Sleep is where so much of this intersects. A 2018 review on sleep and the menopausal transition found that subjective sleep disturbance affects 40-60% of perimenopausal women, driven by night sweats, insomnia, and hormonal effects on sleep architecture [16]. Progesterone, in particular, has sleep-promoting effects through its metabolites, which bind to GABA-A receptors in the brain. As progesterone declines during perimenopause, this natural sleep aid disappears [16]. Oestrogen fluctuations trigger hot flushes that wake women from sleep, often multiple times per night. A 2025 narrative review confirmed that vasomotor symptoms are among the primary disruptors of sleep quality during perimenopause, alongside changes in circadian rhythm regulation [15].
What No One Tells You About Menopause and Hypermobility
If you have hypermobility or Ehlers-Danlos syndrome and you’re somewhere in your 40s or 50s, there’s a very good chance you’ve noticed something changing. The joints that were just about manageable have started misbehaving again. The POTS symptoms you’d worked hard to get under control are flaring. The pain levels you’d brought down are creeping back up. The brain fog is thicker. Sleep is worse. You can’t regulate your temperature to save your life. And on top of all of that, someone mentions hot flushes, and you think: oh, right. I’m also in perimenopause. Great.
The problem is that when you go looking for information, you find one of two things. Either you find general menopause content that doesn’t mention hypermobility once, or you find hypermobility content that barely scratches the surface of what hormonal changes actually do to a connective tissue disorder. Neither is particularly useful when you’re trying to make sense of what’s happening in your body.
So that’s what this article is about. We’re going to go deep. We’re going to look at how hormonal fluctuations across the menstrual cycle affect hypermobile tissue, why perimenopause tends to be more disruptive than menopause itself, what happens to connective tissue when oestrogen drops, what the research actually says about POTS, mast cells, pain, bone health, pelvic floor, and sleep, and what the evidence says about management, including HRT. We’re also going to be honest about where the evidence is thin, because in this area of research, it often is.
This isn’t a menopause 101 guide. If you want a primer on what menopause is and why it happens, there are excellent resources for that. This article assumes you already know the basics and want to understand what it means specifically for a hypermobile body. So, if you’re ready to get into it, let’s go.
Your Menstrual Cycle and Your Joints: The Relationship That Already Exists
Before we can understand why perimenopause is such a disruptive time for those with hypermobility, we have to understand something that often goes completely unremarked: the menstrual cycle is already affecting your joints. Every month. Long before menopause is anywhere near the conversation.
Oestrogen and progesterone don’t just regulate reproduction. They have receptors throughout the musculoskeletal system, including in ligaments, tendons, cartilage, and joint capsules. And when their levels change across the cycle, the mechanical properties of those tissues change with them. A 2021 study examining anterior knee laxity across menstrual cycle phases in 15 women found that joint laxity was measurably higher in the ovulation phase compared to the late follicular phase, particularly in women who already had genu recurvatum (hyperextension at the knee) [9]. Women with baseline joint hypermobility appear to be more sensitive to this oestrogen-driven effect on laxity [9].
A 2022 study in the Journal of Clinical Medicine expanded on this, measuring anterior knee laxity, stiffness, general joint laxity, and genu recurvatum across all four phases of the menstrual cycle in female athletes and non-athletes [10]. The findings were interesting: genu recurvatum was significantly higher in the late follicular, ovulation, and luteal phases compared to the late follicular phase in athletes. And crucially, oestradiol levels appeared to correlate with changes in the stiffness of periarticular muscles around the knee [10]. This is the mechanism in action: oestrogen is genuinely changing how your connective tissue behaves, and it’s doing it every cycle.
Then there’s relaxin. This is a hormone that most people only hear about in the context of pregnancy, but it’s produced in smaller amounts throughout the menstrual cycle, with concentrations peaking in the luteal phase (roughly days 21-24 of a standard cycle). A 2022 scoping review in Frontiers in Endocrinology examined the role of relaxin in musculoskeletal injury risk in women [11]. Relaxin works by activating matrix metalloproteinases (MMPs), enzymes that break down collagen. Higher relaxin levels during the luteal phase are associated with greater ligament laxity, and this appears to be one mechanism behind the well-established finding that women are more vulnerable to ACL injuries during certain phases of their cycle [11]. Relaxin receptors have been found on the acetabular labrum, the ACL, and other joint structures. For someone with hypermobility, where ligament laxity is already the defining feature of the condition, this luteal-phase spike in relaxin is one more variable making things less predictable [11].
Why does this matter for the menopause conversation? Because it explains the lived experience that so many women with hypermobility describe: the predictable pattern of symptoms across the month, the worsening in the week before their period, the slightly better days after it, the particular challenges around ovulation. And it sets up exactly why perimenopause is so destabilising. When that monthly pattern, imperfect as it is, disappears and is replaced by hormonal chaos, the body loses its rhythm. If you’ve read our article on hypermobility and pregnancy, you’ll know that relaxin plays a major role in the increased laxity of pregnancy too, but at least during pregnancy, the levels are high and consistent. The calibration that took years to find suddenly doesn’t work any more.
I want to be clear that the research on menstrual cycle effects specifically in women with hEDS or HSD is very limited. The studies above were all conducted in general populations of women, not specifically those with hypermobility. But the mechanisms are biologically plausible and consistent with what we see clinically, and many of our clients recognise themselves in this description immediately when they hear it.
Oestrogen and Connective Tissue: The Relationship That Changes Everything
To understand why menopause matters so much for those with hypermobility, you first have to understand what oestrogen is actually doing to your connective tissue on a day-to-day basis. And the answer, it turns out, is quite a lot.
A 2019 review published in Frontiers in Physiology examined the effects of oestrogen on musculoskeletal tissue in detail [1]. The findings are illuminating, even if they’re somewhat paradoxical. Oestrogen increases the collagen content of tendons and ligaments, which sounds like a good thing. But here’s where it gets complicated: at the same time, oestrogen decreases the stiffness of those same tissues. It does this by inhibiting an enzyme called lysyl oxidase, which is responsible for cross-linking collagen fibres. Fewer cross-links means more pliable tissue, but also less structural stability [1].
