Could COVID-19 studies already be providing clues about what went wrong with the long haulers and people with post-infectious chronic fatigue syndrome (ME/CFS), fibromyalgia and other diseases?
Two articles in the New York Times – a feature length one, “How Covid Sends Some Bodies to War With Themselves“, and “Scientists Uncover Biological Signatures of the Worst Covid-19 Cases” – present the possibility it is.
Cytokine storms (a very imprecise term) and a tricky immune system are at the heart of it. The feature New York Times piece starts with Dr. Iris Navarro-Millán, a New York rheumatologist who had just watched the health of a 61-year-old COVID-19 patient with mild shortness of breath suddenly plummet. Despite being given oxygen, he’d ended up on a ventilator and requiring dialysis for two months.
Some doctors are using immune suppressants like Anakinra to combat cytokine storms in COVID-19
Navarro-Millán concluded that a cytokine storm had wiped his lungs and kidneys out. She’d seen this kind of thing before in autoimmune patients experiencing a sudden flare. The proper response was simple – knock the immune system down with steroids or other drugs.
COVID-19 patients, though, were fighting off an infection. The accepted wisdom was that tamping down the immune system during an infection would make things worse. Nevertheless, Navarro-Millán tried something different in the next COVID-19 patient showing signs of a rapid decline – a quick-acting immune-suppressing drug called Anakinra.
The patient rapidly got better. In June, Navarro-Millán published a small (n=14) case series report suggesting that Anakinra may have helped prevent mechanical ventilation in about half of the patients. Anecdotal reports from Italy and from several hospitals in the U.S, suggest that glucocorticoids and other immune-suppressing drugs have been helpful. As soon as they see oxygen levels drop, they provide them. Clinical trials are needed, however, to validate her findings.
(An Anakinra ME/CFS study unfortunately failed but in that study Anakinra was given long after initial infectious event occurred.)
If Navarro-Millán is correct, though, antiviral drugs like Remdesevir, that one would intuitively think would be beneficial, will have limited effects in some patients. Studies suggest that Remdesevir does accelerate recovery times, but does not significantly affect mortality; i.e. if you were going to be able to fight off the virus, Remdesivir could help you do that more quickly.
If, on the other hand, if your immune system had turned on you and a “cytokine storm” was the problem, it doesn’t significantly help.
The studies suggest that the people who are dying from COVID-19 may not be dying from the virus – they’re dying from the cytokine storm their bodies have initiated in an attempt to fight off the virus.
If that’s true – and it’s still a hypothesis – effective COVID-19 treatment will depend on identifying just what kind of COVID-19 patient you are – do you need pathogen suppression (or immune enhancement) or immune suppression?
One major study of almost 6,500 patients provided hard evidence that immune suppression was the ticket for some. It found that low to moderate doses of a steroidal, immune-suppressing drug called dexamethasone reduced death rates by a third. Here was solid evidence that in some cases, immune suppression worked.
Of course, it wasn’t as simple as giving everyone the drug.
“Timing is Everything”
After noting that dexamethasone was cheap, widely available and safe, a published comment on that study, titled “After 62 years of regulating immunity, dexamethasone meets COVID-19“, concluded that “timing was everything” with the drug.
TIming is important with COVID-19 drugs (Image by Free-Photos from Pixabay)
The “cytokine storms” don’t happen with everyone. People who are able to mount a strong early immune response to the virus may never experience one. Oddly enough, it’s the people who can’t amount a strong early immune response who may get plastered by a cytokine storm later. At that point – apparently alarmed by all the damage present – they go into overdrive.
The authors believe that the appearance of substances called “alarmins”, which are associated with cell damage caused by the pathogen, sends the immune system into hyperdrive, resulting in inflammation and even more cell damage. An uncontrolled, positive feedback loop then occurs as inflammation-induced damage triggers more inflammation, leaving the COVID-19 patient in real trouble.
The authors proposed that the best course before the alarmins show up is to try and fight the virus off. After they show up, though, immune suppression is needed.
