Is joint hypermobility linked to self-reported non-recovery from COVID-19? Case–control evidence ... , 2024, Eccles et al

Jessica Eccles has been suggesting Long Covid patients are bendy too:

https://www.theguardian.com/society...ay-be-more-prone-to-long-covid-study-suggests

Usual Guardian gossip.

 

BMJ hasn't posted the study yet. Here's a different press release: https://www.miragenews.com/joint-hypermobility-elevates-long-covid-risk-1197939/. Seems like they aren't looking at EDS but at GJH (which according to them 20% of the UK population suffer from, since researchers frame this as being genetic, any thruth to their theories should be picked up by a GWAS).

 

Also, it tends to affect women, and quite a lot of younger women are naturally bendy. Some would probably answer Yes if asked – because it's true, not because it's ever been much of a problem.

 

I would tend to think that, that shouldn't be a problem if they would have a good and well matched control cohort, but who knows. According to them GJH is prevalent in 20% of the general UK population and is even more common in women and furthermore even more common amongst people that have LC. If it was really the case that roughly every third or forth woman would have this and it's then even more prevalent amongst people with LC (and we already know that LC is dominated by woman), I would tend to think their definition would be far too loose to capture anything meaningful (or at least I'd think that if there was something like "more than 40% of people with LC have this or that" based on a questionnaire and that would have any meaning, that meaning would have shown up on multiple studies by now). I simply can't see how this basic math could add up and I currently can't see how it would be any different to something like "so and so many people have long hair", but I'll patiently wait for the paper and then see what they are actually doing.

 

They should do a study on how to understand the dynamics of social media engagement to manage medical uncertainty and misinformation.

This is particularly concerning regarding MCAS when they are being told that this is what they are suffering from by a "user name".

 

This is pure nonsense, propagated by people like Peter Rowe and Rodney Grahame, I'm afraid. Generalised joint hypermobility just means you have relatively stretchy ligaments around joints. 20% of the population are the 20% stretchiest. And 20% are the 20% least stretchy. Women are stretchier on average because they are women. And so on however you like. It is total pseudoscience.

 

#hEDS trending now on Twitter after the Guardian article.

 

Can you please explain the skepticism around HSD or hEDS in connection with MECFS? I am relatively new in the forum but have picked up on this reading a number of posts. I have been interested in it because my son with mostly severe, occasionally moderate or very severe MECFS was diagnosed by a specialist as having hEDS. He has always had an extreme range of motion in many of his joints and we had no idea his party tricks were attributable to this. I have read much of what Peter Rowe and others have published on it. I am also aware that probably most PwME are not hypermobile. However, I am also aware of other teens with MECFS & hEDS who are at the severe end of the spectrum and like my son are the ones who have difficulty maintaining weight and some have been diagnosed with vascular compressions.
It is important to me to be objective. I value and respect your expertise and I am genuine in asking why you consider this to be nonsense.

 

It is a long story, hidden in the threads, but in brief.

I was involved in the hypermobility story early on in 1978 when Rodney Grahame set up a clinic at Guy's Hospital in London. It was my research base. We wrote a paper on cardiac involvement that didn't really make sense. I was too junior at the time to say so. Since then I have seen the hypermobility bandwagon grow but never seen any convincing data that there is a 'disease' or 'illness' based on common polygenic 'hypermobility' - which in practice just means the people who are a bit bendier than average. After leaving Guy's I decided to keep clear of the subject. Around 2000 I was asked if I would take over Dr Grahame's clinic when he retired but declined!

'hEDS' replaced 'EDS III' as a term for hypermobility without internal organ problems. It is inappropriate because EDS is defined as a monogenic disease - caused by one connective tissue protein gene being defective. Hardly any 'hEDS' cases have been shown to be due to a single defective gene. The term is used to cover anything from 1 in 5000 of the population to 1 in 5, so is too ill defined to be any use anyway. (In other words some doctors will diagnose it a hundred times more often than others, for no good reason.)

Lots of children are bendy and can do party tricks - about one in five girls and one in ten boys. It is very normal.

The idea that hypermobility (or EDS) is associated with fatigue seems to have been started off by Peter Rowe around 2000. A supposed association with general pain goes back to 1970 or so. The fatigue story was raised again by the biopsychosocial enthusiast Hans Koop in I think 2009. It got into the folklore. However, inasmuch as there are any reliable studies they show little or no association. The UK ME Biobank did not pick up hypermobility. Some large studies of children failed to show anything much (I think in Scandinavia) - not even a link with pain much.

I was close to all this much of my career, since Dr Grahame moved to UCL, where I was, and a number of our clinical trainees worked in his clinic (which I decided not to take over). Over the years I heard endless claims about links with pain and dysautonomia and fatigue but never saw any data. Having taken an interest in ME in retirement I looked again and there doesn't seem to be any - beyond a few case reports that are almost certainly related to clinic attendance bias.

There is absolutely no reason that I know of for hypermobility being associated with ME. Stories about neck subluxation and vascular compression appear to be baseless. Unfortunately there are a good number of doctors and therapists, particularly private physicians who sell HSD or hEDS as an explanation for just about anything. Even in mainstream rheumatology it is common for doctors to check for hypermobility and then blame whatever the person's symptoms are on it - it sounds knowledgeable but has no basis.

A very small number of children have major laxity problems with certain joints - often just one pair - knees or shoulders for instance. Subluxation and gait problems can occur. I used to see people like this about once in ten years. They have very real problems with that specific joint but otherwise tend to be quite normal.

