Dr Markov CBIS Theory of ME/CFS - General Discussion

[godlovesatrier]

You know I just had a thought. Surely urine would have these bacteria in them anyway? And this might be a complete red herring.

Because there could be literally anything in there from the urethra. It might be worse/better for women because of the anatomical situ and potential for cross contamination?

I wonder how many women he's treated successfully?

Also another thought if he's sees milder patients there's a very good chance they could make a full recovery inside 3 years. If they are beyond the first 3 years of being sick then I think it's highly unlikely. And therefore treatment could well be working. I don't believe there's any science to backup the 3 year rule though.

I made a decent recovery inside my first 3 years. Only for a general anesthetic to totally fuck me over which I've never really recovered from. Even if it only took 10% that was a lot at the time.

 

[lint7]

@Hip Did Markov identify the same type of bacteria that you identified?

 

[Hip]

Surely urine would have these bacteria in them anyway? And this might be a complete red herring.

Because there could be literally anything in there from the urethra. It might be worse/better for women because of the anatomical situ and potential for cross contamination?

Dr Markov found that only 7% of adult healthy controls are positive for bacteria using his high sensitivity urine culture. Whereas 95% of ME/CFS patients are positive. All these facts and figures are found in the Markov summary post.

Contamination from bacteria on the skin is a possibility in any urine test, and Dr Markov recommends washing skin area around the urethra before passing urine for the culture. I went one step further, and washed the skin with soap and water, and then afterwards applied some disinfectant 10% povidone-iodine solution I had (surgeons use this to disinfect their hands before surgery).

 

[Hip]

@Hip Did Markov identify the same type of bacteria that you identified?

Yes, there was a good correspondence.

I was able to partially identify the bacteria growing on my dipslides, by transferring the bacteria to some chromogenic agar plates, which turn different colors depending on the species of bacteria.

Using Brilliance UTI chromogenic agar, I partially identified three species:

• Enterococcus species (blue-green color on the chromogenic agar)
• Coliform bacteria (dark blue color)
• Staphylococcus or Streptococcus (white color)

See this post for pictures of my chromogenic agar tests.

Note that coliform bacteria include: Escherichia, Klebsiella, Enterobacter, Citrobacter and Hafnia. So the coliform bacteria I found could be any one of these species (except E. coli, as that appears as pink/red on the chromogenic agar).


When I sent all my dipslides and agars to the Markov Clinic, their bacteriology department said were able to identify with "complete certainty" three species:

• Enterococcus faecalis
• Klebsiella pneumonia
• Pseudomonas aeruginosa

So the Enterococcus faecalis the clinic found corresponds to the Enterococcus species I found.

The Klebsiella pneumonia the clinic found corresponds to the coliform bacteria I found.

The Pseudomonas aeruginosa I did not see myself on the chromogenic agar (it turns brown/green on the agar), so that is one I missed, but the clinic picked up.

Dr Markov commented that this was a "good catch" of bacteria.


The clinic said they would create an autovaccine from these 3 bacteria (all three in the same autovaccine). Plus they are prescribing Dr Markov's own off-the-shelf Staphylococcus vaccine (Staphylo-PrimaVac), so I presume they found evidence of Staphylococcus on my agars too, which corresponds to the Staphylococcus or Streptococcus I found on the chromogenic agar.

 

[Hip]

My dipslide was positive too at room temperature.

I will add you to the list of positive ME/CFS patients in my post. So now that is 6 out of 6 patients positive.

 

[Hip]

I wonder how many women he's treated successfully?

The intriguing thing is that in Dr Markov's clinic, he sees roughly equal numbers of male and female CBIS ME/CFS patients. Of the 2340 adult ME/CFS patients in his clinic who satisfied the CDC 1994 Fukuda criteria, 1287 (55%) were men, and 1053 (45%) were women.

That is at odds with the more usual ME/CFS male to female ratio of 1:4 that studies tend to observe. I don't know if that could be a cultural thing, with men more likely to seek help when they get ME/CFS symptoms in the Ukraine, or maybe men have more money than women, so can more afford private doctors.

