Paradigm Shift for Long COVID Patients (and people with ME/CFS)?
The dramatic announcement that Congress is going to appropriate over a billion dollars (a billion dollars!) to study the COVID-19 long haulers was just one sign that long COVID is being taken seriously. Hopefully, along with that will come a new recognition regarding chronic fatigue syndrome (ME/CFS).
So much of what is being written and done about long COVID, after all, could have been written and done about ME/CFS, but we just didn’t have the sudden, worldwide event to spur the medical profession into action.
We don’t know how many people are usually added to the ME/CFS community every year but we can take a shot. Approximately150,000 people in the U.S. reportedly come down with infectious mononucleosis (IM) every year. If five percent of them come down with an ME/CFS-like condition, IM adds about 7,500 people with ME/CFS to the U.S. every year.
IM, however, is apparently responsible for only about 8% of young people with a sore throat. Tens of millions of people in the U.S. come down with the flu every year. Many more people come down with other colds and infections. Plus, a substantial number of people with ME/CFS do not have an infectious onset. Year after year, then, a lot of people are probably being added – under the medical profession’s radar – to the ME/CFS rolls in the U.S. and elsewhere every year.
The difference with the coronavirus is its sudden impact and its visibility. There’s something about a worldwide “pandemic” that concentrates the mind! One editorial from a leading medical journal wrote:
“Given the scale of the pandemic, if even only a small percentage of the tens of millions of infected people worldwide develop long COVID, a staggeringly large number of people would need long-term follow-up and treatment.”
The pandemic appears to be finally forcing the medical community to acknowledge and grapple with post-infectious illnesses – which, it turns out, are not uncommon at all. Even the really hard cases. Even the most resistant part of the medical profession – the doctors – are starting to change their ways.
Doctors have come down with ME/CFS before – but not in the numbers they are coming down with long COVID now. Those doctors are pushing for more and better research and better support from the medical community.
They, after all, are getting sick too. Thirty-nine long COVID doctors in the U.K. recently got together to write a “manifesto”, “From doctors as patients: a manifesto for tackling persisting symptoms of covid-19“, to the British Medical Journal (BMJ). If 39 sick doctors in Britain wrote a letter, then hundreds of doctors in the U.S. must be ill.
They weren’t messing around. How often do you see doctors using a term like manifesto. That’s the kind of language that someone uses to try penetrate through the everyday thinking – the tranquilized obliviousness – of a profession. They’re trying to transform the way doctors and the medical profession operate. They are asserting that it’s not feasible anymore to treat only the infection and leave the patient to deal with its long-term consequences. The BMJ letter states:
“death is not the only important negative consequence of SARS-CoV-2 infection. It has become increasingly clear that many patients, even those with mild cases, may go on to develop lasting symptoms that can have disabling consequences for those affected.”
We argue that this means accepting an emerging picture that prolonged symptoms are having a substantial impact on a significant minority of people and acknowledging that death is not the only outcome to measure.
A Nature editorial, “Meeting the Challenge of Long COVID”, felt similarly.
Both editorials pushed for more and more research.
“Failure to understand the underlying biological mechanisms causing these persisting symptoms risks missing opportunities to identify risk factors, prevent chronicity, and find treatment approaches for people affected now and in the future.”
Recognition is also starting to creep in there that ME/CFS has been poorly treated by the medical profession – and some are vowing that history is not going to repeat itself.
Take this Nature editorial, “Long COVID: let patients help define long-lasting COVID symptoms“, which apparently is coming straight from Nature itself – and is going to be widely read. The photo atop the editorial – is from a #Millions Missing patient. The caption below the picture reads:
“Research funders were reluctant to engage with groups representing people with ME/CFS (pictured). The same mistake must not be made with those experiencing long COVID.”
The editorial asserts that:
“researchers and policymakers must take heed of what happened in the case of myalgic encephalomyelitis, also called chronic fatigue syndrome (ME/CFS).”
Unfortunately, the editorial then strangely presents ME/CFS as a kind of problem solved. It states that “It took sustained advocacy from patients’ organizations — who had to organize their own independent science advice — to persuade research funders to listen.” – as if they are listening. It goes on: “And although COVID is well known, long COVID isn’t — at least, not yet. It is crucial that those with the condition are listened to in a way that, tragically, people with ME/CFS were not.” – as if people with ME/CFS are being heard.
It been past time for change for the ME/CFS community. Some in the medical community are now recognizing that.
Interestingly, it was Peter White (of CBT/GET fame or someone else?), who pointed out that the use of the past tense resulted in a “dangerous misconception”; i.e. that the situation has been solved. “The reality”, White correctly wrote, “is that the tragic situation continues” – that patients still aren’t being listened to, and that funding still sucks.
White asserted that ME/CFS’s causes are unclear, that it’s an intractable illness, and that the “urgent need for high-quality, imaginative and ambitious research should therefore not be undermined by downplaying the current impact of this condition (ME/CFS) on millions of people around the world.”
