Dr Markov CBIS Theory of ME/CFS - General Discussion

Hip

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I am about half way through the 10 injections of Dr Markov's polyvalent urological vaccine (which targets various UTI pathogens), and depression levels have increased quite noticeably. I am taking multiple antidepressant drugs and supplements to try to compensate.

I think though this depression could actually be a good sign, as I've previously found that certain immune boosting-supplements have ramped up my depression. So perhaps the increased depression may indicate this vaccine is stimulating the immune response.
 

GlassCannonLife

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Has anyone else had complement levels tested? I had slightly low C3 (normal C4) for a few years now..

Just saw that low C3 and normal C4 can be linked to staphylococcal glomerulonephritis and I'm wondering how this may fit in with the Markov theory..?

@bensmith @Hip @Hipsman @BrightCandle

Just tagging people I know are doing/looking into doing the Markov stuff..!


Edit: just checked a different result and actually it was as I said in 2019 and 2020 then normal for one test in 2021 and now low/normal C3/C4. Something causing low C3 but yeah not constantly.
 
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BrightCandle

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Has anyone else had complement levels tested? I had slightly low C3 (normal C4) for a few years now..

Just saw that low C3 and normal C4 can be linked to staphylococcal glomerulonephritis and I'm wondering how this may fit in with the Markov theory..?

No idea, don't think they ever tested it and I haven't done so.
 

Hip

Senior Member
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18,133
Just saw that low C3 and normal C4 can be linked to staphylococcal glomerulonephritis and I'm wondering how this may fit in with the Markov theory..?

I have not yet really investigated whether immune deficiencies might be a factor which predisposes to bacterial dysbiosis, but I suspect certain deficiencies might.


Mannose-binding lectin deficiency is an immune deficiency prevalent in ME/CFS, with 32% of patients having MBL deficiency, versus 7% of healthy controls. Ref: here. MBL deficiency is also quite common in the general population (7%).

One of the symptoms of MBL deficiency is recurrent sore throats, which ME/CFS patients tend to have (chronic or recurrent sore throat is often found in ME/CFS).

Mannose-binding lectin and the lectin pathway is one of the 3 pathways of the complement system.


Antibody deficiencies, such as IgG3 and IgG4 subclass deficiencies, are common in ME/CFS too.

IgG deficiencies can result in increased infections such as sinus or respiratory infections, gastrointestinal infections, ear infections, etc.
 

Hip

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18,133
I received an email from the Markov Clinic today saying that remote patient treatment services from the clinic (ie, sending them your dipslides, and receiving custom autovaccines in return) can resume as soon as air flights to Kyiv resume.

Obviously air flights are necessary for courier transport of these items.
 
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Hipsman

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Location
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I received an email from the Markov Clinic today saying that remote patient treatment at the clinic (ie, sending dipslides and receiving custom autovaccines) can resume as soon as air flights to Kyiv resume.

Obviously air flights are necessary for courier transport of these items.
That might take a year, or at least till September, the normal aviation is one of the last things that will resume I heard...
 

Hip

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I’d imagine the war would have to end for fedex etc I o start up again.

Fedex say they have suspended shipment to the Ukraine, for the safety of their employees.


However, it looks like EMS is still a viable option to send to the Ukraine: I just went to the local EMS provider in the UK, which is ParcelForce, and their website was able accept a 3-day shipment to the Ukraine.

So I imagine the local EMS provider in the US, which is Priority Mail Express International, will ship the Ukraine also. These items will be delivered by the local EMS provider in the Ukraine, which is Ukrposhta.

Ukrposhta apparently resumed operations in March 2022.
 

Garz

Senior Member
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374
thought people on this thread might be interested in this story from Yale that came out a few days ago - it seems other researchers are finding bacterial communities in the organs of people who have or have had "leaky gut" - and that these distributed communities are thought to add to illness including auto-immune disease.

story here - https://news.yale.edu/2022/07/13/how-gut-microbes-can-evolve-and-become-dangerous
not sure where the actual scientific report is yet

please post up if you find it
 

Hip

Senior Member
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18,133
I had an email from Dr Oleg Markov of the Markov Clinic today, saying that the clinic is now up and running again.

He said the clinic are now shipping their vaccines to remote patients in the US, going via Poland.

If I understood correctly, the clinic are not yet in a position to receive dipslides sent in from remote patients, because at the moment it is taking 2 weeks for courier shipping to Kyiv, and this is too long, as the bacteria will dry out a die during this time.

However, the clinic suggest that remote patients can expose their dipslides to urine as per normal, and when the bacterial colonies have grown on the dipslides, patients can take pictures of the dipslides, and based on the photos the bacteriological department of the Markov clinic will be able to identify the bacteria.

Then vaccines can be made using museum strains of bacteria, registered at the State Depositarium Ukraine, which match the patient's bacteria.

Shipping time for the vaccines is "2-4-5 weeks" (I presume that means 2 to 5 weeks).

This is what Dr Oleg Markov said in the email.
 

bensmith

Senior Member
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1,547
Thinking about trying this, their office contacted me as well. I would categorize my experience as a success. Although i am having a bad crash the last month.

I also had issues with musuem strains, the autovax seems to be what has worked. Still, thinking of trying again. Hopefully that probiotic or whatever you mentioned(@Hip) will help. I dont think i’ll do the extra work you mentioned, but i have it in my fridge.
 

Hip

Senior Member
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18,133
Dr Oleg Markov also said that when taking pictures of bacterial colonies growing on a dipslide, in order to help the bacteriology department to identify the bacteria, you would want to take at least 3 different pictures on each side of the dipslide, with each picture taken from a different position or a different angle, and with a different angle of lighting.

