Hypermobility Spectrum Disorder and hEDS: What Lies Beyond Being Flexible

There’s a common misconception that hypermobility is simply a matter of being “double-jointed” or particularly flexible — and that it’s always a good thing. After all, ballet dancers, gymnasts, and yoga teachers are often celebrated for their extraordinary range of motion. But for a significant number of people, joint hypermobility is not a party trick or a competitive advantage. It’s a source of daily pain, fatigue, instability, and significantly reduced quality of life.

What Is Joint Hypermobility?

Joint hypermobility refers to joints that move beyond their normal range of motion due to laxity in the connective tissues — tendons, ligaments, and the joint capsule itself. This laxity is often caused by variations in collagen structure, which affect the mechanical properties of connective tissue throughout the body.

Hypermobility exists on a spectrum. At one end, you have individuals with asymptomatic generalised joint hypermobility (aGJH) — flexible people who experience no problems whatsoever. At the other end lies hypermobile Ehlers-Danlos Syndrome (hEDS), a heritable connective tissue disorder with systemic involvement. Between these two poles is what clinicians now call Hypermobility Spectrum Disorder (HSD).

Understanding this distinction is clinically important. The terminology has changed considerably over the past decade, and even many healthcare practitioners haven’t fully caught up.

The Beighton Score: Useful, But Limited

The most widely used clinical screening tool for generalised joint hypermobility is the Beighton Score. It assesses 9 points across five tests:

• Passive dorsiflexion of the little finger beyond 90° (1 point each side)
• Passive apposition of the thumb to the flexor surface of the forearm (1 point each side)
• Hyperextension of the elbow beyond 10° (1 point each side)
• Hyperextension of the knee beyond 10° (1 point each side)
• Forward flexion of the trunk with knees extended so the palms rest flat on the floor (1 point)

A score of 5/9 or above is commonly used to diagnose generalised joint hypermobility in adults (4/9 in those over 50, and 6/9 in children).

However, the Beighton Score has significant limitations. It doesn’t assess the hip, shoulder, or ankle — three joints frequently affected in hypermobile patients. It doesn’t capture the day-to-day fluctuation of symptoms, and it misses the many people whose hypermobility is localised rather than generalised. High scores in isolation don’t confirm pathology; low scores don’t rule it out. The Beighton Score is a useful starting point, not a complete answer.

From Flexible to Symptomatic: What Changes?

Not everyone who scores high on the Beighton test will develop symptoms. What appears to trigger the transition from asymptomatic hypermobility to symptomatic HSD often includes:

• A significant increase in physical load — a new sport, a sudden increase in training intensity, pregnancy
• Sedentary periods that lead to deconditioning of stabilising musculature
• Repetitive strain or cumulative micro-trauma
• A single significant injury that initiates a pain cycle
• Hormonal changes — oestrogen is known to influence ligament laxity, which is why many women with hypermobility report symptom flares around menstruation, pregnancy, and menopause

When joints lack adequate passive restraint from ligaments and capsule, the burden of stability falls disproportionately to the surrounding musculature. Over time, this creates persistent muscular overactivation, fatigue, and the development of myofascial trigger points. Pain becomes complex and widespread. Patients often describe a paradox: they feel stiffest and most uncomfortable at rest, and have a constant urge to move or “click” their joints for relief — only for symptoms to return shortly afterwards.

Hypermobility Spectrum Disorder (HSD)

HSD was formally defined in the 2017 International Consortium on Ehlers-Danlos Syndromes as a diagnosis for individuals who have symptomatic hypermobility that does not meet the full diagnostic criteria for hEDS or another heritable connective tissue disorder. It is not a lesser condition — it can be equally disabling — but it lacks the full systemic feature profile required for an hEDS diagnosis.

HSD subtypes include generalised HSD (G-HSD), where widespread hypermobility produces musculoskeletal symptoms across multiple joints; peripheral HSD (P-HSD), limited to the hands and feet; localised HSD (L-HSD), affecting one or a small number of joints; and historical HSD (H-HSD), a history of hypermobility in patients who appear to have “tightened up” with age but retain symptomatic sequelae.

Hypermobile EDS (hEDS)

hEDS is the most common form of Ehlers-Danlos Syndrome and is distinguished from HSD by additional clinical criteria, which must be met in combination. These include:

• A positive family history — at least one first-degree relative with a confirmed hEDS diagnosis
• Systemic features: skin hyperextensibility, atrophic or papyraceous scarring, piezogenic papules (fatty papules visible on the heel under weight-bearing), dental crowding, high palate, or Gorlin’s sign (ability to touch the tongue to the tip of the nose)
• Generalised joint hypermobility on the Beighton Score (thresholds vary by age)
• Musculoskeletal complications: recurrent joint dislocations or subluxations, chronic widespread pain, fatigue

Critically, a formal hEDS diagnosis requires all three criterion groups to be met simultaneously. It is a clinical diagnosis — there is currently no genetic test that confirms hEDS. Diagnosis is typically made by a clinical geneticist, rheumatologist, or specialist with connective tissue expertise.