 

The study has now been published.

Abstract

Objectives This study sought to explore whether generalised joint hypermobility (GJH, a common marker of variant connective tissue) was a risk factor for self-reported non-recovery from COVID-19 infection.

Design Prospective observational study.

Setting COVID Symptom Study Biobank (https://cssbiobank.com/) UK

Participants Participants were surveyed in August 2022. 3064 (81.4%) reported at least one infection with COVID-19. These individuals self-reported on recovery and completed a self-report questionnaire to detect GJH (Hakim and Grahame 5-part questionnaire, 5PQ).

Main outcome measures The primary outcome was the presence of self-reported non-recovery from COVID-19 infection at the time of the survey. Additional outcomes included scores on 5PQ and self-reported fatigue level (Chalder Fatigue Scale).

Results The presence of GJH was not specifically associated with reported COVID-19 infection risk per se. However, it was significantly associated with non-recovery from COVID-19 (OR 1.43 (95% CI 1.20 to 1.70)). This association remained after sequential models adjusting for age, sex, ethnic group, education level and index of multiple deprivation (OR 1.33 (95% CI 1.10 to 1.61)) and further adjustment for vaccination status and number of vaccinations (OR 1.33 (95% CI 1.10 to 1.60)). Additionally, including in a model adjusting for all covariates, hypermobility significantly predicted higher fatigue levels (B=0.95, SE=0.25, t=3.77, SE, p=0.002). Fatigue levels mediated the link between GJH and non-recovery from COVID-19 (estimate of indirect effect=0.18, 95% bootstrapped CI 0.08 to 0.29).

Conclusions Individuals with GJH were approximately 30% more likely not to have recovered fully from COVID-19 infection at the time of the questionnaire, and this predicted the fatigue level. This observation is clinically important through its potential impact for understanding and identifying sub-phenotypes of long COVID for screening and personalised targeted interventions. More generally, greater awareness of GJH and its extra-articular associations is needed for effective patient stratification and implementation of personalised medicine.

https://bmjpublichealth.bmj.com/content/2/1/e000478

 

The hypermobility story never made much sense to me. Presumably you’ve always had this very common condition without suffering from debilitating symptoms. And then one day out of the blue you develop ME/CFS. What’s the causal link? I don’t see how having bendy joints explains brain fog, hypersensitivity to light, sound, meds etc.

 

There is absolutely no reason that I know of for hypermobility being associated with ME.
Thanks for your thoughtful and clear response to my question. It is helpful to know that your conclusion is based on an in-depth understanding and experience in this field. As you know PwME or, as in my case, their mothers, are desperate for information that could lead to treatments or cure and find ourselves swamped with conflicting information that we do not have the expert knowledge to fully understand. For the last few years I have been under the the distinct impression there was an association between the two conditions but your feedback has made me reconsider this and now I would say I am on the fence. I hope that at some point in the not to distant future there would be a robust study that would either clearly establish any association and the mechanism for it or refute it entirely. I am grateful for the collective wisdom in this forum.

 

I think it's driven by people seeing an apparently strong association being highlighted by apparently knowledgeable people online, and it piques their interest.

Add to that the fact that they're desperate for answers but there are none, and there are charlatans who know this but make money out of offering them anyway, and you can end up with memes that circulate with little resistance and even less questioning.

And of course there's no ad revenue or brand value or share potential in articles pointing out that you can use statistics to link any common attribute with any condition you want, but it doesn't make it real.

 

When I was hospitalised for ME 2 years ago, there was a big fuss made over an apparent POTS and ME specialist, a big-time professor who just happened to be doing a rare round in the hospital. When I finally saw him, he claimed that POTS is caused by excessively stretchy blood vessels, which are in turn caused by a kind of EDS that also is linked to autism and ADHD. Oh and he diagnosed me with POTS without any testing whatsoever. I got the impression that every other clinician had so little experience with any of these things that they fell over themselves to defer to him on any point.

So it's propped up in-person too, by supposed experts!

 

Interesting. What are the alternative hypothesis for blood pooling in the extremities in POTS again? I know SFN is a potential cause but is there anything else?

 

Thanks for that reply Hutan. It is helpful & makes me feel a little more comfortable sitting on the fence.

 

Come on @Hutan, the things you mention make no sense in terms of explaining why PWME are unwell. There are people with gross collagen abnormalities of all sorts who do not feel as if they have ME. You can dream up 'vague indications' for anything. Why on earth should flexibility make you more vulnerable to ME?

People with hypermobility show no evidence whatsoever of collagen defects - they just have a greater range of movement. People with monogenic EDS with connective tissue protein defects look quite different in my experience - you can see that the tissues are abnormally structured.

If you trace this story through the Rowe cases and Knoop it is pretty obvious that the whole thing is a case of Chinese whispers - the story changes every time. I won't go in to the details but I had first hand experience of data being gerrymandered. Maybe it is because of my early contact with the hypermobility crowd that I am so aware of how easy it is to manipulate data and how easy it is for people to believe it or at least 'keep an open mind'.

Remember the old saying:
'Keep an open mind but not so open your brain falls out'!!

We have spent six years on this forum collectively learning just how much hooey there is around in medicine and how much more sceptical we need to be than we ever thought because people find whatever way they can to distort reality. I cannot prove that there is absolutely no link between ME and bendiness. But I cannot prove that there is absolutely no link between politics in Peru and the date that daffodils first flower in Golders Hill Park.