What are all the theories of what causes ME CFS?

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It's the fact that he detects these bacteria in the urine, and when he targets these bacteria he finds in the urine with autovaccines, the patient's health improves, and eventually is cured.

So that's the main evidence, the fact that his treatment is keyed on bacteria in the urine.

Of course autovaccines would also work on the same bacteria if they were found elsewhere in the body, like in the intestines. But I think Dr Markov has found that his autovaccine treatment does not seem to alter the gut microbiome, but does alter the kidney microbiome (in that after treatment, these bacteria can no longer be found in the urine).


However, I think Dr Markov would admit that he cannot be 100% sure at this stage that the kidney is the culprit. The gut could also be involved.
would itbe ridiculous to suppose that a gut leakiness could cause intestinal bacterias to go from the intestine to the kidney and then bladder, and that his autovaccine could fix that ?
 

nerd

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May I ask how you experience it?
Like a worse version of my baseline. No clear thoughts, word finding issues, leas cognition, muscle fatigue, more air hunger, headache, oversensitivity to light, dysautonomia, numbness in my finger tips, tachycardia. It takes one night to become notable though. There's another immediate fatigue I experience, which feels like I'm on too many antihistamines. So I explored the possibility that this is maybe histamine-related. Microglia activation might be one explanation.


I did experience an entirely psychologically generated severe "pain" which my body produced. Not an "illness" but a symptom.
I wouldn't call this psychological. If you look at it from this perspective, asthma is psychological as well because it's triggered the same way as your episode. We're generally hypersensitive and this doctor provided the necessary overload. But the mechanism is neurological.

phone really makes me feel more ill really quickly. Holding it, focusing on it if its a video chat (often is, my grandaughter), I often get PEM the next day if the call is very long. And I don' t do that much of the talking
I think it's the subconscious pattern that goes along. We've learned to subconsciously prepare for a talk and a phone call. But our brain might not be ready for this task. So even if we don't consciously focus, our subconscious might be overdoing it. It doesn't mean it's psychological. It's just a physiological process that can't work properly because of the pathophysiology of ME.

From my experience, PEM is neurological, and probably involves glial cells. Cognitive exertion could trigger my PEM within an hour (variable delay).
Same idea. Glutamate activates the glial cells. If the neurons send too much glutamate or if the glial cell receptors are hypersensitive to glutamate, it's a natural response. The question is what mechanism is really at play. It could as well be a dysfunction of GABAergic system as the antagonist of glutamate. This intrigues me about the Coetene theory. But maybe their success is just an indirect one related to glutamate or GABA. I'm certain that antihistamines interact with the pathogenesis, though I'm not sure if it's in a positive or negative way.

would itbe ridiculous to suppose that a gut leakiness could cause intestinal bacterias to go from the intestine to the kidney and then bladder, and that his autovaccine could fix that ?
That's a typical explanation for bladder infection in males. In fact, it's E. Choli that end up in the kidneys, bladder, prostate and urinary tract. In my case, it basically began with a UTI and I've had many UTIs in my relatively young life. Sometimes, I can detect high amounts of blood in the urine, so it's definitely more than just a general inflammation of the urinary tract. I also have traces of coliform bacteria in my drinking water. I think the main issue here is that the reduced acidity in the stomach opens the door to bacterial infections of the GIT and UT.
 

Hip

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would itbe ridiculous to suppose that a gut leakiness could cause intestinal bacterias to go from the intestine to the kidney and then bladder
See this paper:
Bacterial translocation is defined as the passage of viable bacteria from the gastrointestinal (GI) tract to extraintestinal sites, such as the mesenteric lymph node complex (MLN), liver, spleen, kidney, and bloodstream.

The three primary mechanisms promoting bacterial translocation in animal models are identified as: (a) disruption of the ecologic GI equilibrium to allow intestinal bacterial overgrowth, (b) increased permeability of the intestinal mucosal barrier, and (c) deficiencies in host immune defenses.

