One thing worth investigating in the cholinergic activities of ME/CFS patients in the fact that 50% of patients have have auto-antibodies to the acetylcholine muscarinic receptors. Reference: here, and also in this following study:
See also this study of anti-muscarinic autoantibodies in ME/CFS:
Autoantibodies against muscarinic cholinergic receptor in chronic fatigue syndrome
Autoantibodies to muscarinic receptors and beta-adrenergic receptors are also found in orthostatic hypotension:
Autoantibody activation of beta-adrenergic and muscarinic receptors contributes to an "autoimmune" orthostatic hypotension
And in Sjgren's syndrome (dry mouth), which a lot of ME/CFS patients suffer from, signal transmission in the parasympathetic nerves is inhibited by these muscarinic receptor autoantibodies, and this is the likely reason the saliva glands do not get fully activated:
Inhibitory effects of muscarinic receptor autoantibodies on parasympathetic neurotransmission in Sjgren's syndrome
Antimuscarinic antibodies in primary Sjgren's syndrome reversibly inhibit the mechanism of fluid secretion by human submandibular salivary acinar cells
Inhibitory effects of autoantibodies on the muscarinic receptors in Sjgren's syndrome
I believe an underactive parasympathetic can also cause circulation problems: cold hand and feet common symptoms in ME/CFS
So if in Sjgren's syndrome, these anti-muscarinic antibodies inhibit signal transmission in the parasympathetic nerves such that the saliva glands remain under activated, then these anti-muscarinic antibodies in ME/CFS patients will presumably be causing body wide inhibition of the parasympathetic nervous system.
I believe that the sympathetic/parasympathetic balance has an impact on the Th1/Th2 immune system balance, so a parasympathetic nervous system inhibited by these anti-muscarinic antibodies may shift the immune response away from Th1 and towards Th2, thus impeding viral clearance.
I would not be surprised if these anti-muscarinic antibodies were deliberately triggered by invading viruses as a means to stop the immune system from attacking them (ie, as an immune evasion tactic).
So it would seem that for ME/CFS with anti-muscarinic auto-antibodies, it might be a good idea to take supplements that boost the parasympathetic nervous system; or better still, find some medications that can treat this ME/CFS autoimmune condition that targets the muscarinic receptors. Rituximab can treat of autoimmune diseases; perhaps this is the reason rituximab benefits ME/CFS patients: because it helps reduce auto-antibodies to muscarinic receptors.
Actually, this is probably along the right lines, as it seems rituximab can treat Sjgren's, and its anti-muscarinic auto-antibodies:
Rituximab treatment in patients with primary Sjgren's syndrome
I don't agree with your conclusions. The auto-antibodies do not block the receptors - they cause increased activation of them. That's why you get increased vasodilation: "Activating autoantibodies to ?1/2-adrenergic (AA?1/2AR) and M2/3 muscarinic receptors (AAM2/3R) produce vasodilative changes in the vasculature that may contribute to OH". In the PMID 22130180 study, they actually stopped the increased vasodilation by blocking muscarinic and beta adrenoceptors, but patients found the side effects intolerable.
This is also my own personal experience. I also do not have particularly dry mouth or eyes, even though a have severe POTS. And the cold hands and feet is caused by blood pooling, which can result from both excessive vasoconstriction (sympathetic) or vasodilation (parasympathetic). That is also why there are several types of POTS, including high-flow and low-flow. I am pretty sure my case is the high-flow type. Read this:
But you're right that the solution to the problem is getting rid of the auto-antibodies.