Personalised Support for Ehlers-Danlos Syndrome & Hypermobility
At the Autoimmune Clinic, we support individuals living with hypermobile Ehlers-Danlos syndrome (hEDS) and Hypermobility Spectrum Disorders (HSD), conditions that extend far beyond joint hypermobility alone.
HYPERMOBILITY IS LINKED WITH A WIDE RANGE OF ASSOCIATED CONDITIONS. WE LOOK BEYOND THE DIAGNOSIS TO UNDERSTAND HOW CONNECTIVE TISSUE AFFECTS IMMUNITY, NERVOUS FUNCTION, DETOXIFICATION, AND OVERALL HEALTH.
Many of our clients have spent years collecting multiple labels such as chronic fatigue syndrome, fibromyalgia, depression, anxiety, IBS, or “unexplained pain” before hypermobility is ever identified as a core underlying factor.
Many of our clients have spent years collecting multiple labels such as chronic fatigue syndrome, fibromyalgia, depression, anxiety, IBS, or “unexplained pain” before hypermobility is ever identified as a core underlying factor.
Our functional medicine approach is holistic and personalised.
We explore the root causes, work systematically across all affected systems, and create a bespoke support plan that helps stabilise the body, reduce inflammation, support resilience, and improve quality of life.
What Is Ehlers-Danlos Syndrome (EDS)?
Ehlers-Danlos syndromes are a group of inherited connective tissue disorders affecting collagen structure and function. Collagen forms the scaffolding of the body, influencing joints, blood vessels, fascia, the gut lining, and even immune system architecture.
Connective tissue is not “dead” tissue.
It is metabolically active and constantly communicates with the immune system through biochemical signalling. Disruption in connective tissue can increase inflammatory signalling molecules such as MMP-9, influence cytokine activity, and alter how the immune system senses and responds to perceived threats. This helps explain why many individuals with hypermobility experience widespread inflammation, immune dysregulation, and heightened sensitivity to stressors.
Common features of hEDS include:
• Generalised joint hypermobility
• Instability, sprains, and subluxations
• Muscle tension, pain, and fatigue
• Poor proprioception
• Immune system dysregulation and
• Heightened sensitivity to medications and supplements
• Gut symptoms such as bloating, reflux, constipation, or diarrhoea
• Autonomic instability such as dizziness and palpitations
Because collagen underpins multiple systems, hEDS naturally leads to
a broader pattern of dysregulation rather than symptoms occurring in a
single area.
Why Co-Morbities Are Common in Hypermobility and hEDS?
Many individuals with hypermobility receive multiple diagnoses over the years as different symptoms emerge across several body systems. It is common for clients to spend years seeking answers and to accumulate labels that never really explain the underlying issue(s).
These often include chronic fatigue syndrome, fibromyalgia, anxiety or depression, IBS, migraines, “unexplained inflammation”, and various forms of sensory hypersensitivity. The reason for this is that hypermobility affects far more than joints. Differences in connective tissue influence immune and cytokine signalling, mast cell behaviour, gut barrier integrity, blood vessel stability, detoxification capacity, autonomic nervous system function, and mitochondrial energy production. When these systems are disrupted simultaneously, a wide and seemingly unrelated constellation of symptoms can appear, leading to the long list of diagnoses that many hypermobile clients recognise all too well.
Taken together, these can create a complex clinical picture that is often misunderstood in a conventional care setting. Below, we explore the co-morbidities we most frequently see in hypermobile clients and how we support them through a functional and systems-based approach.
Hypermobility, Chronic Fatigue Syndrome & Fibromyalgia
Chronic fatigue and fibromyalgia are two of the most frequently reported diagnoses in individuals with hypermobile EDS and HSD. In many cases, these labels are given long before hypermobility is recognised, and they reflect underlying multisystem dysfunction rather than isolated conditions.
Why Chronic Fatigue Is So Common in hEDS
Fatigue in hypermobility is rarely due to a single cause. Instead, it often arises from the combined effects of:
• Undiagnosed autoimmune disease or CIRS.
