Menopause, Perimenopause, and Hypermobility: How Hormonal Changes Affect Your Body

If you have hypermobility or Ehlers Danlos syndrome, and you’re somewhere in your 40s or 50s (or possibly younger), there’s a decent chance something has shifted in your life. Joints that were just starting to get manageable have started misbehaving again, the POTS symptoms you’d finally got under control are flaring up again, and the pain you’d brought down over years of rehab is slowly creeping back up. The brain fog is thicker, sleep is worse, and you can’t regulate your temperature to save your own life. Then, someone mentions hot flushes and the penny drops. The same hormonal swings nudge other things around too, and throat and voice symptoms can indeed fluctuate with them.

If you’ve also been told you have PCOS, the picture gets even more layered, and we’ve written about that overlap separately in PCOS to PMOS: what the new name means for women with hypermobility article if you want to go deeper.

The problem is that when you go looking for information, you find one of two things: either general menopause content that doesn’t mention hypermobility once (happens all the time), or hypermobile content that barely touches what hormonal change actually do to connective tissue. Neither is much use if you’re trying to work out what’s actually happening in your body.

Two things are worth saying before we get into this article, as they shape everything you will find below. The first is that the menopause transition is a multisystem event, rather than a hot flush problem, and joint and muscle discomfort is the single most commonly reported physical symptom from it worldwide ^[1][2]. The second is that almost none of this has ever been studied “directly” in people with hEDS or HSD. There’s one reasonably large body of self reported data in hEDS, covering hormonal life events, and after that we’re reading across from general menopause science, from sports medicine, and from mechanism ^[1][3].

Where something is established, we’ll say so, and where it’s plausible but untested in a hypermobile body, we’ll say that instead, as the honest version is a lot more use to you in a ten minute appointment, rather than a confident one that falls apart under questioning (no one wants to look silly).

A quick note before we go on: this is educational. It isn’t medical advice, it doesn’t replace a clinical assessment, and it shouldn’t be used to change treatment you’re already on.

Your Menstrual Cycle and Your Joints: What Actually Changes, and What Does Not

Long before perimenopause gets anywhere near the conversation, hormones are already acting on your musculoskeletal tissue, as oestrogen and progesterone receptors are present through out it: in ligaments, tendons, cartilage and joint capsules, and oestrogen has measurable effects on collagen content and on tissue stiffness ^[4].

The interesting part is that those two effects pull in different directions all together. Oestrogen increases the collagen content of tendons and ligaments, which sounds rather protective, and it also reduces their stiffness by inhibiting lysyl oxidase, the enzyme that cross links collagen fibres. Fewer cross links means both more pliable tissue, and less structural stability at the same time ^[4].

The question that actually matters is whether any of that shows up as measurable looseness, across a normal cycle, and the picture there is a good deal messier than it’s usually presented online and in the many instagram posts on the subject.

Some measurements do move though, like “Genu Recurvatum”, which is hyperextension at the knee, and whole body joint laxity have both been recorded as higher in the ovulatory phase, rather than the late follicular phase tracking the rise in oestradiol ^[5]. Anterior knee laxity and stiffness, measured in the same work, didn’t differ between those phases ^[5]. Genu recurvatum has also come out higher in the late follicular, ovulatory and luteal phases than the early follicular phase in athletes, with oestradiol appearing to track the stiffness of the muscles around the knee ^[6].

Pool all of that work together though, and the picture changes a fair bit. As across the sex hormone and ligament evidence there’s no overall effect of menstrual cycle phase on knee laxity or anterior tibial translation ^[7]. Pooled work on cycle phase and ACL injury risk, rates the underlying evidence as relatively low to very low quality, with studies disagreeing on whether there’s an effect and sometimes on its direction ^[8]. Older work measuring knee laxity alongside collagen markers found laxity moving with oestrogen, and that’s one input rather than a settled answer ^[9].

The honest read is this: hormonal effects on ligament biology are real, and the cycle phase effects on clinically meaningful laxity are inconsistent at best. So, anyone telling you which phase your knee is most vulnerable in, is going well past what the data supports. And none of it was measured in people with hEDS or HSD anyway.

What about progesterone and relaxin?

Progesterone gets a lot less attention than it actually deserves here, and the evidence for it is weaker than the confident version you’ll read online suggests.

Progesterone increases the expression of relaxin receptors in ligaments and tendons, so tissue responds more strongly to relaxin, even when relaxin levels haven’t changed. That finding comes from female rats though, so it’s a read across from animal tissue rather than a measurement in you ^[10]. Relaxin itself is produced in small amounts across the cycle, peaking in the luteal phase (well some stages and it also depends on a few things), and it activates the enzymes that break collagen down. Higher relaxin has been associated with greater ligament laxity in some joints, and much of the mechanistic detail comes from animal and laboratory work rather than from women who aren’t pregnant, in whom circulating levels are far lower: that evidence isn’t yet strong enough to draw firm conclusions ^[11].

