million? GWAS looks for smaller genetic influences — a recent GWAS in migraine found the key gene/pathway to target with drugs.
GWAS can be delivered relatively cheaply — why is NIH not running them in Lyme, ME/CFS & Long Covid – then combine the data?
*
https://www.s4me.info/threads/suppose-you-have-%E2%82%AC5-10-million-for-me-cfs-research-what-would-you-spend-it-on.30357/#post-445820
I love the way Nath calls ME/CFS, Fibro, Post-Lyme Syndrome the “Mysteries of Medicine”. They are only mysteries because the NIH refused to fund studies to find a bio- marker. Those chose not to listen to patients, or encourage instruction on ME/CFS in Med School. They acted as if the disease did not exist, despite the millions of disabled. Women who had glandular fever followed by ME/CFS were dismissed as “hysterical” for 50 years. The Gulf War tankers and infantry vets were told that they had Post Traumatic Stress Syndrome, when Sarin gas detectors were going off all over the place. I would rather see Dr. Systrom funded privately, as it is going to require a “clinician” with extensive knowledge of both Cellular Biochemistry a s Human Physiology to treat this. The NIH has known for decades that ME/CFS patients’ legs turn purple/blue when showering. They chose to ignore that. Too difficult to study. Dr. Systrom has the intellectual curiosity to attack “Medical Mysteries”. The preload failure problem should have been tackled by NIH years ago!!
If Dr. Nath is certain that he has found blood vessel endothelial tissue inflammation in the BBB of Long Covid patients, then we need to be ready to immediately examine the endothelial tissue in know ME/CFS patients during autopsy. There may be several causes of ME/CFS, but at least we can nail one of them down. I’ll be the first donate my brain. The Gulf War vets nervous systems were damaged by low levels of Sarin gas. ME/CFS is probably immune system related. The Third Reich supposedly did not employ their huge stock piles of this nerve agent, because it is a tasteless, non- visible, odorless gas. Thought too dangerous to handle.
Hear, hear for Rich Grisius. “Medical mysteries” indeed. Nonetheless, I’m dying to read about any insights yielded by applying NIH’s advanced devices to the unknowns of ME. That, after all, seemed to be the rationale for bringing the ME research into the intramural program.
Regarding Long Covid, I’m baffled as to why an NIH clinical trial — presumably big and expensive — would concentrate on such broad-brush and basic remedies as steroids and IVIG versus placebo. I thought NIH was focusing on hypothesis-driven research, not empirical data-gathering.
Ronnie, Dr. Prusty is pointing right at the villains in his abstract printed in Frontiers in Molecular Biosciences.
They found active and abundant HHV-6 and EBV transcripts in postmortem neuronal tissue of ME/CFS patients by using microRNA probes. These tissue specific infections seen in the three ME/CFS patients, were not seen in the controls
I agree with Rich.
For a number of years I have had a few contacts with Professor Nath. I have a lot of faith in him. But it all takes a very long time. Still, I’m glad someone with his status is investigating ME/POTS. I look forward to his publications. I know he knows these are real illnesses. Prove that to the entire medical community.
Considering how many people are effected by this disease, there should be 20 labs the size of Nath’s studying this at the NIH. I live across the street from the campus. It is bigger than 95% of the Universities in this country. The Dental Research Institute in building #10 has vastly more funding than those in “Neuro and Stroke” working on ME/CFS.
Blood coagulation seems to me 5to be the simplest of these possible “causes.”
Is there any indication that it is a unique cause of CFS, or that it has been created by some other factor?
I don’t think anybody thinks coagulation is the cause; if it plays a role and my guess is that it does, it will do so in combination with other factors. Microclots have been found in ME/CFS but they’re weren’t as prevalent as those found in long COVID.
Thank you Cort,
Over 20 years ago a special microscope found that my blood cells were overly clustered together. And since about that time I have had CFS.
2 questions.
1) CAN blood cells be UNclustered? And
2) Would it do me any good to have that done?
