You probably have an autoimmune disease...

[crypt0cu1t]

I actually tried plasmapheresis earlier this year. I did 4 plasmaexchanges in 1 week. I was positive for 3/4 of celltrend Antibodies + Tpo-antibodies. The result: I had no improvement at all.

That’s why I don’t believe that antibodies play a major role in this disease, at least in my case. Beside my case I know at least 2 other cases who did plasmaexchange and immunadsorption with positive antibodies and no improvement.

What symptoms do you have? Mine are almost all mental/cognitive (encephalopathy type)

 

[Canned]

What symptoms do you have? Mine are almost all mental/cognitive (encephalopathy type)

I’d say my main symptom is fatigue. I also have severe cognitive problems (not brain related but nervous system related), muscle weakness, stomach problems, PEM.

 

[crypt0cu1t]

I’d say my main symptom is fatigue. I also have severe cognitive problems (not brain related but nervous system related), muscle weakness, stomach problems, PEM.

I seem to be very different from most here, all of mine are purely cognitive and mental (Derealization, confusion, headaches, dizziness, frequent urination, blurry/double vision, weakness in arms)

 

[JES]

I seem to be very different from most here, all of mine are purely cognitive and mental (Derealization, confusion, headaches, dizziness, frequent urination, blurry/double vision, weakness in arms)

Many people have cognitive problems here, brain fog is probably the most predominant. The type of cognitive issues that ME/CFS brings is in my case quite different than something like, say, dementia. I typically don't keep forgetting things or become disorganized, it's more like a lack of drive or energy to perform cognitively demanding tasks or even something simple like socializing for an extended period of time.

Regardless, I think autoimmunity and neuroinflammation can be tied to lots of different symptoms, whether it would be brain fog, headaches or orthostatic issues . It may be that the exact location and type of inflammation is what differentiates the symptoms. ME/CFS patients seem thankfully quite spared of permanent brain damage as in some other neuroinflammatory diseases. I have noticed a rapid improvement of symptoms following various protocols, which shows at least a great deal of reversal is possible.

 

[Wishful]

Regardless, I think autoimmunity and neuroinflammation can be tied to lots of different symptoms, whether it would be brain fog, headaches or orthostatic issues .

It could also be that many kinds of immune activation, whether autoimmune or not, viral or physical cell damage or whatever, can trigger some other mechanism, such as glial cells, that in turn generate the ME symptoms.

 

[sometexan84]

I still don't know if my ME/CFS/fibro is auto-immune or not, and I don't think we have definite proof it's an autoimmune disease.

You're right, the proof does not yet exist.

Grave's thyroiditis is an evident auto-immune disease; it is tightly associated with a single Ab type (anti TSH receptors) and resolves when these Ab are cleared.

Thyrotropin Receptor antibodies (TRab) are found in 90% of Graves' disease. But Thyroid stimulating immunoglobulin (TSI) antibodies are also found in Graves', 79%.

Saccharomyces cerevisiae antibodies were found in 12%.

Did you know that you can have Graves' and Hashimoto's?

Graves' disease is also associated w/ a ton of other things involving auto-immunity, like polyglandular autoimmune syndromes, pernicious anemia, vitiligo, diabetes mellitus type 1, autoimmune adrenal insufficiency, systemic sclerosis, myasthenia gravis, Sjögren syndrome, rheumatoid arthritis, and systemic lupus erythematosus.

My point is, your Graves' disease example is understandable.... but it's an oversimplified (and outdated) approach to autoimmunity.

The fact anti-muscarinic and anti-adrenergic Ab are associated with ME/CFS is not a proof ME/CFS is a primary auto-immune disease. These Ab are not specific, they happen in many auto-immune and neuro-degenerative diseases.

Again, you are correct. It isn't proof. If I had 100% definitive proof available, I would share it of course. But I do not. And of course you are more than free to not believe what I'm saying.

You know, the majority of auto-antibodies are not disease specific. The Graves' disease example you gave is sort of an exception. There are some antibodies that strongly correspond to a specific disease like:

Graves' disease - Thyrotropin-receptor antibody​

Crohn's disease - Anti-Saccharomyces cerevisiae antibodies (ASCA)​

Rheumatoid arthritis - Rheumatoid factor​

Most aren't like that though. And I don't believe there are any ME/CFS specific autoantibodies. I don't think ME/CFS is a thing, at all. I wrote more about that elsewhere.

Again, I think we are all different, but most of us have undiagnosed autoimmune conditions. They'll mostly be different. I think we even have auto-antibodies that have yet to be discovered, linked to auto-immune conditions/syndromes that do not yet exist, and that this will start coming to light more and more over the next few years in the research.

 

[sometexan84]

I did 7 rounds of plasmapheresis and noticed a decent improvement about a week later.

