Dr Igor Markov Says ME/CFS Is Caused by a Bacterial Dysbiosis in the Kidneys, and Says Autovaccine Therapy Cures 93% of ME/CFS Cases

[Hipsman]

did the dr find a marker of some kind, so he knows you have bacteria?

I think Dr Igor Markov found multiple things that suggest I have bacterial infection in kidneys, but I only remember that he saw mucous in my urinalysis test from 2019, witch he says suggests I have bacterial infection in kidneys.

In my most resent urinalysis test (after 7 Staphylo-Primavac vaccine shots) the mucous was still there, but urine bacteria cultures did not show staph aureus this time, so I guess that suggests that there is something else...

He just doesn’t know which one?

He did not tell me.

 

[MaximilianKohler]

@Hip I'll comment here instead of replying by PM.

Yes, someone shared this thread with me some time ago. And it was the first I recall hearing the term "autovaccines". From what I know, it seems that gut dysbiosis is the crux of the issue, and then impacts and spreads out to other body sites. If you have dysbiosis or a pathogen at any given body site it seems that addressing the gut is generally the way to fix it.

I'm very doubtful of his claims that he can identify and target the exact microbes causing the problem.
1. The microbiome and dysbiosis are extremely complex.
2. Current technology and knowledge are extremely limited

93% cure rate is also extremely suspicious. If he's able to do such a thing he should publish his results. He would be world renowned and I'm sure would win huge amounts of praise, funding, and awards.

 

[Martin aka paused||M.E.]

1. The microbiome and dysbiosis are extremely complex.

I know it's very unpopular on this board to say but the whole thing about the microbiome and it's impact on our health: there is still no consensus in science about this. Especially as it comes to leaky gut in fact we don't have sufficient evidence to support it.
https://www.nhs.uk/conditions/leaky-gut-syndrome/

I don't want to say that anybody is right or wrong because I think we can't really judge it yet. But I agree with you that he should publish his results. I asked him to do a study and publish it but he refused to do it.

 

[Learner1]

I know it's very unpopular on this board to say but the whole thing about the microbiome and it's impact on our health: there is still no consensus in science about this. Especially as it comes to leaky gut in fact we don't have sufficient evidence to support it.
https://www.nhs.uk/conditions/leaky-gut-syndrome/

I don't want to say that anybody is right or wrong because I think we can't really judge it yet. But I agree with you that he should publish his results. I asked him to do a study and publish it but he refused to do it.

There are definitely some combinations of microbiome constituents that can negatively impact health. The challenging thing is there's no perfect microbiome - there lots of healthy people that have a lot of different combinations of microbiome constituents.

 

[Hip]

I'm very doubtful of his claims that he can identify and target the exact microbes causing the problem.

Doesn't it make intuitive sense that when a microbiome is in dysbiosis (meaning certain specific bacterial species have become overgrown with respect to the other species living in the microbiome colony), selectively targeting the overgrown species might help return the microbiome to balance?

The species that are found in the urine test used by Dr Markov are presumably going to be the species that are in overpopulation, as you would expect these overpopulated species to be in relatively high abundance in the urine. So the urine test would tend to isolate and identify the bacteria causing the dysbiostic overgrowth.

Once these overgrown bacteria are reduced in numbers due to a targeted immune attack on them induced by the autovaccine, then you might expect that to address the overgrowth.

Autovaccines are highly targeted, whereas antibiotics are broad-spectrum, so antibiotics would target both the overgrown species of bacteria, and the species of bacteria which are the underdogs of the microbiome. Presumably you don't want to inhibit the underdogs, you only want to inhibit the overgrown bacteria. So I believe that is why antibiotics are not able to fix a dysbiosis, but autovaccines can.



If you wanted to use autovaccines to target a dysbiosis in the gut, I guess that would be feasible, provided you found a lab that could perform a stool analysis which identifies the bacterial species in overpopulation, and then provides you with isolated of those bacteria, from which you could then make an autovaccine.



In my investigations into autovaccines, I found out that the late Dr Bill Rae at the Environmental Health Center Dallas (EHCD) used to treat ME/CFS using autovaccines. I contacted the EHCD to try to find out further details of his approach, but was not able to get much information. So it's not clear what Dr Rae did, or how successful he was, but I would imagine that he probably targeted gut bacteria in overpopulation, rather than kidney bacteria.

When I was communicating to EHCD by email to tell them about the Markov CBIS theory and treatment of ME/CFS, they said to me tat Dr Elizabeth Seymour at the EHCD has expressed an interest in Dr Markov's treatment. So I promised to pass on any further details to Dr Seymour.

93% cure rate is also extremely suspicious. If he's able to do such a thing he should publish his results.