For most people, this is a manageable trade-off that comes with being female. For those of us with hypermobility or EDS, where the connective tissue is already struggling with laxity, this oestrogen effect takes on a different significance entirely. Your ligaments are already working at the edge of their tolerance. Add in hormonal fluctuations that further reduce stiffness, and you start to understand why things go sideways.
The 2012 study we referenced in the first version of this article remains relevant here. It measured knee joint laxity and collagen markers across the menstrual cycle in 20 women [6]. The researchers found that knee laxity fluctuated in line with oestrogen levels, with measurable changes in collagen production markers and the mechanical properties of the joint. This study was in a general population, not specifically those with hypermobility, so we should be careful not to overextend the finding. But it does confirm the mechanism [6].
Now, here’s a nuance worth sitting with. The relationship between oestrogen and connective tissue is not simply “more oestrogen equals worse joints.” After menopause, when oestrogen is consistently low, many women with hEDS notice something unexpected: they feel stiffer. The same tissues that were more lax under oestrogen’s influence become less pliable once oestrogen drops. Some women report joints that feel almost too stiff, particularly in the morning. This is because oestrogen was actually contributing something positive in terms of tissue hydration and collagen maintenance, even while it was also reducing stiffness. Remove it, and you lose both sides of that equation. This is one of the reasons why the picture is so much more complicated than “oestrogen bad, low oestrogen good” or vice versa.
Why Perimenopause Hits Harder Than Menopause for Hypermobile People
There’s something counterintuitive about perimenopause and hypermobility that’s worth understanding clearly. For many women with hEDS and HSD, perimenopause, not menopause itself, tends to be the most disruptive phase. And when you look at what’s happening hormonally, it makes complete sense.
Perimenopause is not a slow, gradual decline in oestrogen. It’s a period of wild fluctuation that can last anywhere from four to ten years. Oestrogen levels can spike to abnormally high levels one cycle and then crash to near-zero the next. Progesterone becomes erratic. FSH surges and falls. A 2015 review in Nature Reviews Endocrinology described perimenopause as a “neurological transition state,” characterised by persistent variability in circulating 17-beta-oestradiol that can manifest as persistently low, abnormally high, or erratically oscillating levels [4]. That variability is the problem. It’s not the destination, it’s the journey, and it’s a bumpy one.
For those with hypermobility, connective tissue has already adapted to a lifetime of suboptimal structural support. That adaptation, however imperfect, is at least somewhat calibrated to a predictable hormonal environment. When that environment becomes chaotic, the calibration falls apart. Joints that had been relatively stable become less predictable. Pain levels fluctuate more. The nervous system, already sensitised, has to contend with rapid hormonal changes on top of everything else [4].
This is why the data from a 2016 cohort study of 386 women with hEDS is worth examining, even with its limitations [2]. The study, published in the Orphanet Journal of Rare Diseases, found that 22% of postmenopausal women with hEDS reported an improvement in their symptoms after menopause. This is actually a reasonable finding when you think about it: once oestrogen settles at a consistently low level, the chaotic fluctuation stops. A smaller number, 15% of those who used menopausal hormone therapy, also reported improvement in hEDS symptoms [2]. But the majority reported no improvement, and the study had significant limitations, including its observational nature and relatively small postmenopausal subgroup. What it does suggest is that the hormonal instability of perimenopause, rather than simply low oestrogen per se, may be the primary driver of symptom worsening in this population.
There’s also the unpredictability factor, which is deeply underrated as a source of distress. Those with hypermobility have already spent years learning to read their bodies, working out which activities cause flares, which days to push and which days to rest. Perimenopause blows that system up. You can do everything right and still have a terrible day, because the variable you’ve been optimising around, your hormonal baseline, has become completely unstable. That’s genuinely demoralising, and it’s worth acknowledging before we get into the physiology.
POTS and Autonomic Changes During Perimenopause
For those with hypermobility who also have POTS or dysautonomia, perimenopause introduces a particularly complex set of challenges. The overlap between POTS symptoms and menopausal symptoms is striking, and it creates real difficulties in working out what’s going on and what to do about it.
A 2026 narrative review in the Journal of Clinical Medicine, specifically examining POTS, menopause, and hormone replacement therapy, laid out this overlap clearly [5]. Symptoms common to both POTS and perimenopause include heat intolerance, flushing, sleep disturbance, palpitations, headache, brain fog, fatigue, and mood changes. When these symptoms are appearing or worsening in a perimenopausal woman with POTS, distinguishing which condition is causing which symptom becomes genuinely difficult [5]. And the danger is that clinicians attribute everything to menopause and miss what might be a significant worsening of the underlying autonomic dysfunction.
Why does POTS worsen during perimenopause? Oestrogen plays a significant role in autonomic nervous system regulation. When oestrogen levels drop and fluctuate, there is evidence that sympathetic nervous system activity increases while parasympathetic activity decreases. The autonomic instability this creates overlaps substantially with the pathophysiology of POTS. In effect, the hormonal transition can tip an already vulnerable autonomic nervous system into greater dysregulation [5].
There’s also the blood volume angle. Oestrogen contributes to plasma volume maintenance. Declining oestrogen is associated with reduced plasma volume, which makes orthostatic symptoms worse. If you’re already dealing with the volume management challenges of POTS, losing one of your hormonal allies in maintaining that volume is not helpful at all.
Hot flushes are worth talking about separately here, because they’re not just an inconvenience. They represent an actual dysregulation of the hypothalamic thermostat, and for those with hypermobility who already have impaired autonomic thermoregulation, they can be genuinely debilitating. The autonomic nervous system dysfunction that makes heat intolerance a problem in hypermobility intersects with the hypothalamic dysregulation of perimenopause. Some women notice that cold intolerance also fluctuates more during perimenopause, which reflects the instability of thermoregulatory control in both conditions simultaneously. So yes, you can feel boiling hot one hour and freezing the next, and that’s not in your head.
