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].