Does EDS get worse as you age?

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Adam Foster

Director at The Fibro Guy

Adam Foster is the founder of The Fibro Guy and one of the leading voices in hypermobility, EDS, and chronic pain rehabilitation. A former Reconnaissance Soldier, he developed chronic pain after an IED blast in Afghanistan and built his approach from the ground up when the medical system had no answers. Since 2009 he has worked with thousands of people across eight countries, drawing on pain neuroscience, motor learning, and sensorimotor rehabilitation. He co-authored "No Pain, No Pain" with trauma psychologist Dr Mairi Harper, directed the documentary "Invisible Monster," and has been featured in Forbes, BBC Radio 4, ITV News, LiveScience, and The Telegraph.

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Most people asking this have already decided roughly what the answer is and are bracing for it, so let’s get the useful version out of the way first. For a lot of those with EDS the total burden does go up across adulthood, as pain, fatigue, gut trouble, autonomic symptoms and the slowly growing pile of other diagnoses all tend to accumulate rather than clear up. It isn’t a steady slide though, and it doesn’t happen to everybody, and the part of you that changes the most is very often not your joints.

When people with EDS were followed for about a decade, the average symptom scores barely shifted, which sounds reassuring right up until you look inside that average, because sitting in it were people who improved a great deal and people who got dramatically worse over the same stretch of time ^[1]. So the group answer and your answer are two completely different things, and anybody telling you confidently which of those two you’re going to be is well ahead of what can actually be shown.

What’s below is what the evidence supports about getting older with EDS: what tends to change, what tends to get blamed on ageing with very little behind it, and what has actually been tried.

The Average Is Hiding Two Groups

A flat average across a decade is usually read as “nothing much happens”, and here it means very nearly the opposite, as the flatness came from improvement and deterioration cancelling each other out in the same group of people ^[1]. That’s a genuinely different message. It’s the single most useful thing in this whole area really, because it means a diagnosis doesn’t come with a trajectory attached to it.

Asked to describe what the years had actually been like, rather than to score themselves on a form, most people with EDS said their general function had declined and their symptoms had got worse. What they described though wasn’t a line going downwards, it was cycles: a period of decline, then a reprieve, then another decline, with the reprieve never quite getting back to where the last one started ^[3]. A fair few also said they couldn’t separate what EDS was doing from what ordinary ageing was doing, which is a pretty reasonable thing not to be able to separate, given nobody hands you a control version of yourself to compare against.

Pull back from the individual stories and the same shape appears in the wider picture, as the authors of ^[2] describe the age related picture in EDS as heterogeneous, multisystemic and unpredictable. They also describe the clinical impact of ageing itself as mostly speculative, because none of the work they gathered up had been designed to ask about ageing in the first place. That’s a limitation of what’s been done, and it’s the reason everything below is a “tends to” rather than a “will”.

The Hypermobility Gets Quieter and Everything Else Gets Louder

If there’s one thing the older women in this literature say that nobody warns them about in their twenties, it’s what happens to them in their late twenties and early thirties. A third phase tends to set in around then, where the hypermobility itself becomes less visible and the pain and multisystem trouble become considerably more so ^[4]. The joints stop being the headline. They’re still involved, they’ve just stopped being the thing that’s ruining the week.

That matters clinically, and not in a good way, because a great deal of assessment still keys off how far a joint opens up. If you were obviously hypermobile in your twenties and only moderately so by midlife, you look on paper like somebody who’s improved (and there’s a fair chance you’ve been told exactly that). You usually haven’t though, you’ve just moved into the part of the condition that doesn’t show up on the examination that gets used.

Past forty, the authors of ^[4] say there’s much less to go on (nobody has rushed to fix that). What does exist points the same way as the rest: in women aged forty and over with hEDS and HSD, symptom burden was high, quality of life was poor, and the physical side of quality of life scored worse than the mental side ^[6]. Symptoms had usually started in childhood, and diagnosis had usually waited until the mid forties ^[4]. Which reframes the whole question, as a good chunk of what looks like decline with age is really two or three decades of an unmanaged condition finally arriving somewhere visible.

Across a large group of adults with hEDS and HSD, the same three things turn up again and again: a long wait for the diagnosis, a heavy load of other conditions collected over a lifetime, and frequent autonomic, gut and pain symptoms ^[5]. The accumulation is the pattern, and it accumulates across adulthood rather than waiting for old age. It starts earlier than that as well. Children with joint hypermobility syndrome and hypermobile EDS who came in with more pain, more fatigue, more multisystem complaints and poorer postural control, went on to have worsening disability and worsening quality of life over the next three years ^[13]. So the stacking begins in childhood for some, and “does it get worse with age” turns out to be a question about how long the load has been building rather than a question about birthdays.

What Actually Decides How Bad a Decade Feels

Pain, fatigue and psychological distress are strongly tied to disability in adolescents and adults with hypermobility related conditions ^[7]. It isn’t joint laxity, and it isn’t how many points you scored on an examination. The thing that actually predicts whether you can work, cook, socialise and sleep, is the symptom load and how it’s grinding on you, which is why two people with pretty much identical joints can be living entirely different lives.

