PCOS to PMOS: What the New Name Means for Women with Hypermobility

• About
• Latest Posts

Adam Foster

Director at The Fibro Guy

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

Latest posts by Adam Foster (see all)

• PCOS to PMOS: What the New Name Means for Women with Hypermobility - 25 May 2026
• Hypermobility and Exercise Part 2: Proprioception, Brain Maps and Why Your Body Feels Lost - 19 May 2026
• Hypermobility, EDS and Constipation: Why Your Gut Won’t Cooperate and What Actually Works - 18 May 2026

Prague, 12 May 2026. One of the most common endocrine conditions in women got a new name. PCOS, the label that’s followed women around for decades, is now PMOS: Polyendocrine Metabolic Ovarian Syndrome [1]. Not a rebrand. A 14-year international consensus, 22,000 stakeholders, 195 countries, led by Helena Teede at Monash and the AE-PCOS Society [1]. Diagnostic criteria haven’t changed. Treatment recommendations haven’t changed [1, 2]. The framing has. And for the hypermobile community, framing matters. PMOS bumps up against a symptom set we already see day to day in our studios: pain that moves, fatigue that doesn’t shift, sleep that breaks, joints that complain. So this piece walks through what’s actually changed, what the science says, and what’s still missing.

What’s actually changed on 12 May 2026

Worth starting with the timeline. The noise around this rename has been loud. The substance, in most coverage, has been thin.

The announcement came at the European Congress of Endocrinology in Prague on 12 May 2026 [1]. The accompanying paper, in The Lancet that same day, formalised a name change that’s been quietly cooking for years [1]. Polyendocrine Metabolic Ovarian Syndrome. The new label deliberately moves the centre of gravity away from the ovary as the defining feature [1]. “Polyendocrine” because more than one hormone axis is involved. “Metabolic” because insulin and glucose handling are central to what’s going on. “Ovarian” because the location still matters, even if it isn’t the whole story. “Syndrome” because, well, that part stays [1, 3]. If you’re new here, our primer on what hypermobility actually is is a sensible starting point before going further.

Why the change? Because the word “cystic” has been misleading clinicians, women and policymakers for years [1]. The “cysts” the old name describes aren’t cysts in the way most people imagine. They’re small follicles on imaging, and they’re not even necessary for diagnosis [2, 1]. A 2026 commentary published in Metabolism Open puts it plainly: the rename reflects the metabolic and multi-endocrine reality of the condition rather than the ovarian morphology that gave it its old name [3]. And a 2025 commentary in Endocrinology and Metabolism, looking at the 2018 to 2023 guideline shift, had already started shifting the diagnostic emphasis in the same direction, with AMH allowed as an alternative to ultrasound in adults, simpler algorithms, explicit recognition of weight stigma, and elevated mental health screening at diagnosis [4].

A 2025 longitudinal international online survey in eClinicalMedicine asked women living with the diagnosis and the clinicians treating them whether the name needed to change [5]. The answer was clear. Strong support, on both sides, for replacing the term [5]. The “cystic” bit, in particular, came in for stick. If you want a sense of who we are and why we write these pieces from a rehab angle rather than a clinical one, that’s worth a minute.

On the actual diagnostic criteria? Nothing’s been ripped up. The Rotterdam approach still stands: two of three out of hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology (with AMH allowed instead of ultrasound in adults) [2]. The 2018 international guideline that established Rotterdam as the global diagnostic standard hasn’t been thrown out, it’s been built on [6]. Treatment principles also haven’t moved. Lifestyle interventions remain first line. Letrozole stays first line for ovulation induction. Psychological screening at diagnosis is still mandated [2].

What’s different is the three year transition timeline. Full uptake is tied to the 2028 International Guideline update and the ICD-11 alignment that follows [1]. If you’re sitting in front of a GP who still says PCOS for the next while, that’s expected. Adoption is gradual. It always is.

Wider context worth flagging. PCOS, now PMOS, is one of the most common endocrine conditions affecting women, with around 1 in 8 women globally meeting diagnostic criteria [1]. A lot of women, carrying a diagnosis whose name was misleading them, their doctors, and the policymakers writing screening protocols. The clinical community has been edging toward this rename for years. The 2018 international guideline tightened diagnostic clarity [6]. The 2023 update broadened the diagnostic options (AMH as an alternative to ultrasound) and explicitly elevated mental health screening at diagnosis [2, 4]. The 2026 rename is the next logical step in the same direction.

The bit worth sitting with is the reframing itself. “Metabolic” pulls the conversation toward insulin resistance, androgen excess and chronic low grade inflammation [3, 7, 8]. “Polyendocrine” forces clinicians to stop thinking ovary first and start thinking hormones across systems [3]. The moment we start thinking hormones across systems, the people in our studios with hypermobility, EDS, hEDS and the whole HSD spread start to look very relevant.

Why this matters specifically if you’re hypermobile

Hormones and connective tissue aren’t separate systems. Shared receptors. Shared inflammatory pathways. Shared insulin and androgen signalling. So a condition framed as hormonal and metabolic, sitting alongside a condition framed as connective tissue, almost certainly overlaps at the biological level. Long before we get to symptom overlap.

Here’s where it gets interesting. Hypermobility isn’t an isolated thing. It clusters. A 2024 review pulled together the data showing hypermobility detected in 30 to 57% of people with ME/CFS, fibromyalgia, POTS and Long COVID [9]. That’s a lot of overlap. And the proposed shared pathophysiology (connective tissue fragility, mast cell activation, dysautonomia, systemic inflammation) is the same biological neighbourhood PMOS science is now wandering into [9].

We’ve got plenty of evidence the hypermobile population carries elevated multisystem disease burden. A US claims database of nearly 20,000 young people with hEDS, matched against a control pool of nearly 5 million, found endocrine disorders significantly more common in the hypermobile group [10]. Gastrointestinal hit 54.6% versus 28.5% in controls. Cardiovascular 43.6% versus 10.3%. Anxiety around 25% versus 15% [10]. The endocrine category, the one most relevant for PMOS, sat elevated too [10].