Progesterone may also do the opposite job in some tissues, suppressing the enzymes that degrade collagen and supporting collagen synthesis, though that work comes from skin fibroblasts and specific joint fibrocartilage rather than from ligament or tendon directly ^[12][13].

Put it all together: progesterone plausibly makes tissue more responsive to relaxin, and plausibly supports collagen maintenance, and both of those are inferred rather than demonstrated in a hypermobile human. What isn’t in doubt is that once progesterone becomes erratic, whatever it was doing becomes unpredictable.

All of that matters for the menopause, as it explains the pattern that so many people describe: worse in the week before a period, easier after it, and rather odd around the ovulation phase. It also sets up why perimenopause is so destabilising, as when that monthly rhythm, imperfect as it is, breaks down, the calibration that took years to find can stop working. If you’ve read our article on hypermobility and pregnancy, you’ll know relaxin has a much larger role there, and at least in pregnancy the levels are high and consistent.

Oestrogen, Androgens, and Connective Tissue

The version of this story that circulates online is simple: oestrogen loosens tissue, oestrogen falls, everything gets worse. Unfortunately it’s too simple, in two separate ways.

The first is that oestrogen’s effects on connective tissue are tissue specific rather than uniformly good or bad, as it raises collagen content and lowers stiffness in the same tissue at the same time ^[4]. Which is why a lot of people notice the opposite of what they expect after menopause (we see this in our clients all the time), in that tissue which felt loose under oestrogen feels stiffer once oestrogen is consistently low, particularly first thing in the morning.

The second one is more interesting, and it’s fairly recent. When steroid hormones were profiled in women with hEDS, oestrogen and progestogen was largely no different from the controls, and what was actually different was androgen metabolism: lower androgen sulfate metabolites, alongside downregulated androgen pathway enzymes in skin fibroblasts ^[14]. That’s a single line of work and it’s rather mechanistic as opposed to clinical, so it settles nothing really. It does mean though, that the tidy oestrogen first model of hypermobility, isn’t particularly the only candidate on the table, and that’s worth knowing before somebody sells you a hormonal explanation with more confidence than the field has actually earned.

Why Perimenopause Can Be the Harder Part

Perimenopause isn’t a smooth decline, not really, it’s a period of large fluctuation, in which oestradiol can sit persistently low, run abnormally high, or even oscillate erratically, while progesterone becomes irregular and cycles lose their pattern ^[15][1].

For a body that’s spent decades adapting to imperfect structural support, that matters, as the adaptation is at least calibrated to something predictable, and once the input becomes chaotic the calibration stops holding, and a nervous system that’s already sensitised, has to absorb all that variability on top of everything else.

The self reported hEDS data points the same way as well, without ever proving it. In a large group of women with hEDS, symptoms were reported as worsening around puberty, before periods, and after childbirth, which is exactly the pattern you’d expect if hormonal change moves symptoms. Among those past menopause, 22% reported that their symptoms improved afterwards ^[3], and some report fewer injuries after menopause too ^[16].

What this doesn’t establish though, is that perimenopause is generally worse than menopause for hypermobile folk. It’s a plausible reading, however, of a consistent pattern, rather than a large population level finding, so just note that. The alternative reading, that stability matters more than absolute hormone levels, fits the same data equally well.

The unpredictability itself is badly underrated as a source of distress, too, as you’ve spent years learning which activities cause flares and which days you can push, and perimenopause takes the one variable you were optimising around, and completely destabilises it. You can do everything right, and still have a terrible day.

POTS and Autonomic Changes During Perimenopause

For those with hypermobility who also have POTS or dysautonomia, this transition is genuinely difficult to interpret, mostly because the two symptom lists overlap almost completely, so it adds a huge amount of nuance, into an already complicated picture.

Heat intolerance, flushing, disturbed sleep, palpitations, headache, brain fog, fatigue and mood change all turn up on both lists ^[17]. So, when those symptoms worsen in a perimenopausal woman with POTS, working out which condition is driving which, is genuinely hard. And, the risk that the lot gets attributed to menopause while a real worsening of autonomic dysfunction goes unmanaged is real ^[17].

The background burden here isn’t small as well, as in women with HSD and hEDS autonomic symptom scores come out severe, 58.3% report a physician diagnosis of POTS, and 98.8% report chronic pain ^[18]. Cardiovascular autonomic dysfunction is also a recognised feature of hEDS, rather than an add on ^[19].