Autonomic symptoms sit right in the middle of it, as in hypermobile EDS a heavier autonomic symptom burden went alongside worse quality of life, more fatigue and more severe pain ^[8]. A more recent group of women with HSD and hEDS reported severe autonomic dysfunction, poor quality of life, more than half of them reporting POTS and nearly all of them living with chronic pain ^[9]. Nobody has shown which one is dragging the others along, and in practice it probably doesn’t matter a great deal to you, because you’re carrying all of them at once.

Quality of life itself is reliably poor, and it’s poor across the board: adults with the hypermobility type of EDS scored worse than comparison groups on every single quality of life domain measured, the mental ones included ^[10]. Adults with joint hypermobility syndrome and hEDS also had lower physical quality of life, more pain and worse shoulder function ^[11]. That’s an unpleasant set of findings to read, and there isn’t a version of it that reads any better. So there it is.

Among a very large group of adults with hEDS and HSD in the United States, lower satisfaction with healthcare went alongside lower quality of life and feeling less able to manage your own symptoms ^[12]. Those three things turning up together doesn’t prove that bad medical care makes people worse. It does mean that a meaningful slice of what gets recorded as “quality of life in EDS” is shaped by how you’ve been treated by the system rather than by what your collagen is doing, and that part isn’t fixed and it isn’t inevitable.

Bones, Fractures and the Bit That Gets Overstated

This is where the internet gets incredibly loud and the evidence, at the same time, gets pretty awkward, so we’ll go through it slowly.

In a group of women with hEDS and HSD around midlife, fractures had been more common than in the comparison group, the cortical bone (the dense outer shell of a bone, the bit that does most of the load bearing) was smaller in both area and thickness, and there was less muscle across the limb. But bone mineral density, the number a DEXA scan actually gives you, was no different, and over the following eight years there was no sign of bone being lost any faster than normal ^[14]. A separate group found the same shape: less muscle, smaller cortical bone measures, and no meaningful difference between an hEDS label and a hypermobility spectrum disorder label on any of it ^[15]. So if you’ve been told HSD is the lesser diagnosis and you needn’t think about your bones, that isn’t what the bone measurements say.

Now, spinal fractures are the one that comes up most, and they’re real. Among adults aged thirty to fifty with classical or hypermobile EDS, bone density and bone structure scores were lower than in matched comparisons, and fractures in the vertebrae that show up on imaging were several times more common ^[16]. In a mixed group of adults with EDS the same thing appeared, with those who had fractures reporting more severe back pain, and no clear density difference between the ones who’d fractured and the ones who hadn’t ^[17]. That last detail is the interesting one though, as it points at bone quality rather than bone quantity (or at least it would appear that way). The scan can come back fine and the bone can still break.

Pull the wider picture together and it stays messy in a specific way. In rare types of EDS, low bone density and fractures do appear frequently, while in hypermobile and classical EDS any reduction in density is usually mild and the increase in fracture rates is much less certain, though odd vertebral shapes may still be common ^[18]. Pooling across hereditary connective tissue conditions, fracture prevalence came out high and fracture risk came out clearly raised, with no clear link to osteoporosis and a great deal of disagreement between the pieces being pooled ^[19]. So: fractures go up more reliably than bone density goes down. Which is not the story most people are given.

Joints do degenerate in some settings, and among adults with classical or hypermobile EDS in midlife, more than four in ten had early osteoarthritis in the hands visible on x ray, more often in classical EDS than hypermobile, with the thumb joints worst affected ^[20]. Take that gently though please, as it was exploratory and the group was small. Rarer subtypes can show clearer degeneration, with early onset osteoarthritis and reduced bone density reported in EDS type VIII ^[21], and progressive skeletal fragility with age related changes in the hand bones and osteoarthritis in the upper limb in musculocontractural EDS ^[22]. Rare subtype findings stay rare subtype findings though. They don’t transfer across to hEDS just because the two of them happen to share a surname.

Hormones, Menopause, and the Things That Get Blamed on Age

Hormonal transitions get held responsible for an enormous amount of what happens to women with EDS in midlife, and the evidence underneath that is a great deal lighter than the confidence it tends to get asserted with.

Among a large group of women with hypermobile EDS, a subset reported their symptoms worsening at puberty, before their periods, after giving birth, or on the contraceptive pill ^[23]. A subset though, not all of them, and reported rather than measured. That’s a real signal that some women are hormonally sensitive, and it’s a long way from proof that everybody’s midlife decline is hormonal.

Menopause specifically is a gap, and the authors of ^[24] make the case for a dedicated research field covering menopause in rare conditions precisely because of gaps like it. Which is a polite way of saying that if a clinician tells you confidently that your menopause is or isn’t driving your EDS symptoms, they’re working from the same thin material you are.

What Age On Its Own Actually Tracks

This one cuts against everything above, and it gets the same airtime as the rest. In a large group of adults with hEDS, older age went alongside better wellbeing, while a higher count of other conditions went alongside worse wellbeing ^[25]. Older, in that group, was not worse. The likely explanations are unglamorous, as it could be who survives to be surveyed, who’s still willing to fill in a questionnaire, or genuine adaptation after decades of practice, but whichever it is, the number of other things wrong with you tracked wellbeing and your age didn’t.

