[Thought experiment] In a random cohort of 100 ME/CFS patients (recent diagnosis via CCC), what can you know about them with 90%+ certainty?

Very interesting study, I thought I would mention that measures to increase volume (saline, desmo,fludro,..) worked well for me in the earlier phase of my illness but stopped working after a while. Recently I started a retrial of desmopressin and was quite surprised when it made me feel MUCH worse. What was really surprisig though was that it led to an elevated NTproNB, which is a biomarker for heart failure. This biomarker works essentially by indirectly (an overly 'stretched' heart muscle will lead to its expression) measuring fluid overload!

The whole blood volume issue is a bit of an enigma as you know, the best 'simple' explanation from a mere structural perspective, that could be a common/shared phenotype in IACCs, I believe is that there is 1. not enough capacity to hold the necessary blood volume, i.e. a literal lack of blood vessels (especially microvascular) unable to meet metabolic demand and/or 2. a stagnation/sagging of blood in the venous compartment that could be partially overcome by more volume. In a sense, ADH could be low because blood vessels are overly 'stretched' in some compartments but not others leading to a kind of paradoxical situation (from a central command perspective) of too much AND too little volume. Afaik nobody has looked at the issue from this perspective; maybe for good reasons.

I think it could be interesting to consider because such a scenario would ultimately lead to hypoxia, and what we see metabolically looks a bit like hypoxia?