The reason perimenopause would make any of that worse is fairly mechanical, as Oestrogen has a role in autonomic regulation and in plasma volume maintenance (I bet you saw that one coming), so falling and fluctuating levels plausibly shift the balance toward sympathetic activity and reduce circulating volume. And both of those worsen standing tolerance ^[17]. If you’re already dealing with the volume management challenges of POTS, losing a hormonal buddy in holding onto volume really doesn’t help.

Hot flushes sit here rather than in a box of their own as well, as they’re a thermoregulatory event rather than just an inconvenience. Menopause changes temperature regulation directly ^[20], and that lands on top of the autonomic thermoregulatory problems that already make heat intolerance and cold intolerance such a feature of hypermobility. Boiling hot one hour and freezing the next is a real physiological state.

It’s also worth noting, that three patterns get described in perimenopausal women with POTS: worsening through the transition, improvement once hormones settle at postmenopausal levels, and new onset POTS appearing during the perimenopausal years. Those are clinical impressions rather than trial results though, and the course of POTS through peri and postmenopause hasn’t actually been studied ^[17]. They’re worth knowing because they tell you which questions to ask, and they aren’t just predictions.

Palpitations deserve a specific mention here as well, because they frighten people the most. Menopausal palpitations tend to travel with flushes, cluster in the evening, and often settle on their own. Orthostatic palpitations are triggered by positional change, they involve a heart rate rise of 30 beats per minute or more on standing, and usually come with other orthostatic symptoms. So, if yours are clearly positionally dependent, that’s worth getting checked out.

Pain: Central Sensitisation Meets Hormonal Disruption

Let’s start with the general population, as around 71% of perimenopausal women report musculoskeletal pain, which makes them roughly 1.63 times more likely to experience it than premenopausal women ^[21]. In the largest pooled picture available, muscle or joint pain rises from 40% before the transition to 57% during perimenopause and 59% afterwards ^[22]. Musculoskeletal change is now discussed as a defined part of the menopause picture rather than a coincidence of ageing (I know it just keeps getting better)^[26].

And that’s all in women without hypermobility keep in mind, before you get anywhere near the baseline this population starts from.

For those with hypermobility, pain is already shaped by central sensitisation, which is documented in Ehlers-Danlos syndrome and fibromyalgia, among other persistent pain states ^[23]. In hEDS specifically, the degree of central sensitisation tracks with fatigue, pain and cardiac autonomic symptoms, which is a genuinely useful way of understanding why all of those move together rather than separately ^[24].

Layer perimenopause on top of that, and Oestrogen receptors are distributed through out the central nervous system, including regions involved in pain modulation, and oestrogen appears to influence the descending inhibitory pathways that damp incoming signals from the body ^[25]. So, when oestrogen falls and fluctuates, that damping gets less reliable, and for a nervous system that’s already amplifying, the margin gets thinner and thinner.

There’s a clinical pattern also, in that Fibromyalgia diagnoses are “anecdotally” more common around the menopause transition, and the overlap makes mechanistic sense, being that reduced descending inhibition, disrupted sleep and heightened autonomic arousal all push the system in the same way. What the evidence doesn’t support is inevitability, as plenty of people go through this transition with a sensitised nervous system and don’t develop fibromyalgia, and framing it as unavoidable is both wrong and unhelpful.

The pain is usually both the hypermobility and the menopause, and the split doesn’t change what helps. Loading tissue, protecting sleep, downregulating an aroused nervous system, and appropriate hormonal support where it’s indicated all apply either way.

Fatigue, Sleep, and the Brain Fog You Cannot Describe

Brain fog in EDS and POTS is something we’ve covered in great length already, so have a little look if you want to go deeper into this topic.

Perimenopause adds its own layer to it though, and for a lot of people, it’s the symptom that frightens them most, because it feels like something fundamental has shifted.

Cognitive symptoms during the transition are widely recognised, as they usually involve working memory, processing speed and word finding, and in general populations, they tend to be temporary rather than progressive ^[1][27]. That last part is worth keeping in mind though, as the fear underneath brain fog is nearly always about permanence (at least in our work with people). Oestrogen receptors are present in the prefrontal cortex and hippocampus, which is the mechanistic reason the transition touches cognition at all ^[15].

Sleep is where most of this intersects, as subjective sleep disturbance affects 40 to 60% of perimenopausal women, driven by night sweats, insomnia, and changes in sleep architecture (this is a big one). And progesterone metabolites acting at GABA-A receptors are part of what disappears, once progesterone declines ^[28]. Vasomotor symptoms are among some of the main disruptors of sleep quality across this transition, alongside circadian changes and mood ^[29].