Dr Markov says he often finds prolonged early childhood antibiotic use in those with CBIS ME/CFS. He thinks antibiotics in childhood may promote the development of dysbiosis in the kidneys, with the antibiotics causing bacterial biofilms building up in the kidney.

This idea of childhood antibiotic use setting the stage for chronic disease later in life is not new: if you Google for early childhood antibiotic use chronic disease, you will find quite a few studies on this.

This article for example says:
Children under age 2 who take antibiotics are at greater risk for childhood-onset asthma, respiratory allergies, eczema, celiac disease, obesity and attention deficit hyperactivity disorder, according to a paper written jointly by Mayo Clinic and Rutgers researchers.
When I was 2 to 4 years of age, I was given many round of antibiotics, due to chronic tonsillitis. So that may fit the pattern of childhood antibiotic use leading to chronic disease later.
 
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I have pharyngitis as well and a general ill feeling, but not the flu-typical fluid secretion at mucus membranes, no airway obstruction except for my nose mucus being inflamed and swollen and making nose breathing more difficult.
No me either. It feels more like a high fever without having a fever.
 
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See this paper:



Dr Markov says he often finds prolonged early childhood antibiotic use in those with CBIS ME/CFS. He thinks antibiotics in childhood may promote the development of dysbiosis in the kidneys, with the antibiotics causing bacterial biofilms building up in the kidney.

This idea of childhood antibiotic use setting the stage for chronic disease later in life is not new: if you Google for early childhood antibiotic use chronic disease, you will find quite a few studies on this.

This article for example says:


When I was 2 to 4 years of age, I was given many round of antibiotics, due to chronic tonsillitis. So that may fit the pattern of childhood antibiotic use leading to chronic disease later.
You remind me that I still have to do my dipslites test. It's an interest theory.
 
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I read (but forgot the source) that EBV deactivates the ability to get a fever to sustain its own survival.
I never got a fever since my infection...but it kinda feels like i agree.
 

nerd

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I wonder if it's possible for the vagus CNS/NTS pathogenesis to develop just by having a prolonged exposure to a vagus nerve stimulus such as a long mononucleosis or prolonged physical trauma.

During exposure, there would be an increased glutamate threshold in the NTS, this might consequently change the homeostasis of the microglia. These would then contribute to the problem by releasing cytokines which then stimulate the NTS again, which then triggers the microglia again. Trauma or viral infection could also be part of the feedback because they are also enhanced by the downstream effects of this neurological dysregulation. Monocytes might migrate into the CNS just because of the cytokine signaling but not because there are pathogens necessarily.
 

sometexan84

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I wonder if it's possible for the vagus CNS/NTS pathogenesis to develop just by having a prolonged exposure to a vagus nerve stimulus such as a long mononucleosis or prolonged physical trauma.
Prolonged Gut Dysbiosis will do this.

https://www.linkedin.com/pulse/gut-...l-nerve-tone-imbalance-directly-sheri-thoman/
The Vagus nerve reads the gut microbiome which initiates a response to modulate inflammation based on whether or not it detects pathogenic versus non-pathogenic organisms
 

nerd

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Yes, that as well. Beside other things that form indirect feedback loops. I'm not sure if we'll ever find a causal treatment that it's precision or broadband medicine, targeting multiple of the defective systems. Purely logically, it seems to be trivial that you need to combine at least two therapies - one for the pathogenesis, one for the etiology.
 
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Yes, that as well. Beside other things that form indirect feedback loops. I'm not sure if we'll ever find a causal treatment that it's precision or broadband medicine, targeting multiple of the defective systems. Purely logically, it seems to be trivial that you need to combine at least two therapies - one for the pathogenesis, one for the etiology.
What would be a treatment for the etiology? Thats a good point of view honestly.

Drugs that reduce glutamate or microglial activation?
 

nerd

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What would be a treatment for the etiology? Thats a good point of view honestly.

Drugs that reduce glutamate or microglial activation?
No, these treat the presumed pathogenesis. The etiology varies, as we know, from trauma to viral infections to vaccinations to drug/supplement use to cancer. There's no way to find a single drug that treats all of that.