Why Rheumatologists Should Care About Hypermobility, EDS and Shared Mechanisms
Long COVID and hypermobility are more connected than most people, and many clinicians, realise. People with hypermobile Ehlers Danlos syndrome (hEDS), hypermobility spectrum disorders (HSD) and connective tissue variants are significantly more likely to develop Long COVID after infection, and more likely to experience prolonged, complex symptoms when they do. A 2025 study in BMJ Public Health found that generalised joint hypermobility is a statistically significant predictor of Long COVID, with extreme hypermobility carrying an even stronger association.
The reason comes down to shared biology. Both conditions disrupt the same underlying systems: autonomic regulation, mast cell behaviour, microvascular function and connective tissue integrity. The symptom overlap is not coincidental. It reflects a genuine mechanistic connection involving fatigue, orthostatic intolerance, brain fog, gastrointestinal dysfunction, pain and post exertional symptom worsening, all appearing in both conditions for related physiological reasons.
For patients this matters because it explains why Long COVID can feel so catastrophic for people who were quietly struggling before COVID arrived. For clinicians it matters because standard investigations remain normal despite significant functional impairment, and recognising the connective tissue piece changes how that picture should be read.
If you were ever called double jointed as a child, if your joints twisted a little too easily, if you felt tired in ways your friends did not, and then COVID happened and everything became unmanageable at once, this article is for you.
Key Takeaways
- Hypermobility appears to increase Long COVID risk.
- hEDS and HSD frequently overlap with POTS and dysautonomia.
- Shared mechanisms include autonomic dysfunction, mast cell activation and vascular instability.
- Pacing remains central to management.
- Recognition of hypermobility may improve care.
What is the connection between Long COVID and hypermobility?
Research suggests people with hypermobility, including hypermobile Ehlers-Danlos syndrome (hEDS) and Hypermobility Spectrum Disorder (HSD), may be more likely to develop Long COVID and experience more severe symptoms. Shared mechanisms include dysautonomia, mast cell activation, connective tissue abnormalities and microvascular dysfunction.
Long COVID and Hypermobility: When Your Body Was Already Playing on Hard Mode
Here is something a lot of people with Long COVID have had said to them over the years, often in childhood, usually by a PE teacher or a doctor doing a routine check: “You are very flexible, aren’t you?”
Some were called double jointed. Some were excellent at gymnastics or ballet and thought nothing more of it. Some quietly noticed that their ankles twisted a little too easily, that their knees ached after walking, that their stomach was unpredictable, that they felt tired in ways their friends did not.
And then COVID happened, and everything that had been quietly manageable became unmanageable all at once.
If this sounds familiar, you are not alone, and there is now real evidence explaining why.
Research published in BMJ Public Health in 2025 found that people with variant connective tissue, the umbrella term covering hypermobile Ehlers Danlos syndrome and hypermobility spectrum disorders, are significantly more likely to develop Long COVID after a COVID infection than those without these features. The association was even stronger in people with what the researchers called extreme hypermobility. This is not coincidence. It is biology.
What hypermobility actually is and what it means day to day What is hEDS and what is HSD Why hypermobile people were already at a disadvantage before COVID arrived What the research says about hypermobility as a Long COVID risk factor Why these two conditions look so similar on paper The shared mechanisms driving both What this means practically if you have Long COVID and are hypermobile What actually helps Frequently asked questions
What hypermobility actually is and what it means day to day
Hypermobility is more common than most people realise and more complicated than it sounds.
In simple terms it means your joints move further than they should. Elbows that extend past straight, thumbs that bend back to meet the forearm, knees that hyperextend slightly with every step. On a standard assessment called the Beighton score, clinicians check nine of these features and score them, though the score alone does not capture the whole picture.
For some people, being hypermobile causes no significant problems. For others, it comes with a cost that has nothing to do with joint flexibility and everything to do with what connective tissue actually does in the body.
Connective tissue is not just ligaments and tendons. It is everywhere. It lines blood vessel walls. It wraps around nerves. It holds organs in place and helps maintain pressure throughout the circulatory system. When connective tissue is less structurally rigid than it should be, the downstream effects can show up in places that seem to have nothing to do with joints: heart rate that races on standing, digestion that never quite works properly, skin that bruises from nothing, a nervous system that seems permanently on alert.