It gets more complicated. Many types of immune responses may show up – each with an optimal treatment protocol.
Subtypes
In “Scientists Uncover Biological Signatures of the Worst Covid-19 Cases“, Katherine Wu of the New York Times reports that the immune systems of some people with COVID-19 appear to have trouble marshaling the right kind of immune response. In a massive, but largely fruitless effort, their immune systems are spraying bullets all over the place – but missing the target. (A similar process has been suggested in ME/CFS).
In fact, one study suggests that these dysfunctional immune systems appear to have been tricked into mounting an immune defense more suited to bacteria and fungi than viruses. The immune system’s misguided efforts leave the virus intact and a long-term immune response stuck on the on-button.
Adequate early immune response to the virus – Interestingly, the dexamethasone study found that the drug actually made people with mild cases of COVID-19 worse but did not increase their mortality rates. This suggests that if your immune system is already successfully fighting off the virus, you don’t need dexamethasone.
Poor early immune response to the virus – People with an insufficient early innate immune response (people who are older or who have immune issues) may suffer later when their immune system finally gets into gear and then compensates by going into hyperdrive – flooding the body with cytokines and causing a vicious cycle of inflammation-induced damage to occur.
These people may need to get their immune or antiviral response boosted early in order to avoid a cytokine storm that comes later. Because immune responses will vary, identifying and then boosting the specific immune deficiency they have would be the most effective.
People in the throes of a cytokine storm – these people need immune suppression. Broad spectrum immune suppressants such as dexamethasone can be helpful, but a more precise reading of the immune system could allow doctors to target the specific part of the immune system that has overheated and tamp that down.
The inability to distinguish immune subsets may explain why immune suppression appeared to fail to work with the first coronavirus that appeared in 2003, or in sepsis. In two cases, researchers who have gone back and re-analyzed old trial results have found that immune suppression did work – but only in those patients whose test results suggested they had high levels of inflammation.
Clues for ME/CFS and the Long Haulers?
With many immune drug trials underway, we should learn much more about their impact on COVID-19. Early into the pandemic, though, without the results of any long-hauler studies published, we may be getting some clues as to what may have gone wrong very early in the disease process in ME/CFS and the long haulers.
People with initial poor responses to the virus may have set themselves up for a devastating cytokine storm later – which could then set the stage for a prolonged illness. Ron Davis has said that he believes the damage that sets ME/CFS in motion probably begins very early – hence his desire to get a hold of coronavirus patients very early in the game.
Could an early cytokine storm in ME/CFS (and some long haulers) be triggering the microglial to fry brain circuits?
While the Dubbo studies may not have tested their participants early enough to catch that, they represent a landmark effort to understand what happens in post-infectious illness. They tracked an extensive cohort of people (n=253) who’d experienced various infectious events (Ross River virus, Epstein-Barr virus, Q fever (Coxiella burnetii ) over the course of year in the mid-2000’s. All appeared to have been successfully treated for the pathogen they’d encountered; i.e. testing suggested it had been vanquished.
They found, though, that 35% of people still had “post-infectious illness” (e.g. chronic fatigue syndrome) at 6 weeks, 27% did so at three months, and 9% were still sick at 12 months. The studies also found that while the initial symptom set was different in all three infections, it evolved over time to a general pattern characterized by fatigue, musculoskeletal pain, and neurocognitive issues.
The study found that more severe symptoms early were associated with an increased risk of coming down with a post-infectious illness. That could suggest a hyperactive immune response (cytokine storm?), which set off a strong case of “sickness behavior”.
That finding was buttressed a bit by a genetic study which found that small changes (single nucleotide polymorphisms (SNPs)) in two immune genes involved in the early immune response were associated with a 8-fold increase in a person’s chance of having a “severe illness response”; i.e. ME/CFS.