• Autonomic dysfunction (POTS or low blood pressure stability)
• Mast cell activation and chronic inflammatory signalling
• Mitochondrial inefficiency and impaired energy production
• Sleep disruption or non-restorative sleep
• Gut dysbiosis, SIBO/SIFO, or poor nutrient absorption
• Viral reactivation, mould exposure, or immune dysregulation
• Increased MMP-9 and cytokine activity affecting tissues and nerves
• Constant muscular compensation for joint instability
Why Fibromyalgia Often Coexists With hEDS
Fibromyalgia is characterised by widespread pain, tenderness, and heightened sensory processing. In hypermobile individuals, several mechanisms contribute:
• Connective tissue fragility leads to micro-instability and increased muscle tension
• Central sensitisation amplifies pain signals in the brain and spinal cord
• Chronic inflammation and mast cell mediators activate pain pathways
• Autonomic instability affects blood flow to muscles and tissues
• Poor sleep quality increases pain sensitivity
• SIBO/SIFO and gut permeability can drive systemic inflammation
Fibromyalgia in hEDS is, therefore, not simply “muscle pain”, but a reflection of systemic overload and altered signalling between connective tissue, nerves, immune cells, and the brain.
MORE ABOUT CHRONIC FATIGUE AND FIBROMYALGIA HERE >
Hypermobility & Mast Cell Activation Syndrome (MCAS)
MCAS is extremely common in individuals with hEDS. Connective tissue instability affects mast cells, making them more prone to inappropriate activation and mediator release. This contributes to unpredictable inflammatory “flares”, reactivity to foods or supplements, and general system overload.
MCAS may present with:
• Flushing, itching, hives
• Food reactions or multiple sensitivities
• Bloating, abdominal discomfort, diarrhoea or constipation
• Temperature dysregulation
• Palpitations or anxiety-like symptoms
• Brain fog and difficulty concentrating
People with hEDS often have mast cells embedded throughout loosened or fragile connective tissue structures, amplifying reactivity. MMP-9, a connective tissue remodelling enzyme, can be elevated in states of chronic inflammation and mast cell activity, contributing to sinus issues, gut inflammation, or neurological symptoms.
Our support includes:
• Identifying triggers such as histamine, mould, chemicals, or stress
• Mast cell stabilisation
• Low-histamine or modulated diets where appropriate
• Detoxification and liver support to reduce burden
• Nervous system regulation to calm mast cell-nerve interactions
CIRS & Mould Illness in Hypermobile / hEDS Individuals
CHRONIC INFLAMMATORY RESPONSE SYNDROME
Clients with hEDS often experience stronger or more prolonged responses to environmental and biological stressors, including mould exposure. Genetic susceptibility and altered immune signalling can make it harder for the body to regulate inflammation and clear biotoxins when they are present, which may increase the risk of developing Chronic Inflammatory Response Syndrome (CIRS) in a subset of individuals.
Common features we see include:
• Persistent fatigue
• Brain fog and difficulty processing information
• Increased reactivity to foods or supplements
• Sinus congestion, recurring infections, or MARCoNS
• Hormonal and sleep disruptions
• Temperature instability
• Poor tolerance of detoxification interventions
Our clinical approach focuses on stabilising the system and addressing root drivers.
This often includes:
• Shoemaker Protocol style screening including HLA genes, VCS, and inflammatory markers
• Guidance on assessing the home environment and determining whether remediation is needed
• Calming and regulating the immune system before introducing binders
• Supporting detoxification pathways
• Reducing overall reactivity so that deeper healing can take place
This framework ensures that mould is considered within the wider context of hEDS physiology rather than treated as the sole cause of symptoms.
Hypermobility, Postural Orthostatic Tachycardia Syndrome (POTS) & Dysautonomia
Autonomic nervous system imbalance is one of the most common and disabling challenges in hEDS, and it often appears long before individuals receive a diagnosis. Because connective tissue provides structural support to blood vessels, lymphatics, and the surrounding nerves, any laxity or fragility can impair the body’s ability to regulate circulation. This means that hypermobile individuals frequently struggle to maintain stable blood pressure and heart rate, particularly when moving from sitting to standing or when spending prolonged periods upright.
For many, this presents as a constant feeling of physiological instability. The body must work much harder to push blood back to the brain and vital organs. As a result, even small physical tasks can trigger a disproportionate stress response, leaving individuals feeling depleted, shaky, or unwell.
Common symptoms include:
• Dizziness and lightheadedness
• Palpitations or a racing heart
• Fatigue after minimal activity
• Heat intolerance or temperature dysregulation
• Nausea, bloating, or gut dysmotility
• Exercise intolerance or “crashing” after exertion
These symptoms do not occur in isolation. Autonomic dysfunction often overlaps with mast cell activation, impaired gut motility, electrolyte imbalance, and chronic low-grade inflammation. Each of these factors places additional pressure on an already sensitive nervous system, creating a loop where the body becomes increasingly reactive and less resilient.
