Hello Dr. P.,
what an honour to have you here with us. Congratulations for publishing this paper!
Do you think that people with a non sudden onset and a continous deteoriation also fit your model?
What about the high number of EDS patients (like myself) in the severly ill subset? You wrote that NO is a strong inhibitor of IDO, to my knowledge NO will rise in a state of hypoxia in any given cell.
We do know that there is a hypoxic state in muscles and nerve tissue in me/cfs. Could this be the reason for mitochondrial damage and/or increased oxidative stress? What else could account for the low energy state (it is not fatigue) and does your theory account for that?
I am sure it does - but I do not see it from reading the paper?
I think Dr. Birch found genetic issues for NO metabolism in a subset of me/cfs patients.
Infections will dramatically increase NO in tissues. High NO would also explain POTS and a chronic compensatory sympathetic state.
EDS and it laxitys in any given structure but also the high numbers of Small Fiber Neuropathy seen in this syndrome seem to be a very good predisposition for a hypoxic state, hence a high NO state, especially with exertion.
The main question will be what drives what, and how much of the damage accumulated is reversible?
THANK YOU.
@HTester