In real daily life, before COVID, this might have looked like:
Waking up stiff despite sleeping well, because muscles work overtime all night holding joints where they belong. Feeling unexpectedly wiped out after a day that looked fine from the outside. Eating something ordinary and spending the afternoon bloated and uncomfortable. Sitting at a desk for two hours and needing to shift position every fifteen minutes because something quietly aches. Being told you are anxious when you are actually dizzy.
The disconnect between how someone looks and how they feel is one of the most characteristic and most exhausting features of hypermobility related illness. And then Long COVID arrives and layers the same experience, but amplified and newly named, on top of a system that was already working harder than it appeared.
What is hEDS and what is HSD?
Hypermobile Ehlers Danlos syndrome, or hEDS, is the most common of the thirteen recognised types of Ehlers Danlos syndrome. It is a hereditary condition affecting how the body produces and structures collagen, the protein that gives connective tissue its strength and elasticity. Unlike several other types of EDS, there is currently no confirmed genetic test that can diagnose hEDS, which means diagnosis is clinical, based on a structured assessment of symptoms and family history. This has made it consistently underdiagnosed.
Hypermobility spectrum disorder, or HSD, sits alongside hEDS as a diagnosis for people with symptomatic joint hypermobility that causes real functional impairment but does not quite meet the full criteria for hEDS. HSD is not a lesser condition. It is a recognition that hypermobility exists on a spectrum and can cause significant illness at any point along it.
Both conditions are far more common in women than in men, and both are often diagnosed late, commonly in the thirties or forties, sometimes because symptoms were always present but put down to other things, and sometimes because a significant health event, such as pregnancy, surgery, or a viral illness, pushed a previously managed system past the point where it could compensate quietly.
Why hypermobile people were already at a disadvantage before COVID arrived
A 2024 review published in Frontiers in Neurology mapped the shared pathophysiology between Long COVID and hypermobility spectrum disorders in detail. It found that hypermobility has been detected in up to 30 to 57 percent of people with conditions including Long COVID, POTS, ME/CFS and fibromyalgia, compared with 10 to 20 percent of the general population, as documented in this review of shared pathophysiology of Long COVID and hypermobility spectrum disorders.
That clustering is not a coincidence. It reflects something about the underlying biology.
People with hEDS and HSD already have autonomic nervous systems working harder than average. Because blood vessels have less structural support, maintaining stable blood pressure and blood flow during posture changes requires more compensatory effort. The heart may beat faster. Blood may pool in the lower limbs. Digestion slows when blood is redirected elsewhere. The nervous system sends out more signals trying to keep up.
This background overload matters. Because before COVID, it could often be managed, perhaps imperfectly, with enough fluid, compression, rest and pacing. But the body was already closer to its physiological limit than it appeared. COVID did not have to push very hard to tip it past the point where compensation was possible.
What the research says about hypermobility as a Long COVID risk factor
The key study here was published in BMJ Public Health in September 2025, led by researchers from Brighton and Sussex Medical School and King’s College London. A case control survey of 1,816 adults across the UK and US found that generalised joint hypermobility was a statistically significant predictor of developing Long COVID after infection. People with what the researchers classified as extreme hypermobility showed an even stronger association. The study also found that hypermobility predicted higher symptom burden and a greater likelihood of ongoing fatigue, as described in this BMJ Public Health case control study on variant connective tissue and Long COVID risk.
An earlier study by Eccles and colleagues in BMJ Public Health had already found a link between joint hypermobility and self reported non recovery from COVID in the British COVID Symptom Study Biobank, which this larger study built on and strengthened.
This is still emerging research. Case control studies using self reported data have limitations, and the team is appropriately careful about stating what the data can and cannot confirm. But the direction and consistency of the findings across multiple cohorts, combined with the clear mechanistic reasons why this association would exist, makes it increasingly hard to dismiss as coincidence.
Why these two conditions look so similar on paper
Anyone who has spent time in a Long COVID patient group and in an EDS support group will notice something quickly. The symptom lists are almost identical.
The 2024 Frontiers review described extrapulmonary symptoms appearing in both conditions, including musculoskeletal pain, autonomic disorders, cognitive difficulties and fatigue, as a key feature of the overlap. Importantly it noted that these symptoms were present across ME/CFS as well, suggesting shared biological pathways rather than diagnostic confusion.