The results were published earlier this year here.

 

[andyguitar]

Autovaccines are highly targeted, whereas antibiotics are broad-spectrum,

And antibiotics dont always work.

 

[Hip]

I think what makes this approach interesting is, that the most effectiv treatment for mecfs was a vaccine against bacteria. And the clinical effect of that vaccine correlated with antibodies against toxins in the blood of patients.

But I wonder, wouldn’t patients improve on antibiotics when a bacterial infection is the cause?

I am replying to your above comment in this Markov Summary thread, in order not to take the other thread off topic.

I think that's a good question regarding why antibiotics do not seem to help clear this putative kidney dysbiosis. I suspect the answer may be that the bacteria in the kidneys are living in a biofilm community, which antibiotics cannot really touch.

In addition, these kidney bacteria may be living in the L-form state, against which antibiotics have little effect. Many bacterial species have the ability to change their morphology into an L-form, and then live inside the cells of the host.

L-forms and biofilms are the two main tactics that bacteria use to avoid the immune response, and also avoid antibiotics.

Enterococcus, the bacterium which Dr Markov most frequently finds as the culprit bacterium in his CBIS ME/CFS patients, has the ability to live as an L-form intracellular infection, as well as live in a biofilm community.

 

[Garz]

interesting thread Hip

on biofilms - I have been researching the topic recently and the amount of scientific knowledge has moved on quite a bit - but more in the field of microbiology than medical research ( there seems to be a quite surprising large disconnect between what is known to microbiologists and what is practiced in medicine )

it seems that, as you suggest, many bacteria species are able to form and exist long term in biofilm communities - often mixed species and even cross kingdom communities ( eg fungal species together with bacterial ).

initially it was thought that biofilms were mainly a physical barrier to antibiotics and slowed their diffusion through the biofilm to such a degree that antibiotic concentrations at the heart of the biofilm were always below MIC's for the organism.

subsequent work has show that the biofilms actually have channels though which to respire liquids in and out and the biofilm matrix itself is actually highly permeable to antibiotics with experiments showing full antibiotic concentrations being reached at the core of biofilms within minutes.

the actual explanation for bacteria in biofilms having tolerance to antibiotics is more interesting and at the same time concerning. it has more to do with your L-Forms.

gene activity testing studies on common bacterial species have shown that they often have two modes - and they switch from one genotype that is free swimming to an entirely different one when they become part of a biofilm.
these studies show that in doing so these bacteria may switch off 80-90 genes and switch on a similar number of hitherto unused genes. As a result the organism may have switched off entire arms of its metabolism that most antibiotics were designed for - and is happily living on a new set.
the bacteria also specialise in their functions and create networks to channel nutrients in and waste products out - and communicate with each other through chemical signalling network analogous to a primitive nervous system - it really quite a remarkable thing.

the bottom line is that tests have shown that the same antibiotics that work well for a bacterial species when it is in its free swimming form - need to be increased in concentration between 500 and 10,000x to kill all of the same species that are in the biofilm.

biofilm researchers make the point on how this situation has come about: because all anti-biotic research through the early antibiotic era was conducted on bacteria that could easily be cultured ( bacteria in biofilms are notoriously hard to culture ) and hence all the antibiotic developed were targeting the free swimming forms and little was known about the biofilm forms and in any case were hard to grow and work with in the lab - so the assumption was made that if an antibiotic worked for the planktonic bacterial cultures it would work for all bacterial infections. But we now know this is not the case

it seems we should be thinking of the planktonic forms ( singular free floating or free swimming forms ) as just one life stages of many bacteria and the bacteria of the same species living in biofilms as a second all together different life stage - such that the planktonic phase is more its means of translocation and propagation - a bit like seeds - and the biofilm form is more the final sophisticated form of the organism.

sorry for the lack of references - this is all from memory - but if you were to start with Dr Bill Costerton - he is regarded by many as one of the pioneers of biofilm research - you will get most of the above.

 

[Garz]

I guess one question i have is - why do the toxins flow into the body in the blood rather than out in the urine - as that is what the kidney is designed to do after all - preferentially move toxins out - while keeping the good stuff in .

 

[Hip]

subsequent work has show that the biofilms actually have channels though which to respire liquids in and out and the biofilm matrix itself is actually highly permeable to antibiotics with experiments showing full antibiotic concentrations being reached at the core of biofilms within minutes.

the actual explanation for bacteria in biofilms having tolerance to antibiotics is more interesting and at the same time concerning. it has more to do with your L-Forms.

gene activity testing studies on common bacterial species have shown that they often have two modes - and they switch from one genotype that is free swimming to an entirely different one when they become part of a biofilm.
these studies show that in doing so these bacteria may switch off 80-90 genes and switch on a similar number of hitherto unused genes. As a result the organism may have switched off entire arms of its metabolism that most antibiotics were designed for - and is happily living on a new set.

