Preprint: Broken Connections: The Evidence for Neuroglial Failure in ME/CFS

Learner1

Learner1

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Pyrrhus said:
Related discussion:

https://forums.phoenixrising.me/thr...yndrome-may-come-with-pem.83473/#post-2358524
Click to expand...
All these threads on the same thing are confusing. I'm not sure where to answer.

Reading through the paper, I find I have several disagreements with many of his assumptions, based on other things I've read as well as my own experiences. I don't doubt that a few people may have whatever disease he's talking about, but do not find it describes what I have and others I know. And, he says:

"As a caveat and for clarification we want to add an important qualifier. It is unknown if ME/CFS can be legitimately conceptualized as manifestation of a single, underlying pathophysiological process. Indeed, many ME/CFS researchers question a universal pathological matrix especially across the
different etiotypes of the disease. This may be seen as a discouragement or even fatal blow to the approach presented in this working paper."

There are patients with mycotoxins, Epstein Barr, Cocksackie B, CCI, arsenic toxicity, thiamine or B12 or iron or tyrosine or citrulline deficiency, adrenal insufficiency, lipopolysaccharides, oxidative and nitrosative stress and many other etiologies and drivers of their disease.

Furthermore, not all of us experience PEM has he describes it, not do our physical symptoms equate with our mood. I don't doubt that glial cells play a role, but I'm not convinced that his assumptions and then the conclusions he derives from those somewhat questionable assumptions neatly explain our problems across the board.
 
V

VisualEffect

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Learner1 said:
All these threads on the same thing are confusing. I'm not sure where to answer.

Reading through the paper, I find I have several disagreements with many of his assumptions, based on other things I've read as well as my own experiences. I don't doubt that a few people may have whatever disease he's talking about, but do not find it describes what I have and others I know. And, he says:

"As a caveat and for clarification we want to add an important qualifier. It is unknown if ME/CFS can be legitimately conceptualized as manifestation of a single, underlying pathophysiological process. Indeed, many ME/CFS researchers question a universal pathological matrix especially across the
different etiotypes of the disease. This may be seen as a discouragement or even fatal blow to the approach presented in this working paper."

There are patients with mycotoxins, Epstein Barr, Cocksackie B, CCI, arsenic toxicity, thiamine or B12 or iron or tyrosine or citrulline deficiency, adrenal insufficiency, lipopolysaccharides, oxidative and nitrosative stress and many other etiologies and drivers of their disease.

Furthermore, not all of us experience PEM has he describes it, not do our physical symptoms equate with our mood. I don't doubt that glial cells play a role, but I'm not convinced that his assumptions and then the conclusions he derives from those somewhat questionable assumptions neatly explain our problems across the board.
Click to expand...
I don’t think any of his assumptions are questionable. He is trying to reverse engineer the problem and find dysfunctional part of the brain which is responsible for all the symptoms we have. That’s the key to solving this disease.

Author is saying that understanding “neuro-orthopedic” ME etiotype is crucial because it localises the problem. If I understood correctly, author means any process that leads to brainstem perfusion abnormality will consequently lead to ME. I believe this is 100% correct.
 
Learner1

Learner1

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VisualEffect said:
I don’t think any of his assumptions are questionable. He is trying to reverse engineer the problem and find dysfunctional part of the brain which is responsible for all the symptoms we have. That’s the key to solving this disease.

Author is saying that understanding “neuro-orthopedic” ME etiotype is crucial because it localises the problem. If I understood correctly, author means any process that leads to brainstem perfusion abnormality will consequently lead to ME. I believe this is 100% correct.
Click to expand...
Both genetic and environmental factors can play a role.

At this point, it seems EBV, HHV6, mycoplasma pneumoniae, chlamydia pneumoniae, and arsenic, cadmium, platinum, and mold toxicity leading to immunodeficiency, autoimmunity, endocrine dysfunction, nutrient deficiencies and mitochondrial dysfunction, with stress and the aftermath of a car accident caused my illness. Being celiac and having Hashimotos and hemochromatosis didn't help.

It would take a lot of reverse engineering to unwind that. Most patients who have had thorough diagnostic testing have similar lists of issues.

I think it's great that this guy and Dr. Van Elzakker are figuring out how these things can affect the brain and create symptoms, but unfortunately, it takes doing the individual detective work and treating the problems driving the abnormal brain function so that they're not impacting the brain any more to start to get well.

The sooner we figure out that individualized medicine is the answer, picking from a Chinese menu of common suspects as well as investigating more esoteric issues for some, and treating us as individuals, the more patients will get better.
 
bertiedog

bertiedog

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@Rufous McKinney said "this presentation, including Dr. Proal's discussion towards the end: is really great and complements all this."

I would love to know how many other researchers have come out confirming Van Elzakker and Dr Proal's ideas? We seem to have so many papers/speakers talking about their current theories but what we need desperately is confirmation via successful trials based on these theories. I know the pace of research of scientists interested in ME/CFS has picked up over recent years but it is hard to understand why there isn't more of consensus as to what is definitely going on.

After all it was 10 years ago when our community thought that the retrovirus XMRV was the answer and stimulated interest amongst scientists but it turned out to be a theory that was a huge letdown because it could easily be debunked.

Pam
 
C

Consul

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Interesting patient generated hypothesis on astrocyte dysfunction

https://patientresearchcovid19.com/...ovid-and-me-cfs-patients-pghj-issue1-may2023/

Abstract

An overactive sympathetic nervous system (SNS) may cause one subtype of Long COVID. People who are genetically at risk for noradrenergic nerve problems may develop an overactive SNS after an infection. Alternatively, genetic or virus-induced dysregulation of astrocytes could lead to overactivation of the SNS. An overactive SNS could disrupt regulation of immune cells, energy metabolism, sleep homeostasis, respiratory rate, gastrointestinal function, and systemic and cerebral blood pressure, causing fatigue and cognitive dysfunction.
 
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