Over time, this imbalance can affect daily functioning, cognitive clarity, sleep regulation, and the ability to tolerate physical rehabilitation. Understanding the interconnected nature of these systems is essential, as supporting autonomic stability typically requires addressing circulation, hydration, electrolytes, mast cells, gut inflammation, and overall neuroimmune balance together rather than focusing on one pathway alone.
Hypermobility, Long COVID & Post-Viral Syndromes
Hypermobile individuals frequently experience worsened or prolonged symptoms following viral infections. The immune system is often already operating in a heightened or unstable state, which means that a viral trigger can tip the balance further and make recovery slower, more reactive, and more complex. Connective tissue plays an active role in immune signalling, so when it becomes dysregulated, the body may struggle to switch off inflammatory pathways after the initial infection has resolved.
In clinic, we commonly see:
• Post-exertional malaise
• Severe fatigue
• Brain fog and sensory overload
• Heightened MCAS symptoms
• Food and supplement intolerance
• Dysautonomia and POTS-like features
These patterns are intensified by the close relationship between hEDS, MCAS, dysautonomia, and chronic inflammatory states. Viral infections, including COVID, can provoke strong mast cell activation. In some individuals, components such as the spike protein appear to keep mast cells primed, contributing to prolonged sensitivity, inflammation, and reduced tolerance to interventions.
For a subset of hypermobile clients, a viral illness can also reveal difficulties with shutting down the inflammatory response, leading to a CIRS-like pattern. This can amplify mast cell activity, alter neuroimmune communication, and further destabilise autonomic function.
Inflammatory markers may rise due to persistent immune activation, contributing to vascular permeability, tissue irritation, and impaired recovery.
Addressing these intertwined pathways requires stabilising mast cells, supporting antiviral and anti-inflammatory responses and assessing for biotoxin-related drivers where appropriate.
Hypermobility & Neurodiversity: ADHD, ASD & Sensory Profiles
There is a well-recognised correlation between hypermobility and neurodiversity, and for many clients this becomes one of the most impactful aspects of daily life. Differences in connective tissue do not only influence joints; they affect the scaffolding around nerves, sensory receptors, and the microcirculation that supports the brain and autonomic nervous system. As a result, proprioception, sensory processing, autonomic balance, and immune–nervous system communication can all be affected.
For many hypermobile individuals, the nervous system is working much harder than average to interpret sensory input, maintain stability, and regulate internal signals. This heightened baseline load can make the brain more sensitive to changes in environment, stress, temperature, hormones, inflammation, or mast cell mediator release.
It is therefore common for clients with hEDS to identify with traits associated with ADHD, autism spectrum profiles, or sensory processing differences, even if they have never received a formal diagnosis.
Clients often describe:
• Sensory sensitivity, including sound, light, temperature, or texture
• Difficulties with focus, organisation, or sustaining attention
• Emotional reactivity or rapid shifts in internal state
• Sleep problems due to autonomic arousal or mast cell activity
• Fatigue after cognitive effort, often described as “my brain shuts down”
These patterns rarely occur in isolation. They frequently overlap with MCAS, POTS, impaired gut motility, and neuroinflammation. Mast cell mediators can directly affect the brain and sensory pathways, contributing to irritability, overwhelm, and difficulty filtering incoming stimuli. Autonomic instability can reduce cerebral blood flow, worsening attention, processing speed, and sensory tolerance. Gut inflammation and altered vagal signalling can further influence mood, cognition, and emotional regulation.
Together, these mechanisms create a distinctive neurodivergent profile seen in many hypermobile clients, where the combination of structural, immunological, and autonomic factors shapes how the nervous system perceives and responds to the world. Recognising this interconnected physiology allows us to approach care in a way that supports both the body and the brain, rather than viewing these experiences as unrelated or behavioural in nature.
Hypermobility & Autoimmune Disease
Autoimmune conditions are notably more common in individuals with hEDS, and this is likely driven by several mechanisms. Increased gut permeability, altered connective tissue signalling, and a baseline tendency toward immune activation all contribute to a terrain where the immune system is more likely to misidentify self-tissue as a threat.
Chronic inflammation, impaired barrier function, and autonomic dysregulation further compound this risk, creating an environment in which autoimmune processes can take hold more readily.
