Dr Markov CBIS Theory of ME/CFS - General Discussion

[Hip]

The only thing that would make it fine, in my eyes, is only if he tested all patients on all other issues like hormonal/vitamin deficiencies, celiac disease, mold issue, adrenal issues, other known infections, and other blood tests. Basically make ME/CFS diagnosis of exclusion.

Yes, in order to be reasonably sure of an ME/CFS diagnosis, it is always important to perform the necessary tests to exclude the common diseases which can produce ME/CFS-like symptoms, such as hypothyroidism, celiac disease, lupus, anemia, hepatitis B or C virus infection, major depression, and others.

The CDC 1994 Fukuda criteria state that all other known causes of chronic fatigue must have been ruled out before you can be confident in a ME/CFS diagnosis.

The Open Medicine Foundation compiled a list of diseases (see page 3) which can cause similar symptoms to ME/CFS.

 

[Hip]

One thing I'm a bit confused about - why would you need repeated vaccines for the treatment to work? Surely if the body's immune system is being trained to recognise a particular bacteria as a threat then it wouldn't forget it? Is the idea the bacteria mutate, or that different strains arise in its place?

It's not uncommon to require a course of vaccinations against a bacterium.

Some years ago I was experimenting with the Russian Medgamal® Staphylococcus toxoid vaccination (in order to try to replicate Prof Gottfries's good results putting ME/CFS into remission with the Staphypan® Staphylococcus toxoid vaccine).

This Russian Medgamal Staphylococcus vaccine is designed to protect against Staphylococcus infection, or to treat these infections.

In the instructions of the adjuvant-free version of this Russian Staphylococcus vaccine it says:

A full course of treatment includes 7 injections carried out with every 2 days, following increasing doses: 0.1 - 0.3 - 0.5 - 0.7 - 0.9 - 1.2 - 1.5 ml.

So you can see the course of injections start at low doses, and slowly builds up the dose in subsequent injections.

I understand that low doses are used first for cautionary reasons: if you happened to have a significant Staphylococcus infection somewhere in your body, then starting with a high dose of the vaccine could be dangerous, as it could trigger a sudden fierce immune response against that infection.

In order to guard against the risk of provoking a sudden very strong immune response, low doses are used first, and the dose is slowly built up.



Professor Carl-Gerhard Gottfries in Sweden used this scheme of gradual dose build up when treating ME/CFS patients with the Staphypan Staphylococcus toxoid vaccine. The Gottfries introductory dosing protocol is detailed in this post.

Prof Gottfries found that the benefits of the Staphypan Staphylococcus vaccine for ME/CFS would fade after about 4 weeks, so to maintain remission from ME/CFS, the Staphylococcus vaccine needs to be given one every 3 or 4 weeks indefinitely.

By contrast, Dr Markov's autovaccine treatment of ME/CFS appears to be curative: once you go through the full cycle of the autovaccine treatment, it requires no further injections (except he says in this post that some patients can have a relapse 5 to 7 years later, and may require another cycle of treatment with the autovaccine to address the relapse).



Dr Markov also uses gradual dose build up: in this post he says that one cycle of autovaccine treatment involves 2 or 3 courses of immunization with the vaccine.

One course involves 10 subcutaneous injections given every other day, in increasing doses, over a period of 20 days.

Between courses there is a rest period of 3 or 4 weeks where patients do not receive any injections. So a whole treatment cycle lasts for about 100 days or so.

 

[Hip]

It is interesting that in Professor Carl-Gerhard Gottfries's published 2002 clinical trial of the Staphylococcus vaccine for ME/CFS patients (detailed in my post here), Prof Gottfries found that 33% of ME/CFS patients obtained a 50% reduction in symptoms from the Staphylococcus vaccine.

Whereas Dr Igor Markov says he finds his autovaccine treatment is curative for 93% of the ME/CFS patients he treats who have CBIS.

Why does Dr Markov appear to have a higher success rate?

Well it could be because each ME/CFS patient has an issue with a different bacterium.

For some ME/CFS patients, the issue may be Staphylococcus. But for other patients, their issue may be due to different bacteria, such as Enterococcus, Escherichia coli, Klebsiella, Streptococcus, Enterobacter — which are all bacteria that Dr Markov routinely finds in the urine samples of ME/CFS patients.


So if you happened to be an ME/CFS patient with a Staphylococcus issue, then Prof Gottfries Staphylococcus vaccine protocol should work.

But if you have another bacterium, or issues with two or more bacteria, then the Gottfries protocol may not help, but in principle Dr Markov's protocol would help, because autovaccines are tailor-made for each patient, to target the actual bacteria they had.

So this could explain the higher success rate of Markov's protocol compared to Gottfries's protocol.

 

[Perfson]

If I didn't have PEM I wouldn't be here, every time I tried pushing myself over what's comfortable at the beginning of my illness, it would backfire and I would end up a bit worse at baseline!

Thanks for the answer, tbh im also getting much better physically, which hopefully will leave me without pem from physical activity at some point.
Sorry for doubting you. Good luck with treatment!