Even though the editorial got some key facts wrong, it did get a lot right. It brought ME/CFS into the middle of the discussion and used the problems people with ME/CFS encountered in the medical profession to argue for a different response to the long COVID patients. Another silver lining to the COVID-19 catastrophe is surely going to be a recognition of how poorly ME/CFS has been treated.
Even The Lancet – for years the bugaboo of the ME/CFS community for its refusal to address the problems of the PACE trial – has stepped up on the long hauler issue. The recent “Facing up to long Covid” editorial stated that “long COVID is a burgeoning health concern and action…” (and that) “large and long-term cohort studies (which contain both hospitalized and non-hospitalized patients) are urgently needed”.
While it couldn’t bring itself to directly mention myalgic encephalomyelitis, it did acknowledge that “Many patients already feel dismissed or overlooked”, and referred to “poorly understood conditions (such as chronic pain and functional disorders)” as examples of how that has happened in the past. Basically, it said that the mistakes of the past should not be repeated.
When editorials from three major medical journals vow that things will be different this time – maybe they will be. Widespread change is a process that takes place over years, but one wonders if we will look back in five years and say – that was the defining event.
For now, it appears that long COVID is getting attention from major opinion makers in the medical field. While ME/CFS may not be mentioned as much as we might want in connection with long COVID, it’s certainly in the mix.
It was encouraging, for instance, to see ME/CFS experts in abundance in the NIH Post-COVID Sequelae workshop. It was very encouraging to see Emily Taylor and the Solve ME/CFS Initiative get a strong coalition to back a long COVID letter which emphasized the role ME/CFS and allied diseases should play in understanding it. It was even more encouraging to her that Emily Taylor and Solve M.E. played an instrumental role in educating legislators about the dangers of long COVID, which supported the enormous amount of long COVID funding for the NIH.
The next year is going to be very interesting. The time “to strike”, to make our mark, is now when the pandemic is in full force and the attention of the world is on it.
The Autoimmunity or Friendly Fire Hypothesis
Did the fight against the coronavirus unleash a swarm of autoantibodies which are causing long COVID?
An autoimmune process must be high on many researchers’ list of what’s happening to the long haulers. Autoimmune processes are often triggered by infections and can attack virtually any part of the body, and cause diverse symptoms. A recent study not only had some fascinating results but suggests we are going to see some studies the likes of which we’ve rarely seen before. It also demonstrates how important the mountain of work done, not on the long haulers, but on people who are still fighting off the virus, will be to understand the long haulers.
The Diverse Functional Autoantibodies in Patients with COVID-19 study is the kind of big study that we see all too rarely in ME/CFS. Featuring about 30 Yale researchers and almost 200 patients, the authors used the latest technology to look at a specific kind of protein – extracellular and secreted proteins (which are called the “exoproteome”) – which has not been assessed in ME/CFS. The study assessed thousands of these proteins.
The patients ran the gamut from those with mild, or even asymptomatic, infections to the seriously ill.
Right away, the study highlights what an opportunity a raging pandemic presents! It presents the opportunity to catch so much in the act. In typically understated terms, the authors state:
“While pathological innate immune activation is well documented in severe disease, the impact of autoantibodies on disease progression is less defined.”
In other words, medical science well knows how destructive autoantibodies can be in autoimmune diseases, but it doesn’t know all that much about how the immune system gets itself into that fix.
What they found shocked them in a number of ways. First, they found startling autoantibodies present that were able to attack an array of human tissues. The autoantibodies appeared to make a difference: the more “functional” (dangerous) they were, the sicker the person was, and the more tweaked their immune system was. For instance, some of the autoantibodies were blunting the immune response to the virus – not exactly what the immune system was set up to do.
Interestingly, and perhaps importantly, they did not find a specific autoantibody signature in the COVID-19 patients. Instead, they found a complex array of autoantibody responses that were often specific to individual patients. These included many uncommon or rare autoantibodies which appeared to have a big impact on the person they were found.
That’s a very interesting finding given the difficulty thus far in pinning down the autoantibodies at work in ME/CFS. Besides the adrenergic and muscarinic antibodies that Scheibenbogen discovered, I’m not aware of any significant leads. I have a memory, though, of it being reported that lots of antibodies being found in ME/CFS patients, but no specific ones have stood out. Instead, there’s this weird mass of antibody activity.
It appeared that the body’s effort to mount an attack on the coronavirus had let loose a massive escape from the immune mechanisms designed to keep the body from attacking itself. Interestingly, the higher amount of inflammation present and therefore the tissue damage found (in the form of ferritin, CRP, lactate), the more autoantibodies to tissues were found. That made perfect sense. As tissues get damaged during inflammation, they let loose proteins which can then trigger an autoimmune reaction.
Not only were a host of new autoantibodies formed during this process, but the researchers found that old autoantibodies that had been kept in check prior to the infection may have been let loose.
So many autoantibodies were found that the authors asserted that it was critical that future studies employ “unbiased proteome-scale surveys” (i.e. very broad based analyses that could pick up all the unusual autoantibodies floating around).
