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/