Sleep is already compromised for a lot of people here by pain, dislocating joints, and autonomic arousal and sensory sensitivity, which our article on hypermobility and sleep goes through it all in detail. So, this is a hard extra load for your body. Poor sleep amplifies central sensitisation, worse pain disrupts sleep, and perimenopause tends to accelerate that loop at exactly the point where there’s the least capacity to absorb it.

The fatigue that comes out of that isn’t ordinary tiredness, as the body is working harder to regulate itself in the first place, the overnight repair isn’t finishing the job, and daily life carries on regardless. Pacing strategies matter much more during this period rather than less, and they usually need recalibrating and really looking at, rather than just repeating.

Mast Cells, Oestrogen, and MCAS Flares

For those you who also have mast cell activation syndrome, perimenopause can be completely baffling until you know the mechanisms behind it.

Oestrogen can activate mast cells directly, acting through oestrogen receptor alpha to trigger calcium influx and degranulation, releasing histamine and other mediators, while progesterone appears to have a somewhat stabilising effect (depending on the model, so it depends) ^[30]. That predicts a pattern across a cycle: more reactivity in the first half when oestrogen is rising and progesterone is low, relative calm in the luteal phase, then another wave as oestrogen drops before a period. In perimenopause, when oestrogen spikes and crashes without any pattern, that reactivity plausibly becomes more erratic (plausibly) ^[30].

Unfortunately, as you would expect, there’s no research on perimenopause triggered mast cell flares in hEDS, so what exists is just the mechanism, plus a consistent clinical observation. And, there’s no agreed protocol for managing MCAS specifically through this transition. What clinicians actually do, is manage MCAS the way it’s normally managed, with antihistamines, leukotriene blockade, mast cell stabilisers and trigger management, all whilst dealing with the hormonal instability separately where it’s appropriate ^[31].

Practically: if you have MCAS and you’re heading into perimenopause, raise this with your team whether your management needs adjusting, and track symptoms against your cycle while you still have one. Knowing that hormonal fluctuation may be driving flares, makes the apparently random bad days a lot less bewildering.

Bone Health: A Risk Worth Measuring Rather Than Assuming

Bone health feels like a distant problem when pain, fatigue and POTS are the daily reality. But, it does deserve attention during these years anyway, as the picture in hypermobility is genuinely unresolved. Oestrogen regulates bone density, its loss after menopause accelerates bone loss, and that much isn’t in dispute. What is in dispute though, is the starting point in those with hypermobility.

Some of the evidence points to a lower baseline, as bone mineral density at the femur and lumbar spine has been recorded as lower in premenopausal women with hEDS or HSD than in matched controls ^[32]. Vertebral fractures have turned up far more often in Ehlers-Danlos syndrome than in controls, 38.5% against 5.1%, and that excess wasn’t reliably predicted by standard density measurement, which suggests bone quality rather than bone quantity is part of the problem ^[33]. Bone fragility also comes out increased across hereditary connective tissue disorders once the work is pooled ^[34].

Other evidence points the other way. Across hypermobile and classical Ehlers Danlos syndrome, the reductions in bone density come out rather mild, with fracture risk described as uncertain and heterogeneous ^[35]. And set against women with classical EDS, women with hypermobile EDS, show no meaningful difference, and no increased risk of low bone mass specific to the hypermobile group ^[36].

Those aren’t the same comparison, which is a fair part of why they disagree, in that one set compares hypermobile people with healthy controls and the other compares one the EDS subtype with another. So, rather than assuming the worst or even the best, the sensible thing is to actually measure it, and to ask for a scan earlier than you otherwise might do, if you carry additional risk: low body weight, gut problems affecting absorption, limited exercise tolerance, or a history of stress fractures.

Loading exercises also matter a great deal here too, and so do all the boring fundamental stuff, so get your vitamin D checked and corrected if it’s low, and keep dietary calcium in good stead. Our article on EDS and ageing covers more of the long term picture.

The Pelvic Floor: Already Compromised, Now Under More Pressure

The pelvic floor is connective tissue like everywhere else, so the problems start well before menopause. Pelvic floor dysfunction is very common in Ehlers Danlos syndrome, with rather high reported rates of urinary incontinence, prolapse, bladder pain, and sexual dysfunction ^[37]. Pooled data now puts prolapse risk in joint hypermobility syndromes at more than twice that of the general population ^[38].

