More on that, the rabbit study above reported the endothelin-1 synthesis is decreased by alcohol.
About endothelin-1:
There is a bit of evidence that endothelin-1 is increased in ME/CFS e.g. in two studies by different teams:
What if over-production of endothelin-1 in ME/CFS was an adaptation to poor control of blood vessels because the peripheral vascular nerves aren't working properly? (or maybe a deficiency of effective endothelin-1 receptors?) And what if alcohol stopped that adaptative increased endothelin-1, resulting in even worse vasodilation and lack of a constrictive response?
About endothelin-1:
ET-1 is a potent vasoconstrictor, meaning it causes blood vessels to constrict or narrow. ET-1 has been shown to be one of the most potent vasoconstrictors. Vasoconstriction is mediated principally by ETA receptors on the underlying smooth muscle, where a small proportion of ETB receptors may also be present.
There is a bit of evidence that endothelin-1 is increased in ME/CFS e.g. in two studies by different teams:
The ET-1 concentration was significantly elevated in both ME/CFS and PCS patients compared to HCs and PCHCs.
But they did find some differences between the two groups of patients combined and the healthy controls. It looks like patients had lower activity levels, worse sleep quality, a worse lipid profile and higher levels of endothelin-1 and VCAM-1.
What if over-production of endothelin-1 in ME/CFS was an adaptation to poor control of blood vessels because the peripheral vascular nerves aren't working properly? (or maybe a deficiency of effective endothelin-1 receptors?) And what if alcohol stopped that adaptative increased endothelin-1, resulting in even worse vasodilation and lack of a constrictive response?
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