Then there’s the gynaecological story specifically. A 2016 French cohort study (Paris) followed 386 women with joint hypermobility syndrome and hypermobile EDS. Single arm, no control group, but the in-cohort frequencies are striking: menorrhagia in 76%, dysmenorrhoea in 72%, dyspareunia in 43% at intromission, and endometriosis in 6% [11]. A 2019 scoping review of 105 studies covering pelvic and urogenital complications in EDS reported pelvic organ prolapse and urinary incontinence each in 45% of the included studies, with dyspareunia in 36% and dysmenorrhoea in 27% [12]. A 2023 narrative review of female reproductive health across Long COVID and associated illnesses (ME/CFS, POTS and EDS) reported dysmenorrhoea in around 72% of women with EDS, dyspareunia in 43% to 64%, and noted elevated rates of ovarian cysts, pelvic congestion, uterine fibroids and endometriosis in the wider ME/CFS and POTS cohorts overlapping with EDS [13]. A 2024 cluster analysis of a hEDS registry identified phenotypic clusters that included endocrine and reproductive comorbidities [14]. An online cross sectional survey of 1,146 women with EDS and HSD reported probable vulvodynia at roughly 50% against an 8% general population figure, and within the subset reporting painful intercourse, 47.5% also reported ovarian cysts, fibroids or abdominal/pelvic scarring [15].

That’s a lot of signal. Here’s the catch. None of it adds up to a published prevalence rate of PCOS (or PMOS, going forward) inside a hypermobile cohort. Nobody’s done the dual diagnosis prevalence study. We can’t tell you that X% of women with hEDS have PMOS. What we can tell you, honestly, is this: the symptom overlap is meaningful, the mechanisms are plausible, the clinical experience is consistent, and the formal prevalence work hasn’t been done yet. The clustering picture in the hypermobility population is well documented elsewhere, including in our overview of the POTS, EDS and MCAS trifecta.

Had a client last month. Runner, early thirties, diagnosed hEDS. She’d been told for two years that her cycle related joint flares were “just hormonal”. Separately, she’d been told her acne, irregular periods and fatigue were “probably PCOS, mild”. Two different doctors, two different filings, no joined up picture. She’s not unusual. We see this a lot. The women walking in with the hypermobility label are also, frequently, the women walking in with a PCOS or now PMOS file open in another corner of their record, and nobody’s holding the two together.

That’s the gap this piece is trying to nudge. Not by claiming we know more than the literature does, but by pointing out that two stories the medical system tells in separate offices are almost certainly the same story, told from different angles.

The shared biology: androgens, insulin resistance, and connective tissue

Right. The mechanism bit. Patience needed, because the science here is genuinely interesting but also, almost entirely, mechanism level rather than clinical outcome level. Most of what follows is cell, tissue or laboratory work, with a couple of clinical cross sections. None of it has been done in a hypermobile PCOS or PMOS cohort yet. Treat it as a plausible biological story that maps onto what we observe in practice. Not as a clinical claim.

The androgen and insulin feed forward loop

The metabolic part of PMOS isn’t decorative. Androgen excess in PCOS directly impairs insulin signalling in muscle, fat and liver, which raises insulin. High insulin then raises androgen production further [7]. A feed forward loop. It’s been the central pathophysiological model in the better mechanism reviews for years [7].

A 2026 cross sectional study (n=445, single centre in China, 301 women with PCOS, 144 controls) made the point bluntly. HOMA-IR, the index of insulin resistance, independently predicted the hyperandrogenic phenotype, with adjusted odds ratio 1.35 and p value of 0.003 [8]. BMI, in the same multivariable model, did not [8]. Worth a second read. In that dataset, insulin resistance was driving the high androgen presentation regardless of body weight. Which is a big deal for hypermobile women. Often slim. Often told they “don’t look like” they’d have a metabolic problem. Under screened, as a result, for the metabolic side of things. For more on how the metabolic side intersects with day to day choices, our piece on diet and metabolic considerations in hypermobility goes further.

So the question we get a lot, “do I even need to think about insulin resistance if I’m not overweight?”, keeps getting answered the same way. Yes. The Wang 2026 data lines up with the broader PMOS literature [8, 7]. It also lines up with what we see in the studios. Slim hypermobile women with fatigue, cycle chaos, brain fog and joint flares who, when they finally get the metabolic markers checked, are sitting on insulin and androgen patterns nobody had bothered to chase.

What androgens might do to connective tissue

The dose specifics matter here, so slow down.

In laboratory work on human fascial cells, dihydrotestosterone applied at female level concentrations (around 0.4 ng/mL) shifted the collagen ratio: collagen I rose from about 2% to nearly 5% of cell area, while collagen III dropped from roughly 10% to 3% [16]. At male level concentrations (4 to 10 ng/mL), the effect blunted [16]. Striking finding, but the scope flag is non negotiable. Cultured fascial cells. Mixed sex, non hypermobile donors. Mechanism evidence, not clinical evidence. We can’t say it explains joint symptoms in PCOS or PMOS, because that experiment hasn’t been done.

Collagen I is the stiffer, load bearing fibre. Collagen III is the more elastic one. A shift toward more I and less III is a shift toward a stiffer, less elastic tissue. In a healthy woman that might mean very little. In a hypermobile woman whose connective tissue is already structurally different, the relevance is at least worth asking about.

The same Italian group has shown, in further laboratory work, that fascial collagen ratios shift across hormone concentrations matching the menstrual cycle phases [17, 18]. At low beta oestradiol, collagen I rises and collagen III plus elastic fibres fall. Around the ovulatory peak, collagen III rose 2.4% to 6.8% in their cultured cells, while collagen I fell 5.2% to 1.9%, with the tissue moving toward a softer baseline [18]. Again, in cell studies, not in women in clinic. But the directional signal is there.

Why does the fascia care about hormones at all? Because the receptors are there. Tissue immunohistochemistry has shown that human fascial fibroblasts express oestrogen, relaxin and androgen receptors, with expression lower in postmenopause [19]. That’s a direct biological route for hormonal effects on connective tissue. It doesn’t tell us what happens in chronic hyperandrogenism. It tells us the machinery is in place for hormones to act on fascia at all.

