By Cort Johnson in Health Rising.
This new ME/CFS / long-COVID paper, “Endothelial Senescence and Chronic Fatigue Syndrome, a COVID-19 Based Hypothesis”, highlights something we’d hoped would occur with COVID-19: new eyes being placed on, and new perspectives being produced on chronic fatigue syndrome (ME/CFS).
The group that wrote this paper is an interesting case in point. Their June 2020 paper, “Intoxication With Endogenous Angiotensin II: A COVID-19 Hypothesis“, proposed that endothelial dysfunction was a key aspect of COVID – and linked it to high angiotensin II (Ang II) levels. They suggested that the high Ang II levels in COVID-19 had caused “premature vascular senescence”.
That was intriguing given the really interesting place that high Ang II levels, and something called the RAAS or RAS paradox, inhabits in the ME/CFS/POTS universe.
The paradox concerns the renin-angiotensin-aldosterone pathway that’s supposed to kick in when low blood volume levels occur. Even in context of the very low blood volumes found in ME/CFS/POTS, the pathway doesn’t kick in, and its critical endpoint, aldosterone, remains at normal or even low levels. This is despite the fact that the levels of Ang II – found in the middle of the pathway – tend to be very high.
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