Finally, they suggested that given the remarkable diversity of autoantibodies which showed up early in the disease process, more studies need to examine this in infectious diseases. The authors suggested that the persistence of these autoantibodies over time could help explain why some people may fail to recover from COVID-19. The senior author of the study stated that:
“Because antibodies can persist for a long time, it’s conceivable that they may contribute to the development of long-Covid diseases”.
This early study, then – as other early studies will do – will be able to inform long COVID studies on what to monitor for – in this cause autoantibodies. They have never, to my knowledge, been studied in post-infectious ME/CFS studies.
Autoimmunity is getting a lot of play in the COVID-19 research literature. In “Autoimmunity as the comet tail of COVID-19 pandemic“, two researchers report that hyper-activation of the immune system – particularly in younger individuals – could be triggering autoimmunity.
That’s an interesting idea, given results from the Dubbo studies which suggested that those individuals with the most severe symptoms were most likely to come down with ME/CFS after an infection.
These researchers believe the atypical forms of COVID-19 which may affect everything from the skin, to the heart and skeletal muscles, blood cells, central and peripheral nervous system, etc., could reflect the diverse autoimmune processes unleashed by the virus.
Another recent review suggested that the wide variety of clinical presentations suggests an overexuberant autoimmune response may have occurred.
Speaking of autoimmunity, a German company called “Berlin Cures” reportedly offered to screen the German long COVID group, “Covid 19 Langzeitbeschwerden”, for their autoantibodies to the adrenergic and muscarinic receptors that Carmen Scheibenbogen first found. In November, a doctor with the group reported that they were finding these antibodies in all long COVID patients tested so far…
Conclusion
Major stakeholders in the medical world have taken up the plight of the long COVID patients. Several editorials doing so have rued the mistakes of the past, where post-infectious patients have not been believed, and some have directly mentioned ME/CFS. Sick doctors are even writing “manifestos” charging the medical profession to change its ways and not consign them and their illness to the wastebasket, as it has in the past.
Meanwhile, COVID-19 studies may be uncovering clues as to what’s happening to the long COVID patients. One large study examining the exoproteome was shocked at how many autoantibodies both to the immune system and to other tissues were found. The fact that the autoantibody levels were correlated with illness severity suggested they were making a difference.
Interestingly, no autoantibody signatures stood out. Instead, the fight against the virus seemed to have triggered the production of a wide array of antibodies that often differed from person to person. Rare autoantibodies which appeared to have functional significance were found. New autoantibodies were formed, and at times, old ones were unleashed. The authors suggested that the persistence of these autoantibodies could help explain long COVID.
One report to a patient group in Germany indicated that the adrenergic and muscarinic antibodies Scheibenbogen found may be turning up frequently in the long COVID patients as well.
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Very interesting on so many different levels. Maybe this is why I’m feeling a bit bamboozled. I sense a shift is happening and for me it’s important to try and understand what’s happening, who’s doing what and where are we trying to go and what are we trying to achieve? There seem to be opportunities arising from this horrible illness Covid-19, that would be a terrible shame to miss, amongst the chaos and misery.
Yes, great opportunities – not just for us but for many diseases that can be triggered by infections. COVID-19 is giving us the opportunity to catch that disease process in the act if we look hard enough. Hopefully we are and will be.
It is astonishing indeed that so little attention has been directed to ‘post viral fatigue syndrome,’ (often becoming CFS/ME) something that was known for so many decades but not adequately explored. Now, that there is a threat that Long covid –CFS/ME may become more rampant there is finally a little movement. I do hope there will be help forthcoming for the long suffering CFS/ME population soon. And I hope that the explorations of long covid include CFS/ME! Thanks Cort for all your magnificent work. Best to you for 2021.
Thanks! We shall see. I am – an eternal optimist it seems – am very hopeful. There is so much potential here.
Interesting.
Combining
“two researchers report that hyper-activation of the immune system – particularly in younger individuals – could be triggering autoimmunity…
…studies which suggested that those individuals with the most severe symptoms were most likely to come down with ME/CFS after an infection.”
And
“they did not find a specific autoantibody signature in the COVID-19 patients. Instead, they found a complex array of autoantibody responses that were often specific to individual patients.”
Sort of sounds like an immune system that is taken by surprise in strength and very rapid onset at the start of a strong and quick infection and not finding any good way to deal with it. Read: not finding any antibody to get the immune system produce a targeted and very efficient antibodies to get the fast and vastly expanding infection under control.
Making antibodies to pathogens is IMO sort of a trial and error proces by making antibodies to whatever and “sees what sticks” and works agaist the infection.
If nothing works soon enough in a quickly expanding infection that the body fears could overwhelm it within days, it might decide to set the “try and invent antibodies against whatever” knob to maximum and have every immune cell produce its own variants and see what sticks.
My understanding of the immune system is limited, but if I get it right many immune cells, once specialised against a certain danger, do not “unspecialise”.
In normal conditions, less functional “specialisations” get weeded out and (very roughly) only those with a usefull specialisation (for example against the current infection or overwon previous infections) and those without specialisations remain in the body in the long time.
With each new division of immune cells, unfunctional things get poorer chances for being retained then functional or “blank” immune cells.