Tendon, inflammation and metabolic syndrome

Tendon work mostly comes from animal research and pharmacological doses, so we’re careful here. A 2018 review of tendon remodelling drawing on animal work concluded that anabolic androgens alter tendon collagen turnover. The doses studied, though, are pharmacological rather than physiological [20]. The hedge matters. Endogenous PCOS hyperandrogenism isn’t pharmacological. So while the mechanism is suggestive, you can’t read across from a male rat on injected steroids to a woman with PMOS.

What translates better is the metabolic inflammation story. Reviews of obesity, metabolic syndrome and musculoskeletal disease describe chronic low grade inflammation from insulin resistance as a contributor to tendinopathy, muscle loss and pain [21]. PMOS, by its new framing, is a metabolic condition. The bridge between insulin resistance and musculoskeletal misery isn’t speculative. It’s well described in the literature [21]. If pain management is where you’re stuck, our piece on what pain medication actually does for hypermobility and EDS gets into what the evidence shows is helpful and what isn’t.

So when women with PMOS pictures keep turning up at our studios with stubborn tendon irritation, niggling joint pain that won’t shift, and a fatigue floor that feels metabolic? The inflammation and insulin angle is the most defensible mechanistic thread we’ve got.

Honest scope flag

None of the connective tissue work above has been done in human hypermobile tissue under chronic PCOS or PMOS hormonal conditions. The model is this: hypermobile women already have altered connective tissue biology. PMOS adds chronic hyperandrogenism, chronic insulin resistance and chronic low grade inflammation on top. The mechanistic literature suggests these inputs all act on the same tissue systems. A reasonable biological story. Not a tested clinical mechanism in hEDS or HSD.

What does that mean in practice, for a woman sitting at home with a PMOS file and a hEDS diagnosis? The metabolic side of PMOS matters for her connective tissue, even if no study has yet measured the specific interaction. The insulin resistance to inflammation route to musculoskeletal pain is the strongest evidence based bridge [21]. The androgen to fascia route is plausible at the mechanism level but not clinically tested [16, 20]. The cycle linked laxity story is real in the female athlete literature, with one small pilot suggesting it’s more pronounced in those with hypermobility markers [22, 23, 24]. Treat the metabolic side seriously. Don’t read too much into the fascia mechanism story until it’s been done in the right population.

Symptom overlap: pain, fatigue, mood, sleep

The biology is interesting. The day to day symptom overlap is where it bites. This is the bit that lands with most readers.

Pain in PMOS

Pain is more common in PCOS than the textbooks suggest. An EHR analysis pulling from 120 US healthcare organisations (preprint, still pending peer review) reported clinically coded pain in around 19% of women with PCOS overall. Highest rates in Black or African American women at 32.11% and white women at 30.75% [25]. The figure needs the preprint flag. Still, it’s interesting, because the historical narrative hasn’t framed PCOS as a pain condition. With the rename and the metabolic reframing, that’s likely to shift [3].

The mechanism story for pain in PMOS pulls from the central sensitisation literature plus the metabolic inflammation thread. Reviews of metabolic syndrome describe insulin resistance as feeding chronic low grade systemic inflammation, which in turn contributes to tendinopathy and other musculoskeletal pain through shared inflammatory pathways [21]. Layer that on a hypermobile nervous system that already has its own sensitisation story, and you have two pain amplifying loops running in the same person.

Fatigue and the sleep piece

Sleep is one of the most under appreciated PCOS, now PMOS, problems. Reviews of PCOS and sleep report substantially elevated obstructive sleep apnoea risk, with odds ratios in clinic-based studies of around 7 to 10 against control groups, and the risk persisting after BMI adjustment [26]. Reviews of sleep in PCOS report excessive daytime sleepiness over represented, with associations persisting after adjusting for BMI [27]. A 2024 cross sectional study of 309 women with PCOS found about a third (33.7%) screened high risk for obstructive sleep apnoea on the Berlin Questionnaire, with HbA1c, CRP and SHBG (inversely) independently predicting risk in the multivariable model [28]. For the broader picture of how sleep falls apart in hypermobile bodies, our full sleep and hypermobility guide covers the architecture, the dysautonomia piece and what helps.

A 2022 meta analysis pooling multiple studies found women with PCOS had significantly worse sleep quality scores (PSQI mean difference 0.78), more daytime sleepiness (ESS mean difference 2.49), and higher apnoea hypopnoea indices (AHI mean difference 2.68) than controls, with reduced sleep efficiency [29]. The signal is consistent across the meta analytic data [29].

The hypermobility crowd has its own sleep problem. POTS interrupts the night with positional symptoms. Dysautonomia plays havoc with thermoregulation and heart rate. Joint pain breaks deep sleep. Stack OSA risk on top, and you’ve got a sleep picture that’s hard to fix without targeting all of it. The honest gap is that nobody’s run a sleep study on a dual PMOS plus hypermobile sample. But the convergence of two sleep disrupting conditions in the same body is a clinical observation that’s hard to argue with. Cognitive impact is part of this whole picture too, which we’ve covered in brain fog in EDS, POTS and long COVID.

Studio observation, for what it’s worth. The hypermobile clients we work with who get a PMOS or PCOS diagnosis added to their file almost universally describe the fatigue as a different texture from POTS fatigue. Deeper. Slower to lift. Less responsive to electrolytes and posture work. More responsive to sleep optimisation and metabolic work. Not a controlled study, that. Pattern recognition. Take it for what it’s worth.

Mood, anxiety, body image

Depression is the most commonly reported psychiatric comorbidity in PCOS, with reported prevalence varying widely across studies and populations (from around 15% in some cohorts to well over 60% in others), and a risk roughly three to eight times higher than in women without PCOS [30]. A 2025 neuroendocrinology review describes PCOS related depression as having specific biological drivers, including androgen exposure, HPA axis dysregulation, gut microbiome changes and chronic inflammation, distinct from depression in the general population [31]. Reviews of PCOS consistently report heightened anxiety, depression, eating disorders and reduced quality of life, with multiple proposed mechanisms across body image, infertility distress, androgen effects and HPA axis function [32]. A 2024 review described mood disorders, anxiety, eating disorders and cognitive complaints in PCOS alongside specific brain activity alterations, with marked reductions in quality of life [33].