Or the 1:1 ratio seen in the Markov Clinic might mean that the kidney dysbiosis cause of ME/CFS is only one subtype of ME/CFS, a subtype in which affects the sexes equally.

 

[BrightCandle]

UTI's and kidney infections really aren't that common and more importantly they get treated. Dipslides from urine should never show growth. It can be bacteria from the entrance of the uretha but urine is meant to be sterile. If its not in every ME patient that is a big finding and as always I want more people to do this dipslide test. This is something Phoenix rising really can do, bring us together to confirm findings and the faster we do that and confirm underlying medical oddities the quicker medical researchers can work out why.

 

[pattismith]

Just discovered a possible connection between Dr Markov's kidney infection theory of ME/CFS that is detailed in this thread (where LPS and exotoxins leak into the bloodstream, causing ME/CFS according to his theory), and Dr Robert Phair's interest in the mutations of the IDO2 gene found in ME/CFS patients. @HTester

As I understand it, the mutations in the IDO2 gene often found in ME/CFS patients reduce the effectiveness of the IDO2 enzyme.

Well, this study found that IDO2 knock-out mice had increased production of inflammatory cytokines when exposed to LPS.

So this suggests people who have IDO2 mutations which reduce the effectiveness of IDO2 will be more susceptible to the pro-inflammatory effects of LPS in the bloodstream.

this also suggests that iron deficiency may be a risk factor for ME/CFS as IDO are heme enzymes, likely to have their activity correlated with iron availability.

 

[perrier]

this also suggests that iron deficiency may be a risk factor for ME/CFS as IDO are heme enzymes, likely to have their activity correlated with iron availability.

Thanks Patti Smith for this point. Would you be able to elaborate a little more. Our family member has mutations on IDO 1 and 2, and is chronically anemic. Thanks. I found this interesting article: https://www.pnas.org/content/115/13/3249

 

[pattismith]

Thanks Patti Smith for this point. Would you be able to elaborate a little more. Our family member has mutations on IDO 1 and 2, and is chronically anemic. Thanks. I found this interesting article: https://www.pnas.org/content/115/13/3249

I don't know if mutations in IDO1 or IDO2 have any direct relation with any anemic status.

What I understand is that IDO enzymes are Heme enzymes, this means their activity depends on Heme (which is an iron complex). So if heme is deficient, IDO activity will go down.
The same way, red cells need Heme for function. If heme is deficient, then anemia happens.

So anemia and IDO hypoactivity may be associated in iron deficiency, moreover if IDO mutations with loss of function is present.

Do you have your blood iron parameters?

 

[Consul]

@Consul, I have the same concerns as you, that the ME/CFS research community's interest in Dr Markov's theory and treatment of ME/CFS may grow only slowly, and assuming the treatment does indeed work, it will be some time before there are replication studies, and some time before we see the take up of this treatment in other countries.

As you say, Dr Markov's autovaccine treatment is lengthy, and so even for ME/CFS patients like @Hipsman who started the treatment in June 2021, it's will be 2 to 3 years before we know the full results. Although we should have a good sense of whether it is working after about a year of treatment. @Hipsman already feels that his PEM has improved a little, though he says it is hard to tell.

This is one of my motivations for trying to become a autovaccine guinea pig, so that we might at least have some anecdotal accounts of how the treatment went 2 or 3 years from now. If we can open up the possibility of remote treatment at the Markov Clinic, we may find some more ME/CFS patients become interested in trying this treatment.


Do you know which ME/CFS researchers have spoken to Dr Igor Markov?

I sent a volley of emails to a dozen or so ME/CFS researchers who I thought might be interested in Dr Markov's theory and treatment, especially researchers with an interest in bacterial, leaky gut and LPS etiologies of ME/CFS. Only the Morten Group in Oxford replied to my email and showed some interest.

The Morten Group by the way are doing lots of interesting ME/CFS research on a low budget (detailed in this presentation), and I hope they manage to secure more funding, because there are not many good ME/CFS research groups in the UK.