Then menopause changes the tissue itself, as oestrogen receptors are present through out the vaginal epithelium, the urethral sphincter, the levator ani, and the pelvic ligaments, so when oestrogen declines those tissues atrophy and lose tone. That’s the genitourinary syndrome of menopause, and it raises the risk of both prolapse and incontinence in the general population. Where pelvic support is already compromised, a mild prolapse can indeed become symptomatic, and manageable stress incontinence can stop being manageable ^[38].

One nuance that gets missed nearly every time, and it changes what you should be asking for, urinary symptoms don’t all come from prolapse or from the bladder itself, as pelvic floor dysfunction and neurological contributions account for a substantial share of them. The way these conditions affect the bladder and urinary tract varies from person to person instead of being the same for everyone.^[38][39]. Which matters, because the assessment that finds a dysfunctional pelvic floor, isn’t the assessment that finds a prolapse, and being sent down the wrong pathway costs years and years.

Vaginal oestrogen is the first thing that seems to help, as it has minimal systemic absorption, it’s well supported for urogenital symptoms, and it can be used long term, including by women who aren’t on systemic HRT, and UK menopause guidance supports its use. So if you have urogenital symptoms, raise it before they get severe rather than after.

The second helpful thing is pelvic floor physiotherapy, with somebody who actually understands connective tissue disorders. I actually, can’t stress this more! You can save a lot of time and effort, by just going this route straight off the bat. The goal is coordination and appropriate tone, rather than pure strength alone, because an overactive pelvic floor causes as much trouble as a weak one, and both are common with hypermobility. Our pelvic and core stability content covers the background on your pelvic floor and your breathing.

Mental Health: The Layer Nobody Talks About Enough

Hypermobility and anxiety are incredibly closely linked, and the same autonomic dysregulation that drives POTS also primes the system for threat detection. Plenty of people with hEDS name anxiety as one of their most burdensome symptoms, in fact.

Perimenopause also adds to that risk in a very measurable way, a depressive symptoms are around 40% more likely during perimenopause than before it, and that elevation isn’t sustained after menopause ^[40]. Roughly 32% of perimenopausal women report depressive symptoms at any given point ^[41]. That’s a raised risk across a population though, and not a guarantee that your anxiety will worsen.

Then there’s the experience of being dismissed, which changes shape during these years, as women with hypermobility are already more likely to have symptoms put down to anxiety or stress. And now there’s a new catch all: it’s just menopause. Genuine worsening of autonomic function, connective tissue instability or mast cell reactivity gets absorbed into that phrase and quietly stops being investigated.

In reality though, menopause is contributing, and so is the hypermobility, and both deserve real attention. A useful question, if you’re getting the brush off: could this symptom also be related to my connective tissue disorder, and if so, what should we be doing about it?

There’s a grief and identity dimension here to unpack also, as lot of people spend years reaching a place of stability, only for perimenopause to make them feel like they’re starting all over again.

HRT: The Full Picture for Those With Hypermobility

Nobody has run a trial of hormone therapy in people with hEDS or HSD, not one. So anyone telling you definitively that HRT will help your hypermobility, or definitively that it’ll harm it, is going well beyond the evidence.

What does exist, although not really worth at the moment, is self reported data among women with hEDS. In those who had used menopausal hormone therapy, only four reported that their hEDS symptoms improved (386 women with hEDS, 16.8% were postmenopausal, and 41.5% of those had used MHT)^[3]. Four is a hint rather than a finding, and the sample it came from was small and observational, so it can’t support a treatment claim in either direction unfortunately.

There’s also a theoretical concern that systemic oestrogen, by further reducing tendon and ligament stiffness, could worsen joint laxity in hypermobile people ^[4][17]. It’s biologically plausible, and evidence that it causes clinical harm in hEDS is just absent, rather than reassuring. Treat it as a mechanism to raise with your doctor rather than a reason to rule HRT out though.

The practical position that most menopause specialists take, and the one the evidence actually supports, is this: use mainstream menopause evidence to treat menopausal symptoms, and don’t expect it to treat the hypermobility.

Transdermal vs Oral: Why Route Matters

This is the part of the HRT conversation with the strongest evidence behind it, and the one that brings a smile to my face as I write this, because I don’t have to make a million hedges against the evidence.

Oral oestrogen goes through the liver first, which raises clotting factors, and transdermal oestrogen bypasses that entirely, so the consequence is a clear difference in venous thromboembolism risk: oral hormone therapy is associated with raised risk, while transdermal preparations aren’t ^[42][43]. That advantage holds up in women who already carry a raised risk of clots, which is the group where it matters most ^[44]. Progestogen choice modifies the picture too, and the oral versus transdermal contrast survives once that’s accounted for ^[45].

