Hypermobility: Beyond Loose Joints — hEDS, Fascia, Nervous System and Lymphatics
When most people think of hypermobility, they picture “double-jointed” party tricks or extreme yoga poses. But clinically, hypermobility is far more than just flexible joints — it’s a systemic connective tissue difference that affects the fascia, nervous system, proprioception, and even lymphatic circulation.
Understanding hypermobility requires zooming out from the joint itself and looking at the interconnected network of collagen, elastin, fascia, mechanoreceptors, and autonomic regulation that shapes how hypermobile bodies move, sense, and recover.
What Is Hypermobility? A Collagen-Based Perspective
At its core, hypermobility is linked to alterations in connective tissue structure, particularly collagen and elastin:
Collagen Types I and III: Type I provides tensile strength; Type III is more elastic. In hypermobility, the ratio often shifts toward more elastic tissue, increasing extensibility but reducing joint stability.
Extracellular Matrix (ECM) Dysregulation: Fibroblast activity and matrix metalloproteinases (MMPs) may be altered, affecting how collagen is formed and repaired, contributing to tissue fragility.
Result: Joints move beyond the physiological end range without the usual protective tension of ligaments and fascia, predisposing to injuries and chronic strain.
Fascia: The Body’s Sensory Web
Fascia is a living, innervated organ, dense with mechanoreceptors and nociceptors, making it integral to proprioception and pain signalling.
In hypermobility:
Reduced fascial stiffness: Leads to decreased structural support.
Altered mechanoreceptor feedback: The brain receives less precise proprioceptive input.
Muscle compensation: Chronic hypertonicity develops as muscles attempt to stabilize unstable joints, explaining why hypermobile individuals often feel simultaneously “too loose and too tight.”
Fascia is both a culprit and a compensator, influencing joint stability, movement patterns, and pain perception.
Nervous System: Proprioception and Autonomic Regulation
Proprioception is the brain’s ability to sense joint position, movement, and body orientation. Hypermobile individuals often experience:
Impaired joint position sense (JPS): The brain receives inaccurate signals from lax joints.
Motor control challenges: Clumsiness, poor fine motor skills, and higher injury risk.
Autonomic dysregulation: Many hypermobile individuals experience dysautonomia, including postural orthostatic tachycardia syndrome (POTS), due to:
Lax vessel walls → poor venous return
Inefficient baroreceptors → unstable blood pressure
Sympathetic overdrive → fatigue, dizziness, palpitations
The nervous system does more than “read joints”: it also manages cardiovascular tone, balance, and systemic responses to stress and movement.
The Lymphatic System: An Overlooked Connection
The lymphatic system relies on connective tissue and fascial support for optimal function. In hypermobility:
Reduced fascial support: Lymphatic vessels may lack the mechanical scaffolding needed for efficient flow.
Diaphragmatic dysfunction: Hypermobile individuals often breathe with accessory muscles rather than the diaphragm, reducing lymphatic propulsion.
Sympathetic dominance: Chronic stress can constrict lymphatic smooth muscle, slowing transport.
Consequences include:
Localized edema or heaviness
Slower recovery from exertion or illness
Immune dysregulation and increased inflammation
Hypermobility vs. hEDS — When It’s More Than Flexible Joints
While many people experience generalised joint hypermobility, hypermobile Ehlers–Danlos Syndrome (hEDS) is a hereditary connective tissue disorder representing the far end of the Hypermobility Spectrum.
Genetics and Collagen Function
No single gene mutation identified, but differences exist in fibroblast function, collagen fibrillogenesis, and ECM signalling, including TNXB and TGF-β pathways.
Effects: reduced collagen cross-linking, disorganized fibril architecture, and increased tissue compliance and fragility.
Systemic Manifestations
Dysautonomia (POTS)
Gastrointestinal dysmotility
Pelvic floor dysfunction and prolapse
Temporomandibular dysfunction and craniocervical instability
Fascial and Neurological Implications
Reduced fascial density → impaired mechanotransduction
Imprecise proprioceptive feedback → clumsiness, poor movement patterns
Chronic micro-injury → amplified nociception and central sensitisation
Lymphatic Implications
Lymphatic vessels may be too compliant, impairing flow
Venous pooling and low diaphragmatic tone exacerbate lymphatic stasis
Clinical consequences: edema, inflammation, slow recovery
Management and Clinical Approach
Effective management focuses on stability, regulation, and supportive interventions, not restricting movement:
Fascia & Proprioception:
Eccentric and isometric strengthening
Proprioceptive training: closed-chain exercises, unstable surfaces, eyes-closed drills
Nervous System:
Diaphragmatic breathing and vagal tone activation
Neuromotor retraining: Tai Chi, Feldenkrais, Pilates
Lymphatics:
Manual lymphatic drainage (MLD)
Rhythmic movement: walking, rebounding, swimming
Postural awareness to reduce pooling
Additional considerations: pacing, education, and gradual load progression to prevent injury.
Conclusion
Hypermobility is far more than loose joints. It is a systemic connective tissue variation affecting fascia, proprioception, the autonomic nervous system, and lymphatic circulation. Including hEDS provides a framework for understanding when hypermobility is part of a broader hereditary disorder.
By addressing fascial support, nervous system regulation, and lymphatic flow, individuals can enhance stability, reduce pain, and improve overall function, moving beyond the misconception that hypermobility is merely a “fun flexibility trick.”
References
Castori, M., et al. (2017). A framework for the classification of joint hypermobility. Am J Med Genet C, 175(1), 148–157.
Malfait, F., et al. (2017). The 2017 international classification of the Ehlers–Danlos syndromes. Am J Med Genet C, 175(1), 8–26.
Schleip, R., et al. (2019). Fascial system research: A narrative review. J Bodyw Mov Ther, 23(4), 555–567.
Rombaut, L., et al. (2010). Musculoskeletal complaints in hEDS. Disabil Rehabil, 32(16), 1339–1345.
Russek, L. N., et al. (2019). Recognizing and managing hypermobility-related conditions. Physiother Pract Res, 40(1), 1–14.
Chopra, P., & Tinkle, B. (2015). Pain management in EDS. Am J Med Genet C, 169(1), 84–96.
Voermans, N. C., et al. (2011). Fatigue in EDS. Semin Arthritis Rheum, 40(3), 267–274.
Levy, H. P. (2023). Ehlers–Danlos Syndrome, Hypermobility Type. GeneReviews.