Systemic Features: Beyond the Joints

One of the most important aspects of hypermobility disorders that healthcare practitioners frequently underappreciate is that these conditions are not purely musculoskeletal. Connective tissue is present throughout every organ system in the body, and in those with heritable variants in collagen or associated proteins, the effects can be wide-ranging and deeply interconnected.

Dysautonomia and POTS

Postural Orthostatic Tachycardia Syndrome (POTS) is significantly overrepresented in people with hEDS and HSD. When moving from lying or sitting to standing, heart rate increases by 30 beats per minute or more (or exceeds 120 bpm), without a corresponding drop in blood pressure. Symptoms include dizziness, pre-syncope, fatigue, brain fog, palpitations, and nausea. Many patients with POTS are misdiagnosed with anxiety or panic disorder for years before POTS is identified. The mechanism linking hypermobility to POTS is thought to involve laxity of blood vessel walls and impaired venous return, combined with dysregulation of the autonomic nervous system.

Mast Cell Activation Syndrome (MCAS)

There is a well-documented high rate of co-occurrence between hypermobility disorders and MCAS, a condition in which mast cells release excessive mediators in response to triggers such as heat, stress, foods, medications, exercise, or environmental chemicals. Symptoms can include flushing, urticaria (hives), gastrointestinal disturbance, fatigue, and in severe cases, anaphylaxis. The triad of hypermobility disorders, POTS, and MCAS — sometimes called the “hypermobility trifecta” — has gained significant recognition as a clinically meaningful cluster warranting specialist co-management.

Gastrointestinal Dysmotility

Symptoms of irritable bowel syndrome, gastroparesis, chronic constipation, and gastro-oesophageal reflux are disproportionately common in hypermobile patients. Connective tissue laxity affecting the gut wall, combined with autonomic dysregulation of smooth muscle, is thought to impair normal motility. Many patients with hEDS and HSD have received prior diagnoses of IBS or functional gut disorders without the underlying connective tissue component being identified.

Fatigue

Not the ordinary tiredness of a busy life, but a profound, often post-exertional fatigue that does not resolve with rest. Post-exertional malaise — where exertion, even mild exertion, triggers a significant worsening of symptoms lasting 24 hours or more — is a feature that significantly overlaps with ME/CFS. The mechanisms are multifactorial: the additional muscular effort required to stabilise hypermobile joints is metabolically expensive, autonomic dysfunction impairs energy regulation, and disrupted sleep compounds the picture.

Mental Health

Anxiety is particularly prevalent in hypermobility disorders — at rates far exceeding what would be expected from chronic pain alone. Research suggests this is not purely a psychological response to difficult circumstances. There may be shared neurobiological pathways involving interoception (the brain’s awareness of internal body signals), connective tissue mechanoreceptors, and the autonomic nervous system. Clinicians should be aware that treating anxiety without addressing the underlying hypermobility presentation will have limited benefit.

Why Diagnosis Takes So Long

Studies have reported an average time from symptom onset to diagnosis of over 10 years for hEDS and related conditions. This is not an accident — it is a predictable consequence of several systemic failures:

• Symptoms are varied, fluctuating, and not obviously connected to a single organ system
• Many practitioners have not received specific training in connective tissue disorders
• Joint pain in young flexible women is frequently attributed to anxiety, deconditioning, or “benign hypermobility”
• There is no biomarker or definitive diagnostic test for hEDS or most forms of HSD
• Patients — disproportionately young women — may have their pain minimised, dismissed, or attributed to mental health without adequate investigation
• Comorbidities such as POTS and MCAS are often managed in silos without the connecting picture being recognised

If you have been told you are “just flexible” but experience chronic joint pain, recurrent sprains or subluxations, fatigue, and symptoms spanning multiple body systems, it is worth asking specifically about hypermobility spectrum disorders. Bringing a prepared symptom history, including the Beighton Score self-assessment and a description of systemic symptoms, to a GP appointment can help facilitate an appropriate referral.

Management: What Actually Works?

There is no cure for hypermobility disorders. However, with the right approach, most people can significantly improve their function, pain levels, and quality of life. Management is multidisciplinary and requires patience — this is a long-term condition requiring a long-term strategy, not a quick fix.