Increased incidence of a SNP which boosts interferon gamma (IFN-y) was especially intriguing because IFN-y administration has been show to produce the array of symptoms associated with an infection; i.e. “sickness behavior”. Similarly, the over-representation of an IL-10 SNP, which muffles it’s anti-inflammatory effects, might set the stage for an early heightened immune response.
While the study never found direct evidence on increased cytokine levels, cell cultures confirmed that people with these SNPs did indeed produce more pro-inflammatory cytokines. That finding sent the authors were looking not to the body but to the brain. They believed that an active cytokine response early in the illness tweaked the microglia to sensitize central nervous system pathways and produce ME/CFS.
That’s an interesting conclusion given that some COVID-19 researchers are already tentatively linking cytokine storms to central nervous system dysfunction. They believe it may be possible to identify cytokine profiles that are likely result in long term central nervous system issues and use anti-inflammatories or other drugs to knock them down.
The fact that the genetic polymorphisms identified appeared to have the same effect on each of the infections was striking and left the authors wondering they’d identified something that could be applied to many post-infectious illnesses.
“Because of the highly varied characteristics of the pathogens studied here, these findings may plausibly be generalized to the host response to many infectious agents.”
If they’re right, some of the COVID-19 long haulers might have the same immune genetic predispositions that this study suggested people with ME/CFS do.
The Upshot
It’s important to note that COVID-19 studies published thus far have not assessed long haulers – they’re focused exclusively on what’s happening early in the illness.
Are COVID-19 studies already providing clues for ME/CFS and the long haulers?
The Gist
- Rheumatologists experienced in treating “cytokine storms” began successfully using immune suppressants like Anakinrin and dexamethasone in COVID-19 patients who’s oxygen levels were falling.
- Studies and anecdotal reports suggest that immune suppressants work when the virus has caused so much tissue damage that an inflammatory positive feedback loop has formed. When people with COVID-19 die, it appears it’s the immune system that is killing them.
- Before that inflammatory process has gotten started – when the body is focused on fighting off the pathogen – antivirals and immune enhancing drugs appear to be more helpful.
- The Dubbo studies in Australia did not test their subjects early but found evidence suggesting that ME/CFS patients are predisposed to produce a very active immune in response to an infection. That response could have produced the more severe symptoms that most people who came down with ME/CFS experienced.
- The Dubbo authors hypothesized that this hyperactive immune response activated microglial cells in the brain which then produced the symptoms found in ME/CFS. They noted that all the symptoms in ME/CFS could be produced by the brain.
- The COVID-19 studies have already opened up several possibilities. 1) a poor early response to the virus results in a cytokine storm later. The bigger the cytokine storm the more likely one is to be hospitalized and suffer from organ damage.
- Smaller cytokine storms, on the other hand, in non-hospitalized patients, could have triggered several outcomes: an autoimmune process, neuroinflammation, herpesvirus reactivation. It’s also possible that the virus had not been completely vanquished.
- COVID-10 is already illuminating the different immune responses to the virus that are occurring it’s critical for the ME/CFS community, as well as for the non-hospitalized long haulers, that they be represented in studies so that we can learn what exactly went wrong with them.
While few long hauler studies have been published thus far, think how easy it would be so easy to turn these early COVID-19 studies into long hauler studies. All the researchers need to do would be to follow the progress of the patients in the study – and then look back and see if they can identify what was happening in people who turned out to be long haulers.
Several scenarios have been presented. All involve some period of strong immune activation
- Poor early immune response leads to a massive cytokine storm later that damages the lungs and other organs and causes hospitalization. Researchers focused on hospitalized patients may, however, conclude that the fatigue, PEM, etc. that is present is the result of organ damage.
- Poor early immune response leads to a smaller cytokine storm later. The patient is able to fight off the virus while at home but has trouble recovering. Various hypotheses have been presented: the cytokine storm has triggered an autoimmune reaction (Nath), it has altered central nervous system functioning, or the virus has not been completely neutralized, or it has reactivated herpesviruses.