That's interesting. Though I can't seem to find any info online about this new discovery that antibiotics can successfully penetrate into biofilms. All the stuff that comes up in Google says there is poor penetration.

But certainly the bacterial mode change inside biofilms is a major factor in protecting bacteria from antibiotics. I read that about 1% of bacteria in biofilms turn into persister cells. These persisters are in a dormant state, and are metabolically inactive, and that protects them from the antibiotics.

biofilm researchers make the point on how this situation has come about: because all anti-biotic research through the early antibiotic era was conducted on bacteria that could easily be cultured ( bacteria in biofilms are notoriously hard to culture ) and hence all the antibiotic developed were targeting the free swimming forms and little was known about the biofilm forms and in any case were hard to grow and work with in the lab - so the assumption was made that if an antibiotic worked for the planktonic bacterial cultures it would work for all bacterial infections. But we now know this is not the case

Yeah, I guess we need the drug companies to invest in new antibiotics which work on biofilm bacteria. Unfortunately the pharma companies are reluctant to invest in any new antibiotics, as there is no money in it (because most people rarely need antibiotics, and even when they do need them, it's usually only a 5 to 10 day course that is given, so very little opportunity to sell their pills).

However there are now some government schemes designed to support pharma research into new antibiotics.

I guess one question i have is - why do the toxins flow into the body in the blood rather than out in the urine - as that is what the kidney is designed to do after all - preferentially move toxins out - while keeping the good stuff in .

I am not sure, but perhaps the answer lies in the fact that most of the fluid flow in the kidneys is actually the blood returning to the systemic circulation, rather that the waste products being removed in the urine.

Around 2000 liters of blood pass through the kidneys each day for cleaning; whereas only 1 or 2 liters of urine are passed each day.

I think it might also depend on where the dysbiotic bacteria are living in the kidney.

The tiny blood vessels which pass blood through the kidney for filtration are called glomeruli. There is a specific type of kidney infection which involves these glomeruli, called glomerulonephritis. Now a dysbiosis is not an infection, but maybe the kidney dysbiosis Dr Markov refers to might be one located on the glomeruli, which would then explain why these bacterial toxins enter the bloodstream.

 

[Garz]

hi Hip,
Costerton presented the findings of their groups experiments with probes inside biofilms an the time dispersion data in one of his presentations.

ref the economics of antibiotic drugs - i agree - but its even worse than that - i was talking to someone involved in the R&D side of abx and funding models for new abx just the other day - it turns out historically several companies developed new abx and then promptly failed - due to doctors not using the new abx because they wanted to keep it in reserve in case of abx resistance - so there was no demand - and the investors have all burned their fingers once - so the subject is a really really hard sell in investor circles.

hopefully this could be avoided if they were super targeted abx for biofilm type infections - but we need new funding models - some interesting patient funded stuff is happening in a few places

 

[Garz]

I found the preso where he talks about the abx diffusion experiments - its ages old - maybe the 70's or 80's ?
he died a very old man in 2012

the whole thing is good - but goto 1:06 for the diffusion stuff

funny how this stuff was known even then - but not made its way into medical science - despite the hardcore microbiologists studying it for 20 years - silos i guess!

 

[Hip]

This paper from 2016 says that antibiotic penetration into biofilms depends on the antibiotic, and on the bacteria involved.

But it says even when penetration occurred, the antibiotics did not kill the bacteria:

antibiotics failed to kill the biofilm cells independent of penetration, indicating that other factors contributed substantially to biofilm resistance.

 

[Garz]

But certainly the bacterial mode change inside biofilms is a major factor in protecting bacteria from antibiotics. I read that about 1% of bacteria in biofilms turn into persister cells. These persisters are in a dormant state, and are metabolically inactive, and that protects them from the antibiotics.

persister cell behaviour is another super interesting area of microbiology - as you indicate closely related to biofilm behaviour.