I don’t know. I’ve had a few readings suggesting of blood clots and my blood from what I’ve gleaned from tests tends to run thick. I think it must be a piece of the puzzle.
Since they talk of clot-busters I assume these things can be unclustered.
Encouraging news Cort. Interesting to see the paper and good that it has also generated smaller papers. I like the idea that if you solve one you solve all. I feel hope that things are beginning to move at last.
I see that pwME from stress were screened out of his study. It’s not surprising given that long covid is a post-viral illness. But since I’m a stressed out pwME it’s a little disappointing. Are there any studies which exclude post-viral pwME and focus on the stress-induced ones?
Not that I know of. Consider, though, that while you were stressed you were almost certainly at risk of viral reactivation, if not at more risk of an infection – which you may or may not have known was happening. I’m in a similar boat by the way. I just gradually got sicker and sicker over several months with no evidence of an infection (sore throat, fever, etc.) – but who says that infections can only cause those symptoms. I read there’s a form of mononucleosis that produces alot of muscle pain but not typical flulike symptoms.
Stress- and immune system are also closely linked, and stress is an epigenetic mediator. I’ve read about at least one other (autoimmune) disease for which stress has been established as an initial onset trigger. My guess is that for ME/CFS, high stress events (or high chronic stress) can act as an immune trigger quite similar to an initial onset infection event. But of course this would not preclude that viruses like for example reactivating herpes viruses are involved too, or that we do not remember an asymptomatic infection.
2 Things. 1)Not having been know to have a viral beginning appears to keep you out of research, and 2) if you are sick with ME it must be related a an unknown virus. That makes it likely that it well eventually fall under “post viral syndrome”, excluding those with non-viral cause. Many of us will never be diagnosed with ME for that reason even if we have ME. For me it was a lot of things all at one time, pregnancy, complication in labor, risk to baby’s life followed immediately by emergency surgery, and severe pain with intense physical and mental stress. We’ve been pushed over to the side and will eventually pushed out.
@Sue and Cort, I too would like to see this decoded one day. But I feel that it might be the right way of doing studies first for cases that are so clearly post-infectious that it becomes very difficult to make any allegations of psychological factors at play, and then hopefully show the same ME/CFS pathomechanism applies for other onset trigger too. But if you’re interested I think that there’s already papers out there that review the effects of stress on the body (I think that stress is often commonly thought to only be a transient state of mind, neglecting that it is also a systemic state of the body that can induce changes in the body). Also I am quite fascinated by German researcher Prof. Elisabeth Binder who researches stress-induced psychiatric and post-traumatic disorders on a molecular and epigenetic basis. https://www.psych.mpg.de/2733202/home , https://www.psych.mpg.de/binder . She is doing for psychiatric diseases what biomedical researchers are doing for ME/CFS, namely looking for an actually treatable biomedical pathomechanism https://www.youtube.com/watch?v=18H-eaS4PK4. Maybe at some point of time, when the biomedical picture of ME/CFS has become even clearer, an exchange of findings between her and ME/CFS researchers would be a good idea just out of curiosity if there’s any areas of overlap regarding stress-induced mechanisms. I really would not be surprised if there were some undiagnosed ME/CFS patients among her cohorts.
Definitely, someone to keep an eye on. With the stress response system acting up, the PEM and high functional impairment, the natural hypervigilance that ensues – I, quite frankly, don’t see how PTSD could NOT be involved in this disease.
Wow…. I’m impressed that you have such access! ! As someone who shares all the same symptoms of ME/CFS but arrived here post toxicity rather than post viral , I was happy with “ if you solve one you solve them all “ comment. I was severely damaged by a Fluroquinolone So I probably share more with the GWS population with regards to the trigger. The science uncovered by these studies should benefit us all . Fingers crossed ! Thank you Cort !
Fingers crossed indeed. I hope he’s right about the solve one – probably solve them all idea. Wouldn’t that be something?