Clinically, three patterns tend to be observed in perimenopausal women with POTS: symptoms worsen significantly during the transition, symptoms actually improve once hormones stabilise at lower postmenopausal levels, or new-onset POTS symptoms appear during the perimenopausal years for the first time [5]. That third pattern is important. Some women who were managing perfectly well with undiagnosed borderline autonomic dysfunction are pushed over the threshold into clinical POTS by the hormonal chaos of perimenopause. This isn’t a coincidence. It’s biology.
Palpitations deserve a specific mention because they’re one of the most alarming symptoms in this crossover territory. Heart palpitations are common in both perimenopause and POTS. The question of which is which matters clinically. Menopausal palpitations tend to be associated with hot flushes, occur more frequently in the evening, and often resolve without treatment. POTS-related palpitations are more consistently triggered by position change (particularly standing), tend to involve a rate increase of 30 beats per minute or more upon standing, and may be accompanied by other orthostatic symptoms. If you’re experiencing palpitations that are clearly position-dependent, it’s worth asking your doctor to check for orthostatic heart rate changes, not just to reassure you that it’s “just menopause.”
Pain: Central Sensitisation Meets Hormonal Disruption
When it comes to pain, the menopause transition creates a set of challenges that are distinct from but massively amplified by existing hypermobility-related pain sensitisation. Understanding this layering is important, both for managing the experience and for explaining it to healthcare providers who may be tempted to attribute everything to one cause.
First, the general population data. A 2020 systematic review and meta-analysis of 16 studies, covering 5,836 women, found that 71% of perimenopausal women reported musculoskeletal pain, with perimenopausal women being 1.63 times more likely to experience it than their premenopausal counterparts [3]. A more recent 2026 systematic review and meta-analysis covering 37 studies and 93,021 women across 22 countries found that over half of perimenopausal women (57%) and postmenopausal women (59%) experience muscle or joint pain, compared with 40% of premenopausal women [8]. That’s a 1.35-fold increased risk at perimenopause and a 1.40-fold increased risk postmenopause [8]. And again, this is in women without hypermobility. Now consider the baseline.
For those with hypermobility, the baseline pain experience is already shaped by central sensitisation. A 2021 review in The Lancet Rheumatology specifically noted that central sensitisation has been documented in Ehlers-Danlos syndrome, fibromyalgia, and other chronic pain conditions [7]. Central sensitisation means the pain-processing system is already running hot. The nervous system has developed a kind of hypersensitivity where pain signals are amplified and thresholds for triggering pain responses are lowered [7].
Now layer on top of that the effects of perimenopause. Oestrogen receptors are distributed throughout the central nervous system, including in brain regions involved in pain processing. A 2025 review on gonadal hormone changes and chronic pain summarised the evidence on oestrogen and descending pain inhibition: oestrogen appears to modulate the activity of the periaqueductal grey, a key region in the brain’s descending pain inhibitory pathways [13]. When oestrogen levels drop and fluctuate, these pain-modulating effects become disrupted. The brain’s ability to damp down pain signals is reduced [13]. For someone with an already sensitised pain system, this disruption can tip the balance significantly.
The fibromyalgia overlap is worth flagging here, because there’s a clinical pattern that we see repeatedly: women who are going through perimenopause get a new diagnosis of fibromyalgia. This isn’t a coincidence. Fibromyalgia most often develops during the menopausal transition, and the mechanisms for why are becoming clearer. The combination of oestrogen withdrawal affecting descending pain inhibition, disrupted sleep amplifying central sensitisation, and anxiety driving nervous system hyperreactivity creates conditions where fibromyalgia symptoms are almost inevitable in vulnerable individuals [3][7]. If you received a fibromyalgia diagnosis during your perimenopausal years, and you also have hypermobility, it’s worth considering that these are not separate conditions. They’re overlapping manifestations of the same sensitised nervous system responding to a hormonal transition.
Then there’s the muscle and joint pain that’s harder to characterise. Is it the hypermobility? Is it the menopause? The honest answer is usually both, and trying to attribute every symptom to one cause or the other isn’t particularly useful. What matters is understanding that both are real, both are physiological, and both respond, at least in part, to the same management approaches: exercise to maintain muscle stability, sleep protection, nervous system downregulation, and appropriate hormonal support where relevant.
Fatigue, Sleep, and the Brain Fog You Can’t Describe
Brain fog in hypermobility is something we’ve covered in detail in our article on brain fog in EDS and POTS. Perimenopause adds its own distinct contribution to this, and for many women, it’s the symptom that scares them most because it feels like something fundamental is changing in how their mind works.
Oestrogen receptors are present in the prefrontal cortex, hippocampus, and other regions involved in memory and executive function. The 2015 Brinton et al. review described oestrogen loss as associated with a 15-25% decline in brain metabolic function in some areas [4]. Oestrogen fluctuation during perimenopause disrupts working memory, processing speed, and word-finding ability. The resulting cognitive symptoms sit directly on top of the autonomic and sleep-related brain fog that many with hypermobility already experience [4]. It’s layered, and the layers are not always distinguishable.
Sleep is where so much of this intersects. A 2018 review on sleep and the menopausal transition found that subjective sleep disturbance affects 40-60% of perimenopausal women, driven by night sweats, insomnia, and hormonal effects on sleep architecture [16]. Progesterone, in particular, has sleep-promoting effects through its metabolites, which bind to GABA-A receptors in the brain. As progesterone declines during perimenopause, this natural sleep aid disappears [16]. Oestrogen fluctuations trigger hot flushes that wake women from sleep, often multiple times per night. A 2025 narrative review confirmed that vasomotor symptoms are among the primary disruptors of sleep quality during perimenopause, alongside changes in circadian rhythm regulation [15].
