@Jonathan Edwards - I think EDS is clearly real (as I believe you do) - just that it's overdiagnosed. Most EDS is related to specific known defects in collagen genes. I agree with most of what you are saying - I think there is some bias based on what doctors think they will find. EDS3 is a bit more of a mystery, although at least a subset have mutations (3 known as last I heard) in the TNXB gene (tenascin-X - TNXA is a pseudogene on the RCCX cassette on chromosome 6 and isn't functional). The RCCX is on chromosome 6 in the MHC between HLA-B and HLA-DRB1. I think if we can find an actual mutation in the TNXB gene and correlate to symptoms, then the person does have a form of EDS, or at least some form of hypermobility. It's inherited in an autosomal dominant fashion.
That said, most with EDS3 diagnoses are negative for all known EDS3 mutations. We need a good study to actually genotype them (sequence the genes). These are very tricky genes to sequence because of the nearby pseudogene with high sequence homology. As such, SNP typing may not give accurate results. Also, the copy number for the RCCX cassette is highly variable, ranging from 0-5, as meiotic crossing over is notoriously error prone when dealing with duplicated and deleted areas of high sequence homology.
POTS is not about blood pressure - it's about heart rate. I have POTS. When I stand my HR can go to 150, and usually jumps about 50 for a few minutes, then normalizes somewhat. I have syncope on a tilt test without adrenergic stimulation, usually in under 1 minute. This was first noticed in 1997 or so, shortly after I developed ME. My ID specialist read the paper from Rowe et al from Hopkins on the connection between CFS and NMH (neurally mediated hypotension) and decided to order the test. Actually, he was pretty shocked it was positive. I asked him if CFS was real. He told me that a few years prior he would have said no, but he's seeing too many cases that look alike, and look like it, and for which he cannot find other explanations. I have never tested positive for orthostatic hypotension with the standard tests, although it's all over my file - mostly because of confusion by doctors as to what the difference is, and because POTS was only really known by Dr. Low at Mayo and a few others in the mid-late 90's. I did have an unusual drop in bp on valsalva noted by a very talented neurologist at the med school where I did my undergrad work. I improved a great deal on florinef and atenolol, as in the Rowe paper. Later small studies failed to duplicate the efficacy of florinef, but I suspect they were too small and the population too heterogeneous, because the effect was quite dramatic in me. We also documented hypovolemia (>2 standard deviations below normal for my age/gender/BSA - about 2/3 of normal plasma volume, normal red cell mass) by radiolabeled dilution assay at a top university med school. This was AFTER I started florinef! Florinef is the only reason I was able to finish my undergrad, and I take it today. All through the process I've had undetectable vasopressin levels, but no endo has ever wanted to treat with desmopressin as the florinef maintains osmolality better - desmopressin can induce hyponatremia.
I think the POTS/EDS connection is that if you cannot properly constrict veins in your legs, then you pool blood, which can be compensated for by increasing heart rate - which is what those of us with POTS do. I think the best POTS researchers right now are at Mayo with the exception of Dr. Julian Stewart, who has done some really brilliant work on it at NYMC and published extensively. He has a very useful and information rich website (if not always easily navigated).
I do not have EDS. I do have POTS. My mom had ME when she was 15 for about 2 yrs, but recovered (mostly). At that time she developed POTS. She still has that - but she has no abnormal reaction to exercise, which I consider the defining feature of ME. She and I run low bp in general, we increase HR on standing, and we experience syncope and presyncope. My maternal grandmother also required florinef or experienced extensive syncope, although not until later in life (70+). She had labile bp (as do mom and I - e.g. all 3 of us have/had systolic bp move over 100 points in a day in the absence of exercise).
My father, sister, and remaining grandparents are/were unaffected, both in terms of ME and POTS. In this case, it seems to pass as autosomal dominant or possibly X-linked dominant (men/women affected equally).
Thus, if POTS were caused by EDS3, then it is peculiar than mom and I do not have hypermobility. I think my Beighton score was like 1-2 (out of 9). Mom is in her 60's and has absolutely no joint paint complaints of any kind. My maternal grandmother had a bit of osteoarthritis but generally was in very good health until her death at ~87 and said she never had any pain. So in our case, we have familial POTS with possibly simple mendelian inheritance in the absence of EDS or hypermobility.
That doesn't mean hypermobility affects some with POTS or that it's not a cause of some cases of POTS. Most POTS docs describe subsets. I'm not sure if any of Dr. Stewart's research (very high quality stuff, and published/peer-reviewed) has identified EDS in some but not other subsets, or at varying frequencies.