Unfortunately ME/CFS research does go far more slowly than we would like. If we look at the rituximab research, for example, which was the great hope of the ME/CFS community for many years, the very first paper published by Fluge and Mella was in 2009, and their final phase III clinical trial was published ten years later in 2019 (and unfortunately showed rituximab was not generally beneficial for ME/CFS). So that rituximab saga took a full ten years from beginning to end.

Hi, i was a bit drained yesterday so i had to postpone the reply. The only info i have on Dr Markov is from this forum, i think its mentioned in your summary thread that Dr Markov have spoken to some ME associations, i dont know if he talked to any researchers.

Looks like we have the same thoughts regarding this, stuff needs to go faster. I personally struggle to see the scam element in this though, i dont see what he would gain from it nor why he would bother writing that huge document, and now its verified that he actually has a real medical office where he indeed is making auto vaccines. So the possibility of this being a scam has shrunk quite alot. Would be awesome if this was indeed the solution. Another random worry is that russia seems to be amassing forces on the ukraine boundary now according to news reports so if something military were to go down in the region i would prefer if someone had adopted Dr Markovs technique to the west before its too late.

I have been watching the Karl Morten video you linked and a few other, very interresting indeed. In one video he displays a graph showing me/cfs patients consulting doctors at a consistently higher rate than controls already 15+ years ahead of getting the diagnosis. It does take alot of time to be diagnosed but it still looks like something is going on a long time before ppl get me/cfs.

The rituximab took a long time and failed but the drug does cure some individuals even if it doesnt generally work, as im sure you know. And that seems to be true for a whole lot of different stuff like mitochondria supplements, anti virals, stress reduction through e.g meditation, circadian rythm and sleep interventions, ketogenic diet, etc.

Very weird. What do you think is the common denominator, bacteria in L-form / low grade infection?

Im not well educated in this field so i really have no clue, trying to educate myself more on this stuff.

Also what was Dr Mortens reply to your email?

 

[Hip]

What do you think is the common denominator, bacteria in L-form / low grade infection?

Numerous causal theories have been proposed for ME/CFS. This illness nearly always begins with a viral infection, and chronic viral infections have been found in most ME/CFS patients, so the viral theory of ME/CFS is one of the oldest and best researched.

Then there are gut microbiome dysfunction theories, and leaky gut (intestinal hyperpermeability) theories, where bacterial toxins seep out of the gut. There are autoimmune theories, immune dysfunction theories, and mitochondrial dysfunction theories. And many other theories. I recently posted a list of all the ME/CFS theories I could recall in this post.

Dr Markov's kidney dysbiosis CBIS theory is similar to one of the ideas of Prof Michael Maes, who was examining whether a certain bacterial toxin called LPS found in the gut might seep into the systemic blood circulation from a leaky gut to cause ME/CFS.

In these bacterial toxin theories of Maes and Markov, the bacterium itself does not cause any major issues, but the toxins it secretes are thought to cause system-wide poisoning and dysfunction. A bacterial toxin in the blood could disrupt numerous systems in the body. And this is exactly what what we see in ME/CFS: a disease in which multiple systems are dysfunctional.

Bacterial toxins are some of the most potent toxins known to man. The lethal injected dose of LPS is only around 1 microgram, yet we have about 10 grams or more of LPS in our gut. 1 The LPS causes no harm while it remains in the gut, but if even a tiny amount leaks out, it can cause trouble. And LPS is just one of hundreds of different toxins bacteria make. Each species of bacteria may produce half a dozen toxins just on its own.

Also what was Dr Mortens reply to your email?

Dr Karl Morten said Dr Markov's theory sounds interesting, as it fits the thinking of the Morten Group, who are focused on bacterial etiologies of ME/CFS. Dr Morten thinks intestinal hyperpermeability is the likely source of leaking bacterial toxins in ME/CFS, but found Markov's idea that the kidneys are the source of the leak interesting. He said he would have a good look at Dr Markov's published work.