For those with hypermobility, who already struggle with poor sleep quality due to pain, autonomic arousal, and sensory processing differences, this additional hit is particularly brutal. Our article on hypermobility and sleep covers the baseline challenges in detail, but the short version is this: poor sleep and pain exist in a bidirectional relationship. Poor sleep amplifies central sensitisation. Worsened pain disrupts sleep. Perimenopause often kicks this cycle into high gear precisely when the hypermobile nervous system is least equipped to handle it [4].
The fatigue that results is different from ordinary tiredness. It’s the bone-deep, unrestorative exhaustion that those with hypermobility know well, but amplified. The body is working harder to regulate itself. The hormonal fluctuations are metabolically expensive. The disrupted sleep means recovery never quite happens. And then there are the demands of daily life on top of all of that. The pacing strategies that work in hypermobility become more, not less, important during perimenopause, but they may also need recalibrating. What felt sustainable before may not be sustainable during the transition, and that’s not a failure. It’s a physiological reality.
Mast Cells, Oestrogen, and the MCAS Flare Nobody Warned You About
For those who also have mast cell activation syndrome, perimenopause may introduce a layer of complexity that’s genuinely baffling if you don’t understand the mechanism. And the mechanism is this: oestrogen directly activates mast cells.
A 2012 review in Frontiers in Immunology examined the role of female sex hormones in mast cell behaviour [12]. The authors found that oestrogen, acting via oestrogen receptor alpha in a non-genomic pathway, can trigger calcium influx and mast cell degranulation, promoting histamine release and other inflammatory mediator release. Progesterone appears to have a somewhat stabilising effect on mast cells [12]. This creates a predictable pattern across the menstrual cycle: the first half of the cycle (follicular phase), when oestrogen is rising and progesterone is low, may be associated with more MCAS-type reactivity in susceptible individuals. The luteal phase, when progesterone is higher, may feel more stable. And then, the sharp oestrogen drop just before menstruation can trigger another wave of mast cell activation.
Now, what happens during perimenopause? The oestrogen spikes that characterise early perimenopause can, in theory, drive increased mast cell degranulation. Some women notice that their histamine intolerance worsens significantly during this time, with reactions to foods and environments that they’d previously tolerated fine. This is not necessarily a new condition developing. It may be the existing MCAS becoming more volatile due to hormonal instability [12].
I need to be honest here: the research specifically on MCAS and perimenopause in women with hEDS is essentially non-existent. What we have is the mechanistic data on oestrogen and mast cells, combined with widespread clinical observation that MCAS symptoms tend to worsen during the perimenopausal transition in women who have it. There are no randomised controlled trials. There is no agreed treatment protocol for managing MCAS specifically in perimenopause. What clinicians typically do is focus on MCAS management as usual (antihistamines, mast cell stabilisers, trigger avoidance) while also addressing the underlying hormonal instability where appropriate.
What does this mean practically? If you have MCAS and you’re entering perimenopause, it’s worth having a conversation with your team about whether your MCAS management needs to be adjusted during this transition. Tracking symptoms in relation to your cycle (while you still have one) can help identify patterns. And being aware that hormonal fluctuations may be driving flares, not just the usual environmental triggers, can help you make sense of why some days are so much worse than others for no apparent reason.
Bone Health: A Risk That Compounds With EDS
Bone health is one of those things that feels distant and abstract when you’re dealing with immediate problems like pain, fatigue, and POTS. But for those with hypermobility, it deserves serious attention during the perimenopausal years, because the risk profile is more complex than it is in the general population.
Oestrogen is a key regulator of bone density. Postmenopausal oestrogen deficiency accelerates bone loss, and this is a well-established risk factor for osteoporosis. But here’s the thing about EDS: the bone density picture in this population is already complicated before menopause even enters the equation. A 2022 study published in the Journal of Clinical Densitometry examined bone mineral density in 18 premenopausal women with hEDS or HSD and 18 matched controls [14]. The women with hEDS/HSD had significantly lower bone mineral density at the femur and lumbar spine compared to controls, despite being premenopausal and age-matched [14]. This matters because it means those with hypermobility may be starting from a lower bone density baseline when they reach the menopause transition.
A 2016 study published in Bone added further complexity. Examining 52 consecutive EDS patients, the researchers found that vertebral fractures were significantly more prevalent in EDS patients compared to controls (38.5% versus 5.1%), and crucially, this elevated fracture risk was not reliably predicted by standard bone mineral density measurements [17]. Bone quality, not just bone quantity, appears to be impaired in EDS [17]. Standard DEXA scan results may underestimate the true fracture risk in this population. The altered collagen structure that defines EDS may affect bone quality in ways that aren’t captured by density measurements alone.
What does this mean for someone with hEDS approaching perimenopause? It means bone health is not a “deal with it later” issue. It means asking your GP for a DEXA scan earlier than you might otherwise, particularly if you have any of the additional risk factors: low body weight, GI complications affecting nutrient absorption, limited exercise tolerance, or a history of stress fractures. It also means that bone-loading exercise, the kind that stimulates bone density maintenance, is non-negotiable during and after the perimenopausal transition. You need to be building on whatever bone capital you have while oestrogen is still present, because the accelerated loss phase is coming.
Vitamin D and calcium matter here too. Vitamin D deficiency is common in those with chronic pain conditions who tend to limit outdoor activity, and it’s essential for bone health. Getting your vitamin D levels checked and supplementing appropriately if needed is a simple intervention that’s entirely evidence-based. Calcium intake from diet is preferable to supplementation for most people, but if dietary calcium is genuinely inadequate, supplementation is reasonable. These are the fundamentals, not the whole story, but skipping them is not an option when you’re already at elevated risk. Our article on EDS and ageing covers some of this longer-term picture in more depth.
The Pelvic Floor: Already Compromised, Now Under More Pressure
When it comes to the pelvic floor and hypermobility, the challenges start well before menopause. For those with hEDS and HSD, the pelvic floor is connective tissue just like everywhere else, which means the same collagen dysfunction that affects joints affects the fascial support structures of the pelvis. A 2023 international survey study of cisgender women with EDS found that pelvic floor dysfunction was nearly universal in this population, with high rates of urinary incontinence, pelvic organ prolapse, bladder pain, and sexual dysfunction [18]. A 2026 narrative review for urogynaecologists noted that meta-analytic data now shows a more than twofold increased risk of pelvic organ prolapse in women with joint hypermobility syndrome [19].