There’s a caveat on a lot of the older adult work too, which is that worsening has sometimes been inferred by comparing older women against younger cohorts instead of following the same women through time ^[2]. Comparing an older group against a younger one tells you about different generations of diagnosis, treatment and expectation, rather than about what happened to the older group over the intervening decades.

So age is a poor predictor and comorbidity count is a better one. That’s genuinely good news though, as the second thing has a great deal more handles on it than the first.

What Actually Helps

Now, the part you came for, and it’s more encouraging than the bone section made it sound. Across the exercise and rehabilitation work in EDS, hEDS and HSD, every piece of it reported improvement in at least one physical or psychological outcome, with a single non serious adverse event linked to an intervention across the lot of it ^[26]. Much of that work wasn’t well enough designed to lean on hard, and the authors of ^[26] say so plainly, but the direction is consistent, and the safety picture is reassuring in a population that is constantly told movement is dangerous. Looking specifically at physiotherapy in hypermobile EDS, pain or proprioception improved across the trials that randomised people properly, and quality of life improved consistently ^[27].

The specific programmes are where this gets concrete.

Nine weeks of outpatient rehabilitation: in hypermobile EDS this improved functional exercise capacity, fatigue, balance and quality of life immediately afterwards, and some of those gains were still there half a year later ^[28]. That’s not forever. But it’s long enough to matter and long enough to rebuild on.

Rehabilitation and fear of movement: an earlier look at the same kind of programme found people walking further in a timed walking test, less afraid of moving, less affected by fatigue and with better vitality ^[29]. Fear of moving is not a small side issue in this population, it’s frequently the thing holding the whole pattern in place.

Six months of home shoulder exercise: in hEDS and HSD with unstable shoulders, shoulder function improved, and it improved on both of the programmes tested rather than just the clever one ^[30]. Across the shoulder work more broadly, pain, daily activities and strength all showed positive effects over time, though there isn’t enough there yet to say what the ideal dose is ^[31].

Which leaves the bone question, and that one needs care rather than encouragement.

The smaller cortical bone and the raised fracture rate in hEDS and HSD have been interpreted as possibly related to lower mechanical loading and less muscle, rather than to bone being lost quickly ^[14]. That’s an interpretation and it’s a plausible one, particularly since lower physical activity, fear of movement and deconditioning are so common in this group ^[10][32]. If it’s right, loading is exactly the lever you’d want.

But it hasn’t been tested in EDS, and what we have instead is general population evidence, which needs the label on it. In older adults at risk of fracture, progressive resistance training improves bone mineral density at the hip alongside strength ^[34]. In postmenopausal women with low bone mass, supervised high intensity resistance and impact training improved bone density at the lumbar spine and femoral neck ^[33]. Both of those are real findings in people who don’t have a connective tissue condition, which makes them a reason to suspect that loading helps EDS bone rather than a reason to believe it. Nothing in the EDS work above shows that resistance or weight bearing training slows bone degeneration or prevents a single fracture.

So the position is this: strength and rehabilitation work in EDS have decent, consistent support for pain, fatigue, function, balance and quality of life, which are the things that actually decide how your decade feels ^[7]. Their effect on your bones is an extrapolation. Do it for the first reason, and treat the second as a hopeful maybe.

What To Do With Any Of This

The question was whether EDS gets worse as you age, and the closest thing to a straight answer is that the load usually grows while the trajectory stays unpredictable, and the things that grow most are not the ones that got you diagnosed.

If the number of other conditions you’re carrying tracks wellbeing better than your age does ^[25], and if pain, fatigue and distress track disability better than joint laxity does ^[7], then the useful work, in our opinion, is on the load rather than on the ligaments. That means taking the autonomic symptoms seriously early, staying loaded and strong for the sake of function rather than in the hope of saving your bones, and getting the medical relationships into a state where you’re not fighting for basic care, since that turns up alongside quality of life too ^[12].

None of that stops you getting older, it just changes what you’re carrying while you do it.

The Fibro Guy

References

[1] Schubart, J.R., Mills, S.E., Schaefer, E.W., Bascom, R. and Francomano, C.A. (2022) ‘Longitudinal analysis of symptoms in the Ehlers‐Danlos syndromes’, American Journal of Medical Genetics Part A. https://doi.org/10.1002/ajmg.a.62640

[2] Anderson, L.K. and Lane, K.R. (2023) ‘Clinical trajectory of hypermobile Ehlers–Danlos syndrome/hypermobility spectrum disorders in older adults’, Journal of the American Association of Nurse Practitioners. https://doi.org/10.1097/jxx.0000000000000900

[3] Schubart, J.R., Mills, S.E., Francomano, C.A. and Stuckey-Peyrot, H. (2024) ‘A qualitative study of pain and related symptoms experienced by people with Ehlers-Danlos syndromes’, Frontiers in Medicine. https://doi.org/10.3389/fmed.2023.1291189