So I guess when taking dipslide pictures, it would be a good idea to use a camera with the highest megapixel resolution you can find, and to ensure good strong lighting, and make sure you take sharp, well-focused pictures. And then you want to change the position of the dipslide in order to take pictures from different angles.
 

BrightCandle

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1,213
Identification definitely requires all 3 different coloured windows from the identification chart I saw and the green one especially has lots of different styles of growth. I found when taking my picture that angle seemed to impact the how the raised yellow bump appeared as well as the appearance of the overall yellow background and you'll want to capture that detail as the 3d aspect is important for identification.
 

Garz

Senior Member
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374

The author kindly sent me a copy of the article I linked to above that was investigating the in-host evolution of commensal bacteria into pathogenic variants that can escape the gut, invade tissues and live in internal organs.

I was interested as it sems to link quite well to this topic – as most of the organism discussed in Markov’s work are of gut origin - and so some form of escape and colonisation of tissues outside the gut are theorised as the root cause. As such some independent confirmation that this can indeed happen would be useful – and also any clues as to why and how may be of interest to us here.

The paper is quite dense and took me some effort to work through – and most of it is dedicated to their main model organism - which was Enterococcus gallinarum - I don’t think this was one of the main ones Markov finds – but it is a known “pathobiont” found in the guts and tissues of both mice and humans – so that was the reasons for their choice.

The main finding were that through lots of in depth sequencing technologies they were able to demonstrate that pathogenic strains that differ substantially from original wild type strains can develop in mice in a single lifetime - and that some of these strains can translocate to the liver where their adaptations make them more resistant to immune clearance - and that these tissue adapted strains cause more inflammation than wild / original strains in both gut and liver tissues.

In the last few paragraphs, they acknowledge this is just one model organism – but they mention something interesting and relevant to us here -

“Notably, analogous instances of within-host evolution may also occur in humans. For example, Clostridium innocuum strains recovered from the intestinal mucosa versus mesenteric adipose tissue of patients with Crohn’s disease were genetically divergent30; bloodborne isolates of the Enterococcus faecalis acquired resistance to immune clearance through mutations in the transcriptional regulator gntR31; and, compared with nose-colonizing strains, infecting variants of Staphylococcus aureus accumulated adaptive mutations in rsp or agr genes, which regulate bacterial quorum sensing and toxin production32”.

So they refer to other known cases where tissue invasive strains of staph (which I think is on Markov’s list) have adapted in regions of their genomes that govern quorum sensing and toxin production – both of which behaviours are known to be associated with biofilm formation.

Overall it seems likely that within host genetic adaptation is involved in any translocating organism that may be living in say the kidney of ME/CFS patients – and these mutations will likely contribute difficulty in clearance by the immune system
 

Garz

Senior Member
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374
there is some coverage in the news of some recent studies that i think might be relevant here

it may be covered elsewhere on PR but basically the study is claimed to be the first large scale study showing a consistent biomarker in ME/CFS vs controls.

the researchers found 10 times the number of micro clots in the blood of CFS patients vs controls
( they also found them in long COVID patients and they are known to occur in many other chronic inflammatory conditions - from diabetes to Alzheimer's)

i mention it here as there was some interesting points raised in terms of how these micro clots - which appear be be a mix of fibrin and amyloid proteins and are resistant to normal breakdown by enzymes.

the author of this paper found evidence that these clots are triggered formed by contact between elements of the immune system and bacterial or perhaps viral proteins - and more interestingly that the micro clots themselves contain inflammatory compounds that trigger inflammation when these clots are eventually broken down by various methods.

these micro clots could be driving the very wide symptom array in CFS via their affects in many different tissues - eg in the brain causing brain fog and cognitive deficits - in the organs - reduced organ function etc

the authors go on to propose a theory of PEM based upon an ischemia reperfusion response - that accounts for the delayed response of symptoms in PEM - where inflammatory compounds are released only after improved perfusion is restored - eg by exercise - or fibrinolytic therapies

"Of particular interest was a substantial increase in α(2)-antiplasmin (α2AP), various fibrinogen chains, as well as Serum Amyloid A (SAA) that were trapped in the solubilized fibrinolytic-resistant pellet deposits."


this finding of micro clots in CFS would be consistent with the Markov theory of CFS via biofilm communities in the kidney - as such a biofilm community would be an appropriate trigger for micro clots to form - especially given how much blood flows through the kidney

but would also account for the great deal of overlap with other conditions - such as chronic Lyme, Bartonellosis, Brucellosis etc - ie anything that creates a long term stable bacterial biofilm community/communities in the body ( all chronic bacterial infections do this - and bartonella in particular also stimulates dramatic excess fibrin in the microvasculature ) and so would qualify as an appropriate trigger for this mechanism

anecdotally those with these conditions typically have a flare of inflammatory symptoms when taking fibrinolytic agents ( i have experience of this myself and witnessed the corresponding reduction in clotting and artefacts in my blood as a result)

i have also seen accounts of those with CFS apparently curing themselves of the condition with fibrinolytic agents- Ken Larsessen writes about it i believe in his blog

It also links to the PEM reactions experienced by those experimenting with the breakdown of biofilms here - as breaking up biofilms via ultrasound or any other method would also lead to improved reperfusion - and potentially trigger the same ischemia reperfusion response.

apologies if it is seen as off topic - but i felt it was connected enough to the discussion thus far to be worth adding.

article outlining how micro clots may lead to PEM symptoms in CFS
https://portlandpress.com/biochemj/...otential-role-of-ischaemia-reperfusion-injury

article describing the micro clots in long covid vs controls and resistance to trypsin digestion - and that they contain inflammatory chemicals
https://pubmed.ncbi.nlm.nih.gov/34425843/
 
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