For someone with hypermobility who may be less active, may have autonomic instability affecting their vascular tone, or may have other reasons for vascular caution, transdermal is by far the logical default. It also delivers steadier levels without the peaks and troughs that come with oral dosing, which matters quite a lot if you react badly to hormonal fluctuation in the first place ^[17].

Body Identical vs Synthetic Progestogens

If you have a uterus, oestrogen has to be combined with a progestogen to protect the lining, and the type you’re given isn’t neutral.

Micronised progesterone, sometimes prescribed in the UK as Utrogestan, appears to have a more favourable profile than some synthetic progestins for clotting and possibly for breast risk. And its metabolites act at GABA A receptors with sleep promoting and anxiety reducing effects ^[45][28].

Two caveats though:
That comparison rests largely on observational data rather than actual trials, so treat it as a reasonable preference, and whichever one you end up on, the dose has to be adequate for endometrial protection. If you’ve tried HRT and felt worse on the progestogen component specifically, it’s worth asking whether or not micronised progesterone is an option.

Testosterone: What It Is and Is Not For

Testosterone gets talked about with a great deal more enthusiasm than the evidence justifies. Women produce testosterone in the ovaries and adrenal glands, levels decline gradually with age, and they drop sharply after surgical menopause. What the pooled trial evidence supports is one single indication: low sexual desire causing distress in postmenopausal women ^[46]. It doesn’t support testosterone for cognition, for energy, for muscle, or for hypermobility symptoms, and where trials have looked at those outcomes the case isn’t made.

Now, the muscle argument is superficially attractive for those with hypermobilility. As muscle is how hypermobile joints are protected, and with muscle getting harder to maintain during this transition, you can see why it would be appealing. But, none of it adds up to evidence that prescribing testosterone will do that job, as resistance training has evidence behind it, and testosterone for muscle in women doesn’t.

Testosterone for women isn’t licensed as a specific product in the UK, and is prescribed off label. UK primary care guidance sets out how that’s done and for whom, and the national guidance supports considering it for low sexual desire where HRT alone hasn’t worked ^[50].

Vaginal Oestrogen

This gets a separate mention here, because it’s so consistently underused, time and time again. With vaginal oestrogen, systemic absorption is minimal, it can be used long term, it can even be used by women who aren’t on systemic HRT, and it addresses vaginal dryness, urethral discomfort, recurrent urinary infections and painful sex. If you have urogenital symptoms, ask for it specifically, you may just be really surprised.

The Timing Window

Now there’s a real concept buried in here, and a lot of overstatement around it, because, the benefits generally outweigh the risks most clearly in symptomatic women under 60. Well, within ten years of their final period, and starting earlier is associated with more favourable cardiovascular outcomes ^[47][48]. What’s far less certain is cognitive protection, which gets claimed a lot and isn’t established ^[49]. Hormone therapy isn’t recommended as primary prevention for heart disease, dementia or cognitive decline ^[47].

The practical version: if you’re 45, with irregular cycles and increasing symptoms, that’s the point to start speaking up, rather than at 60 once things have gone awry.

What to Discuss with Your GP

Tell them you have hypermobility or EDS, and why that changes the conversation: meaning the potential connective tissue effects, POTS if it’s relevant, and the vascular considerations. Ask about transdermal rather than oral oestrogen. Ask about micronised progesterone, rather than a synthetic progestin, particularly if sleep and anxiety are already problems, and ask about vaginal oestrogen for urogenital symptoms, whether or not you take systemic HRT. If your GP isn’t familiar with the hypermobility side, asking for a referral to a menopause specialist is entirely reasonable, and there’s a searchable directory of accredited menopause specialists in the UK if you want to find somebody local. You can find the British menopause specialist list here, so that you don’t need to go searching for it.

What Actually Helps: Practical Management for the Hypermobile Perimenopausal Body

There’s no single intervention that fixes this unfortunately, and that includes HRT. What there is instead, is a package: loading, proprioceptive work, motor learning, sleep treated as its own problem, autonomic support, and pacing that’s been recalibrated rather than just repeated.

Resistance Training, Done Properly

The temptation is to reduce activity because everything feels harder, which is completely understandable and also the wrong direction, as muscle is the main mechanism by which hypermobile joints are protected, that and sensori-motor control.

Exercise and motor function training improve pain, proprioception and quality of life in hEDS and HSD, though the trials are small, varied and short ^[51][53]. Targeted home exercise has improved shoulder instability in hEDS and HSD, which is one of the few properly randomised findings in this space, but just keep in mind that this entire area is completely lacking^[52]. Supervised heavy resistance work in hypermobile women with knee pain was tolerated, with improvements in pain, fear of movement, strength, proprioception and tendon stiffness ^[55]. But, I would personally recommend you see this as an advancement, once you have some good motor control. Everyone is different, I don’t want anyone jumping into anything they aren’t quite ready for just yet. Self guided resistance training in generalised joint hypermobility produced no strength advantage over the control group, despite good adherence and few adverse events ^[54].

