If there was a consensus this broad, I'd think the disease would be much easier to treat.
I'm no expert on autoimmune diseases but the presence of some antibody is not necessarily an open and shut case that shows POTS is caused by autoimmunity. Some people have some levels of antibodies that dont correlate with anything clinically.
Also some of the private labs that do antibody panels for adrenergic antibodies and autoantibodies in general are somewhat controversial.
I seriously don't mean to be rude, but it's a bit brash to assume that you have the answer to a complex syndrome figured totally out when it's fairly opaque even to top researchers. And I dont know where you get the 95 percent figure. Rowe is one of the top pots researchers for example and he takes the cervical spine compression connection to POTS seriously.
Imo, pots can have many causes. When it occurs in Me/cfs I think it tends to be paired with low blood volume and I think it could be caused by brainstem inflammation from toxic exposure, or brainstem compression, or both. But that's just a theory
Never heard of Rowe, must not be affiliated with Dysautonomia International
What I say, or think, it's not relevant, it's relevant that there is strong indication that it's autoimmune and of course there will be another few years before that's accepted.
You can easily find more information, they don't base that opinion only on antibodies, there are certain criteria when disease is accepted as autoimmune, POTS is very close to fullfill all the criteria. Like passive transfer of antibodies to animal , causes POTS.
Exactly for the reasons you mentioned like questionable antibodies testing. But they are using various methods to circumwent that.
I personally tested via 2 methods, enough for me next to Sjogrens and Hashi and extremely good response to IVIG .
Tested with CellTrend ELISA, which has problem with adrenergic antbodies, but not muscarinic.
and tested with dr Wallukat's method from BerlinCures, bioassay where he measures activity of those antibodies - how much they change activity of the adrenergic/muscarinic receptors.
I was positive on both, although on Wallukat i didnt have alpha adrenergic, but I had beta and Muscarinic 2.
Btw no, those antibodies are not one of those that appear in other people too (like probably invalid Cunningham panel!) it's quite specific for POTS and for rheum.diseases in general, and the cut off is of course set at 2st dev anyway.
BTW, another funfact is that Dysautonomia International also did study for early Sjo antibodies and found them in almost 50% of POTS patients who don't test positive for ANA/SSA.... I had POTS for 20 years befoe EVER feeling any eye/mouth dryness or any non-neuro symptom except bit of parotid swelling 15 years ago when my POTS got activated, and now it turns out I have Sjogrens all this time.
My ME friend, without POTS, without any dryness symptoms, turns out he has Sjogrens too, with negative ANA. i forced him to do lip biopsy because of SFN and positie SSA, and lip biopsy -which is gold standard for Sjogrens, was extremely positive! He has 99.9% neuro sympotms.
I was intentionally blunt because I don't want people to undergo extrremely invasive surgeries like CCI while the underlying cause of the disease is totally something else.
Not speaking of all people, ME probably is not autoimmune. I had ME of varying levels - at some point couldn't even read, and for me it's related to gut, when they destroyed my gut with antibiotics (ceftriaxone) I got quite severe ME, luckily, it reduced with essential oils -again for gut/SIBO and with time that slowly recovered my gut.
But if I had POTS, man, and i test positive on more than 1 of those antibodies, I'd seriously think about the real cause of my disease.
Even if CCI, as i remember -it's found in 50% of RA people?!