I think the 'causal link' was manufactured by Peter Rowe, Rodney Grahame and Hans Knoop, among others. Rodney Graham has been travelling the world saying people with hypermobility have widespread pain for decades, without ever showing any evidence.
What I wonder is if it’s a problem of “selecting on the dependent variable.” You see people who are hypermobile and sick. (Sick in many different but still some predictable ways, namely ME, MCAS, POTS, dysautonomia, fibromyalgia, etc.) You start to describe this and eventually say, “Ah, you are sick because you are hypermobile.” Few people ask, “What about all the people who are hypermobile and not subluxating, not in pain, not sick?” Because they have no complaints, they don’t come into the clinic, and so are largely unobserved. They aren’t even in the study I posted above. Our entire conception of the problem is then based on looking at this truncated sample of people who are both hypermobile and sick. Missing are the hypermobile + well and the not hypermobile + sick
in precisely the same ways. If we compared these three groups to non-hypermobile, healthy controls, perhaps we could learn something.
One of the ways some people with hEDS get sick that seems unique to them and some other CTDs is that they can have severe and frequent subluxations. These can be very painful and debilitating. Maybe some people who are hypermobile get sick for some totally independent reason Z but their symptoms and complications differ because of the hypermobility. Their hypermobility didn’t necessarily
cause their illness. Rather, it poses some specific challenges, given that they are sick.
I am thinking here of the people who were hypermobile and well up until
something happened, where the something might be an accident, fluroquinolone antibiotics, or an infection. There are of course people with hEDS who have been subluxating and getting injured or had gradual onset of dysautonomia and other symptoms since they were kids. They strike me as being in a perhaps a very different situation from the person who was fine until they had an infection. I worry that for the sudden onset case, hypermobility becomes a post-hoc explanation for their symptoms when, as others have said, hypermobility is common in the population.
There is one theory going around that it’s all about mast cell activation and collagen breakdown, which might have different implications for someone with hypermobility v. w/o. I think this is an interesting idea and might explain why hypermobility could be a risk factor for developing ME. Remember that in this sample, everyone is hypermobile. We know hypermobility doesn’t correlate with disability, but there might be other unseen genetic factors that correlate with hypermobility but are also present in people without a hypermobile phenotype, and that predispose people to developing certain chronic illnesses.
In sum: This study suggests it’s not about how hypermobile you are, but that doesn’t mean that hypermobility doesn’t matter. Hypermobility may affect your clinical presentation in important ways without actually
causing your illness. It may also correlate with something else that
does have some explanatory power but is unlikely to be unique to hypermobility or to be a sufficient condition for developing a chronic illness.