Now stack that on the hypermobility mental health load already there. A 2026 German EDS clinic cross section of 99 participants found 85% reporting moderate to severe mental health burden, with PHQ-9 depression scores above clinical cut off in around 60% and DASS anxiety above cut off in around 45% [34]. The lifetime psychiatric diagnosis figure was 58.6%. The mechanism side of why hypermobility and anxiety tend to travel together is worth a read if you’re trying to make sense of a mood and joint picture that doesn’t add up.

Two diagnoses. Two independent mood loads. Added together in the same person. The dual diagnosis additive piece hasn’t been formally quantified, but the convergence isn’t subtle.

Cognitive symptoms and brain fog

The cognitive piece deserves its own paragraph. Brain fog isn’t a recognised diagnostic feature of PCOS or PMOS, but it shows up in the symptom lists women bring to us, and the underlying mechanisms (insulin resistance affecting glucose handling in the brain, chronic low grade inflammation, disrupted sleep, mood load) all sit in territory the literature has covered for adjacent conditions [21, 31]. Hypermobile women with POTS already deal with cognitive impact from cerebral blood flow shifts when standing. Layer PMOS related insulin resistance and sleep disruption on top, and the cognitive picture often gets worse rather than better. Gut symptoms also overlap heavily in this population, which we’ve gone into in the hypermobility and constipation overlap.

Gut symptoms deserve a mention too. Constipation, bloating and gut motility issues are well represented in hEDS cohorts, and the gut microbiome is one of the proposed contributors to the PCOS related depression picture [31]. The dual diagnosis gut story hasn’t been published, but the overlap is hard to miss in practice.

The summary picture

What hypermobile women with PMOS describe to us in the studios isn’t a coincidental cluster. Pain that doesn’t behave like simple joint pain. Fatigue that doesn’t lift with rest. Sleep that breaks for multiple reasons. Mood pulled in several directions at once. A cognitive load that compounds the other three. The mechanism stories sit underneath. The clinical observation matches. The formal dual diagnosis prevalence work is still missing.

Hormonal cycling and joint stability

This section exists because hypermobile women have been telling us, for years, that their joints behave differently across the cycle. And the literature has finally caught up enough to say something useful.

Bulk of the cycle and laxity literature, though, has been done in mainly non hypermobile female athletes and dancers. So we’re extrapolating. But the mechanism work and the population studies line up in the same direction.

A 2026 systematic review of 17 studies on female athletes reported the pre ovulatory and ovulatory phases as linked to greater knee laxity and elevated ACL injury risk, mediated by reduced passive stability and impaired neuromuscular control [22]. An earlier 2017 systematic review of menstrual cycle effects on lower limb biomechanics concluded ACL injury risk peaks in the pre ovulatory phase via a combination of greater laxity and altered knee mechanics [35]. A 2019 review of oestrogen’s musculoskeletal effects describes a dual pattern: oestrogen increases muscle mass and strength, but in ligament and tendon it reduces stiffness and increases laxity [24]. That dual pattern is important, because it means the same hormone has opposite effects on the two tissues that have to coordinate to keep a joint stable. For the broader piece on why traditional strength training falls short for hypermobile bodies, that’s where the loading principles get unpacked properly.

Relaxin biology pulls in a similar direction. Reviews of relaxin show its receptors are present in hip and knee joints, and relaxin activates matrix metalloproteinases that degrade collagen, providing a plausible mechanism for cycle linked tissue vulnerability [36]. Relaxin peaks mid luteal in a normal cycle [36]. So in a typical ovulatory cycle you’ve got one window of high oestrogen near ovulation pushing ligament laxity up, then a mid luteal relaxin window doing the same through a different route.

Now to the hypermobility relevant bit. A small Japanese laboratory study (15 young women, pilot level) found no overall cycle effect on anterior knee laxity across the group [23]. But within the sample, the subset of women with genu recurvatum, a marker of hypermobility, showed significantly greater anterior knee laxity at ovulation [23]. Sample size means this is signal, not certainty. The direction is consistent with the broader cycle literature, though, and it suggests hypermobile women may carry more cycle linked laxity than the general female population [23].

Work in female contemporary dancers (n=11, cycle phase tracked by basal body temperature and LH surge kit) found that oestrogen and relaxin were associated with greater musculoskeletal compliance, while progesterone was associated with increased muscle stiffness [37]. Dancers as a population probably enrich for hypermobility even though they weren’t formally screened for it [37]. So the dancer finding is suggestive in our direction.

The PMOS twist

This is the bit nobody’s written up properly. In a normal cycle, the luteal phase brings progesterone and relaxin peaks, then a withdrawal that triggers menstruation. In anovulatory PMOS, the luteal phase is often absent or blunted, because ovulation didn’t happen [2]. So the normal relaxin and progesterone rhythm doesn’t run. Chronic hyperandrogenism sits on top of chronic low grade oestrogen exposure, rather than the cyclical peak and trough pattern that drives the laxity changes described above [1, 2].

What does that mean for joint stability? Honestly? We don’t know. Could mean the cyclical laxity issue described in non PMOS women is less of a problem, because the cycle isn’t cycling. Could mean the chronic hormone baseline creates a different tissue state altogether. The mechanistic fascia work suggests chronic hyperandrogenism might shift collagen ratios toward a stiffer baseline [16], while a chronic low oestrogen state would shift fascia toward stiffer too [17]. Combine that with hypermobile connective tissue biology, and the prediction is messy. Nobody’s done the cycle laxity study in a PMOS plus hypermobile sample [22, 23]. If you’re heading into the next chapter of hormonal change, our piece on menopause, perimenopause and hypermobility walks through what shifts and what to do about it.

What we tend to find with hypermobile women working through PMOS symptoms is that the symptom variability across the cycle is less predictable than in non PMOS hypermobile clients. Some report flatter symptoms across the month (no cyclical worsening, but a higher baseline). Others report unpredictable flares that don’t track with any cycle phase. Pattern recognition, again, not controlled data. But worth saying out loud.