it turns out that the % of persister cells in a population is highly variable - and since its an adaptive behaviour - as you would expect, this percentage depends of a host of factors in any given population
-the bacterial species and or strain involved
-the environmental conditions - eg abx / other drugs/ nutrient availability / oxygen content/quorum sensing/etc
-the age of the microbial community - larger persister cell % correlated with stationary growth phase

in general most bacteria like to grow rapidly - a more or less logarithmic growth trajectory while conditions are favourable - as nutrients start to become more scarce - or other conditions limit or impinge on their growth - or as the community grows biofilm - then the % of cells that are persister cells typically increases.
in some cases this may be 50% of the population or more

if you introduce an antimicrobial - then typically the easy to kill portions of the population are killed off - leaving only the persisters - so in these conditions it can be close to 100%

the persister cells as well as using different genes, and presumably different metabolic pathways - also dramatically reduce their overall metabolism - and stop replicating or at least dramatically slowed down replicating. Most abx mechanisms of action require them to be taken into the bacterial cells as the cell respires, or as it divides, in order to have their effect - so it is this combination of behaviours that make them so much more resilient to the effects of abx. Once they have entered the persister states and susceptible bacterial killed off with normal levels of abx - additional increases in dose of that abx often does little or nothing to this population and in In-Vitro experiments they can often remain viable even at 500-1500x the concentration.

the mechanism for this switch to persister behaviour is complex and multifactorial - but from the studies i have read appears to be driven by cell stress signalling inside the bacteria - which makes a lot of sense - as then any stressor - be it heat, chemical, nutrient reduction etc - will tend to trigger higher transformation into persister states. This has been studied quite well in certain bacteria including things like E. Coli and Borrelia

its also notable that for persister cell behaviour to work as an evolutionary advantage - the cells must, while in their very low metabolic state, still have an ability to sense when the environment has become more suitable again and they can return to log growth behaviour. This they are also able to do.

its an active area of research and there is a great deal we still do not know about how exactly they do some of these things - but in general persister states and biofilm formation tend to go hand in hand.

its important to note that this complex behaviour is not limited to some rare or obscure small subset of bacterial species - persister cells and biofilm formation are present in many common species relevant to human health. eg Escherichia coli, Pseudomonas aeruginosa, Bacillus subtilis, and Staphylococcus aureus to name just a few.
Estimates i have read are that 90% of bacteria are capable of forming biofilm communities.
This paper says its actually a universal attribute of all bacteria, and wherever we find biofilm we typically find persister cells.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2890205/

and yet - how many of us have been told by a primary care physician that - if we have had a 2-3week course of antibiotics than that will have taken care of whatever infection we may have had .........

hope this is not too far off topic - its something i have been researching recently - and i thought it was relevant to the question of how such an dysbiosis discussed here could remain active in the kidney for so long despite abx treatments

 

[Wishful]

I wonder whether my type IV food sensitivity was due to a persistent biofilm in my intestines, which survived antibiotics, but got flushed out by food poisoning. A quick googling showed plenty of hits about diarrhea-causing biofilms, but maybe no one has studied how diarrhea might remove existing biofilms. Just something to think about ... if you're really into thinking about diarrhea.

 

[Rim1]

@Garz Do you know if phages could work for these persister cells instead?

 

[Garz]

@Garz Do you know if phages could work for these persister cells instead?

yes - I believe phage's have efficacy against persister cells
- they have been used in bacterial infections known to have persister behaviour
- they do not seem to rely on the bacteria's metabolism to gain entry to the cell - but have their own machinery to do that

 

[Hip]

I guess one question i have is - why do the toxins flow into the body in the blood rather than out in the urine - as that is what the kidney is designed to do after all - preferentially move toxins out - while keeping the good stuff in .

One other interesting fact about the kidneys is that their blood supply is not filtered by the first pass metabolism (the hepatic portal system), whereas the blood supply issuing from the intestines is cleansed of toxins by the first pass metabolism before it enters the systemic circulation.

The first pass metabolism is known to filter out up to 99% of LPS, and we might imagine that it similarly filters other bacterial toxins.

Therefore, bacterial toxins leaking into the bloodstream from the intestines will be mostly (99%) filtered out by the first pass metabolism before they can reach the systemic circulation. Whereas bacterial toxins leaking into the bloodstream from the kidneys will enter the systemic circulation unfiltered. This makes any bacterial toxins leaking into the blood from the kidneys are 100 times more potent/dangerous than the same amount of toxin leaking from the intestines.

 

[borko2100]

Bacterial dysbiosis has always been a possibility. I don't know about the kidneys, but there were some studies that showed remissions from fecal transplants. The frustrating thing though is, if I remember correctly those studies were not very well designed (eg. no control group).

Has anything changed recently? Wasn't there a large, controlled study planned on this somewhere?

 

[Garz]

thanks Hip - that's a fair point -
This first pass circulation to the liver argument makes more sense to me than purely the surface area and blood flow rate explanation.
but something still concerns me in this area - as the kidneys are supposed to selectively pass toxins one way - so the question still exists - why aren't they doing this with the bacterial toxins

is it because of the location of the bacteria vs the barrier ?
or
is it because the kidneys cannot process and excrete the toxins in the form they are being made ?
or
some other explanation