Now add menopause into this picture. Oestrogen receptors are present throughout the pelvic floor: in the vaginal epithelium, the urethral sphincter, the levator ani muscles, and the pelvic ligaments. When oestrogen declines postmenopause, all of these tissues change. The vaginal and urethral epithelium atrophies. The pelvic ligaments lose some of their tone. The levator ani becomes less responsive. This is the genitourinary syndrome of menopause (GSM), and it dramatically increases the risk of both prolapse and urinary incontinence in the general population.
For those with hypermobility, where pelvic floor support is already compromised, this is a compounding risk that deserves specific attention. Prolapse that was mild or subclinical may become symptomatic. Stress incontinence that was manageable may become problematic. Pelvic pain may worsen as tissues that were providing some support lose their hormonal stimulus [19].
What can be done? First, vaginal oestrogen. This is one of the most consistently evidence-based interventions available and carries negligible systemic absorption. Local vaginal oestrogen (in the form of pessaries, cream, or a ring) maintains the health of the vaginal and urethral tissues without the same risk considerations as systemic HRT. The NICE menopause guideline supports its use and notes that it can be used long-term. For those with hEDS who have significant urogenital symptoms, this is a conversation worth having with your GP proactively, not waiting until symptoms are severe.
Second, pelvic floor physiotherapy. The evidence for pelvic floor physiotherapy in both incontinence and prolapse is solid. For those with hypermobility, the approach needs to be tailored, because the goal isn’t just strength, it’s coordination and appropriate tone. An overactive or inappropriately tense pelvic floor can be as problematic as a weak one, and in hypermobility, both presentations are common. If you haven’t already connected with a pelvic physiotherapist who understands connective tissue disorders, doing so before or during perimenopause rather than after a prolapse has become significant is preferable. Our pelvic and core stability content provides some of the background, but working with a specialist is worth it for this area specifically.
Mental Health: The Layer Nobody Talks About Enough
Anxiety and hypermobility are already closely linked, and we’ve covered the mechanisms in our article on hypermobility and anxiety. The short version is that the same autonomic nervous system dysfunction that drives POTS also primes the nervous system for heightened threat-detection and anxiety responses. Many people with hEDS report anxiety as one of their most burdensome symptoms, often out of proportion to what they’d expect given their psychological circumstances.
Perimenopause adds to this significantly. Oestrogen modulates serotonin, dopamine, and GABA activity in the brain. When oestrogen drops and fluctuates, these neurotransmitter systems become destabilised. The result is that perimenopause is associated with markedly increased rates of new-onset anxiety, depression, and mood instability, even in women with no previous mental health history. For those who already have hypermobility-linked anxiety, this is not a theoretical risk. It’s a practical certainty that their existing anxiety is going to worsen during perimenopause, at least for a period.
There’s something else worth naming here, and it’s the experience of medical gaslighting. Women with hypermobility are already statistically more likely to have their symptoms attributed to anxiety, stress, or “just being that way.” During perimenopause, a new version of this emerges: “it’s just menopause.” Symptoms that represent genuine worsening of POTS, connective tissue instability, or MCAS get written off as menopausal. The worsening brain fog gets attributed to hormones rather than to a combination of hormonal and autonomic factors. This is frustrating, and it delays appropriate management.
The honest reality is that yes, menopause is contributing. And so is the hypermobility. And both deserve to be taken seriously. If you find yourself being told that everything is “just menopause,” it’s worth asking specifically: “Could this symptom also be related to my connective tissue disorder, and if so, what should we be doing about it?” Finding clinicians who understand both is the ideal, and we’ll address that below. Finding them can take effort, but it’s worth it.
There’s also a grief and identity dimension here that I don’t want to skip over. Many people with hypermobility spend years getting to a place of stability: understanding their body, finding management strategies that work, accepting the limitations and working within them. Perimenopause can feel like starting over. The body you’d finally learned to manage is changing again, and the rules have shifted. That’s genuinely hard. It doesn’t need solving with an evidence-based study. It needs acknowledging.
HRT: The Full Picture for Those With Hypermobility
This is the question that most people want answered, and the honest answer has to start with this: there are no randomised controlled trials specifically examining HRT in women with hEDS or HSD. None. The evidence base simply doesn’t exist yet. Anyone who tells you definitively that HRT will help your hypermobility, or definitively that it will harm it, is going beyond what the evidence actually supports.
What we do have is observational data from the 2016 cohort study of 386 women with hEDS [2]. Of the postmenopausal women in that group, 42% had used menopausal hormone therapy. Of those who used it, 15% reported an improvement in their hEDS symptoms, while the majority reported no change. Some reported worsening. The study was observational, the sample size for the postmenopausal subgroup was relatively small, and we can’t draw firm conclusions. What it suggests is that adding oestrogen back in doesn’t consistently improve hypermobility symptoms, but it doesn’t appear to worsen them in most cases either [2].
There’s a theoretical concern that systemic oestrogen supplementation, by further reducing tendon and ligament stiffness via LOX inhibition, could worsen joint laxity in hypermobile individuals [1][5]. This is biologically plausible. But the evidence that this specifically causes clinical harm in people with hEDS who use HRT is extremely limited. It’s a mechanism to be aware of and to discuss with your doctor, not a reason to categorically avoid HRT.
Transdermal vs Oral: Why Route Matters
If someone with hypermobility and POTS is going to use systemic HRT, the form it takes matters significantly. A large nested case-control study published in the BMJ in 2019, using data from over 80,000 women in the QResearch and CPRD databases, found that oral HRT was associated with a significantly increased risk of venous thromboembolism (adjusted odds ratio 1.58 compared to no HRT), while transdermal preparations were not associated with any increased VTE risk [20]. This is a crucial distinction [20].