That's pretty cool.

Had you tested positive for any particular auto-antibodies?

 

[sometexan84]

I actually tried plasmapheresis earlier this year. I did 4 plasmaexchanges in 1 week. I was positive for 3/4 of celltrend Antibodies + Tpo-antibodies. The result: I had no improvement at all.

That’s why I don’t believe that antibodies play a major role in this disease, at least in my case. Beside my case I know at least 2 other cases who did plasmaexchange and immunadsorption with positive antibodies and no improvement.

Guys, you have got to take a step back from the whole 1-to-1 linear cause/effect rationale.

There are multiple reasons why your symptoms might not have improved. Btw, if you had 3/4 celltrend antibodies plus TPO antibodies, I'd bet $1 Million that you have other auto-antibodies.

Also, I'd like to make it clear that I am not saying auto-antibodies are causing everyone's fatigue. I'm saying that most ME/CFS have autoimmunity that caused and/or perpetuated the set of conditions.

 

[sometexan84]

One more autoimmune association... (just saying)

Female Prevalence

ME/CFS: 75 - 85% women

Autoimmune Disease: 80% women

Numerous studies have found the rates of ME/CFS to be substantially higher in adult women than in men, with estimates ranging from 75-85%

Approximately 80% of all patients diagnosed with autoimmune diseases are women

 

[Wishful]

One more autoimmune association... (just saying)

While I'm not convinced that ME is an autoimmune disease, the observation about prevalence in females is certainly interesting.

 

[sometexan84]

Well, maybe one more thing that might convince you further is to Google "autoantibodies long covid"

 

[Wishful]

Okay, I checked one paper. It convinced me that the autoimmunity hypothesis was worth further research, but didn't convince me at this time that it's 'the answer'.

"In summary, the evidence for autoimmunity in ME/CFS is indirect or circumstantial. It rests on the effect of immunosuppression (although unsubstantiated in a double-blind trial) of anti-CD20, comorbidities with known autoimmunity (thyroiditis, thyroidism) or possible autoimmunity (FM, POTS, IBS), probable improvement after immunostimulation, and an increased frequency of certain autoantibodies and of B cell lymphomas. Of the Witebsky–Rose criteria for autoimmunity (270), direct; transfer of disease by antibody, and indirect; transfer of disease by cells to SCID mice, induction of disease by autoantigen, identification of antibodies within lesions, genetic predisposition, autoantibodies or self-reactive T cells, a few (genetic predisposition and increased frequency of autoantibodies) are partially fulfilled. Much work remains."

I'll await further developments.

 

[sometexan84]

The research will get there. But it's going to be SLOW!

More studies will come out where they'll find low but "statistically significant" autoantibodies in ME/CFS. Not significant enough to make the front page.

They'll do more studies on autoimmune condition comorbidities in ME/CFS. And I'm sure some will find low but "statistically significant" patterns. That won't be a head turner either.

Maybe they'll do more general autoimmune-type treatments (e.g. immunoadsorption). But those will never be conclusive.

As long as people think of ME/CFS as a single, unique, standalone disease, research will continue moving in the wrong direction, with desperate attempts to find a common denominator that does not exist.

 

[dave11]

A recent study found that only two cytokines working together may be responsible for the severe effects of covid - TNF-a and IFN-y. This finding may offer insight into potential treatment for covid and autoimmune diseases.

https://www.sciencedirect.com/scien...ptosis,damage through inflammatory cell death.

 

[Wishful]

One problem I have with the paper I clipped from is that their evidence is partly based on 'some people show some improvement on treatments targeting antibodies'. To me that's the kind of response I expect from the placebo effect, or from reducing some other health problem that makes ME worse. If ME is supposed to respond to anti-antibody treatments, there should be some major improvements or even full recoveries reported.

 

[sometexan84]

Well, there have been some major improvements in some.

But I don't think a single treatment is going to 100% cure an entire group of people, just because they have an autoimmune condition.

Some autoimmune treatments have resulted in terrible outcomes.

 

[wastwater]

Would eculizumab be worth trialling,would this target immune activation at the source

 

[sometexan84]

A recent study found that only two cytokines working together may be responsible for the severe effects of covid - TNF-a and IFN-y. This finding may offer insight into potential treatment for covid and autoimmune diseases.

It's possible. But they do have an overactive immune system.

"Hyper-activation of the immune response against severe acute respiratory syndrome coronavirus 2 may result, in some cases, in development of unwanted autoimmune disorders"
https://www.wjgnet.com/2307-8960/full/v8/i17/3621.htm

ME/CFS (and those w/ Long Covid) have an overactive immune system and auto-antibodies before getting sick.

