EDS Flare Ups

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Adam Foster

Director at The Fibro Guy

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

Latest posts by Adam Foster (see all)

• Why ADHD and Hypermobility Keep Turning Up Together - 16 September 2026
• Hypermobility and Early Development: Milestones, Motor Delay, and Predictions - 12 September 2026
• Fibromyalgia and Itching: Why It Happens, What the Science Actually Says, and What You Can Do About It - 9 September 2026

A flare up, in the most useful sense of the word, is a temporary worsening of several things all at the same time, and it’s that “all at the same time” part that makes it so hard to explain to anybody who has never had one. Pain climbs, fatigue gets heavy, joints feel less trustworthy than they did last week, the gut plays up, standing gets harder, and thinking slows right down, all inside the same few days. There isn’t actually an agreed definition of a flare anywhere in the hypermobility literature, which is genuinely worth knowing before somebody tells you very confidently what one is ^[1][2]. What the research does support is a fairly consistent shape: a whole body event with several contributors loading up together, rather than one switch getting flipped ^[1][2][3].

So, the short answer. A flare is very rarely one trigger, it’s usually two or three loads arriving at once, and the ones you can actually get your hands on are sleep, orthostatic symptoms, activity that outran your current tolerance, gut symptoms, and whatever else life happens to be doing to you that week. Which is also why hunting for the single cause tends to go nowhere, as a lot of the time there simply isn’t one to find.

What an EDS Flare Up Actually Is

The honest definition is the loose one: a temporary intensification of symptoms, which varies enormously from one person to the next ^[1][2][3]. That variation is the actual finding, as hypermobile Ehlers-Danlos syndrome and hypermobility spectrum disorder both present across a lot of systems at the same time, and different people carry different combinations of them, so a single uniform flare phenotype has never turned up in the research ^[1][2][3].

For one person a flare is mostly gut: cramping, reflux, nothing sitting right, appetite gone. For another it’s mostly upright symptoms, so dizziness, a racing heart, and that particular exhaustion that comes with standing in a queue. For plenty of people it’s all of the above, plus a run of subluxations. All three of those are the same phenomenon, which is admittedly a slightly unsatisfying thing to be told, but it’s where the evidence sits.

The biggest shift in this field over the last few years is that hEDS and HSD are now supported as genuinely whole body conditions, rather than isolated joint problems ^[2][4]. Pain, fatigue, autonomic symptoms and digestive symptoms cluster together in these groups rather than arriving separately ^{[2][5][6][7][8]}. So, once you know that, a flare that takes out your gut, your standing tolerance and your shoulder in the same week stops looking like three coincidences.

Pain itself isn’t one thing either, as across the reviews it gets separated into joint pain, muscular pain, neuropathic pain, back and neck pain, abdominal and pelvic pain, and headache, with subluxations, dislocations, muscle weakness, proprioceptive problems, spinal instability and previous surgery all named as contributors ^[9][10]. Which matters practically, as “my pain is worse” can mean six different mechanisms, and they don’t all respond to the same thing.

Why a Flare Takes the Whole Body With It

What disability actually tracks in hypermobility is pain and fatigue, not how hypermobile you are ^[11][12][13]. That finding turns up repeatedly, in adults and in children, and it holds when physical and psychological burden are measured alongside each other, so how much a flare costs you is not a readout of your Beighton score ^[11][12][14].

There are also signs of central sensitisation in these groups, meaning the whole system runs at a lower threshold, and in adolescents with HSD or hEDS those signs have been looked for and found ^[15]. It’s been linked to the broader whole body symptom picture as well, though that link is an association rather than a demonstrated chain of cause and effect ^[16].

Now, the sensory side. Joint position sense is measurably worse in hypermobile Ehlers-Danlos syndrome, and that’s the mechanism sitting underneath a lot of what gets called clumsiness ^[17]. A brain working from a less precise signal about where a joint is, makes worse decisions about how to load it, and during a flare, when you’re tired and sore and moving differently, that signal gets no better. This is the part of the picture our own work sits on, so treat the mechanism as our reading of it rather than as settled, as nobody has tested whether improving joint awareness reduces flare frequency (surprise, surprise).

Fascia gets raised as another possible contributor, and there is emerging work on it in HSD and hEDS, but it’s genuinely emerging rather than established, and we’d be getting ahead of the evidence if we built anything on it yet ^[18].

Sleep, and Which Direction It Runs

Sleep is the load we see doing the most damage in the studios, and it’s also the one that gets overstated most often. You’ll see it written that poor sleep directly causes more pain, which is a good deal stronger than the evidence actually supports. What the chronic pain literature shows is a strong two way relationship, where sleep impairment and pain each make the other worse, and sleep impairment often predicts pain more reliably than pain predicts sleep ^[19].