Why? Oral oestrogen undergoes first-pass liver metabolism, which increases coagulation factors including fibrinogen and factor IX, and reduces natural anticoagulants. Transdermal oestrogen bypasses the liver and avoids these coagulation changes. For those with hypermobility who may have some vascular vulnerability, who are less active due to their condition and therefore already at somewhat higher VTE risk, and who may have autonomic instability that affects vascular tone, the preference for transdermal oestrogen is logical and well-supported by evidence [20].
The 2026 review on POTS and menopause reached similar conclusions, noting that transdermal oestrogen is preferable for those with POTS or autonomic dysfunction, and that it also provides more stable oestrogen levels without the peaks and troughs of oral dosing [5]. Stable levels matter particularly for those who react badly to hormonal fluctuations.
Body-Identical vs Synthetic Progestogens
For women with a uterus, oestrogen must be combined with a progestogen to protect the uterine lining. The type of progestogen matters. Micronised progesterone (body-identical progesterone, sometimes called Utrogestan in the UK) appears to have a more favourable profile for sleep and anxiety compared to synthetic progestins like norethisterone or medroxyprogesterone acetate. Progesterone metabolites bind to GABA-A receptors and have anxiolytic and sleep-promoting effects. For someone who is already dealing with anxiety and sleep disruption, this distinction is clinically meaningful [5][16].
Synthetic progestins don’t have the same GABA effects. Some women find that certain synthetic progestins worsen mood, anxiety, and sleep. If you’ve tried HRT and felt worse on the progesterone component, it may be worth discussing whether switching to micronised progesterone is possible.
Testosterone: The Forgotten Hormone
Testosterone is often overlooked in the menopause conversation, but it’s worth understanding what it does and why it might matter for those with hypermobility. Women produce testosterone in the ovaries and adrenal glands throughout their lives. Levels gradually decline with age and drop more abruptly following oophorectomy (surgical menopause). By the time most women reach natural menopause, they’ve already lost a significant proportion of their testosterone relative to their younger years.
A 2020 guide published in the British Journal of General Practice summarised the clinical evidence for testosterone supplementation in perimenopausal and postmenopausal women [21]. The authors noted that the most commonly described symptoms of androgen insufficiency include unexplained fatigue, dysphoric mood, changes in sexual function, cognitive changes, vasomotor symptoms, bone loss, and decreased muscle strength [21]. A 2024 pilot study examining transdermal testosterone therapy in 510 perimenopausal and postmenopausal women at a UK menopause clinic found that mood improved in 47% of women and cognition improved in 39%, with significant improvements also noted in libido and energy over a four-month period [21].
For those with hypermobility, the specific relevance of testosterone is in muscle strength and tone. Muscle strength is the primary mechanism by which people with hypermobility protect their joints. When testosterone declines, maintaining muscle mass becomes harder. The combination of declining testosterone and the general deconditioning risk of perimenopause (when exercise often drops off because everything feels harder) creates a real risk of significant muscle loss at exactly the time when muscle is most needed.
Testosterone supplementation for women isn’t currently licensed in the UK as a specific product, but it can be prescribed off-label. NICE guidance supports considering testosterone supplementation for women with low sexual desire if HRT alone isn’t effective. Some menopause specialists will consider it more broadly for the symptoms described above. It’s worth raising with a menopause specialist if fatigue, cognitive symptoms, and muscle weakness are prominent concerns.
Vaginal Oestrogen
Vaginal oestrogen deserves specific mention because it’s often underused, it has minimal systemic absorption, and it significantly reduces the urogenital symptoms that particularly affect those with hypermobility-related pelvic floor dysfunction. Vaginal dryness, urethral discomfort, recurrent urinary tract infections, and dyspareunia are all amenable to vaginal oestrogen. It can be used safely by women who aren’t using systemic HRT, and it can be used long-term. If you’re experiencing urogenital symptoms, don’t wait for them to become severe. Ask your GP specifically about local vaginal oestrogen.
The Timing Window
There’s a concept sometimes called the “window of opportunity” in menopause medicine: the idea that HRT started early in the menopausal transition may have benefits (particularly cardiovascular and cognitive) that are not available when it’s started later. The evidence here is complex and still evolving, but what it suggests practically is that having the HRT conversation with your doctor during perimenopause, rather than waiting until well after menopause, gives you more options and likely more potential benefit. If you’re 45 with irregular cycles and increasing symptoms, now is the time to have that conversation. Not at 60 when the symptoms have become entrenched.
What to Discuss with Your GP
When you have an HRT conversation with your GP, specific information will help get you the most appropriate response. Tell them you have hypermobility or EDS, and why that changes the conversation (connective tissue effects, POTS if relevant, VTE risk considerations). Ask specifically about transdermal rather than oral oestrogen. Ask about micronised progesterone rather than synthetic progestins, particularly if sleep and anxiety are concerns. Ask about vaginal oestrogen for urogenital symptoms regardless of whether you’re taking systemic HRT. If your GP isn’t familiar with the hypermobility-specific considerations, asking for a referral to a menopause specialist who can take a more nuanced view is entirely reasonable. The British Menopause Society maintains a directory of accredited practitioners.
What Actually Helps: Practical Management for the Hypermobile Perimenopausal Body
Here’s what we can say with reasonable confidence actually helps, based on the available evidence and clinical experience with hypermobile bodies specifically. Some of this overlaps with general menopause management. Some of it is specific to the combination of hypermobility and hormonal transition.
Resistance Training Becomes Non-Negotiable
The temptation during perimenopause is to reduce activity because everything feels harder and more unpredictable. This is understandable, and it’s also one of the worst things you can do for a hypermobile body. Muscle strength is your primary joint stability mechanism. When muscle declines, joints become less supported, pain increases, and the fear of movement often follows. Core stability work and progressive resistance training become more important during the perimenopausal transition, not less.