Exercise and rehab: how the standard PMOS prescription needs adapting

On exercise prescription, the PCOS literature’s actually in decent shape. A 2022 meta analysis of 18 randomised controlled trials with 593 women showed exercise significantly improved cardiorespiratory fitness (VO2max) and waist circumference in PCOS [38]. A 2020 systematic review found moderate certainty evidence that aerobic exercise reduces BMI in PCOS (standardised mean difference around minus 0.35), with weaker evidence for reproductive outcomes [39]. A 2025 trial reported combined resistance and endurance training in women with PCOS improved fasting glucose, insulin, HOMA-IR, QUICKI and lipid profiles, and reduced inflammatory and androgen markers [40]. Systematic reviews of exercise and hormones in PCOS recommend vigorous aerobic exercise and resistance training as the most consistent ways to improve insulin sensitivity and reduce androgen markers [41]. Recent reviews conclude that aerobic, resistance, HIIT and combined protocols all benefit PCOS metabolic and reproductive markers, with combined training providing the most comprehensive effect [42].

Right. Headline’s not subtle. Exercise works for PMOS. Combined aerobic and resistance training has the most consistent support across recent reviews for cardiometabolic and reproductive outcomes [42].

Here’s the catch. None of those trials screened for hypermobility. So when a PMOS guideline points at “vigorous” aerobic work, high impact loading and ballistic protocols, it’s pulling from data that didn’t include the population we work with [38, 41]. The metabolic mechanism isn’t wrong. The metabolic mechanism is the same in a hypermobile body as in a non hypermobile one. What changes is the implementation. The motor control side of why hypermobile bodies need a different approach is covered in proprioception, brain maps and why hypermobile bodies feel lost.

What we actually see is this. Women who plough into a “vigorous PCOS exercise plan” off the internet, when they’ve got undiagnosed or partially managed hypermobility, end up flared. Injured. Demoralised. Or all three. We’ve had clients walk in pre flared from a six week running build. Others from a CrossFit foundations programme that defaulted to box jumps and ballistic loading. Not because the prescription was wrong in principle. Because the prescription wasn’t tailored.

Principles for hypermobile women working with a PMOS picture

In practice, the adjustments we make in our studios are these.

First, build motor control and joint co activation before adding speed or load. Hypermobility doesn’t mean weakness, but it does mean the central nervous system map of where the joints are sitting often needs work before adding velocity, because velocity without control is where joints end up at the wrong end of range. The other side of that coin is fear of movement in hypermobility and EDS, which has to be addressed in parallel.

Second, manage range of motion actively rather than relying on passive end range. The hypermobile joint already has the range, what it needs is the capacity to control the range. Static stretching toward end range, beloved of generic flexibility advice, is mostly the wrong direction. Strength through full range is the better target.

Third, use compound, controlled tempo loading. The metabolic returns shown across PCOS exercise reviews are most consistent when resistance training is paired with aerobic work [42]. Resistance training delivers those returns whether you’re loading at 3 seconds down 3 seconds up with controlled tempo or whether you’re hammering it on a barbell. For hypermobile bodies, the controlled tempo route, with longer time under tension, gets the metabolic adaptation without the joint risk of ballistic loading.

Fourth, avoid ballistic plyometric work as a default starting point. Plyos are a tool. They have a place, but not as an entry point for someone whose joint stability is already a moving target. Build the base first.

Fifth, cycle load, not just calories. Load tolerance varies with sleep, hormones and inflammation. Hypermobile bodies don’t respond well to a fixed plan run rigidly for twelve weeks regardless of how the person is feeling that week. The PCOS exercise evidence supports a range of intensities and protocols, so flexing load around how the body is responding is well within what the literature backs [42].

Sixth, respect rest and adaptation from a metabolic perspective, not just a muscular one. The PMOS picture brings with it elevated inflammatory markers, disrupted sleep architecture, and a baseline metabolic stress that interacts with training stress in ways that aren’t always intuitive [21, 29]. Two hard sessions back to back, which a body without hypermobility or PMOS might absorb fine, can stack into a flare that takes a week or two to settle. We programme rest days as deliberately as we programme training days. In our experience, the women who buy into the rest day discipline early get further in the rehab journey than the ones who push through.

Seventh, screen for OSA if symptoms warrant. Daytime sleepiness, witnessed apnoeas, morning headaches, persistent fatigue despite good sleep hygiene, these warrant a conversation with the GP about a sleep study [26, 28]. Untreated OSA undermines every training and metabolic adaptation you’re trying to build. The week to week management of load and energy is where pacing for chronic pain and EDS becomes essential.

On modalities, swimming and cycling deliver the cardiometabolic load with less joint impact than running, which matters in the early phases of building tolerance. Walking is underrated. Long, steady walking shifts insulin sensitivity, doesn’t tax joints, and is something hypermobile women with PMOS can generally do without flaring.

Resistance training, for our money, is the most important single piece. Recent PCOS exercise reviews put combined aerobic plus resistance training as the protocol with the broadest cardiometabolic and reproductive returns [42]. For hypermobile bodies, resistance work also drives the joint control and motor mapping changes that everything else depends on. Progressive overload, controlled tempo, full range under load. That’s the spine of the programmes we run in our studios, and it’s the same spine whether or not a PMOS picture is part of the story.

The bit we want clients to leave with is this. The metabolic mechanism that makes exercise work in PMOS is the same mechanism that needs to work in your body. Not “don’t exercise because you’re hypermobile”. Instead: “load well, build the base, train your nervous system to control the range, and treat the metabolic side seriously”. Educational framing, not a treatment claim.

What this changes in practice

Pulling the threads together.

On day to day clinical reality, the honest version is this.

The diagnostic path hasn’t changed. Rotterdam criteria still apply [2]. AMH is still allowed as an alternative to ultrasound in adults [2]. Two of three out of hyperandrogenism, ovulatory dysfunction and polycystic ovarian morphology still defines the syndrome [2]. The 2023 International Evidence based Guideline, developed across 39 organisations and 71 countries, remains the standard until the 2028 update [2, 1].

The treatment path hasn’t changed. Lifestyle first line. Letrozole first line for ovulation induction. Psychological screening mandated at diagnosis [2]. For how we think about the EDS side specifically, how we approach EDS rehab lays out the broader framework.