In daily life this means:
The profound fatigue that does not respond to sleep, and worsens the moment you do slightly too much. The brain fog that makes finding a word feel like searching for something in a dark room. The stomach that rebels without warning. The heart that races when you stand up from the sofa, then gradually steadies once you are still, then races again. The sensitivity to heat, to certain foods, to scratchy fabrics or strong smells. The sense that your nervous system is perpetually sitting somewhere between alert and overwhelmed.
Clinicians sometimes see these patients and reach for an anxiety diagnosis, because the symptom pattern can read as hyperactivation. And while anxiety is indeed common in both conditions, it does not explain the postural heart rate changes, does not explain the digestion, does not explain the post exertional crashes that happen like clockwork eighteen hours after anything that felt like a mildly active day.
The shared mechanisms driving both
Autonomic dysfunction
In hEDS and HSD, structural differences in the connective tissue supporting blood vessel walls make it harder for the autonomic nervous system to maintain stable circulation under demand. POTS, postural orthostatic tachycardia syndrome, is found in up to 57 percent of people with joint hypermobility in some studies, compared with roughly two to three percent of the general population, according to the Frontiers review.
In Long COVID, autonomic instability appears to arise from post viral disruption of the same regulatory systems, a disruption so structurally similar to the dysautonomia seen in ME/CFS that a 2026 study from the Brigham and Women’s Faulkner Hospital comparing 143 Long COVID patients with 170 ME/CFS patients could not distinguish the two groups on the basis of their autonomic test results. Patients with hEDS in that study did show more severe peripheral nerve changes, which is worth noting: the three conditions overlap but are not identical, as detailed in this study on the shared autonomic phenotype of Long COVID and ME/CFS including hEDS comparisons.
The practical result in daily life is the same regardless of cause. Standing up in the morning feels like a full cardiovascular event. A shower uses up more energy than a shower should. Walking to the kitchen and back can require a sit down.
Mast cell activation
The connection between mast cell activation and both Long COVID and hypermobility conditions is one of the more fascinating and frustrating areas of current research, fascinating because it explains so much, frustrating because the directional question of which comes first is still genuinely unresolved.
Mast cells release histamine and other inflammatory signals in response to triggers. In Long COVID, this process appears dysregulated. In hEDS, mast cell activation is a known associated feature, with some researchers proposing it may actually contribute to connective tissue laxity rather than just accompany it. The same 2024 Frontiers review specifically proposed that mast cell activation in Long COVID and ME/CFS may produce hyperinflammation that damages connective tissue, potentially inducing or worsening hypermobility in some patients.
In everyday terms, mast cell involvement explains the food sensitivities that appear out of nowhere, the flushing, the night sweats, the reactions to smells and medications that never caused problems before.
Connective tissue, blood vessels and microcirculation
Because hEDS and HSD affect the collagen that lines blood vessel walls, the vascular system in these patients has less structural support. This contributes to impaired microcirculation and unstable regulation of blood flow during activity or posture changes.
Long COVID independently produces endothelial dysfunction and reduced capillary density, as documented in recent vascular research, some of which is covered in our other articles on this site. In someone who already had connective tissue related vascular fragility, adding post viral endothelial injury may compound the problem considerably.
This is partly why standard investigations so often come back normal in both populations. The issue is not usually a discrete structural abnormality that a scan or blood test will catch. It is a dynamic instability that shows up under demand and resolves when the demand is removed, which is precisely when you are lying down calmly in a hospital clinic.
What this means practically if you have Long COVID and are hypermobile
The first and most important thing it means is that your symptoms are not disproportionate to what is happening in your body. They are exactly proportionate. You just have two systems pulling in the same direction at once, and the compound effect is bigger than either one alone.
For clinicians: recognising this overlap changes the risk profile significantly. Someone with Long COVID and underlying hEDS may have a higher burden of autonomic instability, more pronounced post exertional symptom exacerbation, and a greater sensitivity to interventions like graded exercise that would be contraindicated anyway in the post exertional context but particularly so here. Joint instability also creates its own physical demands that can be invisible in a standard consultation.
For patients: if you have Long COVID and have ever been told you were flexible, or if you can touch your palms flat to the floor without bending your knees, or your thumbs bend back to your wrists, or your elbows go past straight, it is worth raising hypermobility as a possibility with your clinician. It is not always relevant, and hypermobility alone does not explain everything. But if it fits the pattern of your life before COVID as well as after it, it deserves proper assessment rather than being set aside.
What actually helps
Management here requires thinking about both conditions at once rather than treating Long COVID as a clean slate.