Now what if the immune system had such a hard time or was panicking and near all immune cells tried to specialise against something in the hope something would work and then that antibody could be multiplied in huge numbers? Then there would be very few “blank” immune cells left, or at least far less then after a normal clearing of an infection.
That IMO could make “weeding out” the unfunctional specialisations in immune cells a very slow process and give many different sort of “unfuncional specialised” immune cells the chance to become a long term line of antibody producing immune cells.
Just some thoughts. I lack sufficient knowledge on the immune system but I am good at numbers and seeing how selective growth and weeding out might work. And it sort of has a ring to it.
Thanks for putting this so well, DeJurgen.
“not finding any antibody to get the immune system produce a targeted and very efficient antibodies to get the fast and vastly expanding infection under control.”
“Making antibodies to pathogens is IMO sort of a trial and error process by making antibodies to whatever and “sees what sticks” and works against the infection.”
It does seem like an overwhelmed immune process is either engaged in a trial and error process – pumping out antibodies like mad in hopes that some will stick – or is reacting to a lot of tissue damage or – the virus is fooling the immune into producing autoantibodies that attack and disable parts of the immune system that are tasked with getting it under control.
It’s amazing that a piece of genetic code which is not even alive can wreak so much havoc…
I think you hit on what the authors of that paper were indirectly saying. The body can pull back on those autoantibodies or allow them to lapse or disappear over time. That’s why the authors were not sure that they were going to persist.
Is there really such a thing as an autoantibody? Or — like microbes that can be commensal until a fluctuation in the microbiome/virome tips them into a pathogenic state — are autoantibodies just regular antibodies that are in a state that’s harmful to the host?
I have been so confused by the term autoantibody in particularly in cases where it and antibody are used interchangeably. I think you are probably correct – it’s an antibody which is harmful to the host.
Cort, I notice someone on your Facebook page has commented that it isn’t THAT Peter White who pointed out that the use of the past tense resulted in a “dangerous misconception”.
I had a bit of a look Fay and what I found was Peter White from Berkhamsted, UK – who was featured in the Readers respond, Correspondence section within Nature. He made the comment ‘dangerous misconception’. A different Peter White?
Thanks. It would be strange indeed if there was another Peter White out there that got a comment in about ME/CFS but it is possible. I don’t think this Peter White gave his credentials which often happens in comments. I will amend the blog.
1918 epidemic was deadliest to young healthy people— and some thought healthiest give strongest immune response (too strong cytokine storm) others, that the lungs were damaged, and no penicillin then.
https://www.smithsonianmag.com/history/why-did-1918-flu-kill-so-many-otherwise-healthy-young-adults-180967178/
With covid, it is known that lungs damaged, and we have penicillin, but still is deadly. So perhaps the two epidemics have more in common—- in their effects on the body—-than previously thought.
Penicillin is NOT of any use in virus infections. It is used against bacterias. It destroys their cell walls.
I have said it many times, CFS is an autoimmune disease. There hasn’t been enough focus on this, there’s been far too much on all sorts of fluffy, speculative theories.
A lot of time and money wasted.
Autoimmune disease is supposedly when the immune system attacks healthy cells. Or is the immune system attacking virus infected cells which are going undetected by viral serology which are not reliable. Even with Covid PCR tests some have been false positive and false negatives.
I find the idea of autoimmunity in post viral illnesses very intriguing. Basically autoimmunity is the body attacking the wrong thing (itself) in the wrong way (causing damage).
If I understand correctly, people with serious Covid are dying from the body’s overreaction to the virus which binds to ACE2 receptors–of which many are in the lungs but are also in other areas of the body. The body’s immune response is to produce antibodies which cause inflammation in the form of excessive fluids which overwhelm the lungs. The patient, in effect, drowns from their immune system’s over response and not from the virus itself.
Given the results mentioned in your article, to theorize that long Covid is from a tweaked immune system makes a lot of sense. Add to this the recent finding that people who have had recent cosmetic fillers are experiencing extra symptoms in those areas! Fillers are foreign implants and have probably already been tagged by the immune system. https://www.foxnews.com/us/moderna-covid-vaccine-side-effects
The idea that I’m entertaining is that each of us has our own bodily weak spots, whether from genetics or environmental exposure or what ever, so that might account for the variation in long hauler antibodies. I’m thinking that somewhere in the body’s immune system is a master chemical ‘switch’ which gets turned on but never turned off. It may take one illness to do it or perhaps just continuous exposure to something unhealthy or perhaps multiple small insults to create a continuous production of (auto)antibodies. Those differences might account for all the different types of ME/CFS onset.
Pardon me, but that’s my mind mulling about fluffy speculative theories. 😉 Wish I knew more about in-depth immunity because these researchers could really be on to something–a sort of unifying theory. However, I wonder how PEM and prolonged recovery might fit into this idea of autoimmunity. Correct immune function; such a delicate balance…
Hmm,
“I’m thinking that somewhere in the body’s immune system is a master chemical ‘switch’ which gets turned on but never turned off.”