 

[Diwi9]

But i know stories of people believing that have ME/CFS for 20 years, but then they did some more tests and found out that they actually had some underlying health problem, all this time.
It's all fine if we assume that PEM for ME/CFS is not mandatory indeed. But i guess we can't know this for sure yet?

I don't want to sidetrack this thread, but your statement is true. Even during the screening for candidates for the NIH's intramural study, multiple patients were found to be misdiagnosed with ME/.CFS I believe Dr. Nath is quoted stating that one person had Parkinson's and two others had mitochondrial disorders. It goes to show just how neglected the ME/CFS patient population is. If you complain of fatigue and get ME/CFS in your chart, there is a high likelihood all diagnostics will stop unless one is lucky enough to have a dedicated physician willing to keep exploring.

 

[Martin aka paused||M.E.]

Then you have ME, no doubt! Happy to support you in Kiev

I've learned that it is spelled Kyiv. I'm sorry

 

[Hipsman]

I've learned that it is spelled Kyiv. I'm sorry

Kiev is also correct (at least many call it that), Kyiv is just spelled more often.

 

[perrier]

Kiev is also correct (at least many call it that), Kyiv is just spelled more often.

Hipsman
Kiev is the Russian spelling not the Ukrainian

Ukraine is now an independent country and has lobbied international media to use the Ukrainian transliteration of the name
Київ

 

[Hip]

NOTE: if the bacterial dysbiosis infection in your kidneys is from Enterococcus, Staphylococcus or Streptococcus — bacteria which Dr Markov finds in 37%, 10% and 5% of ME/CFS patient's urine respectively — these bacteria will NOT release any LPS into the bloodstream, because these are all gram-positive bacteria, and gram-positives do not contain any LPS.

It is only gram-negative bacteria which contain and release LPS.


However, gram-positive bacteria release their own toxins.

For example, Staphylococcus (which I am most familiar with), releases nasty toxins such as alpha toxin and enterotoxin B and others.

Alpha toxin seems to interact and modulate coxsackievirus B infections. Ref: here. So that could explain its relevance for ME/CFS.

Enterotoxin B is one of the most potent bacterial superantigens that exerts profound toxic effects upon the immune system. Ref: here. Enterotoxin B may also play a critical role in the pathogenesis of autoimmune disorders. Ref: here.

Each bacterium makes a range of toxins, which can have subtantial effects in the human body.



Thus even if your blood LPS levels are low, this would not rule out nephrodysbacteriosis (kidney dysbiosis infection) and CBIS, from what I can work out, because your problems may be due to other bacterial toxins.



I would like to get more info on the blood tests which Dr Markov uses to detect bacterial toxins in the blood, in order to confirm nephrodysbacteriosis and CBIS in ME/CFS patients.
@ME/CFS - Mystery No More! Under ME/CFS hides CBIS

 

[BrightCandle]

While I have been suffering ME/CFS I have had quite varied Kidney function tests showing something was going on with the Kidneys. My GP was dumbfounded when it went up 15 GFR but I felt better while that test was done so I can well believe infection of the kidneys is a factor in ME/CFS. It seems to be a fairly common thing for some amount of kidney function loss, plenty of researchers have mentioned it.

 

[Martin aka paused||M.E.]

NOTE: if the bacterial dysbiosis infection in your kidneys is from Enterococcus, Staphylococcus or Streptococcus — bacteria which Dr Markov finds in 37%, 10% and 5% of ME/CFS patient's urine respectively — these bacteria will NOT release any LPS into the bloodstream, because these are all gram-positive bacteria, and gram-positives do not contain any LPS.

It is only gram-negative bacteria which contain and release LPS.


However, gram-positive bacteria release their own toxins.

For example, Staphylococcus (which I am most familiar with), releases nasty toxins such as alpha toxin and enterotoxin B and others.

Alpha toxin seems to interact and modulate coxsackievirus B infections. Ref: here. So that could explain its relevance for ME/CFS.

Enterotoxin B is one of the most potent bacterial superantigens that exerts profound toxic effects upon the immune system. Ref: here. Enterotoxin B may also play a critical role in the pathogenesis of autoimmune disorders. Ref: here.

Each bacterium makes a range of toxins, which can have subtantial effects in the human body.



Thus even if your blood LPS levels are low, this would not rule out nephrodysbacteriosis (kidney dysbiosis infection) and CBIS, from what I can work out, because your problems may be due to other bacterial toxins.



I would like to get more info on the blood tests which Dr Markov uses to detect bacterial toxins in the blood, in order to confirm nephrodysbacteriosis and CBIS in ME/CFS patients.
@ME/CFS - Mystery No More! Under ME/CFS hides CBIS

Great post!

 

[Martin aka paused||M.E.]

NOTE: if the bacterial dysbiosis infection in your kidneys is from Enterococcus, Staphylococcus or Streptococcus — bacteria which Dr Markov finds in 37%, 10% and 5% of ME/CFS patient's urine respectively — these bacteria will NOT release any LPS into the bloodstream, because these are all gram-positive bacteria, and gram-positives do not contain any LPS.

Wait. But now your connection to the Metabolic Trap is gone, rright?!