Pacing first, everything else second. Both Long COVID and hEDS are characterised by post exertional symptom exacerbation. The research on graded exercise therapy in ME/CFS, which overlaps significantly with both conditions, has not shown benefit and has in some studies caused harm. The starting point in any management plan needs to respect energy limits. We cover this in more detail in our post exertional malaise article.
Joint support without overexertion. Physical therapy for hEDS focuses on joint stabilisation, meaning building the muscle support around joints to compensate for loose ligaments, rather than on flexibility or general fitness building. This principle needs to be applied very carefully within pacing limits, which means a physiotherapist who understands both hypermobility and post exertional symptom exacerbation is a meaningful advantage.
Autonomic support. Fluid and sodium intake, compression garments for the lower limbs, and careful postural habits such as moving to upright gradually rather than suddenly, are all first line approaches for POTS and dysautonomia that apply equally in Long COVID and hEDS. These are low risk and often meaningfully helpful.
Mast cell awareness. If you have noticed new food sensitivities, skin reactions, or sensitivities to medications since COVID, a low histamine approach to diet, alongside discussion with a clinician about whether mast cell activation syndrome warrants investigation, may be relevant to your picture specifically.
Coordinated rather than fragmented care. Both conditions cross specialty lines in ways that create gaps. Rheumatology may see the joint picture. Cardiology may see the POTS. Neurology may see the small fibre neuropathy. Nobody necessarily looks at the whole. Being explicit with each clinician about the overlap, and asking for care that considers all of it together, is one of the most practically useful things someone navigating this intersection can do.
This is genuinely complicated medicine. Not because patients are complicated people, but because the underlying biology is genuinely interconnected in ways that specialty silos were not designed to capture. The evidence is building. The dots are being connected. And if you have been told for years that you are simply flexible and simply anxious and simply deconditioned, it is worth knowing that a 2025 BMJ study, published by researchers at two leading UK institutions, is now saying something rather different.
Frequently asked questions
Is there a proven link between hypermobility and Long COVID?
Yes, with appropriate caveats. A 2025 BMJ Public Health study found that people with joint hypermobility, especially extreme hypermobility, were significantly more likely to develop Long COVID after COVID infection. The association held even after adjusting for other factors. The research is still developing and this was a retrospective survey study, but it fits the biological picture well.
Can Long COVID cause hypermobility?
The relationship may actually go in both directions. People with hypermobility appear more susceptible to Long COVID, but researchers have also proposed that the ongoing inflammation from Long COVID may damage connective tissue in a way that induces or worsens hypermobility over time. The 2024 Frontiers in Neurology review discussed mast cell activation as a possible mechanism for this.
Can COVID unmask hypermobility that was there all along?
This is one of the more clinically significant findings in this area. For people who were hypermobile but compensating well enough to function, COVID may push the autonomic system past the threshold where compensation is possible. Symptoms that were mild or intermittent before can become central and disabling afterwards. The body did not change. The reserve it was drawing on ran out.
Why do the symptoms of Long COVID and hEDS look so similar?
Because both conditions disrupt the same underlying systems: autonomic regulation, mast cell behaviour, microvascular function and connective tissue stability. When these systems are disrupted in similar ways, the clinical picture looks similar regardless of which condition is driving it.
Should I be assessed for hypermobility if I have Long COVID?
If you have a personal or family history of flexible joints, chronic pain, POTS, digestive dysfunction, or frequent sprains and injuries, it is worth raising. Hypermobility assessment is non invasive and uses structured clinical criteria. Recognising it can change how your management is approached, particularly around exercise and pacing.
Why are tests normal in both these conditions?
Because the dysfunction is usually dynamic rather than structural. The problem shows up under demand, during posture changes, after exertion, in response to triggers, not in a static scan or resting blood test. This is a recognised limitation of standard testing, not evidence that nothing is wrong.
What is the connection to POTS?
POTS is extremely common in both hEDS and Long COVID. The mechanisms differ somewhat, but the clinical result is similar: heart rate rises excessively on standing, blood flow to the brain reduces, and symptoms like dizziness, palpitations, brain fog and fatigue worsen in upright positions and improve lying down. See our separate article on POTS and Long COVID for more detail on management.
Is hypermobility more common in women?
Yes. Both hEDS and HSD are significantly more common in women, as are Long COVID and POTS. The reasons are not fully understood but likely involve hormonal effects on connective tissue, differences in immune regulation, and a history of diagnostic dismissal that has led to research underrepresentation.
