I have a strong feeling that many #POTS patients are in effect in a prodromal phase of #mecfs. Not all #POTS patients will end up with #mecfs, but almost all #mecfs patients had #POTS either before (often unknowingly;"anxiety") or early in their #mecfs course./1
Often these patients with POTS that later develop #mecfs fall into the #hEDS category. Their descent into #mecfs is often but not always triggered by infections or, more generally, inflammatory events (surgery, accidents,..). We don't know what #hEDS is exactly but at /2
Its core the Ehlers-Danlos-Syndrome family might be caused by an inflammatory cascade downstream from a redox imbalance in certain cell types, in effect, a mitochondrial dysfunction. A pre-existing redox imbalance gets further strained by inflammatory stress (like infections)./3
In summary: You start with a #hEDS phenotype (in my view, to some degree a mitochondrial dysfunction) and will at some point get POTS, the more "inflammatory stress," the earlier it will happen. This then results in "mild" hypoxia of brain, muscles, gut etc. /4
Leading to LPS leakage, ANS dysfunction, bodywide inflammaging, and more. At this point, with every new inflammatory cascade, the likelihood of whacking your BBB and the neurovascular- unit increases; at some point, actual #PEM sets in. /5
That is when "peripheral inflammation" resulting from among other things a redox imbalance in muscle, travels "centrally" relatively undisturbed, causing among other things a (hence delayed) reperfusion injury and chronic hypoperfusion. /6
I think viral persistence is a player in #mecfs, but I guess you could get there without it. /7
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