And, (I don't have the article link handy, sorry) supposedly Covid put the autoantibodies into motion.

I think COVID is slightly different. TNF-a is key. But the IFN-y increase might just be a result of the autoantibodies they found in COVID patients against the other Type I Interferons. Or it might not. IFN-y can go up and down quickly, from the research I've seen.

But I think a good ME/CFS comparison is Parvovirus B19 and Enterovirus B.

Parvovirus B19 has been linked to a ton of autoimmune diseases (and ME/CFS). It creates a bunch of auto-antibodies (Collagen II, Phosphatidylserine, Cardiolipin, Angiotensin II type 1 (AT1) receptor, Rheumatoid Factor, DNA (ss and ds), β2-glycoprotein, myelin, etc). There's also a bunch of cross-reactivity to B19 antibodies and its proteins.

So, there's that. And also, acute B19 causes an abnormal immune response, resulting in impaired T cell-mediated cytotoxicity, and irregular cytokine function.

Then later, a bad case of Enterovirus B shows up. It's effect on our immune system results in all those auto-antibodies getting set into motion. If you didn't have reactivated EBV yet, then it will reactive at this time. The auto-antibodies will attack, disrupting your immune system. Dysregulated T cells, other lymphocytes, and cytokine production further disrupts your immune system.

Now you have rare case of non-cytolytic persistent Enterovirus B infection. Of course this will perpetuate your immune dysfunction.

And at this point, you are in a pretty deep hole that is difficult to climb out of. This representation could lead to any number of symptoms and conditions.

(btw - There are still two things about Parvovirus B19 that I'm still researching and have yet to confirm. I'm not sure about the extent of damage and autoimmunity one can get from merely an acute B19 infection. And I still don't know if chronic diseases and autoimmune conditions occur more w/ persistent B19 infections, and/or the best way to test for persistent B19 infections. All I know is there is more to B19 than meets the eye. I will find answers. I will share more when I find out)

 

[Fighttolive]

It's possible. But they do have an overactive immune system.

"Hyper-activation of the immune response against severe acute respiratory syndrome coronavirus 2 may result, in some cases, in development of unwanted autoimmune disorders"
https://www.wjgnet.com/2307-8960/full/v8/i17/3621.htm

ME/CFS (and those w/ Long Covid) have an overactive immune system and auto-antibodies before getting sick.

And, (I don't have the article link handy, sorry) supposedly Covid put the autoantibodies into motion.

I think COVID is slightly different. TNF-a is key. But the IFN-y increase might just be a result of the autoantibodies they found in COVID patients against the other Type I Interferons. Or it might not. IFN-y can go up and down quickly, from the research I've seen.

But I think a good ME/CFS comparison is Parvovirus B19 and Enterovirus B.

Parvovirus B19 has been linked to a ton of autoimmune diseases (and ME/CFS). It creates a bunch of auto-antibodies (Collagen II, Phosphatidylserine, Cardiolipin, Angiotensin II type 1 (AT1) receptor, Rheumatoid Factor, DNA (ss and ds), β2-glycoprotein, myelin, etc). There's also a bunch of cross-reactivity to B19 antibodies and its proteins.

So, there's that. And also, acute B19 causes an abnormal immune response, resulting in impaired T cell-mediated cytotoxicity, and irregular cytokine function.

Then later, a bad case of Enterovirus B shows up. It's effect on our immune system results in all those auto-antibodies getting set into motion. If you didn't have reactivated EBV yet, then it will reactive at this time. The auto-antibodies will attack, disrupting your immune system. Dysregulated T cells, other lymphocytes, and cytokine production further disrupts your immune system.

Now you have rare case of non-cytolytic persistent Enterovirus B infection. Of course this will perpetuate your immune dysfunction.

And at this point, you are in a pretty deep hole that is difficult to climb out of. This representation could lead to any number of symptoms and conditions.

(btw - There are still two things about Parvovirus B19 that I'm still researching and have yet to confirm. I'm not sure about the extent of damage and autoimmunity one can get from merely an acute B19 infection. And I still don't know if chronic diseases and autoimmune conditions occur more w/ persistent B19 infections, and/or the best way to test for persistent B19 infections. All I know is there is more to B19 than meets the eye. I will find answers. I will share more when I find out)

that’s interesting, I had reactivated mono years prior to CFS.

I was never the same after after a horrible virus that made me hallucinate- I always thought that the fever got too high and damaged parts of my brain.

the hypothalamus, mostly

what would one even do knowing about the 2 bouts of mononucleosis?

.

 

[sometexan84]

what would one even do knowing about the 2 bouts of mononucleosis?

Unfortunately, I do not know.

But it sounds very serious, and scary. There are some treatment options for EBV, but overall all I can say is more testing might be in order.