There’s also the bone health angle. Loading exercises stimulate bone density maintenance. For someone approaching postmenopause, when oestrogen-mediated bone loss accelerates, maintaining consistent bone-loading activity is important. This needs to be done appropriately for a hypermobile body: progressive loading, good proprioceptive training, appropriate range of motion guidance, and building from a foundation rather than jumping to heavy loads. Our articles on exercise for hypermobility and managing fear of movement cover the principles. If POTS is a factor, starting with supine or semi-reclined positions and gradually progressing remains the right approach. The principles don’t change during perimenopause, but the execution may need adjustment if symptom levels have increased.
Proprioception and Hormonal Fluctuations
Proprioception, the body’s sense of position in space, is already impaired in hypermobility. During periods of hormonal fluctuation, when joint laxity is less predictable, proprioceptive training becomes even more valuable. Balance work, slow controlled movements, and exercises that challenge position sense help the nervous system adapt to a changing joint environment. This is not glamorous rehabilitation, but it’s genuinely protective against the increased injury risk that comes with perimenopausal tissue changes.
Sleep Is Not Optional, But It’s Hard
We know this is easier said than done when you’re having night sweats and hormonal insomnia. But given the bidirectional relationship between sleep and pain, central sensitisation, and cognitive function, protecting sleep quality during perimenopause is one of the most valuable interventions available. This includes environmental temperature management (cooling mattress toppers, fans, lightweight bedding), sleep hygiene fundamentals, and addressing any identifiable triggers for waking. The hypermobility and sleep article covers the practicalities in depth. If sleep disruption is severe, a conversation with your GP about short-term pharmacological support is worth having. Micronised progesterone, if you’re on HRT, has sleep-promoting effects as noted above. Melatonin may help with sleep initiation. These aren’t magic bullets, but they can make a meaningful difference.
Supplements With Reasonable Evidence
Creatine is probably the most interesting supplement in this space. There’s emerging evidence that creatine supplementation is particularly relevant during menopause and perimenopause, as oestrogen is thought to influence creatine uptake in muscle tissue and postmenopause is associated with reduced creatine synthesis. Some evidence from general menopause research suggests creatine may help preserve muscle mass, strength, and bone density during the postmenopausal transition. Our article on creatine for hypermobility and EDS covers the broader evidence, and this is one area where the interests of menopause management and hypermobility management genuinely converge.
Magnesium is worth considering for sleep and muscle function. There’s reasonable evidence for magnesium glycinate or bisglycinate in supporting sleep quality and reducing muscle cramping and tension. Many people with hypermobility are functionally low in magnesium due to increased musculoskeletal demand on this mineral, and perimenopause adds another reason to ensure adequate intake.
Vitamin D and calcium for bone health, as discussed above. Not exciting, not novel, but genuinely necessary. Get your vitamin D level checked. Supplement if it’s low. Maintain adequate dietary calcium. These are the fundamentals that enable everything else to work.
Volume Management and Compression Garments
For those with POTS or significant orthostatic symptoms, the perimenopausal reduction in plasma volume can worsen standing tolerance substantially. The fundamentals of fluid and salt intake for POTS management become even more important during this transition. Likewise, compression garments, particularly waist-high compression, can provide meaningful support for orthostatic symptoms. If you were previously getting away with knee-high compression, it may be worth trying waist-high during the perimenopausal transition and seeing if that makes a difference.
Cooling Strategies for Thermoregulation
For those dealing with both the temperature dysregulation of EDS/POTS and the hot flushes of perimenopause, cooling strategies are worth taking seriously. Cooling vests can help during exercise and on hot days. Cold water on the wrists and neck during a flush can help activate the diving reflex and reduce the severity. Breathable, moisture-wicking clothing matters more than it used to. Keeping rooms cooler, particularly the bedroom, is genuinely helpful. None of this is glamorous, but when thermoregulation is failing from two different directions simultaneously, these practical interventions make a real difference to daily quality of life.
Pacing Recalibration
Perimenopause is a genuine increase in physiological load. The dysregulated sleep, the hormonal fluctuations, the increased pain sensitivity, the autonomic instability: all of this requires more from your energy reserves, not less. If you were at your activity limit before perimenopause, you may need to reassess your baseline. This is not defeat. It’s sensible adaptation to a changed physiological context. The pacing frameworks that apply in hypermobility are more relevant during this transition, not less, and applying them to the new reality is a practical act of self-management.
When to Seek Specialist Support
There are situations where the interaction between hypermobility and the perimenopausal transition warrants specialist input rather than self-management and general GP care alone.
If your POTS symptoms are significantly worsening during perimenopause, a conversation with a cardiologist or autonomic specialist with knowledge of hypermobility disorders is worth seeking. The evolving landscape of EDS diagnosis and recognition means that finding clinicians with genuine expertise is becoming somewhat easier, though it still requires persistence in most healthcare systems.
If you’re considering HRT, ideally speak with a doctor who has experience in menopause medicine and understands connective tissue disorders. The British Menopause Society maintains lists of accredited practitioners. Not every GP has the level of expertise needed to navigate this combination of conditions, and it’s entirely reasonable to ask for referral to a menopause specialist. Frankly, given how complex the interplay is, you deserve someone who understands both sides of the picture.
If pain levels during perimenopause are significantly above your usual baseline and are not responding to your established management approaches, this is worth investigating rather than simply attributing to hormones. Increased pain that doesn’t track with the hormonal cycle and doesn’t respond to standard management deserves proper assessment. Likewise, if pelvic floor symptoms are worsening, a referral to a pelvic floor physiotherapist with experience in EDS is worth pursuing.
The Research Gap: Why We Don’t Have Better Answers
It’s worth saying explicitly: the research on menopause and hypermobility is genuinely thin. There are no randomised controlled trials. Most of what we know comes from observational studies, patient-reported data, and mechanistic research that we’re extrapolating to this population. The 2016 cohort study of 386 women with hEDS [2] is one of the most-cited papers in this space, and it’s a useful starting point, but it has real limitations. The 2026 review on POTS and menopause [5] is helpful for those with dysautonomia, but it’s a review of existing evidence rather than new clinical trial data specific to hypermobility.