Read together, those say something a good deal more useful than “resistance training is non negotiable”. They say it needs to be individualised, progressive, and supervised enough to actually reach a useful load with decent technique. Generic strengthening advice is what fails for those with hypermobility, over and over.

Perimenopause itself doesn’t block adaptation, by the way. Twelve weeks of supervised low impact resistance work improved hip strength, balance, flexibility and lean mass to a similar degree in premenopausal, perimenopausal and postmenopausal women ^[56]. You haven’t actually lost the ability to get stronger, so every cloud.

Core stability work and progressive loading matter more during this transition rather than less, and there’s a bone argument for loading sitting on top of the joint one. Our articles on exercise for hypermobility and managing fear of movement cover the principles if you want to go a little deeper (this articles nearly finished by the way, I know it was a long one, I make no apologies). If POTS is in the mix, starting supine or semi reclined and progressing gradually is still the right approach.

Proprioception and Hormonal Fluctuations

Proprioception, the sense of where your joints are, is already less reliable in hypermobility, and it improves with rehab ^[51][55]. Whether hormonal fluctuation specifically degrades it in a hypermobile body (surprise, surprise) hasn’t been tested. What’s reasonable to say however, is that when joint behaviour is less predictable, position sense is worth training deliberately: so balance work, slow controlled movement, and tasks that challenge the sense of where you are. Deeply unglamorous I know, and nobody has ever posted a heroic video of themselves standing on one leg by a kitchen counter. Well, my Aunt Suzie, but she was nuts.

Sleep Needs Treating Directly

Easier said than done this one, when factoring in the reality that is night sweats and hormonal insomnia. But, sleep here is a target in its own right, rather than something that will magically fix itself, once everything else improves. Normally, it’s the other way around, better sleep, less pain, better cognitive function during your rehab.

Behavioural treatment is the strongest option, and cognitive behavioural therapy for insomnia in particular has some good support in menopausal women ^[57][58][59]. Exercise helps some people, and the effect is inconsistent, so treat it as a reasonable addition rather than a substitute ^[59]. Supplements are weaker, and omega 3 didn’t improve insomnia when the trial data were pooled ^[60].

The practical measures still count though, don’t make the mistake of thinking they dont. Keep the bedroom cool, deal with anything that reliably wakes you (cats, the partner, Linda next door dragging her bins out at 3am), and if you’re on HRT, micronised progesterone has the sleep promoting effects described above. Our hypermobility and sleep article covers the baseline problems in more depth. And, if sleep disruption is severe, ask your GP about treating it directly, rather than waiting for the hormones to settle.

Supplements: What Holds Up and What Does Not

Less holds up than the internet suggests, and the honest list is pretty short and to the point.

Vitamin D, then calcium has the clearest support, and vitamin D has the best safety profile of anything in this category ^[61][63]. Get your level checked, correct it if it’s low, and keep dietary calcium adequate. Isoflavones have mixed but plausible benefit ^[62]. Black cohosh or Chinese herbal products may help specific symptoms but are not broadly settled, while most other supplements remain low-certainty or product-specific ^[61].

Creatine gets recommended constantly in this space, and our article on creatine for hypermobility and EDS covers what’s actually known about it, It’s a fair bit.

Volume Management and Compression Garments

For those with POTS, the reduction in plasma volume across this life transition can noticeably worsen standing tolerance, so fluid and salt intake matters more rather than less.

Compression is one of the few areas here with direct evidence in hEDS, rather than borrowed evidence from further afield. Adding daily compression garments to physiotherapy improved dynamic balance, with immediate reductions in sway ^[64]. In follow up practice, 80% of people with hEDS or HSD reported a response, most often less pain, with similar benefit in both groups ^[65]. That fits the wider finding that compression improves some aspects of joint position sense, though not every measure of it ^[66].

Our article on compression garments goes into fit and pressure properly. If you’ve been getting by with knee highs, waist high is worth a try through this transition (and yes, getting into them in a heatwave is an event in itself!).

Cooling Strategies: Less Settled Than It Looks

Cooling techniques aren’t recommended for vasomotor symptoms on current evidence, and that’s the position menopause guidance takes rather than our actual opinion ^[67].

Which doesn’t mean throw the fan out, as keeping a room cool and wearing breathable clothing are cheap, harmless, and often very welcome. If you find them helpful, there’s no reason at all to stop. What’s changed is the claim attached to them, as they’re comfort measures rather than a treatment for hot flushes, and if flushes are genuinely disrupting your life, then a comfort measure isn’t the intervention to be leaning on.