In hypermobility specifically, poor sleep is extremely common and it travels with fatigue, concentration problems, worse mental and physical health, and a heavier overall symptom load ^[20][21]. More frequent pain has been associated with taking longer to fall asleep, and with more bad mental and physical health days ^[21]. In hypermobile children, poor sleep and psychiatric diagnoses are both common and both track worse quality of life ^[22]. None of that is causal proof though, and most of it is a snapshot rather than a film, so read it as a strong association that’s worth acting on, rather than a mechanism anybody has nailed down ^[19][21].

Which is enough to act on, honestly, as if a flare has landed and you’ve had four bad nights behind you, you don’t need a study to tell you which one to protect first.

The Autonomic Side of a Crash

When people describe a crash rather than a flare, they usually mean the autonomic version: dizziness, palpitations, exercise intolerance, brain fog, and a flatness that no amount of sitting down fixes. Orthostatic and digestive autonomic symptoms are common in hEDS, and autonomic burden tracks worse quality of life, worse fatigue and worse pain ^[5][23][24]. Among women with HSD and hEDS, a physician diagnosed POTS is common enough to be the majority rather than the exception, and autonomic symptom scores run high across the group ^[5]. Cerebrovascular, autonomic and small nerve features have all been described in hEDS as well ^[25].

Fatigue in these conditions repeatedly links back to autonomic dysfunction, disturbed sleep, pain and deconditioning, in adults and in adolescents both ^[9][26][27]. Which is why “just rest more” is such poor advice, as two of those four contributors get worse with rest.

Heat, dehydration and physical strain making orthostatic symptoms worse is consistent with the wider POTS management literature, where low blood volume and deconditioning are both treated as important contributors, and fluids, salt, compression and graded exercise reconditioning are the usual first line ^[28]. Exercise for POTS in young people with joint hypermobility has been looked at and is used widely, though the evidence base for it is still thinner than the enthusiasm around it ^[29].

One thing worth naming carefully, as it gets passed around as a hypermobility feature with the caveat quietly dropped off it. Coat hanger pain, the ache across the back of the neck and shoulders that comes on with being upright, is well described in autonomic failure and in spinal cord injury with orthostatic hypotension ^[30][31]. It has not been established as a canonical feature of Ehlers-Danlos syndrome specifically. It’s a real phenomenon that plenty of hypermobile people recognise, and the research describing it was done in other populations, which is a reason to suspect it rather than a reason to claim it ^[30][31].

The Gut Side of a Flare

Digestive symptoms are common enough in hEDS and HSD to count as part of the picture rather than a separate problem. Abdominal pain, constipation, diarrhoea, reflux and disorders of gut brain interaction (a phrase doing an enormous amount of heavy lifting) all turn up at higher rates than in comparison groups, and they come with worse quality of life and more autonomic symptoms ^[4][32][33].

Now, reflux usually arrives with a number attached, somewhere upwards of half the hypermobile population, and that number doesn’t really hold up, as the better evidence shows estimates varying widely depending on which group was looked at and how the question was asked ^[4][32]. So reflux and GERD symptoms are common in hypermobility related disorders, and there’s no clean single figure worth quoting.

You’ll also find it claimed that “IBS flares impair nutrition, muscle strength and collagen synthesis”, which reaches a long way beyond anything that has actually been shown. What’s supported is that digestive symptoms travel with a heavier overall symptom burden, poorer quality of life and more autonomic symptoms ^[32][33]. The sensible version, and the one we’d stand behind, is that a bad gut week can worsen your hydration, your appetite, your sleep and your day to day functioning, all of which feed a flare, and that nobody has measured it doing anything to your collagen.

The expert guidance on the digestive and autonomic side of hEDS advises targeted testing based on the symptom pattern actually in front of you, rather than testing everybody for POTS or mast cell activation as a matter of course ^[34].

Mast Cells, and Where That Evidence Stops

Mast cell activation syndrome comes up constantly in hypermobility spaces, usually presented as a fixed trio alongside hEDS and POTS. The reviews do support the overlap being observed, and symptoms genuinely turn up together, but the same reviews say plainly that mechanistic evidence is limited, that shared symptoms on their own can’t establish an association, and that universal testing isn’t supported ^[34][35].

So, the useful version is narrower than the one that gets shared around. In people with suspected or confirmed MCAS, triggers can include foods, odours, temperature changes, emotional distress and some medications ^[34]. That’s genuinely helpful to know if you’re in that group, and it isn’t a rule that applies across everybody with hypermobility, as treating it like one has sent a lot of people down a very expensive elimination diet for no good reason.

Hormones, and What’s Actually Known

A subset of women with hEDS report their symptoms getting worse around puberty, premenstrually, after giving birth, and on oral contraception ^[36]. Puberty, pregnancy, the postpartum period and infections all get reported as contexts where things worsened or first appeared, though these are reported contexts rather than proven causal mechanisms, and that distinction gets lost constantly ^[2][36].

