A Unifying Hypothesis of the Pathophysiology of (ME/CFS): Recognitions from the finding of autoantibodies against ß2-adrenergic receptors: Wirth 2020

Jonathan Edwards said:
There are two problems, though. Firstly, autoantibodies to adrenergic receptors are only very slightly higher in ME patients than healthy people - not the sort of difference that suggests that they matter. Secondly, if this really was a cardiovascular control problem then something consistent should be measurable in ME like a change in blood pressure or heart rate. And it should be a gross difference, not something requiring complicated tests. There is no such difference as far as we know.
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I think I might be able to demonstrate with a simple test that there is a circulatory problem.

If I stand on my feet and reach down to pet my cat, and then after 10 or 20 seconds bring the head back up, I feel unwell (dizzy, malaise, weak). If I repeat this posture change (giving the body some time to adjust to each change) then it gets increasingly worse. After a few times I'm visibly weak and slow so much that it cannot be missed by an outside observer.
 
strategist said:
I think I might be able to demonstrate with a simple test that there is a circulatory problem.

If I stand on my feet and reach down to pet my cat, and then after 10 or 20 seconds bring the head back up, I feel unwell (dizzy, malaise, weak). If I repeat this posture change (giving the body some time to adjust to each change) then it gets increasingly worse. After a few times I'm visibly weak and slow so much that it cannot be missed by an outside observer.
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I find that any repeated movement can reduce me to a paralysed lump eventually. The definition of ME as a disease where you can lift a bag of potatoes over your head once but not lift a spoon to your mouth five times captures much of my disability but does not seem to be well known among scientists and researchers.
 
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