Does treating hypermobility improve Long COVID symptoms?
There is no single treatment for either condition, but addressing the components that overlap, particularly autonomic instability, pacing around post exertional symptom exacerbation, and mast cell activation, can reduce overall symptom burden. Managing hypermobility related joint instability also reduces the baseline physical load on a system that is already overtaxed.
What is the trifecta or trifecta overlap in this context?
The trifecta refers to the clinical observation that hEDS, POTS and mast cell activation syndrome very commonly cluster together in the same patient. Long COVID has brought all three of these into closer clinical view because it can trigger or amplify each of them independently. Patients who find themselves navigating all three at once are not unusual, and are not imagining the complexity of what they are dealing with.
Should hypermobile people take extra precautions around COVID infection?
Based on current evidence, it seems reasonable for people with hEDS or significant HSD to be aware of their potential increased risk of developing Long COVID, and to take prevention and early management seriously. This does not yet translate into specific clinical guidelines, but it is a reasonable consideration to discuss with a clinician.
Can graded exercise therapy help with Long COVID if I am also hypermobile?
No. Graded exercise therapy is not recommended for Long COVID with post exertional symptom exacerbation, and this concern is amplified in someone who is also hypermobile, where inappropriate exercise can cause joint instability and injury alongside post exertional crashes. Pacing and stabilisation based physiotherapy adapted to the specific presentation are the safer approaches.
Why have so many people with hypermobility waited years or decades for a diagnosis?
Because hypermobility, particularly hEDS, has historically been underrecognised by medical training, because its symptoms cross multiple specialties without belonging clearly to any one of them, and because it predominantly affects women who are more likely to have their symptoms attributed to anxiety or low pain tolerance. The same patterns of diagnostic delay and dismissal appear in Long COVID. The overlap extends to the experience of trying to get appropriate care, not just to the biology.
Why Are So Many People With Long COVID Discovering They Are Hypermobile?
One of the more intriguing patterns emerging from Long COVID communities is how many people are discovering they are hypermobile for the first time.
For some, the signs were always there. They were the child who could do the splits without trying, the teenager whose ankles seemed to roll constantly, or the adult who was told they were simply “very flexible.” But because hypermobility is often viewed as a harmless trait rather than a medical condition, it was never investigated further.
COVID appears to have changed that.
Is hypermobility genetic?
Yes. Hypermobile Ehlers-Danlos syndrome (hEDS) and many forms of symptomatic hypermobility tend to run in families. It is common for people diagnosed later in life to realise that a parent, sibling or child has similar traits such as unusually flexible joints, recurrent injuries, chronic pain, dizziness, digestive problems or fatigue. While the exact genetic cause of hEDS has not yet been identified, a hereditary component is well recognised.
About This Article
This article was written for LongCovidJourney, an independent patient-led resource focused on evidence-informed information about Long COVID. It combines lived experience with review of current medical research, including peer-reviewed studies on hypermobility, dysautonomia, mast cell activation and post-viral illness. Medical understanding of Long COVID continues to evolve and this article will be updated as new evidence emerges.
This article is for general information and education. It does not replace personalised medical advice. If you have Long COVID and suspect hypermobility may be relevant to your presentation, please discuss this with a clinician familiar with post viral illness or connective tissue disorders.
Sources and further reading
Key studies Variant connective tissue as a risk factor for Long COVID, BMJ Public Health 2025: https://pmc.ncbi.nlm.nih.gov/articles/PMC12458677/ Long COVID and hypermobility spectrum disorders: shared pathophysiology, Frontiers in Neurology 2024: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11410636/ Shared autonomic phenotype of Long COVID and ME/CFS including hEDS comparisons, Brigham and Women’s Hospital 2026: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12829881/
Background on hEDS and hypermobility What is EDS, the Ehlers Danlos Society: https://www.ehlers-danlos.com/what-is-eds/ Biopsychosocial impact of hypermobility spectrum disorders in adults: https://pmc.ncbi.nlm.nih.gov/articles/PMC10126066/
Mast cell activation and the trifecta Hidden link between inflammation and hypermobility in Long COVID and ME/CFS: https://jeanniedibon.com/me-cfs-eds-long-covid-inflammation-connection/ POTS, EDS and MCAS: understanding the trifecta: https://www.thefibroguy.com/blog/pots-eds-and-mcas-understanding-the-trifecta/