- A strong early immune response causes a smaller but still potent cytokine storm. In the Dubbo hypothesis the patient is able to fight off the virus but the cytokine storm it triggered causes the microglia to go on to hyperalert – producing all the symptoms of ME/CFS, FM and others. We don’t know if this strong early immune response actually occurred but it might have given that stronger symptoms were a risk factor for coming down with ME/CFS.
The Dicey Drug Issue
Thus far some studies and observations suggest that a poor early immune response in some COVID-19 patients may set up them up for a scorching immune response later (cytokine storm) that produces a dangerous positive inflammatory feedback loop. These patients appear to respond to immune suppressants. On the other hand, giving immune suppressants too early – or to people whose immune systems are fighting off the pathogen – is not beneficial.
Depending on where they are in their illness, people with COVID-19 could benefit from antivirals or immune suppressants. These drug studies are providing invaluable insights into the different ways the immune system responds to pathogens. If we can identify which immune mistakes have occurred in the long haulers we will have likely come a long way.
It’s clearly critical for us that long-haulers- particularly non-hospitalized long haulers – get into studies. “Cytokine storms”, for instance, appear to play a major role in sending COVID-19 patients to the hospital – but we don’t know if they’re occurring in non-hospitalized patients. With many COVID-19 studies naturally focusing on hospitalized and more severely ill patients we need more data on non-hospitalized patients.
It’s clear that studies embracing the immune system, genetics, the brain, autonomic nervous system, etc. are needed to study the long haulers. Dr. Nath’s, Ron Davis’s – if it can get the funding – and the Swedish ME/CFS Center study will – and hopefully more will pop up.
Thanks for sharing this Cort.
Speaking of cytokine storm and Covid, I just wanted to share this trial too:
“University of Minnesota first in country to open clinical trial into new COVID-19 treatment”
https://bringmethenews.com/minnesota-news/university-of-minnesota-first-in-country-to-open-clinical-trial-into-new-covid-19-treatment
“The University of Minnesota has become the first institution in the United States to launch a clinical trial into a new kind of COVID-19 treatment.
The U of M announced Thursday it’s treating a patient with COVID-19 and lung failure in a new trial that is aimed at halting the “intense inflammatory response of the body” in the sickest patients with COVID-19.
They will be using mesenchymal stem cells (MSCs) to treat the inflammatory response. MSCs have been used to treat other inflammatory diseases and have been piloted to treat patients with COVID-19 in China and Italy.
Lab research suggests that MSCs can blunt the “cytokine storm,” an intense inflammatory response in the body triggered by the virus which, if unchecked, can lead to extensive organ damage, most commonly lung failure.
The study will determine the effect of MSCs on stopping the cytokine storm,” said John E. Wagner, MD, cancer researcher and director of the Institute for Cell, Gene and Immunotherapy at the University of Minnesota. “In order to determine the real benefit of MSCs in these very ill patients, patients will be randomized to receive three doses of MSC 48 hours apart or a placebo solution.”
Fascinating – thanks Dakota. Very promising for people just coming down with this. I hope they get the study done as quickly as possible.
For me the big question with the cytokine storm is if it produces long term damage somewhere else which then causes long hauling and ME/CFS. If so we have to find out what that is .
If you can nip it in the bud, though – and stop people from used in every infectious event – that’s superb. Plus it might help in other infectious events.
not sure where I read it but melatonin could work as well to calm down the cytokine storm, oddly enough
Check out article in today WSJ today regarding MSC’s. Reference Mesoblast.
Great writeup Cort! Thanks for keeping us well informed in such an understandable way. I’ve been following the long-hauler community when I am able. There was a webinar for long-haulers given on the “Survivor Corps” facebook group page the other day, with a doctor from Mount Sinai in NY.
I originally thought they were only following hospitalized covid patients, but it seems at least some are keyed in to the non-hospitalized cohort. While cautious of naming long-haul covid as something like ME or POTS or MCAS, etc, this doctor seemed confident to assert that what we are seeing in patients who are not recovering is the result of dysautonomia.