Combine that with “a broad and diverse auto immune response to many parts of the body” mentioned in the blog and research.
Would a broad and diverse auto immune response, attacking many parts and types of cells all over the body, be that different perceived by the imune system as a broad and body wide pathogen trying to attack the body?
After all, the results would show quite some similarities: plenty of cells damaged at high rate all over the body. Poor blood flow and recurrent hypoxia (with its very damaging reperfusion injury following in its trail) would further add to the damage all over the body.
Maybe, just speculating a lot here, the body mistakes the combined damage that a variety of auto antibodies (formed in a previous early strong infection) and the damage of poor blood flow, long term low ATP production and recurrent hypoxia and reperfusion injury cause as an unknown strong pathogen it needs to mount a strong immune reaction against. And any strong and long lasting imune reaction risks to create plenty of auto imune issues… creating a vicious circle.
It in sort would even help closing the gap between viral onset ME and gradual onset ME: a strong long lasting imune reaction that risks to create the initial auto antibodies could be both triggered by a strong infection or by long lasting blood flow and oxygenation problems and the like (or rather a combo of them).
@dejurgen, seems as if we both like to riff on research–trying to link ideas. I like your further speculation of a system, with beginning insults, further wobbling out of control (ME/CFS) as each part reacts to the other (your “vicious circle”). The initial insult could begin in any number of places.
I then consider MCAS, which quite a few EDSers (and possibly people with chronic fatigue) seem to have, and wonder how that might affect the trajectory of the illness–and not just Covid. Nobody has explained the inappropriate granulation of these cells and the probable additional cascade of other parts of the immune system.
And then there is the SFPN (small fiber polyneuropathy) which Patricia Price mentions. How can we fold that into these ideas?
And there is the observation (thank you Ron Davis) that there is some factor in the plasma which especially influences our energy mechanisms…
And a side comment for Dennis Copeland; I too sometimes feel as if we are repeatedly shown ‘hope’ only to have it taken away. Personally, better to have some little sliver to hang on to then the idea of no help in our lifetime. And Brent, we will just have to wait and see how all that money will be spent. Could be good, or perhaps a disappointment. Time will tell. I choose to hold on to hope.
@Nancy B. , MCAS research has sort of been one of my research things since its a big issue for me. I’ll list a few post that have some real good info about a new approach I’m using that Bayard brought my attention to.
When in severe COVID illness, appears it has to be addressed fast. But when a daily thing, trying to get Histamine receptors working properly has been a better long term approach for me.
Some really good comments and lots of links within.
https://www.healthrising.org/forums/threads/mast-cell-histamine-immunotherapy-with-histamine.6233/
https://www.healthrising.org/blog/2020/10/10/ras-bradykinin-covid-19-chronic-fatigue-syndrome/
https://www.healthrising.org/forums/threads/pathogen-stimulated-histamine-production-and-release-by-neutrophils-as-a-potential-therapeutic-target-in-preventing-progression-of-covid-19.6353/#post-36645
With me and having known autoimmune issues, seems there can be both over and under activation. Knowing when to tweak what, is a bit tricky.
But histamine, actually triggers the H2 Receptors that turn on Helper T cells. So histamine plays a part in autoimmune function too.
Not sure if people are going back to read these slightly older posts. Anyway, I think dejurgen is correct in saying that the body ‘prunes’ antibodies if they are not useful over time.
It was discovered that the mistaken half dose of the Oxford vaccine plus a later dose gives higher efficacy. They are now thinking that the length of time between doses (longer the better) may also increase the effectiveness. Riffing on dejurgen’s idea, perhaps it is because it takes the body a bit of time to find out ‘what sticks’ and to ‘ramp up production.’
I also wanted to comment on Issie’s most interesting list of links about MCAS. Lots of information–and a bit overwhelming for me as I don’t have much background in that area. I’m one of those people who really doesn’t have much mast cell issues. I do however, have problems with autoimmunity. Like Issie said, (paraphrasing) ‘It is exceedingly difficult to tweak the immune system back to normal function’.
I try to learn about the causes of inflammation which probably influences autoimmune problems. There is a whole long list of culprits–many out of my control. What I have noticed however, is that there is an equally long food and supplement list of anti-inflammatories.
I was shocked when I recently realized that before my partner started living with me, my diet was from the farmers market and almost all fresh fruits and vegetables–and most of them on the list of anti-inflammatories! And then that changed…
What I’m trying to say is if you have trouble identifying all the culprits it might be as good to emphasize the most protective foods and just try to avoid the biggies; sugar, processed stuff with weird chemicals, trans fat.
I need to go back to basics. Takes energy to do this though, but that’s what I think I will concentrate on for the New Year.
Thank you for all that you guys do!
Just curious, I haven’t seen any studies done on Paraprotinemic / monoclonal gammapothies highlighting the autoimmune response as well as Paraprotinemic polyneuropathies therefor tying in the small fibre neuropathy subsets as well as the vagus nerve theory.
I have mecfs and underwent a 6 year investigation into paraprotinemia as a precurser
for myeloma cancer, before I was eventually officially diagnosed with mecfs.