The framing has shifted. The rename pushes clinicians and women toward thinking metabolic and hormonal management, rather than treating the condition as if it’s fundamentally about cysts [1, 3]. That matters, because where you think the disease lives shapes what you screen for, what you treat, and what you take seriously.

For hypermobile women in particular, the shift toward a metabolic understanding of PMOS means the insulin resistance and androgen pieces aren’t optional add ons to the conversation anymore. They’re central [3, 8]. And because the metabolic mechanism is independent of weight, slim hypermobile women shouldn’t get filtered out of the screening conversation by a thin BMI [8].

Practical note. Keep your medical team in the loop on the rename. Records will need to align over the three year transition window. If you’re moving between specialists or geographies, having both PCOS and PMOS in your file avoids future confusion [1]. Don’t expect overnight uptake from clinicians. The transition window is there precisely because these things take time.

Shared management priorities

For PMOS plus hypermobility, the priorities we’d put on the table, evidence wise, are these.

Sleep first. OSA risk is real, fatigue burden is real, and the gains from getting sleep right ripple into everything else [26, 29]. For the autonomic side of the sleep and stability picture, compression garments for hypermobility, EDS and POTS is worth a look.

Strength based rehab over passive stretching. The cardiometabolic returns in PCOS are well documented for both aerobic and resistance training, with combined protocols showing the broadest benefits [42]. The joint control gains are in active loading, not passive end range work.

Lifestyle interventions are evidence based for both conditions independently. The PMOS guideline calls for it [2]. The hypermobility literature agrees on loading principles.

Mental health screening at diagnosis. Mandated for PMOS [2]. Well established as needed in hEDS and HSD [34]. The piece on the hypermobility and anxiety connection covers the mechanism side.

Pain management that respects central sensitisation rather than amplifying it through fear avoidance or over investigation. The medication side is broken down in what pain medication actually does for hypermobility and EDS.

PCOS, now PMOS, is increasingly framed as a lifelong multisystem condition with familial endocrine and metabolic clustering and major implications for type 2 diabetes and cardiovascular risk later in life [43]. A Finnish birth cohort study following 244 women with PCOS and 1,556 without to age 50 found 26% higher overall diagnosis rates and 24% higher medication use in PCOS, with elevations across endocrine, metabolic, nervous system, musculoskeletal and genitourinary disease categories [44]. Some of those elevations persisted even in lean women with PCOS [44]. That’s a long view that, in our experience with hypermobile clients, the day to day management often forgets. Fatigue, often the loudest day to day complaint, has its own physiology, which we’ve covered in the breathlessness, fatigue and chronic pain link.

Where the research is still missing

Worth being clear about the gaps. The honest picture is more useful than a tidy one.

There’s no direct prevalence study of PMOS in hEDS or HSD cohorts. Plenty of hEDS gynaecological data [11, 12, 13, 14, 15]. Plenty of PMOS data in general populations [2, 1]. Nothing that’s measured the rate of one inside the other.

There’s no exercise study run specifically in a PMOS plus hypermobility sample. The PCOS exercise evidence is strong [38, 39, 40, 41, 42]. None of it screened for hypermobility. So adaptation principles, like the ones above, are extrapolated from broader exercise science and clinical observation, not from a hypermobility specific trial.

There’s no cycle laxity study in PMOS. The female athlete cycle and ACL literature is detailed [22, 35, 24]. The hypermobility specific pilot is small [23]. Nobody has combined the two populations [22, 23].

There’s no androgen receptor study in human hypermobile connective tissue. The Italian fascia group has done the cell and tissue work in non hypermobile donors [16, 19, 18]. Nobody has repeated it in hEDS tissue under PMOS hormonal conditions.

There are no longitudinal outcomes studies for women living with both conditions. The Finnish PCOS birth cohort gives us a long view in PCOS [44]. The hEDS multisystem burden data gives us a young adult snapshot [10]. Nobody has joined them.

These are the missing pieces. If you’re a researcher reading this and you happen to have a hypermobility cohort with reproductive endocrine data, please publish it. The clinical community could use it.

In the meantime, the practical posture for women living at this intersection is to take both conditions seriously and to hold the medical team to a joined up conversation. The PMOS literature is moving fast (the rename itself is the proof of that), and the hypermobility literature has, in the last few years, finally started talking to the rest of medicine rather than sitting in its own silo [9, 34]. The two streams are going to converge. They just haven’t yet, in the formal published sense.

The bottom line

The rename is real. PCOS is PMOS. The science underneath the new label is being reframed around metabolic and hormonal drivers rather than ovarian morphology [1, 3]. That reframing is welcome.

For women with hypermobility, the overlap is plausible, clinically observed, mechanistically grounded, and not yet quantified in a single dual diagnosis study. The fascia and androgen mechanism work sits in laboratory studies [16, 17, 19, 18]. The cycle laxity work sits in mainly non hypermobile female athletes and dancers [22, 23, 35, 24, 37]. The pain, fatigue, sleep and mood overlap is real and additive [25, 30, 26, 29, 34, 33]. The prevalence study that would tie it all together hasn’t been done. If you want structured rehab in your own time, our online courses cover the loading, motor control and self management work in a guided format.

What can hypermobile women with a PMOS diagnosis (or a strong suspicion of one) do today? Same thing that works for either condition on its own. Taken seriously. Load well. Sleep well. Screen for mental health. Treat insulin resistance like it matters, regardless of whether your BMI is “normal”. Manage pain without amplifying it. And don’t accept “it’s just your hormones” as a clinical end point.

The Fibro Guy team works with hypermobile women, including many with PMOS or PCOS in their file. We don’t diagnose PMOS, that’s the GP and the endocrinologist’s job. What we do is help women rebuild strength, joint control and confidence through structured rehab, in our studios and through our online programmes. We welcome the rename, because it forces a more useful conversation than “your ovaries have cysts”, which often wasn’t even true [1, 2, 4]. If you’d rather work with the team directly, our in-studio sessions are how we deliver one to one rehab.