They also seem to be treating it using a method that reconditions the autonomic nervous system, starting first with some kind of breath work, then moving on to a kind of physical therapy that uses heart rate variability as a guide for limits, maybe similar to what someone suggested in a dysautonomia community might be the “Levine method.” I’m not really familiar with it.
They are also using an anti-inflammatory dietary intervention, probably pretty simple compared to a lot of elimination diets our community is familiar with, like eliminating sugar and simple carbs and such. However, they are also coaching people how to recognize their own individual inflammatory food triggers using both awareness of symptoms and heart rate variability.
Consequently, they feel as if they are having good results with many patients, some of whom improve very rapidly and others who have shown gradual improvement over time. I think it will be interesting to see if they are eventually left with a cohort that does not respond to these functional approaches.
I hope they will also continue to have interest in such patients. They said they are currently working to disseminate their approach to other doctors and hospitals across the country. I just hope that it doesn’t turn into “graded exercise therapy” as it gets adopted by possibly less experienced practitioners.
Doing everything I can to get folks to support Congressman Rakin’s bill. I have a lot of confidence in our ME/CFS researchers to get to the bottom of things if they are only given adequate resources!
Thanks again!
They’re certainly ahead of where we were. I like the emphasis on the autonomic nervous system and HRV pacing. I think the Levine method is an exercise protocol used sometimes in POTS. I imagine the doctor’s protocol will help some people altho I imagine others will not.
R, I believe my microglia got an awful roasting when I was extremely unwell in 2017. I wonder whether I had Swine Flu?
At the time my overall health was severely compromised as I’d become intolerant to most food, became anaemic due to a gynaecological issue and had also developed a bacterial infection. I’d had IV antibiotics and then two more lots of antibiotics and then, within weeks became very ill with the flu. This lasted for three weeks solidly and took me about three months to even become vaguely normal.
I found after this illness that certain foods set off my brain and I would suffer intense headaches and a sensation that my skull wasn’t big enough. I wouldn’t be able to think, remember and over time I had the horrible feeling that my brain and body were about to just shut down.
I did go to my doctor and to ask if he could give me anything to calm my brain inflammation? However, I think as he already thought that I was on the emotional/hysterical middle aged female spectrum, he just smiled and shook his head…
So, what I discovered myself was that I needed to do everything I could to bring down my inflammation – I used the anti-inflammatory ibuprofen, until my body rejected it – it now affects my heart rhythm. I modified my diet etc used all the functional medicine approaches I knew.
It’s taken me three years but my brain is much calmer and cooler now. I can still wind it up – too much sugar is not good and I don’t eat very much processed food – I really do eat platefuls of leafy green vegetables, extra virgin olive oil etc. I take loads of supplements too.
Quite definitely the nasty flu and the long term very high temperature 41°c/105°f started the very distinct brain energy issues I have now. I had other issues before and after but I associate being on a limited brain energy quota, from that particular illness in 2017.
I am learning to live with it, adapt to it but I have not yet managed to break out of it. I’ve actually stopped trying to break out of it because that’s counter productive. Annoyingly I’ve had to accept that I function better, if I live within my allocation!
Another good article, Cort.
When ever I read about these things I almost always get questions and make hypothetical connections.
This time I was thinking about MCAD and MCAS (mast cell activation syndrome) (and how common a co-morbidity it is in Ehlers-Danlos patients). Seems as if a lot of doctors are thinking along the same lines and in China, Covid patients on H1 and H2 blockers did better than others. You can see all those ideas with a quick Google search.
The list of body systems and organs most commonly affected by mast cell mischief rather parallel some of the same systems affected by Covid; autoimmune, IBS/D, the lungs, blood and tissue, energy (ME/CFS). Mast cells also release/control cytokines, among other things. So what I’m thinking is control the mast cells and perhaps control the severity of Covid. Or conversely mast cell activity may predict Covid outcomes and perhaps be a factor in the development of ME/CFS.