Thanks Cort for this great write up, for for making the trek to DC, I hope it didn’t cost you too much energy
Thanks – it was part of a cross-country trip in the van to visit my brother in Cape Cod. I took it slowly on the way out with many stops and it went great. On the way back I hit some chilly weather and had to push it but it was rougher but I managed. .
Honestly, it was great seeing Nebraska, South Dakota, Minnesota, Illinios, New York – I’d never been to those places.
Thanks as always. Can I ask if the study regarding the 23 vaccine injured patients experiencing severe neurological symptoms was brought up? I would think given his comments here that he should be very interested in studying and helping these individuals. They have purportedly tried to communicate that the immunotherapy treatments they were given at best only had temporary favorable results:
https://www.youtube.com/watch?v=9XGpe6MTaFg&t=349s
https://www.youtube.com/watch?v=Bvssp9uA72A
Unfortunately the interview happened about 6 weeks ago – before I knew about it. I would have loved to ask him about it….
Damn Cort – you are like a super hero!! Just amazing what you are able to do 🙂
I just contributed to the fund raiser. Everybody who can, please help support Cort’s exceptional efforts on our behalf
Thanks Jody!
Nath says it’s important not to jump from one quick study to another but dive deep and yet jump is exactly what he did, once again leaving ME/CFS patients behind and chasing the headlines. Your faith is admirable, Cort, and a huge thank you for your amazing coverage on the behalf of all of us. I find it harder and harder to feel hopeful, or place any faith at all in NIH. They do not have the track record of having our best interests at heart.
I don’t know JG! Here is what I think happened. He couldn’t see patients anymore and wasn’t likely to for awhile so he decided to start analyzing the data. Could he have waited? I don’t know. It is a pity the study wasn’t completed and we’ll see what if any costs there are to that as we go on I guess.
With regards to increased funding – I have no illusions; I’ll believe it when I see it. I expect we’re going to have to fight for it – possibly in Congress.
As someone who has been sick with ME/CFS since 1986 (you do the math) I’m beyond chasing cures and clinging to hopes hyped with every new study. It’s been shameful and we all know it. Accountability might be a new tactic. In Congress? Sure. Why not.
There won’t be funding until there is accountability.
We came close a couple of years ago to getting Congress involved. It would have made a HUGE difference – particularly with the pandemic of long COVID happening. I doubt they would have been happy to see the NIH carry on with their business as usual approach.
I really wish I could figure them out…they are such a puzzle!
How many people at the NIH actually have a say in how much an illness gets in funding?
I’m not sure how many people are in charge of determining whether ME/CFS gets a funding opportunity. It’s probably not many, though – probably a group of people in a Council or other such thing that decide on things like that.
How many people at the NIH actually decide how things are done?
Would it be worth finding out? Might be worth investigating the bureaucratic side of things?
I support holding people accountable as well.
Thanks, Cort, this is good news indeed. It’s becoming clear that protection at the ACE-2 level is key. In a recent post of yours I reiterated the effects of PEA (palmitoylethanolamide) on the Covid virus. We also know that CBD acts on the virus post cell entry and THC does not:
https://www.science.org/doi/10.1126/sciadv.abi6110
We also know that “Cannabinoid acids from hemp (Cannabis sativa) were found to be allosteric as well as orthosteric ligands with micromolar affinity for the spike protein. In follow-up virus neutralization assays, cannabigerolic acid and cannabidiolic acid prevented infection of human epithelial cells by a pseudovirus expressing the SARS-CoV-2 spike protein and prevented entry of live SARS-CoV-2 into cells.” These are CBDa and CBGa. They are available as powdered isolates, but a bit spendy.
https://pubmed.ncbi.nlm.nih.gov/35007072/
Then today I saw this from Science Advances, published 7 December. It is a potential treatment, not preventative:
https://www.science.org/doi/10.1126/sciadv.abq6527
It’s a protein molecule created to be a “decoy” to draw virus particles away from ACE-2 receptors by mimicking an ACE-2 docking site while floating around in your blood. For a simiplified discussion, see:
https://www.dailykos.com/stories/2022/12/9/2140663/-An-ACE2-decoy-irreversibly-inactivates-SARS-CoV-2-even-antibody-resistant-variants
This treatment is not ready for prime time, obviously, and probably will cost you an arm and a leg and various other bodily appendages to get ahold of it, but it might work. In the meantime, I will continue to take PEA, CBD, and CBDa every day. CBGa is too expensive for me, so I haven’t bought any. I haven’t caught the virus yet, but if I do, I have the FLCCC protocol medications on hand. If only they would work on MCAS!