By then I was severely disabled..
If plasmapheresis is the cure (couldn’t be offered to me because they could not find primary cause / what was triggering ongoing infection in my body) surely this could prevent long haulers the ongoing debilitating we have suffered if offered to them in time?
And if this did prove effective, then it would highlight areas for research for effective treatments for MECFS patients if paraprotiens / monoclonal gammapothies were the underlying cause?
For instance with Gullian Barre Syndrome, we know if not detected, diagnosed or treated initially, patients go on to develop chronic inflammatory Demyelating polyneuropathies which clinically mimics Paraprotinemic ployneuropathy.
For such a simple solution.. Its saving millions the debilitating future we have faced.
Yes they think the over response by the immune system could be the difference with severe Covid. And viruses do access through ACE 2 receptors not only in lungs but also on blood vessels endothelial cells. An article by BBC UK said Genes could be the difference between mild Covid or severe Covid. A study of Genes of people in intensive care and healthy people found some Genetic differences. Yes with some people they may have a over response by the immune system but the immune system is still responding to a viral infection.
Cort, what is the status of the supposedly $1B for Covid Long Haulers? You wrote an article a few days ago proclaiming this fantastic new funding building huge hope in your readers. However, there was a debate in the comments if the funding would go to Long covid or just studies of Covid. You repeat the announcement in this article.
Solve ME/CFS has nothing on their website about this funding – WHICH IF TRUE WOULD BE THE BIGGEST DEVELOPMENT IN ME/CFS EVER, and Solve would definitely have it on their website as being part of it. A google search produces nothing on this announcement.
I don’t like getting my hopes up and then dashed. It has happened a hundred times with this disease. With all due respect, I have noticed over the years you write as if some new breakthrough is just around the corner and it never is. That is why I rarely read your website. Creating false hope is a serious offence to chronically ill patients. Now you proclaim $1B in funding for Covid long haulers and there is a debate if it is true and you seem to pretend it is true and now basically ignore it.
See this link: https://www.ncsl.org/ncsl-in-dc/publications-and-resources/covid-19-economic-relief-bill-stimulus.aspx
It says:
“1.25 billion for National Institutes of Health (NIH) to support research and clinical trials related to the long-term effects of COVID-19, as well as continued support for Rapid Acceleration of Diagnostics for COVID-19. “
Am I wrong or is this a complete gamechanger for ME/CFS?
Thanks Soren for clearing that up! Nice find.
You hate to say any definitive but honestly I don’t see how this cannot be a huge gamechanger for COVID-19, for us and likely for other diseases as well.
Thanks Soren, that does make it look like it really is just for long covid. So yes this is finally the game changer we have been waiting for. Sad that it has taken so many more people to get sick for Congress to do something.
Hi Brent, I’m on Solve M.E.’s emailing list and I received an email from Emily Taylor on 24.12.20 on the subject of the over a billion dollar funding, so I suppose Cort received the same email…
Was on my phone and now on the computer and will copy the email from Solve M.E., that I received…
Dear friends,
This is our biggest victory, yet!
Earlier this month, Solve M.E. led the charge for federally funded research into Long-COVID and myalgic encephalomyelitis (ME) — previously known as chronic fatigue syndrome (CFS). We authored this letter, joined by 20 leading chronic disease and health equity stakeholders, and met with dozens of legislators to discuss these federal funding needs. Our message was a warning and call to action about the increasing number of COVID-19 patients experiencing post-viral complications like ME/CFS.
Our message was heard! This weekend, Congress approved $1.15 billion for Long-COVID research and clinical trials, with $100 million specifically used for the Rapid Acceleration of Diagnostics. The funds will remain available to the National Institutes of Health (NIH) until September 30, 2024.
We succeeded because of you! This achievement would not have happened without your support. We are so grateful for your passion in advocating for ME/CFS!
Additional details about the complex weekend budget agreements are slowly emerging from Congress. We’ll have a full ME/CFS budget breakdown for you in the coming weeks.
But we know the fight is not over — we must ensure this $1.15 billion is spent on quality research that will transform our understanding of ME/CFS and post-viral illness and improve the quality of life for millions. Your voice and your support is needed more than ever. Please consider making a gift of any amount to Solve M.E. this holiday season to strengthen our advocacy program next year.
With heartfelt thanks,
(It was signed by Emily Taylor Director of Advocacy and Community Relations)
Here is a link to the ‘letter’ as in ‘We authored this letter’
https://solvecfs.org/wp-content/uploads/2020/12/Long-COVID-Research-Congressional-Letter-Final.pdf
I reported on the announcement which was sent out on an email blast from Solve ME. which they included on their Facebook site on Dec 24th which is still up. (https://www.facebook.com/SolveMECFSInitiative). (Things are more likely to get updated on Facebook sites). It stated among other things:
“This is our biggest victory, yet! Thanks to you, we secured $1.15 billion for Long COVID research, with $100 million specifically used for the Rapid Acceleration of Diagnostics!”