The joint laxity part needs a lighter touch than it usually gets. It’s commonly stated that cycle related laxity results in more frequent and severe subluxations and dislocations, and there is evidence that laxity changes across the cycle, but direct proof that this produces more dislocations in hEDS is weaker than the claim needs it to be ^[36]. So the honest version is that it may contribute to more instability symptoms in some people, and that if you’ve noticed your own pattern, you’re simply ahead of the research on it.

Childbearing brings its own version of all this, and there’s qualitative work on hypermobility and pregnancy which documents how badly the whole thing tends to be handled ^[37].

Stress, Distress, and Where It Gets Used Against You

Stress loading the system doesn’t make a flare psychological, and it doesn’t make the pain any less real, and that needs saying first, as this is the exact ground people get dismissed on. Biology, psychology and circumstance all load the same body, and naming the third one isn’t a polite route to blaming you for the first two.

Stress does appear to worsen symptoms in some people with EDS and HSD, most likely through biopsychosocial and autonomic routes, and direct mechanistic evidence in hypermobility specifically remains limited ^[38]. Psychological distress, pain catastrophising and activity avoidance are associated with worse pain, disability, fatigue and mobility outcomes, and the same literature is clear that they do not explain the symptoms ^[38][39][12]. Depressive symptoms are highly prevalent in HSD and hEDS and track with fatigue and with catastrophising ^[39]. The qualitative work on what living with this actually does to people is, if anything, more useful than the numbers ^[40].

There’s also work outside hypermobility showing the enteric nervous system relaying psychological stress into intestinal inflammation, which is a plausible mechanism for the bad week, bad gut pattern that almost everybody describes ^[41]. It hasn’t been studied in hypermobility though, so treat it as a reason to suspect something rather than a reason to believe it.

Instability, Deconditioning, and the Loop Between Them

Recurrent subluxations, dislocations and general joint instability are repeatedly linked to acute rises in pain and to a heavier symptom load over time ^[42]. No great surprise there, though it’s worth saying that a run of subluxations during a flare is usually a consequence of the flare as much as a cause of it, as a tired body working off a noisier signal, makes worse decisions about how to move.

Physical inactivity and deconditioning appear to worsen symptoms and can set up a loop, where less activity means less tolerance, which means more pain and more orthostatic symptoms, which means less activity again ^[42][29]. That loop is the strongest argument there is for not treating a flare as a reason to stop everything.

One subtype note, because the word flare does real damage here. In vascular EDS, the events that matter are dissections, aneurysms and ruptures, and those are hallmark complications rather than routine flares ^[43][44]. Calling them a flare up makes them sound like something to ride out at home, and they are not. If you have vascular EDS, or a family history that suggests it, acute symptoms are an urgent medical question and nothing in this article applies to them.

What Actually Helps Between Flares

The clearest theme in the prevention literature is active, individualised management aimed at preventing injury and deconditioning, rather than rest, with physiotherapy, exercise, occupational therapy, self management education and psychological support sitting at the centre of care, and the same papers stressing repeatedly that the evidence base is limited and heterogeneous ^[45][46][47]. Care for hEDS and HSD is generally individualised, multidisciplinary and symptom led rather than protocol driven, which is frustrating if you wanted a plan handed to you, and correct given how differently people present ^[48][49].

– Strength and motor control work: The best supported thing on the list. Strengthening, motor control training and stability focused programmes generally improve pain, function or mobility over time in hEDS and HSD ^[45][46]. The caveat is a real one though: evidence quality is limited, controlled comparisons are weak, many of the programmes are small or aimed at one body region, and the optimal dose and progression are genuinely unknown ^[45][46]. So it works, and nobody can tell you exactly how much of it you need.

– Joint protection: Braces, splints, orthotics, adaptive equipment and body mechanics training are all commonly used to reduce strain on unstable joints ^[10][42]. The evidence is stronger for these helping symptoms than for them preventing anything long term, and in the qualitative work clinicians report immediate support and better joint awareness from fabric orthoses while accepting that efficacy remains unproven ^[50].

– Sleep and comorbidity care: Screening and actually treating sleep, autonomic symptoms, digestive problems, headache and mental health, gets framed repeatedly as part of controlling symptoms rather than as a side issue ^[26][34]. The mechanistic links are plausible and the intervention data in hypermobility are limited, which makes this a sensible bet rather than a proven one ^[34].

– Energy management: Pacing gets recommended whenever fatigue, orthostatic symptoms or post exertional worsening are limiting what somebody can tolerate, and in hypermobility specifically, people asked for exactly this when they were consulted about what a self management programme should contain ^[51][52].