This is a critical and cautionary post. Nath is lumping Illnesses. Simon Wessely also did, remember “just one functional disorder“? There’s a reason we have several disease names rather than one, regardless of the overlaps. In my opinion its Unwise to assert that solving pots or FM or gws would solve ME/CFS – the potential disability of ME/CFS vs fibromyalgia are poles apart, some people with Fm Can do and benefit from exercise, the very thing that makes pwME sick. FM has an all over pain that’s not so much reported in LC either. It’ seems To me, NIH still doing the bare minimum for historically neglected and maligned illness, it’s just one step up from nothing – oh just do one to cover all. The thinking that long covid can substitute ME/CFS, in all its stages and severities,and other illnesses, which is what NIH are basically doing, is flawed, neglectful and wrong. The biggest victims from his approach are likely the long-term severely affected/harmed, which long covid research is not enough for. What surprised me is he seems chirpy, nonchalant, remorseless. Does he have any idea of the disability/suffering that’s gone on years in ME, way beyond the high function people he’s met via studies? Of course those dying in bed didn’t deserve any of the treatment trials that nih can overnight do for long covid, & no you don’t die in bed with pots or FM because ME/CFS is different.
Thank you JG Barnes and Kerry Newnham for your comments.
I go back to the mid-eighties with Incline Village, Lyndonville and Simon Wessley. I don’t want us to go back there.
The doctor who diagnosed me knew the whole US history of Incline Village and what was known at that time. He explained they first thought it was chronic Epstein Barr, but finding sporadic non-Epstein Barr cases around the country, they changed their mind. So, he said, “They thought it was Epstein Barr, but now they know it isn’t. They don’t know what it is, but whatever it is, that’s what you have.” The US later named it “Chronic Fatigue Syndrome”. Why not ME, who knows?
I also have reservations about the ‘get one get them all’ remark. There’s an awful lot lot that can go wrong with the human body (just count up all the existing hypotheses and cellular functions involved!). Similar systems being impacted does not inevitably mean identical pathogenesis. Even LC and ME have notable differences by his own admission.
I guess the main positive here is that he obviously feels from the analysis that despite the small sample he has enough clear outcome material to direct follow up work and meet the projects goal of being a directional springboard.
But we need to stop all these little Small sample scattergun study and put out robust studies that actually take us forward on the biomarker and treatment front.
It will be interesting to review his results against the big genetic studies underway leveraging the two together could bring some real insights.
But surely they may shed light on where the blind spots of medicine MIGHT be at eh. 1 blindspot may lead to another?
Besides the fact that some people “with long COVID have organ damage, there appears to be more microvascular disease, blood clots, and blood vessel problems in long COVID. There also appears to be less PEM.”
I wonder if the people being studied for long-covid have been vaccinated as well. If they are, how can you tell apart the effects of the vaccine vs the effects of whatver the ME/CF state.
Or if there are differences between long-covid with vaccine vs long-covid without vaccine.
It brings to mind the Bateman people wrote they saw a difference with the Nasa Lean test between long-covid and long-standing ME/CFS. That the long covid had narrower pulse rates. And that after four years [was it?] of ME/CFS onset, they widen again. They surmised perhaps the body compensates for this after a while of being in that initial mode, as years pass.
I though that was interesting because my pulse rate was narrower both before getting sick with EBV and 5 years after that infection. So somehow my results were not aligning with theirs [it should have been wider]. In gact, I was getting much worse into a severe state, more bedbound state.
As I have been getting better, my pulse pressure is also better.