Exercise and Graduated Loading

This is the single most important intervention. The goal is to build the muscular strength and neuromuscular control that compensates for the body’s insufficient ligamentous restraint. However, exercise must be carefully prescribed and gradually progressed — too much too soon almost invariably triggers a flare. Low-impact resistance training, clinical Pilates, swimming, and targeted proprioceptive exercises are generally well-tolerated starting points. High-impact activities and exercises that take joints to end-range (including aggressive yoga stretching) can worsen symptoms and should be approached with caution.

Key muscle groups to prioritise include the deep cervical flexors, rotator cuff, lumbar multifidus and transversus abdominis, gluteal complex, and intrinsic foot muscles. These are the primary stabilisers for their respective regions — and in hypermobile patients, they are typically underdeveloped relative to the demands placed on them.

Proprioception Training

Hypermobile joints frequently have impaired proprioception — the joint’s awareness of its position in space. Without accurate feedback, the nervous system cannot efficiently coordinate muscular responses to maintain joint stability. Targeted proprioceptive training — balance boards, single-leg exercises, closed-chain exercises that load joints through functional ranges — helps retrain this awareness and reduces injury risk over time.

Pacing

Post-exertional malaise drives the classic “boom-bust” cycle in hypermobility disorders: a good day leads to over-exertion, which triggers a flare, which leads to prolonged rest, which leads to deconditioning, which makes the next good day harder. Pacing involves planning activity levels deliberately — building in rest breaks, setting conservative activity ceilings, and gradually expanding capacity rather than letting symptom fluctuation dictate effort. This is a learnable skill, and working with an occupational therapist or pain psychologist experienced in pacing can be transformative.

Joint Protection

Taping, bracing, and splinting can provide external stability to joints during specific activities — particularly in the hands, wrists, and ankles. Kinesiology taping around the knee or shoulder during sport can reduce subluxation risk. Ring splints for finger joints are widely used by people with hEDS for daily activities. The goal is to protect joints without creating excessive dependence — the focus remains on active muscular stability as the primary long-term strategy.

Pain Management

Multimodal pain management is generally more effective than any single approach. Non-pharmacological strategies include graded exercise, sleep optimisation, heat therapy, hydrotherapy, and psychological support. For pharmacological management, NSAIDs are commonly used for flares; low-dose naltrexone has shown promise in some studies for widespread chronic pain; and in complex cases with significant central sensitisation, a pain specialist referral is appropriate. Opioids are generally avoided in the long-term management of hypermobility-related pain due to poor evidence and significant risks.

Psychological Support

Chronic pain, fatigue, and systemic symptoms inevitably affect mental health and sense of identity. Acceptance and Commitment Therapy (ACT) has the strongest evidence base in chronic pain contexts, and this extends to hypermobility-related pain. CBT and mindfulness-based interventions are also useful. Peer support — through organisations such as the Ehlers-Danlos Society and Hypermobility Connect (in Australia) — can reduce isolation and provide practical strategies from lived experience.

The Role of Osteopathy

Osteopathy can play a meaningful role in managing hypermobility disorders — with an important clinical caveat. The classical approach of stretching, mobilising, and high-velocity manipulation of joints is largely counterproductive for hypermobile patients. These joints do not need more range of motion; they need stability, load tolerance, and proprioceptive control.

What osteopathic management can appropriately offer includes soft tissue therapy and myofascial release for the chronically overworked, hypertonic muscles that attempt to compensate for ligamentous laxity; education on joint protection principles and activity modification; graduated loading programs targeting key stabilising muscle groups; postural and ergonomic advice to minimise unnecessary joint loading; management of secondary musculoskeletal pain (headaches, thoracic stiffness, rib dysfunction) that frequently accompanies hypermobility; and coordination of care with physiotherapy, rheumatology, immunology, cardiology, and psychology as needed.

Screening for hypermobility — including use of the Beighton Score and a brief systemic history — should be a routine part of every new patient assessment. Identifying hypermobility early changes the treatment approach fundamentally and avoids the common clinical error of prescribing stretching and end-range mobilisation for someone whose primary problem is too much range, not too little.

When to Seek Further Assessment

Consider requesting a referral to a rheumatologist or clinical geneticist if you have recurrent joint dislocations or subluxations affecting multiple joints; a first-degree relative with confirmed hEDS or a related connective tissue disorder; systemic symptoms (POTS, suspected MCAS, significant gastrointestinal involvement) alongside joint hypermobility; or symptoms that are significantly impacting quality of life despite a sustained trial of conservative management. A formal diagnosis, while not essential for management to begin, opens access to targeted multidisciplinary support and in some cases disability services and supports not available without a confirmed diagnosis.

Disclaimer: The information provided in this article is for general educational purposes and does not constitute medical advice. If you believe you may have hypermobility spectrum disorder or a related condition, please seek assessment from a qualified healthcare professional.

If you are wondering whether general flexibility alone is ever a concern, our earlier article Hypermobility: Can You Be Too Flexible? covers the basics.