I don’t think researchers entirely understand why some people’s mast cells become so ‘tweaky’ and degranulate at the slightest insult. Those folks also seem to have way more autoimmune disorders too. Genetics? Environmental pollutants? Post viral fragments tripping the alarm? What?
Well, anyway, those are my musings…
I just read the most amazing article about the body’s immune system–and Covid. Makes my previous comments sound like baby talk.
https://www.theatlantic.com/health/archive/2020/08/covid-19-immunity-is-the-pandemics-central-mystery/614956/
Thanks for a clear summary of a topic that I find difficult to understand until I read your article. I did not realize that Ron Davis’ group was studying Covid-19 patients. Such an impressive group of researchers.
He is trying to get the money together to gather the samples over a several year period. Then he will try to get the money together to deeply analyze the samples.. We do have a very impressive group of researchers – it would be great to fully unleash them!
Cort, any ideas on when the results from Dr Nath’s study might come out?
I have no idea. ME Action has more information on this than me. I think they said the study would be starting soon. Nath is so eager to catch people as they’re coming down with an post-infectious. The opportunity to catch the disease in the act is so much greater than with his ME/CFS group which I think required post-infectious ME/CFS patients to have the disease less than two years.
Recently Nath said during the coronavirus they’d been ploughing through reams of data from the ME/CFS study. The really encouraging thing for me is that Nath seems really excited – which suggests that the ME/CFS study has gone well (:)).
I believe the long hauler study will be starting soon but while it’s not as intense as the ME/CFS study – it will probably take quite a while to finish up. I will try and learn more about it.
I believe Nath’s NIH Intramural ME/CFS study targeted more broadly than within first 2 years of illness. If I’m not mistaken it’s at least 6 months but less than 5 years. I took part in the study several months ago right around my 4 year mark.
Sorry, I meant when will the ME/CFS study be published?
Possibly soon-ish?
5 years! I didn’t know that. Thanks for pointing that out. So it’s a really long range. A big acknowledgement to you Winston for being in the study. I hope it was not too stressful.
Got it Matthias. A great question. Nath said that COVID-19 had interrupted the flow of patients into the study and I think maybe half (?) had completed it? He also said the break from COVID-19 allowed them to get at reams of data from the study. I don’t know if they have enough to publish or not.
I assume that many papers focused on the different aspects of the study (exercise, immune functioning, metabolism, gene expression, etc. ) will eventually come out of the study.
We – and the long haulers – were just so lucky that this study started in enough time for Nath to begin to use the results of it on the long-haulers. Already we will have a comparison! Isn’t that something.
I have received significant help from Remicade the tnf alpha cytokine blocker. I just wonder how much better my response would have been had I been able to take it 30 yrs ago when I became chronically ill.
I think that is just the thing that Nancy Klimas in particular would love to do. She’s been talking for years about using immune test result to inform the use of cytokine blockers and similar drugs. In our medical environment it’s hard to do that.
Some COVID-19 researchers, though, think that’s what is wanted and needed – as the study results come out we will see more of this precision approach. Dr. Peterson believes that is the future of medicine. We certainly need it in the very heterogenous ME/CFS population.
Let’s hope!
On research, when ares Klimas’s research results due? It seems quite a few years that she’s been working on it.
I think her trials were probably interrupted by COVID-19 – as everyone’s were. Everything seems to take much longer than one would hope. The answer is I don’t know.
Maybe I’m off on the wrong track here but this topic reminded me of Dominic’s article on Health Rising ‘Neither Dying nor Recovering’.
https://www.google.com/search?q=dominic+health+rising+neither+recovering+or+dying&oq=dominic+health+rising+neither+recovering+or+dying&aqs=chrome..69i57.28990j0j7
I know it’s not quite the same thing but it’s in the same area.
I have more to say but it’s mid afternoon here and my brain has gone onto energy saving/low battery mode… I’ll be back!