Pacing Recalibration

Perimenopause is a genuine increase in physiological load, as disrupted sleep, hormonal fluctuation, heightened pain sensitivity and autonomic instability, all draw on the same reserves. So, if you were already at your ceiling before this started, the ceiling has probably moved (again). Reassessing your baseline is a sensible adaptation. And the pacing frameworks you already use, apply more, rather than less, once they’re pointed at the new reality.

When to Seek Specialist Support

Some of this warrants a good deal more than just self management and general practice. If POTS symptoms are worsening through the transition, then a cardiologist or autonomic specialist who understands hypermobility is definitely worth pursuing. And with the way EDS diagnosis and recognition are changing, it means finding one is becoming slightly easier. It still takes real persistence though, finding the 6 infinity stones, a full moon, and having your weird friend Zoe with all her crystals at the ready.

So, If you’re considering HRT, aim for somebody with menopause expertise who also understands connective tissue disorders. Given how tangled the entire interaction is, that combination is what you actually need.

If your pain is well above your usual baseline and isn’t responding to what normally works, that deserves investigating too, don’t just fob it off. Likewise, worsening pelvic floor symptoms, a physiotherapist with experience in these conditions can help.

Also, if flares appear episodic, multisystem, and consistent with mast cell activation, specialist input is appropriate, though routine testing of everybody isn’t, so expect a fight.

The Research Gap: Why We Do Not Have Better Answers

Research on menopause in hypermobility is thin, I did tell you this at the start: there are no trials. Most of what we have is self reported data (as much use as a chocolate fire guard), mechanism, and extrapolation from adjacent populations, and even the work now being planned in this area expects to find very little on the role of female sex hormones ^[16].

Now, the reason for that is fairly bleak I warn you, but you probably already know. Women’s health research is underfunded (historically so), rare condition research is underfunded (historically so), and putting the two together gives you a gap that leaves clinicians managing people without much guidance at all (historically so). There are researchers working on it I promise you, but we’re probably a decade away at least, from the kind of studies that would answer the HRT question properly in hEDS.

In the meantime, the job is to work with what exists, be honest about what doesn’t, and be careful about how far evidence from other populations gets stretched.

Pulling It All Together

Perimenopause and hypermobility is at an intersection, wherein, the research hasn’t caught up with the clinical reality, but it’s still possible to say something useful. Oestrogen has a hand in connective tissue, autonomic function, pain modulation, mast cell behaviour, pelvic support and sleep, so when it becomes unstable and then declines, all of those may be affected. Where the baseline was already compromised, the effects land harder.

Three things to separate, because they carry very different weights of evidence:
That the menopause transition is a multisystem event with a heavy musculoskeletal component is well established ^[1][2][22]. That hormonal change moves hypermobility symptoms in at least a subset of people is supported by self reported data and no more than that ^[3]. That any specific hormonal treatment improves hypermobility isn’t established at all ^[3]. Knowing which of those three you’re standing on, is what lets you argue your corner in an appointment.

So, don’t abandon the training, treat sleep as its own problem rather than a symptom of the others, keep volume management going if you have POTS, and measure your bone density rather than guessing at it. Ask for transdermal rather than oral if HRT is on the table. And find a clinician who understands both halves of this, because that combination is what you actually need and is really worth the effort of looking.

Go gently with yourself while you do it, this is a real physiological transition, it’s harder in a hypermobile body, and it deserves treating like one. I hope you enjoyed the article, it was a nightmare to write because of the lack good research, and I hope I get to update it again soon with some better research.

The Fibro Guy

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References

[1] Santoro, N., Roeca, C., Peters, B.A. and Neal-Perry, G. (2021) ‘The Menopause Transition: Signs, Symptoms, and Management Options’, The Journal of Clinical Endocrinology & Metabolism. https://doi.org/10.1210/clinem/dgaa764

[2] Fang, Y., Liu, F., Zhang, X., Chen, L., Liu, Y., Yang, L. et al. (2024) ‘Mapping global prevalence of menopausal symptoms among middle-aged women: a systematic review and meta-analysis’, BMC Public Health. https://doi.org/10.1186/s12889-024-19280-5

[3] Hugon-Rodin, J., Lebègue, G., Becourt, S., Hamonet, C. and Gompel, A. (2016) ‘Gynecologic symptoms and the influence on reproductive life in 386 women with hypermobility type ehlers-danlos syndrome: a cohort study’, Orphanet Journal of Rare Diseases. https://doi.org/10.1186/s13023-016-0511-2

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