Pacing is worth a word here, and our own pacing guide covers it at full length if you want the longer version. Direct trials in hEDS are sparse, most of the evidence comes across from ME/CFS and long COVID, and in those populations the reviews suggest possible benefit for fatigue and function while concluding that study quality and consistency aren’t good enough for firm rules ^[53][54]. Outside hypermobility, pacing evidence in chronic pain is low confidence and mixed for both pain and fatigue ^[55][56]. The work with people who actually live with this is more useful than the trials, and it lands on energy management as something to shape around your own life rather than a protocol to follow ^[57].

So, pacing is a pragmatic tool that a lot of people find useful. It’s not a proven treatment though, and anybody presenting it as one is ahead of the evidence.

What Helps While You’re Actually In One

Research specific to what to do during a flare is thin, and the confident flare protocols circulating online are not resting on a literature that exists. What the rehabilitation research and people’s own accounts describe, is a fairly consistent toolkit: temporarily modifying exercises rather than stopping them, using positions that take the load off, dealing with acute or recurrent subluxations, and using mobility aids, braces, splints, heat or cold as supportive measures ^[51][42][10]. Counter pressure manoeuvres for orthostatic symptoms and energy conservation strategies show up in the self management education side of it too ^[51].

Compression is the one supportive tool with some direct evidence behind it, and it’s better evidence than most of what gets recommended for a flare.

– Compression garments and pain: In adults with non vascular Ehlers-Danlos syndrome, mostly the hypermobile type, custom compression garments were associated with lower pain over follow up, along with some improvement in joint awareness and instability measures ^[58]. This was observational without strong controls, so treat it as encouraging rather than settled ^[58].

– Compression added to physiotherapy: Adding compression garments to physiotherapy improved dynamic balance more than physiotherapy alone in hEDS, while pain fell in both groups with no difference between them ^[59]. So the balance effect looks real, and the pain effect probably belongs to the physiotherapy.

– Shoulder specific compression: A compressive jacket reduced reported subluxations and dislocations at the shoulder and increased external rotator power at high speed, though the reduction in pain wasn’t reliable ^[60]. Useful if your shoulder is the joint that keeps going, and not evidence for compression as a general painkiller.

Medication is where expectations and evidence part company most sharply. NSAIDs and paracetamol are commonly used, and the pain management reviews stress that treatment studies in these conditions are few and insufficient for firm guidance ^[10][61]. Data collected from people’s own accounts of what they had tried show mixed and often low rates of improvement across a lot of modalities, with some reporting that specific treatments made things worse, including topical medications, injections, neuropathic agents, opiates and even physiotherapy ^[42]. Read that as heterogeneity rather than as a verdict on any one treatment, but do read it, as it means a treatment failing you is information about you rather than evidence you did it wrong.

What Nobody Knows Yet

The field knows that people with hEDS and HSD get whole body symptom escalation, it still doesn’t have strong prospective work showing which triggers reliably provoke a flare, in which subgroups, and through which mechanism ^[34][32][18]. Most of what exists is observational, clustered by symptom, and mechanistically incomplete, which is exactly why so much flare advice sounds more confident than it has any right to ^[2][32].

The specific open questions, so you know which arguments online are unresolved rather than decided. Whether the MCAS overlap is mechanistic or just co occurrence, nobody has established ^[34][35]. Whether hormonal shifts cause symptom worsening or simply accompany it, nobody has shown ^[2][36]. Which combination of exercise progression, energy management, joint support, sleep treatment and comorbidity specific care actually reduces how often flares happen, or how bad they get, has not been tested in well designed prospective work ^[34][18].

The shift that has already happened is the one to hold on to though, as this stopped being a joint problem with a few extras attached and became a whole body condition where pain, fatigue, sleep, mood, autonomic symptoms and recurrent injury all interact, and where disability tracks that whole picture rather than joint laxity on its own ^{[2][11][12][16]}.

The Fibro Guy

References

[1] Gensemer, C., Burks, R., Kautz, S., Judge, D.P., Lavallee, M. and Norris, R.A. (2020) ‘Hypermobile Ehlers‐Danlos syndromes: Complex phenotypes, challenging diagnoses, and poorly understood causes’, Developmental Dynamics. https://doi.org/10.1002/dvdy.220

[2] Daylor, V., Griggs, M., Weintraub, A., Byrd, R., Petrucci, T., Huff, M. et al. (2025) ‘Defining the Chronic Complexities of hEDS and HSD: A Global Survey of Diagnostic Challenges, Life-Long Comorbidities, and Unmet Needs’, Journal of Clinical Medicine. https://doi.org/10.3390/jcm14165636

[3] Clark, N.L., Johnson, M., Rangan, A., Kottam, L. and Swainston, K. (2023) ‘The biopsychosocial impact of hypermobility spectrum disorders in adults: a scoping review’, Rheumatology International. https://doi.org/10.1007/s00296-023-05298-2