IACFSME 2022 Virtual Medical Conference: Day 3 Presentations: 29 July (9 am to 4.40 pm EDT)

“Do People with Joint Hypermobility Represent a Subgroup of ME/CFS?"
16 pages of slides from a presentation at the recent #IACFSME conference
https://solvecfs.org/wp-content/upl...ve-ME-Research-Slides-Joint-Hypermobility.pdf

ETA: I decided to make a thread for it:
https://www.s4me.info/threads/do-pe...resent-a-subgroup-of-me-cfs-2022-mudie.28923/

 

Continuation of notes from the @s4me_info twitter thread.

This post is a copy of notes made during the July 29 session Immunology of long COVID presented by Akiko Iwasaki.

=== start of comments ===

Iwasaki started with general info on Long Covid. The percentage of symptomatic patients goes down after infection, she explained, but it doesn’t go down to zero. It plateaus.

We need to understand why some people fail to recover.

She also highlighted the problem that there is no universal way to define Long Covid leading to variations in studies and making it difficult to give one number of how many people are affected

Iwasaki talked about the results of a mouse model of mild COVID.

They wanted to know if a mild respiratory infection could affect the brain.

They found that several cytokines were elevated including in the cerebrospinal fluid weeks after the mild COVID infection.

They also found reactive microglia in the brains of the mice which is interesting because they also found this in autopsies of people with a positive test for Sars-Cov-2 (some of these didn't have any COVID symptoms)

One of the elevated cytokines they found in the CSF of the mice is called CCL11.

This cytokine was also found to be elevated in the blood of long COVID patients with brain fog (not in those without brain fog)

Iwasaki concluded that infection of the central nervous system (CNS) is not required to induce significant CNS pathology.

Long COVID might be caused by circulating cytokines that impact the brain in a chronic matter because of epigenetic regulation of the microglia.

Lastly, Iwasaki also presented yet unpublished data from the Mount-Sinai Yale study (MY-Long Covid Study).

This study very extensive testing in patients with long covid, patients with covid who recovered and two groups of healthy controls up to 110 days post-infection.

Long COVID patients had increased B cell activation and increased exhausted T cells.

They also had increased anti-SARS-CoV-2 antibodies, even after controlling for vaccine doses.

There was also reactivation of some herpes-viruses (EBV).

The most striking finding, however, were decreased cortisol levels in long covid patients. They were only about half of controls and also predicted the severity of Long Covid.

Iwasaki said she hopes to extend these analyses to ME/CFS as she thinks there are many parallels and overlaps between Long Covid and ME/CFS.

=== end of comments ===

 

Continuation of notes from the @s4me_info twitter thread.

This post is a copy of notes made during the July 29 session at 1:40 PM and covers presentations by three speakers: Ali Boolani, Liisa Selin, and Deborah Duricka.

=== start of comments ===

The next speaker is Ali Boolani (Clarkson University). His team looked at electronic medical records of patients with a PCR-confirmed diagnosis of COVID-19 from multiple hospitals.

In total they had data on 60.000 patients.

They then looked at how many of these patients got a post-COVID ME/CFS diagnosis.

This turned out to be the case for approximately 8500 patients or around 14%.

Boolani highlighted several limitations to this data.

Not all diagnostic codes were entered correctly and when they looked at some of the records, important things were missed.

The limitations became clear when they looked at predictors of ME/CFS diagnosis.

Being older, male and Caucasian increased the odds of a ME/CFS diagnosis and classification accuracy for machine learning models was low.

Boolani briefly suggested that this could mean that getting a registered ME/CFS diagnosis is subjective: that some people are more likely to receive one than others (regardless of medical condition).

The next presentation is by Liisa Selin (University of Massachusetts) on CD8 T cell over-activation and exhaustion.

Selin says they are seeing similar immune abnormalities in Long Covid as in ME/CFS.

She thinks that Inspiritol (a new patented 5-compound drug) has potential as treatment because it has various immune-modulating effects.

The last presentation before the break is from Deborah Duricka (Neurovision Inc) on how "Stellate Ganglion Block" might help to improve symptoms of Long Covid.

She has previously reported a retrospective case series on this.

A stellate ganglion block is an injection of local anesthetic to block the sympathetic nerves in the neck.

Duricka says she is new to the field of ME/CFS but that she noted that stellate ganglion block improved symptoms in Long Covid patients.

The sample size, however, was limited to 11.

That's the end of tweeting for today.

=== end of comments ===

 

This seems very high! Were there any details about when this research will be published?

 

From Cort Johnson:
The Hugely Predictive Factor for Long COVID...is also found in ME/CFS and Fibromyalgia: the IACFS/ME Conference II

Yale immunologist Akiko Iwasaki swept into the keynote session of the IACFS/ME with some never-before-revealed findings.

She couldn't have chosen a better place. The "hugely predictive" factor for long COVID she found - low cortisol - as well as the EBV reactivation and T-cell exhaustion she also found - have all shown up in ME/CFS as well.

Find out more in

The Hugely Predictive Factor for Long COVID...is also found in ME/CFS and Fibromyalgia: the IACFS/ME Conference II
https://www.healthrising.org/blog/2...ng-covid-factor-chronic-fatigue-fibromyalgia/

Iwasaki is interested in doing a similar ME/CFS study but doesn’t have funding for it.

 

That's very informative, if unfortunate. 14% of one particular cohort. I wish we knew more about this population--hospitalized, non-hospitalized, either, how long they were sick, how age/sex are skewed, etc. Unfortunately, I couldn't find anything about this study online. It must not have been published yet, but I'm guessing it'd be a significant paper, so hopefully he plans to publish it. The fact they used existing diagnoses isn't ideal, but allows them to cast a wider net than looking for diagnoses themselves. I believe we discussed a LC study that used EHR data before, and several people commented that the prevalence of different symptoms seemed very low and skewed towards "concrete" ailments, hinting at potential biases around what was actually diagnosed.