Why is this? Women’s health research is underfunded generally. Rare condition research is underfunded generally. When you put the two together, you get a research gap that’s substantial and that leaves clinicians managing patients without clear guidance. The EDS Society has called for accelerated research into women’s health and hypermobility disorders. There are researchers working on this. But we’re probably at least a decade away from having the kind of large, well-designed studies that would give us definitive answers on HRT in hEDS, or on specific management protocols for perimenopause in this population.
In the meantime, we have to work with what we know, be honest about what we don’t, and be thoughtful about applying evidence from adjacent populations to this specific one. Which is what this article has tried to do. Where evidence exists, we’ve cited it. Where it doesn’t, we’ve said so and explained the clinical reasoning. That’s the best we can offer right now, and it’s considerably better than either pretending the evidence is stronger than it is, or throwing up our hands and saying nothing can be known.
Frequently Asked Questions
For many women it does, particularly during the perimenopause transition when oestrogen levels fluctuate unpredictably. A 2016 cohort study of 386 women with hEDS found that the majority reported no improvement or worsening after menopause, though 22% did report improvement once hormones stabilised. The chaotic hormonal fluctuations of perimenopause tend to be more disruptive than low but stable postmenopausal oestrogen levels. The evidence is limited and individual variation is significant.
There are currently no clinical trials specifically examining HRT in women with hEDS or HSD. The available observational data suggests that a minority of women with hEDS report improvement in their symptoms on HRT, but the majority report no change. HRT may help with the menopausal symptoms that compound hypermobility difficulties, such as sleep disruption, pain amplification, and autonomic instability, but it is not a treatment for hypermobility itself. If HRT is appropriate for you for menopausal reasons, transdermal oestrogen with micronised progesterone is generally preferred for those with connective tissue disorders. Discuss the full picture with a menopause specialist who understands your condition.
Several mechanisms appear to be involved. Oestrogen plays a role in maintaining plasma volume, and declining oestrogen reduces blood volume, worsening orthostatic symptoms. Oestrogen also modulates autonomic nervous system function, and its fluctuation tends to increase sympathetic activity. Additionally, the vasomotor symptoms of perimenopause, including flushing, palpitations, and heat intolerance, overlap substantially with POTS symptoms, making it difficult to distinguish what is driving what at any given moment. Many women with POTS find that once hormones stabilise postmenopause, POTS becomes more manageable, though this is not universal.
Based on current evidence, transdermal oestrogen carries a significantly lower risk of venous thromboembolism than oral oestrogen, because it bypasses first-pass liver metabolism and does not increase clotting factors in the same way. A large 2019 nested case-control study found oral HRT was associated with a 58% increased VTE risk compared to no HRT, while transdermal HRT showed no significant increase in risk. For those with hypermobility who may have vascular vulnerability and reduced mobility, this distinction matters. Transdermal formulations also provide more stable hormone levels, avoiding the peaks and troughs that oral dosing can produce. That said, no formulation has been specifically studied in hEDS or HSD populations.
Oestrogen directly activates mast cells via oestrogen receptor alpha, promoting histamine release and degranulation. Progesterone has a somewhat stabilising effect on mast cells. During perimenopause, the erratic oestrogen spikes and declining progesterone can drive increased mast cell reactivity in susceptible individuals. This means histamine intolerance may worsen, and reactions to previously tolerated triggers may become more frequent. There are no randomised controlled trials specifically examining MCAS management in perimenopausal women with hEDS, but the mechanism is well-documented in the immunology literature. Working with your clinical team to adjust MCAS management during this transition is appropriate.
Several evidence-based approaches are available. Vaginal oestrogen (pessaries, cream, or ring) has minimal systemic absorption and significantly helps with urogenital tissue health, reducing incontinence, recurrent UTIs, and discomfort. It can be used long-term and does not carry the same risk considerations as systemic HRT. Pelvic floor physiotherapy with a specialist who understands connective tissue disorders is also worth pursuing: the goal is coordinated pelvic floor function, not just strength. If prolapse is becoming symptomatic, a referral to a urogynaecologist who is familiar with EDS and its implications for surgical risk is appropriate before proceeding to any surgical management.
Pulling It All Together
Perimenopause and hypermobility is one of those intersections where the research hasn’t caught up with the clinical reality, but we can piece together a reasonably clear picture from what we do know. Oestrogen matters for connective tissue, for autonomic function, for pain processing, for mast cell regulation, for pelvic floor support, and for sleep. When oestrogen becomes unstable and then declines, all of those systems are affected. And for those with hypermobility, the effects are amplified by an already compromised baseline.
What the research tells us, and what clinical experience reinforces, is that perimenopause is not a single event. It’s a transition that can last years, that affects every system simultaneously, and that requires a genuinely comprehensive management approach. There is no single intervention that fixes it, and that includes HRT. What there is, is a toolkit: exercise, sleep protection, volume management for POTS, mast cell management, pelvic floor attention, bone health monitoring, appropriate hormonal support where relevant, and the kind of pacing and self-management that those with hypermobility have usually already learned to do in some form.
The most important thing to take from this isn’t a definitive answer on HRT, because that decision is individual and the evidence base isn’t strong enough to make blanket recommendations. The most important thing is to understand the mechanisms well enough to have better conversations with your healthcare team, to stop blaming yourself for symptoms that have a genuine physiological basis, and to make informed adjustments to your management approach during this transition.
Don’t abandon your exercise. Protect your sleep where you can. Maintain your volume management strategies if you have POTS. Find a doctor who understands both menopause and connective tissue disorders, because that combination of knowledge is what you actually need. And be patient with yourself. This is a significant physiological transition, and it’s harder in a hypermobile body. That’s not weakness. That’s biology, and it deserves to be acknowledged as such.
If you want to explore rehabilitation support that’s specifically designed for those with hypermobility and EDS, our approach to exercise and rehabilitation is built around exactly this kind of complexity. Perimenopause adds a layer, but the foundations remain the same.
— The Fibro Guy Team —