 

[Martin aka paused||M.E.]

Each bacterium makes a range of toxins, which can have subtantial effects in the human body.

Would be great if we knew an inflammatory cascade they have in common.

 

[Hip]

Wait. But now your connection to the Metabolic Trap is gone, rright?!

Yes, the connection might be gone in an ME/CFS patient who did not have any LPS leaking into the bloodstream. Unless of course other bacterial toxins can play a similar role to LPS in their interaction with the IDO2 enzyme.

Note there no connection between LPS and the metabolic trap theory itself (which is an idea put forward by Dr Phair), but rather a connection to the fact that IDO2 mutations are more common in ME/CFS patients (which is the empirical fact that inspired the metabolic trap theory).

The study I citied said IDO2 mutations increase the inflammatory effects of LPS. So I think my idea that IDO2 mutations may be causing increase inflammation from LPS in ME/CFS patients would be an alternative and competing theory to the metabolic trap theory. Both theories seek to explain why these IDO2 mutations are more common in ME/CFS patients.

Would be great if we knew an inflammatory cascade they have in common.

Yes. If it is true that these bacterial toxins are playing a causal role in ME/CFS, maybe the particular bacterial toxins you have determine your ME/CFS subtype.

 

[Martin aka paused||M.E.]

Yes, the connection might be gone in an ME/CFS patient who did not have any LPS leaking into the bloodstream. Unless of course other bacterial toxins can play a similar role to LPS in their interaction with the IDO2 enzyme.

Note there no connection between LPS and the metabolic trap theory itself (which is an idea put forward by Dr Phair), but rather a connection to the fact that IDO2 mutations are more common in ME/CFS patients (which is the empirical fact that inspired the metabolic trap theory).

The study I citied said IDO2 mutations increase the inflammatory effects of LPS. So I think my idea that IDO2 mutations may be causing increase inflammation from LPS in ME/CFS patients would be an alternative and competing theory to the metabolic trap theory. Both theories seek to explain why these IDO2 mutations are more common in ME/CFS patients.





Yes. If it is true that these bacterial toxins are playing a causal role in ME/CFS, maybe the particular bacterial toxins you have determine your ME/CFS subtype.

That’s all very exciting! Idk if I have this mutation but maybe other toxins can also Knock-out IDO without any mutation. In genetics it’s quite often that a mutation seems to be important but then comes out to be absolutely without any impact. Would be funny if the Metabolic Trap would be a coincidental finding.

 

[Boba]

The study I citied said IDO2 mutations increase the inflammatory effects of LPS. So I think my idea that IDO2 mutations may be causing increase inflammation from LPS in ME/CFS patients would be an alternative and competing theory to the metabolic trap theory. Both theories seek to explain why these IDO2 mutations are more common in ME/CFS patients

„Accumulating evidence indicates that IDO2 acts as a pro-inflammatory mediator of autoimmunity, with a functional phenotype distinct from IDO1“

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5119657/

 

[Aidan Walsh]

Has anyone on here approached Dr. Myhill with the Ukraine findings?

 

[Aidan Walsh]

While I have been suffering ME/CFS I have had quite varied Kidney function tests showing something was going on with the Kidneys. My GP was dumbfounded when it went up 15 GFR but I felt better while that test was done so I can well believe infection of the kidneys is a factor in ME/CFS. It seems to be a fairly common thing for some amount of kidney function loss, plenty of researchers have mentioned it.

My left kidney is enlarged on an ultrasound & I was recently sent to a Urology Surgeon thinking it was a Dromedary Hump it was not one but did say it is larger than the right side.

I asked why he said it could be congenital but that to me does not answer the whole issue

 

[Tammy]

But (to info.): in 1999 Markov conclusively proved that the titers of IgG antibodies at chronic viral infections, including at chronic persistence of EBV, regardless of the degree of their increase, do not confirm the activity of EBV and its etiological role in the emergence of CFS.

The fact of presence of IgG antibodies to EBV indicates only on chronic EBV-infectioning. Based on the results of PCR-testing for EBV in more than 5500 immunocompetent (without HIV/AIDS) children and adults, diagnosed with chronic EBV-infection, received in 2009-2020 by Dr Markov, the role of this virus in the emergence of ME/CFS has been conclusively proven to be insignificant or even absent at all.

Don't understand how you ruled out EBV by these statements? You havn't explained how EBV was conclusively proven to be insignificant. How did you come to that conclusion?

 

[Alvin2]

I don't want to sidetrack this thread, but your statement is true. Even during the screening for candidates for the NIH's intramural study, multiple patients were found to be misdiagnosed with ME/.CFS I believe Dr. Nath is quoted stating that one person had Parkinson's and two others had mitochondrial disorders. It goes to show just how neglected the ME/CFS patient population is. If you complain of fatigue and get ME/CFS in your chart, there is a high likelihood all diagnostics will stop unless one is lucky enough to have a dedicated physician willing to keep exploring.

This is what is getting me, how many people could be treated today if they had proper diagnostics
Also how to get proper diagnostics?
Finally if we get an ME treatment many won't respond since they don't have ME...