 

I do not believe that DeMeirleir made mention as of whether he has conflicts of interests or not. I am not sure whether he has shares, owns or is an associate of Red Labs, which has a lab both in Belgium and conveniently in Reno Nevada where he works too. Red Labs' website does not disclose who owns the company and who is on their board of directors.

He mentions that the patients that he sees come from all around the world. But in itself it still represents a self-selection- I did not review the methods of this study he presented and whether patients studied only came from his office. (though your notes @Hutan mentioned Dutch and Belgian patients)

I could not help but notice the next presentations which were difficult case presentations, at one point there was a poll question asking what what the patient's diagnosis, and of all the responses, 1% (probably 1 answer) said the patient had Lyme disease, when the correct answer (or the most probably) was Long-Covid.

So I am taking his study with a grain of salt.

 

Merged thread - This article refers to this talk:

__________________

Could a Major Chronic Infection be Underlying ME/CFS? The IACFS/ME Conference Pt. V
https://www.healthrising.org/blog/2022/10/18/borrelia-miyamotoi-chronic-fatigue-syndrome/

Health Rising blogpost about a very out-there hypothesis.

 

Look under the bed, it's there. I can't even take this seriously anymore.

 

Hey, its better than the Kidney dysbiosis guy at least. (Dr. Igor Markov, who claims ME is caused by kidney dysbiosis and that autovaccines can cure 93% of patients)

 

The infection 'must be gone' idea never chimed with me. I think there are many possible candidates that could be contenders. The symptoms of ME are all symptoms of an ongoing infection(s).

Long term antimicrobial therapy got me pretty near functional (N=1, so not meaningful really) and this it pretty much the only approach that I have seen others improve. Others not.

I doubt very much any medical or research group would test in a rct the type of treatment that I received. Little openness to it or curiosity. That'll change I think only with a decent test showing ongoing infections.

 

Ron Davis

25:47 Now the other thing that we decided to do in this project is to test some of the ideas that patients have had, are they right or not. So I've heard a lot from patients that "Oh I keep getting viral infections . . .I get them all the time, it's really my real problem . . . I'm very susceptible to viral infections". And I ask them what virus do you think you're getting? "Oh I'm sure it's HHv7 or it's another herpes virus and that's what caused my illness in the first place". So we decided to actually test this and we had to develop a technology to really do it and to do what I thought was correct.

28:24 The results of that is basically there aren't virus infections that are different from healthy controls. A few people do have them but healthy controls have more in this small study, so it makes me suspicious that in fact they don't have viral infections. They have something else going on that feels like a virus infection and a lot of inflammation things things will make you feel like that. Most of these viruses probably, by themselves, don't really do anything by themselves. It's not to their advantage to give a signal to the body that they're there. The body is the one that does the signaling that there's something wrong. And I think if you have that signal like inflammation it may feel like a viral infection. The only reason I'm stressing that point is that if it's most likely you don't have a viral infection you shouldn't be taking antivirals probably, because they're probably not that healthy for you. And the reason they're probably not that healthy is that the antivirals generally target the synthesis of the DNA from the virus and it works because it's a very primitive

 

Likewise, treating bacterial infections improves me for a period. If I can get my immune system to go on the march I improve. No doubt I have bacteria in my kidneys from the urine dipstick tests but whether its the cause of the problem or just a side show I have no idea. I think persistent bacterial infection is likely. Chris Ponting was suggesting LPS in the blood of ME/CFS patients caused clotting, if that is right then its bacteria and its a question of where and how to treat it given antibiotics have done nothing for me.

 

I definitely agree with that. I think many of PWME's symptoms are perceptions of feelings without the physical/chemical abnormalities that typically cause them. It probably only takes one misfiring neuron to produce the perception of lethargy, or pain in some part of the body, or some other such symptom.

 

We know of a few bacterial and parasite infections that persist in the face of treatment, and that are commonly failed by diagnostics. Borrelia comes to mind, as do bartonella and babesiosis.

For at least a portion of ME/CFS patients. persistent unresolved infection should remain on the table.

 

It's possible that's why the Covid jabs make me feel great. Also, if I get a bad cold, I'm seized with the energy to clean the whole house the day before I start streaming, croaking, and hacking.

I remember reading somewhere that it's a histamine surge that causes the sudden spurt of energy, but admittedly this was years ago and it might not have been an especially reliable source.

 

Absolutely

 

As a cause of ME, or just as something that worsens existing ME? I suppose there could be some cases where a persistent infection could keep a patient in the ME state whereas they would otherwise be able to switch their ME off, but I think that would be a fairly tiny percentage of PWME. Aside from those few possible cases, I'd say that PWME should be tested extra-well for persistent infections, which could result in a reduction of ME severity, but that it's not a priority for ME research.

 

Technically speaking, both.

A couple things to unpack here.

First, testing extra-well for persistent infections is just not really a thing with some pathogens, including many borrelia species and bartonella strains (ever been around a cat?). Babesiosis is no cake-walk either. And if you assume some pathogens hide out in tissues or are intracellular or have some enhanced capacity at immune evasion, there's a lot more candidates to consider as diagnostic nightmares.

Second, I hope we can define more precisely what ME/CFS is before we try to claim we have the inside track on how to prioritize research. We might have preferences or inclinations, but that's not the same thing, is it. Right now we just afix an ME/CFS label to anyone who shares a cluster of symptoms. That clustering could ALL be pathogen-based, or none of it could be pathogen-based (e.g. immune dysfunction) , or some mix of the two. We don't know yet. So I would personally be reluctant to say what should be a higher priority.