Within a half an hour of the blog post the controversy had shown up and I have amended the blog post twice to reflect that. I have also repeatedly replied to the controversy in the comments section; i.e. I have hardly, as you say, ignored it.
My stance on the controversy remains the same: Emily Taylor has been deeply embedded in the legislative process and she is in touch with lobbying groups and legislators. Since she is closest to what is happening I trust her on this.
While I can understand the concerns about the wording “long term studies” it just doesn’t make sense to me that those would be on anything other than long COVID. Because COVID-19 is a limited infection -as it’s usually vanquished fairly quickly therefore the only long term studies one could possibly engage in involve long COVID patients. Some of that, of course, involves understanding what’s happening to COVID-19 patients BEFORE they become long haulers.
As to my optimism I understand your concern. The research is moving forward in multiple ways all the time and it’s personally exciting for me to see new avenues open up. I do not mean to present, though, that the breakthrough we are all waiting for is imminent and I apologize if that’s the perception you’re getting. (It could be imminent or it may not be – I have no idea).
The blog usually portrays the small advances that are happening – the advances that make up the long arc of progress.
I always try to be careful to point out when more work needs to be done. I always try to point out when studies or clinical trials are too small to be considered definitive. I am careful never to say – this is the breakthrough that will solve ME/CFS.
Science usually moves forward in small steps and I am happy to see those. I do not want to present, though, that ME/CFS or FM is going to be solved in the next year….It likely is not. On the other hand, I would be shocked if progress is not made.
Thanks Cort for the clarification. With what Soren posted and I then read on the State legislator site this IS REALLY A BIG DEAL AND THE REAL THING!
The wording in the appropriations does make it look like it really is just for long covid. So yes this is finally the game changer we have been waiting for. Sad that it has taken so many more people to get sick for Congress to do something.
In fact you should go ahead and make a separate article on this as this is finally the breakthrough we have been waiting for.
Soren just posted this Brent. I hope this clears it up:
See this link: https://www.ncsl.org/ncsl-in-dc/publications-and-resources/covid-19-economic-relief-bill-stimulus.aspx
It says:
“1.25 billion for National Institutes of Health (NIH) to support research and clinical trials related to the long-term effects of COVID-19, as well as continued support for Rapid Acceleration of Diagnostics for COVID-19. “
Cort has been writing for years about the bad flaws in the PACE research too and hopes for that damaging PACE thing to be buried deep under the soil. The Lancet may not have retrackted it yet, but the disastrous CBT/GET combo that made so many of us a lot worse is near everywhere removed from the recomended treatment list.
That may not give a long time patient hope, but it sure is hopefull they will less and less damage new fellow patients with it and fewer and fewer doctors and nurses and psychologist will be able to hide behind the “it’s all in you imagination” nonsense.
So while Cort has written many reports about new developments of PACE being pushed back, it sure ended up in hopefull news.
As I commented before I have since 2002 had seven severe viral episodes and in 2003 diagnosed with viral sub acute thyroiditis obviously the virus was still active, I was prescribed prednisone for inflammation of the thyroid after which I had shortness of breath and prescribed symbicort for inflammation of the lungs. The Symbicort also having a steroid component was affecting my immune system and within one month in 2004 had the second viral episode. Not knowing then that my immune system was compromised by prednisone and symbicort I had another five viral episodes each time getting weaker and more fatigued from each viral episode. After the last viral episode I had a ANCA pathology test which showed positive and antibodies to Vasculitis again inflammation, this time inflammation of the blood vessels. The virus was still active and every so often my immune system would respond and mount a severe immune response. My latest pathology tests show as follows EBV serology IgM positive- Immunoglobulin IgM high, IgA high- PCR DNA test EBV DETECTED. I have been diagnosed with Chronic Active EBV. Whether it’s the only active virus I don’t know but my pathology reports confirm my immune system is responding to viral infection (s) and causing inflammation of Endothelial cells of blood vessels (Vasculitis) and causing blood flow problems and Chronic Fatigue Syndrome.
@Dennis, I know you have Lomatium in your mix already. And probably Red Root for lymph drainage.
There is a company whose herbs I have used quite often and right now am on 3 of them. I’ve tried other brands and find these to work very well. I don’t know if you can get them in your country. With most herbs you rotate on and off them and take a break. (Lomatium you don’t have to do that.)
Link to all their supplements:
https://supremenutritionproducts.com/
I don’t usually list things I’m on, unless I really feel they have made a difference. Because what works for me may not work for someone else. We all have different things going on that may not be a good fit. So do your research and make sure it doesn’t interfere with something else you do. And get your doctors advice.
These are the 3 things that I go on and off more regularly than the others. These can hit both viral, bacterial and some pathogen issues and help modulate the immune system. (I have Hypogammaglobulinemia and several autoimmune diseases. I’m not using IVIG, despite it having been strongly suggested. I manage these myself with supplements and herbals.)
Reishi Supreme
Manjistha Supreme
Scutellaria Supreme
With some of these bacteria and pathogen issues, there can be too thick blood. That is true for me. But genetically, I hav
(I somehow hit submit and wasn’t finished.)