I think that’s a great link and the reason is that it’s something that may very well be happening but which few people know about. Plus it’s happening in sepsis and ICU – and some COVID-19 researchers are looking at COVID-19 and thinking about sepsis. Thanks for mentioning it. I need to put Dominic’s posts in the “Offering to the Long Haulers”
“Neither Dying, nor Recovering”: Learning from ICUs to Solve ME/CFS and Fibromyalgia – A Synopsis –
https://www.healthrising.org/blog/2019/11/21/neither-dying-nor-recovering_icus-fibromyalgia-chronic-fatigue-syndrome/
https://www.healthrising.org/blog/2019/07/24/chronic-fatigue-syndrome-ntis-low-t3-vicious-circle/
https://www.healthrising.org/blog/2019/03/04/hypothyroid-chronic-fatigue-syndrome-thyroid-ntis/
Cort, is anything being done
with the three pronged auto antibodies test
developed by CellTrend, and Carmen Scheibenbogen.
The test was initially for cfs/me.
Are projects using it in any testing/research protocols?
https://me-pedia.org/wiki/CellTrend_diagnostic_test
I wonder if Nath’s is. I would be completely shocked if any non-ME/CFS researchers are checking out those autoantibodies. Maybe with time they will.
I’m also curious on this.
There were these 2 studies last year on it:
https://neurosciencenews.com/pots-fainting-biomarker-14888/?fbclid=IwAR15QKfd3NeRsmwWfGkB6xFCFr-EfKIgy2Q-ZhJFsJUYkmedsjV0B24FdTc
“”In the largest study of POTS patients to date, published Sept. 9 in the Journal of the American Heart Association, Grubb and UToledo research collaborators found 89 percent of patients they examined had elevated levels of autoantibodies against the adrenergic alpha 1 receptor.”
&
https://www.ahajournals.org/doi/10.1161/JAHA.119.013006?fbclid=IwAR0m3EVNwLnOOjmjTehbzVHrRhI517pyk979rClL1eyptYhEkjMcqmnoVfM
“This study demonstrates for the first time a role of adrenergic autoimmunity in the pathophysiology of POTS in two related animal models. The study also demonstrates that the effects of adrenergic autoantibodies are largely reversed using a compound that blocks the autoantibodies, which was developed by the University of Oklahoma researchers.”
Then obviously yesterday’s OMF study release:
https://www.sciencedirect.com/science/article/pii/S2666354620300727?fbclid=IwAR2NLmJlO00XQu2FZ0wBJ3ipMSXbsHjFM3koticSRBU6dAwZlnVTGOBWZ0I
“Autoantibodies to beta-adrenergic and muscarinic cholinergic receptors in Myalgic Encephalomyelitis (ME) patients – A validation study in plasma and cerebrospinal fluid from two Swedish cohorts. Results from this study validated those previously found of an increase of autoantibodies against adrenergic and muscarinic receptors in the blood of people with ME/CFS.”
I hope this will continued to be explored….
Thanks! I missed those. 🙂 A seemingly ever and ever larger focus for ME/CFS.
I have had a lots of diagnosis’ since a fall in the military in 1988. No DNC was done. I had a subsequent infection during operation Just Cause. While I was in the Hospital there in Panama erythromycin was infiltrated into my arm when the needle was placed incorrectly into my arm. I got out not long after that in 1990 and have been fighting for my Veterans Disability since then. I got diagnosed with Fibromyalgia CFS and many other illnesses starting in 1998 after seeing doctor after doctor. I have not had a day free of pain since I was 18 in 1988. I did research with Dr Donald Wood here in Louisville for 8 years before he passed. We had come to some conclusions around his time of death. I believe I was his last patient on the day he died in a car accident. He was a wonderful man and doctor. We found so many underlying conditions that have helped me to keep taking care of my son all these years! He discussed me at all his conferences! He tried so hard to figure out what was wrong and get me out of pain and relieve my issues. I am so very thankful for him!!! I am so very thankful for any help you all could give all of us who have been in daily pain for years with sometimes little to no help. Most of us have been discriminated against ridiculed and poorly treated including myself because of lack of information for these invisible complex illnesses! I know so many people this could help!!!!!!!!! Thank you!!!!!!! Any information is so very much appreciated!!!!