If you’re hypermobile, and you’ve got a PCOS or now PMOS label sitting alongside your hypermobility diagnosis, and nobody’s joined the two stories up for you yet, then this is your nudge. Start asking the joined up questions. The literature’s closer to catching up than it’s ever been [1, 3, 8].

One final thought. The hypermobility community has spent years being told its symptoms are vague, its conditions are rare, and its presentations don’t fit neatly into the boxes the medical system has built. The PMOS rename, in a small way, is the opposite story. A condition that’s been hammered into a too neat box for decades has finally been let out of it, by an enormous international consensus that admits the old framing was misleading [1, 5, 3]. If a condition affecting roughly 1 in 8 women can be renamed because the name was wrong [1, 2], the same intellectual honesty applies to conditions where the name hasn’t been challenged yet. The lesson sits with us. Don’t let outdated terminology shape clinical care if the science has moved past it.

FAQ

References

1. Teede HJ, Khomami MB, Morman R, et al. (2026) Polyendocrine metabolic ovarian syndrome, the new name for polycystic ovary syndrome: a multistep global consensus process. The Lancet. 10.1016/s0140-6736(26)00717-8
2. Teede HJ, Tay CT, Laven J, et al. (2023) Recommendations from the 2023 International Evidence-based Guideline for the Assessment and Management of Polycystic Ovary Syndrome. Human Reproduction, 38(9), 1655 to 1679. 10.1093/humrep/dead156
3. Dalamaga M (2026) What’s in a name? From PCOS to polyendocrine metabolic ovarian syndrome: A metabolic reframing, promise, controversies, and challenges ahead. Metabolism Open, 100479. 10.1016/j.metop.2026.100479
4. Hong AR (2025) Redefining Polycystic Ovary Syndrome: Transformative Diagnostic and Management Changes in the 2023 Guideline. Endocrinology and Metabolism, 40(1), 64 to 66. 10.3803/EnM.2024.2263
5. Teede HJ, Moran LJ, Morman R, et al. (2025) Polycystic ovary syndrome perspectives from patients and health professionals on clinical features, current name, and renaming: a longitudinal international online survey. eClinicalMedicine, 84, 103287. 10.1016/j.eclinm.2025.103287
6. Teede HJ, Misso ML, Costello MF, et al. (2018) Recommendations from the international evidence-based guideline for the assessment and management of polycystic ovary syndrome. Fertility and Sterility, 110(3), 364 to 379. 10.1016/j.fertnstert.2018.05.004
7. Sanchez-Garrido MA, Tena-Sempere M (2020) Metabolic dysfunction in polycystic ovary syndrome: Pathogenic role of androgen excess and potential therapeutic strategies. Molecular Metabolism, 35, 100937. 10.1016/j.molmet.2020.01.001
8. Wang X, Nie H, Cui R, et al. (2026) Divergent pathophysiological drivers of polycystic ovary syndrome: insulin resistance independently predicts hyperandrogenism. Frontiers in Endocrinology, 17. 10.3389/fendo.2026.1758861
9. Ganesh R, Munipalli B (2024) Long COVID and hypermobility spectrum disorders have shared pathophysiology. Frontiers in Neurology, 15. 10.3389/fneur.2024.1455498
10. Kozyra M, Kostyun R, Strecker S (2024) The prevalence of multisystem diagnoses among young patients with hypermobile Ehlers-Danlos syndrome. Medicine, 103(41), e39212. 10.1097/MD.0000000000039212
11. Hugon-Rodin J, Lebègue G, Becourt S, et al. (2016) Gynecologic symptoms and the influence on reproductive life in 386 women with hypermobility type Ehlers-Danlos syndrome. Orphanet Journal of Rare Diseases, 11(1). 10.1186/s13023-016-0511-2
12. Gilliam E, Hoffman JD, Yeh G (2019) Urogenital and pelvic complications in the Ehlers-Danlos syndromes and associated hypermobility spectrum disorders. Clinical Genetics, 97(1), 168 to 178. 10.1111/cge.13624
13. Pollack B, von Saltza E, McCorkell L, et al. (2023) Female reproductive health impacts of Long COVID and associated illnesses including ME/CFS, POTS and connective tissue disorders. Frontiers in Rehabilitation Sciences, 4. 10.3389/fresc.2023.1122673
14. Petrucci T, Barclay SJ, Gensemer C, et al. (2024) Phenotypic Clusters and Multimorbidity in Hypermobile Ehlers-Danlos Syndrome. Mayo Clinic Proceedings: Innovations, Quality and Outcomes, 8(3), 253 to 262. 10.1016/j.mayocpiqo.2024.04.001
15. Glayzer JE, McFarlin BL, Castori M, et al. (2021) High rate of dyspareunia and probable vulvodynia in Ehlers-Danlos syndromes and hypermobility spectrum disorders. American Journal of Medical Genetics Part C: Seminars in Medical Genetics, 187(4), 599 to 608. 10.1002/ajmg.c.31939
16. Fede C, Sun Y, Zhao X, et al. (2025) Effect of Androgens on Human Fascia. Biology, 14(7), 746. 10.3390/biology14070746
17. Fede C, Pirri C, De Caro R, Stecco C (2022) Myofascial pain in females and personalized care: The key role played by sex hormones. European Journal of Pain, 26(4), 939 to 940. 10.1002/ejp.1920
18. Fede C, Pirri C, Fan C, et al. (2019) Sensitivity of the fasciae to sex hormone levels: Modulation of collagen-I, collagen-III and fibrillin production. PLOS ONE, 14(9), e0223195. 10.1371/journal.pone.0223195
19. Fede C, Albertin G, Petrelli L, et al. (2016) Hormone receptor expression in human fascial tissue. European Journal of Histochemistry. 10.4081/ejh.2016.2710
20. Guzzoni V, Selistre-de-Araújo HS, De Cássia Marqueti R (2018) Tendon Remodeling in Response to Resistance Training, Anabolic Androgenic Steroids and Aging. Cells, 7(12), 251. 10.3390/cells7120251