Was saying…..genetically I have things that can cause too thick blood too.
I manage that with enzymes. They can also break down biofilm and fibrin and help with blood flow.
I use Vascuzyme by Empirical Labs.
If already on blood thinners, this does thin blood. You don’t want things too thin. Check with your doctor. (Other herbs thin blood too, like Ginger. So be careful. You also need to stop herbals and enzymes before surgeries. )
@Dennis, My heart went out to you with your last post. I felt the desperation you feel. Been there. It is a difficult thing to manage. Hang in There!
Thanks issie for your support and advice it has been a long journey since 2002 and putting my faith in doctors who with corticosteroids weakened my immune system and kept having recurring viral episodes and immune response causing inflammation damage and further corticosteroids and symbicort treatment only made things worse. Finally researched in 2017 and found what prednisone and symbicort does to immune system. But by then the damage was done. Did manage to cease any further corticosteroids and symbicort late 2017 and with herbal mixture have improved a little. My latest pathology test on October 2020 for Total Lymphocyte Count Subsets. Comment: The majority of lymphoid cells are T cells. The B cells present are polyclonal. Conclusion: Persisting CD8 + T-cell Lymphopenia. Seems my immune system struggles with viral infection. Infectious diseases specialist said they don’t know much and there is no treatment so good bye. Hard to trust or believe anyone not trusting of medical profession or polititains anymore. Once again thanks again issie for your advice.
@Dennis, read the links above on MCAS. The histamine receptors help moderate T cells. H2R turns on the Helper T cells, the ones that turn down the aggressive ones. If the H2R (receptors) are not turning on after a histamine release from the H1R, it doesn’t turn off the mast cell degrandulation. And there will be too high of a build up of histamine. It take histamine to trigger H2R to turn on. (You can do a search on Healthrising blogs and see where I have talked about this. I no longer use histamine blockers, antihistamines. I actually try to add histamine to trigger a H2R turn on. And not have my own body need to activate H1R (histamine) to cause this response. This is very tricky thing to do. If you get timing wrong or use too much, you will trigger your own mast cell degranulation and maybe with faulty H2R, not working properly, cause MCAS attack.) I listed 3 links above. You can Google search “Issie Histamine Healthrising”, it will pull up a lot. You may also do a search with Dejurgen name that same way, he has gotten more into the technical side of things if you want the hard science on it. I’m more the Summary and he is the technical/science writer between the two of us. We research together going on two years now.
That word should be “degranulation” of mast cells. My phone keeps spell checking me wrong and changing things.
For once, Issie talks complex stuff and I’ll do the simple version:
It ressembles a lot that many people with strong and very unpleasant histamine spikes have actually too low *base* histamine levels.
It seems that histamine levels sort of self regulate. Too few histamine seems to make a massive histamine release more likely when something like a food component or poor blood flow triggers it. Then mast cells dump way too much at once in a sort of “panick reaction” and that gets very uncomfortable and likely isn’t as gentle to your body as a more moderate mast cell response.
That may be why many people with allergies (hay fever in particular) have moderate help with drinking daily a cup of nettle tea. Allergic reactions have a clear histamine related response too. Nettles contain both histamine and serotonin. Both can be released in an MCAS event. Note also: both can get the gut speeding up a lot as histamine increases (gut, if that is the place of release) blood flow and serotonin increase gut movement if that is where it is released. That speeds up removal of food one is intolerant to.
So frequent MCAS could be related to a gut with plenty of (often unknown) gut intolerances. The gut is the first to suffer if blood volumes and blood flow are too low. When one has a lot of nor-adrenaline (our fight or flight hormone) blood is further routed away from the gut to “more vital” organs like the brain and liver. So we (ME/… patients) likely near all have poor to very poor gut blood flow and movement when we don’t have combined histamine and serotonin showers.
That is where drinking some nettle tea (somewhere between half to 2 hours???) before a main meal might help both with digestion and against a massive MCAS event.
As we can react to anything, ask doctor advise and go with commercial quality well dosed tea bags rather then own harvest (I hear frequently to never use nettles in seed as they can be rather damaging).
Nettle tea has been one of Dejurgen and my better moderators. I have used a few more things when coming off antihistamines. Having been on them for a straight 8 years, was a hard and risky endeavor. I was successful with it though. I do occasionally still use GastroCrom if I don’t get on top of a degranulation fast enough. But usually can control things. A low histamine diet is important too.
My other MUST HAVE is a combo product of bee Propolis/pollen and royal jelly. I use those several times a day.
Dennis: With regard to using Symbicort……are you referring to the inhaler for COPD?
I use Symbicort and have for nearly 5 years. Is this something I should be wary of? How will I breathe?
Ivermectin used successfully for long covid.
https://www.researchgate.net/publication/344318845_POST-ACUTE_OR_PROLONGED_COVID-19_IVERMECTIN_TREATMENT_FOR_PATIENTS_WITH_PERSISTENT_SYMPTOMS_OR_POST-ACUTE
Might be useful for M.E.
What about Fibromyalgia, a disease I have had since the 1980’s?