Thanks as ever Cort.
Just went back over some of the referenced/linked articles which have resonated with me in that ..one refers to the T3 – rT3 issue. My daughter has such an exceedingly high rT3 reading…(Almost triple the top end of the reference range from memory). No one can suggest what we should do to alter that. I Researched using T3 but was guided away from it as she already has a reasonable amount of free T3..so the issue is conversion, I guess, not availability. (?)
Secondly, a ref to pituitary alterations to growth hormone secretion in the various stages of acute then chronic illness.
My daughter fell ill (virus) at 13yo. She stopped growing and finally did have a later ‘spurt’ of growth when she improved to some degree.
Her fatigue is more brain based. Not so much PEM.
There is so much information it is frying my brain…but I do hope long haulers will get the benefit of much research which may reflect back to the ME/CFS ++ groups for an advancement in their conditions.
That Swedish / German study is fascinating. Seems like they might be on to something. I’ve thought for several years that autoimmunity could be central to CFS. There’s just so much going for the theory in general terms – causation usually through an immune assault, strong dominance among females etc.
I wonder how many CFS patients have had another autoimmune illness, or close family members have. I had juvenile arthritis for one or two years when I was 7, then came down with CFS when I was 19, following a viral infection.
Great question which surprisingly has not been answered yet. It’s one of the questions that the You+ME Patient Registry will surely answer. It’s got a family history section.
My mother had a severe case of Sjogren’s Syndrome.
My family have all sorts of immune issues – it’s what we ‘do’. My mum has fibromyalgia, IBS, and a recurrent dry mouth issue. My dad, at one time, became allergic to treatments used in his work as a vet. We have a lot of asthma, one family member with type 1 diabetes, a few with hay fever (though one didn’t believe in that sort of thing, until they got it!) cold water urticaria, connective tissue disorder, eczema, food intolerances – those are just the ones I know about…
It seems to be Nath’s best guess. It makes me wonder if he’s discovered something in his ME/CFS patients in the intramural study. It’ll be fascinating to see if COVID-19 sparks a range of autoimmune diseases. They would probably have to follow the long haulers for awhile to determine that. Hopefully they will.
Cort do you roughly know when the intramural study might be published?
I was just sent this article in the Guardian from Solve M.E.
“We know too little about Covid-19 ‘long-haulers.’ We need a comprehensive study.”
Oved Amitay and Anthony L Komaroff
https://www.theguardian.com/commentisfree/2020/aug/19/we-know-too-little-about-covid-19-long-haulers-we-need-a-comprehensive-study
How many of us were initially diagnosed with “prolonged post viral syndrome” back in the day when CFIDS, and then ME weren’t familiar to our doctors.
I don’t know. It certainly never came up for my doctors. They went or tried to go straight to depression.
I was diagnosed with being a hysterical female. I do not list CFS/ME as one of my illnesses as when I do, I’m never taken as a patient or asked to leave. I had to have a heart attack from MCAS/Kounis Syndrome to be considered “sick” instead of “nuts.” What a world.
Well, I for one am horrified. There are already 6,000,000 Americans who have caught covid-19 and on today’s CNN website, they say up to 10% of them have post-viral covid-19 (CFS/ME and POTS; I’ve noticed a out of proportion number of them have hypertension – suggesting that lots more than 10% of those POTS patients will have hyperadrenegic POTS. That means up to 600,000 NEW CFS/ME and POTS patients competing for OUR DOCTORS. I can’t find any as it is.
Cort, do we have information on people already with fibromyalgia and ME/CFS that contracted covid and how that affect them?
Hi Stuart,
Health Rising ran a poll a couple of months ago. Most people seemed to be doing OK. I will publish the results in an upcoming blog.