21. Collins KH, Herzog W, MacDonald GZ, et al. (2018) Obesity, Metabolic Syndrome, and Musculoskeletal Disease: Common Inflammatory Pathways Suggest a Central Role for Loss of Muscle Integrity. Frontiers in Physiology, 9. 10.3389/fphys.2018.00112
22. Woźniakowska I, Zambrzycka M, Misarko A, et al. (2026) Training in Sync with the Cycle? The Impact of Hormonal Fluctuations During the Menstrual Cycle on Female Athletes. Quality in Sport, 55, 70927. 10.12775/qs.2026.55.70927
23. Maruyama S, Yamazaki T, Sato Y, et al. (2021) Relationship Between Anterior Knee Laxity and General Joint Laxity During the Menstrual Cycle. Orthopaedic Journal of Sports Medicine, 9(3). 10.1177/2325967121993045
24. Chidi-Ogbolu N, Baar K (2019) Effect of Estrogen on Musculoskeletal Performance and Injury Risk. Frontiers in Physiology, 9. 10.3389/fphys.2018.01834
25. Cherlin T, Mohammed S, Ottey S, et al. (2024) Understanding Pain in Polycystic Ovary Syndrome: Health Risks and Treatment Effectiveness. Preprint, not yet peer reviewed. 10.1101/2024.10.15.24315513
26. Sam S, Ehrmann DA (2019) Pathogenesis and Consequences of Disordered Sleep in PCOS. Clinical Medicine Insights: Reproductive Health, 13. 10.1177/1179558119871269
27. Fernandez R, Moore V, Van Ryswyk E, et al. (2018) Sleep disturbances in women with polycystic ovary syndrome: prevalence, pathophysiology, impact and management strategies. Nature and Science of Sleep, 10, 45 to 64. 10.2147/NSS.S127475
28. Christ JP, Shinkai K, Corley J, et al. (2024) Metabolic and endocrine status associate with obstructive sleep apnea risk among patients with polycystic ovary syndrome. Journal of Clinical Sleep Medicine, 20(6), 871 to 877. 10.5664/jcsm.11012
29. Wang C, Huang T, Song W, et al. (2022) A meta-analysis of the relationship between polycystic ovary syndrome and sleep disturbances. Frontiers in Physiology, 13. 10.3389/fphys.2022.957112
30. Xing L, Xu J, Wei Y, et al. (2022) Depression in polycystic ovary syndrome: Focusing on pathogenesis and treatment. Frontiers in Psychiatry, 13. 10.3389/fpsyt.2022.1001484
31. Dubé-Zinatelli E, Anderson F, Ismail N (2025) The overlooked mental health burden of polycystic ovary syndrome: neurobiological insights. Frontiers in Neuroendocrinology, 78, 101203. 10.1016/j.yfrne.2025.101203
32. Almhmoud H, Alatassi L, Baddoura M, et al. (2024) Polycystic ovary syndrome and its multidimensional impacts on women’s mental health: A narrative review. Medicine, 103(25), e38647. 10.1097/MD.0000000000038647
33. Pinto J, Cera N, Pignatelli D (2024) Psychological symptoms and brain activity alterations in women with PCOS and their relation to the reduced quality of life. Journal of Endocrinological Investigation, 47(7), 1 to 22. 10.1007/s40618-024-02329-y
34. Henning M, Hock M, Shukri A, et al. (2026) Prevalence and management of mental health comorbidities in a German cohort of patients with hypermobile Ehlers-Danlos syndrome and hypermobility spectrum disorder. Orphanet Journal of Rare Diseases, 21(1). 10.1186/s13023-026-04242-4
35. Balachandar V (2017) Effects of the menstrual cycle on lower-limb biomechanics, neuromuscular control, and anterior cruciate ligament injury risk. Muscle, Ligaments and Tendons Journal, 7(1), 136. 10.11138/mltj/2017.7.1.136
36. Parker EA, Meyer AM, Goetz JE, Willey MC, Westermann RW (2022) Do Relaxin Levels Impact Hip Injury Incidence in Women? A Scoping Review. Frontiers in Endocrinology, 13. 10.3389/fendo.2022.827512
37. Pessali-Marques B, Burden AM, Morse CI, Onambélé-Pearson GL (2024) Musculoskeletal Morphology and Joint Flexibility-Associated Functional Characteristics across the Menstrual Cycle in Female Contemporary Dancers. Journal of Functional Morphology and Kinesiology, 9(1), 38. 10.3390/jfmk9010038
38. Breyley-Smith A, Mousa A, Teede HJ, Johnson NA, Sabag A (2022) The Effect of Exercise on Cardiometabolic Risk Factors in Women with Polycystic Ovary Syndrome: A Systematic Review and Meta-analysis. International Journal of Environmental Research and Public Health, 19(3), 1386. 10.3390/ijerph19031386
39. dos Santos IK, Ashe MC, Cobucci RN, et al. (2020) The effect of exercise as an intervention for women with polycystic ovary syndrome. Medicine, 99(16), e19644. 10.1097/MD.0000000000019644
40. Nasiri M, Monazzami A, Alavimilani S, Asemi Z (2025) Modulation of hormonal, metabolic, inflammatory and oxidative stress biomarkers in women with polycystic ovary syndrome following combined resistance and endurance training. BMC Endocrine Disorders, 25(1). 10.1186/s12902-024-01793-0
41. Shele G, Genkil J, Speelman D (2020) A Systematic Review of the Effects of Exercise on Hormones in Women with Polycystic Ovary Syndrome. Journal of Functional Morphology and Kinesiology, 5(2), 35. 10.3390/jfmk5020035
42. Çopuroğlu ÖB (2025) The Effects of Exercise Programs on Metabolic and Reproductive Health in Women with PCOS. Journal of Pharmaceutical Research and Innovation, 5(2). 10.36647/jpri/05.02.a004
43. Louwers YV, Laven JSE (2020) Characteristics of polycystic ovary syndrome throughout life. Therapeutic Advances in Reproductive Health, 14. 10.1177/2633494120911038
44. Kujanpää L, Arffman RK, Pesonen P, et al. (2024) Polycystic ovary syndrome presents as a multimorbid condition by age 50: birth cohort linkage study. European Journal of Endocrinology, 190(6), 409 to 420. 10.1093/ejendo/lvae057