 

[chelsea49]

Has anyone on here tried this yet?

 

[lenora]

@chelsea49....No, I have not and couldn't name anyone who has. I'm not saying that someone's hasn't, I just don't know.

 

[Hipsman]

Has anyone on here tried this yet?

Um, I did, see these posts: (One) (Two) (Three)

 

[Hip]

It's interesting that Staphylococcus alpha toxin, which potentially might be found in the blood of ME/CFS patients with a Staphylococcus dysbiosis in their kidneys, nasopharynx or intestines, has been shown to damage the vagus nerve in an in vitro study:

Injury of myelin sheaths in isolated rabbit vagus nerves by α-toxin of Staphylococcus aureus

Stanislaw Szmigielski, Mayme Blankenship, John P. Robinson, Sidney Harshman

Abstract

Dissected rabbit vagus nerves were incubated in vitro with 0·24-4 μg of purified staphylococcal α-toxin (17,000 H.U./mg protein) per ml. The release of 86Rb from prelabeled nerves and the electrical activity of nerves (action potential) were measured and correlated with morphological changes observed by electron microscopy. At a concentration of α-toxin of 2 μg/ml, 30% of incorporated 86Rb was released from the nerves after 30 min of incubation.

The electrical activity was maintained over this time period and required an additional 30 min before failing completely. Concentrations of α-toxin below 2 μg/ml had no effect on either the release of 86Rb or the electrical activity even after 60 min of incubation of the nerves. In contrast, dramatic changes in the morphology of the myelin sheaths are readily demonstrated after 30 min of incubation and can easily be observed at 0·2 μg/ml, a level of α-toxin which has no effect on 86Rb release or electrical activity. Both non-myelinated nerve fibers and Schwann cell membranes appear to be more resistant to the action of α-toxin.

We conclude that, of the parameters measured, disorganization of myelin sheaths is the first recognizable symptom of injury to peripheral nerves by staphylococcal α-toxin.

I wonder if this damage to the vagus nerve caused by this bacterial toxin might explain the dysautonomia conditions like POTS found in some ME/CFS patients.

I am not sure however if the alpha toxin concentrations of 2 μg/ml used in this study are comparable to the concentrations which might be found in the blood.

 

[chelsea49]

What about bacterias like salmonella why does does he not mention or look for those? I'm asking because I tested positive for salmonella and also have bad kidney issues

 

[Hip]

What about bacterias like salmonella why does does he not mention or look for those?

Dr Markov checks the kidneys for bacterial dysbiosis by examining the bacteria present in the urine. If Salmonella were present in the urine, I presume he would find it. But Salmonella appears to be a rare cause of UTIs. The most common bacterial Dr Markov finds in the urine are listed in the section entitled "The Bacterial Species Involved in Nephrodysbacteriosis" in this post.

 

[BrightCandle]

I took two dipsticks this week, first morning mid streams on two consecutive days, 72 hours and 48 hours old. Both grew nothing, completely clear. Its relatively unlikely that would happen by chance given the previous sticks but still I think plausible. I'll do some more in a few weeks time again and continue with the current cranberry dose.

 

[Hip]

I took two dipsticks this week, first morning mid streams on two consecutive days, 72 hours and 48 hours old. Both grew nothing, completely clear.

Dr Markov says placing the dipslide in the end of stream urine is better than mid stream, although I am not sure how much difference that makes.

What I have sometimes done is placed the same dipslide in my stream of urine several times a day, not just in the morning. So almost every time I go to the toilet, I will expose the same dipslide to the urine. And I may do this for 2 or 3 days in a row, using the same dipslide (for economy reasons). I believe that such multiple daily exposures will increase your chances of catching some bacteria.

Of course, if we want to compare ME/CFS patients to healthy controls, we would need to use the standardized test, which is morning warm end of stream urine for three days in a row using a new dipslide each day.

But if we want to maximize the chances of finding bacteria in the urine, then possibly the multiple daily exposure method I describe might be more effective.