We see a wide range of autoimmune diseases in clinic, such as:
• Hashimoto’s thyroiditis
• Coeliac disease,
• Inflammatory bowel disease such as Crohn's and ulcerative colitis
• Psoriasis
• Rheumatoid arthritis
• Sjögren’s syndrome
• Vitiligo
• Lupus
These conditions often appear alongside MCAS, dysautonomia, and gastrointestinal dysmotility, which together amplify immune instability. Inflammatory mediators, heightened mast cell reactivity, microbial imbalance, and elevated markers place additional strain on the immune regulatory system. Over time, this can lead to reduced tolerance, impaired T-cell regulation, and an exaggerated inflammatory response to everyday stimuli.
Our support focuses on addressing these interconnected drivers rather than treating the autoimmune diagnosis in isolation. This includes:
• Modulating the immune response through personalised dietary strategies, targeted supplementation, and lifestyle interventions
• Identifying and reducing triggers such as infections, mould exposure, environmental stressors, or food sensitivities
• Supporting regulatory T-cell balance to promote immune tolerance
• Restoring gut integrity and improving microbiome diversity to reduce immune activation
• Supporting detoxification and improving inflammatory pathway regulation to reduce overall immune burden
By addressing these underlying mechanisms, we help clients stabilise their immune system, manage symptoms, and create a foundation for long-term recovery and stability.
Intestinal Motility, SIBO & SIFO in Hypermobility & hEDS
Gut issues are one of the most common challenges in individuals with hEDS and HSD. Connective tissue supports the structure of the gastrointestinal tract, the enteric nervous system, and the muscle tone required for coordinated peristalsis. When connective tissue is more lax or fragile, intestinal motility often slows, leading to stagnation, fermentation, and microbial imbalance.
Reduced motility increases the risk of both Small Intestinal Bacterial Overgrowth (SIBO) and Small Intestinal Fungal Overgrowth (SIFO), conditions that frequently appear together in hypermobile clients.
Many individuals with hypermobility report years of digestive symptoms long before receiving an EDS diagnosis, often labelled as IBS, functional dyspepsia, or “sensitive gut”.
Common symptoms include:
• Bloating or distension, often worsening throughout the day
• Abdominal discomfort or cramping
• Constipation, diarrhoea, or alternating patterns
• Reflux or nausea
• Increased food reactions or histamine-type responses
• Fatigue or brain fog triggered by eating
• Difficulty tolerating probiotics or antimicrobials
Why SIBO and SIFO are more common in hEDS?
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Reduced gut motility (sluggish peristalsis)
Connective tissue laxity affects the strength, tone, and coordination of the intestines, slowing movement of food and bacteria. Stagnation provides an ideal environment for microbial overgrowth.
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Impaired Migrating Motor Complex (MMC)
The MMC acts like the gut’s “cleaning wave” between meals. Dysautonomia, vagus nerve dysfunction, and low structural tone all weaken the MMC, increasing the risk of SIBO.
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Mast cell activation and inflammation
Chronic mast cell mediator release can disturb motility, increase intestinal permeability, and contribute to bloating, nausea, and diarrhoea. In sensitive individuals, MCAS can even trigger transient hypermobility through inflammation-driven connective tissue softening.
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Altered connective tissue signalling
Inflammatory mediators such as MMP-9 can degrade extracellular matrix proteins, influencing the integrity of the gut barrier and leading to increased microbial translocation and dysbiosis.
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Higher likelihood of fungal overgrowth (SIFO)
Frequent antibiotic exposure, slow motility, mould illness, and MCAS all increase the likelihood of fungal imbalance in the small intestine.
Our Approach to Hypermobility and Hypermobile EDS
At the Autoimmune Clinic, our approach to hypermobility and hypermobile Ehlers-Danlos syndrome is not to treat the hypermobility. Joint laxity is only one part of a much wider picture. What actually drives symptoms in hEDS are the co-existing layers of immune, neurological, gastrointestinal, and metabolic dysregulation that vary significantly from one person to another. Rather than focusing solely on the structural features of hypermobility, we work to identify what is happening in your unique system that is contributing to the symptoms you are experiencing.
No two people with hypermobile EDS will present in the same way. We take time to understand the individual combination of factors behind your symptoms, whether those relate to mast cell activation, mould exposure, post-viral illness, dysautonomia, impaired motility, microbial imbalance, hormonal disruption, or chronic inflammation.
Our functional medicine approach is holistic and personalised.
We explore the root causes, work systematically across all affected systems, and create a bespoke support plan that helps stabilise the body, reduce inflammation, support resilience, and improve quality of life.
This approach is grounded not only in clinical experience, but also in lived experience.Our Clinic Director, Muriel Wallace-Scott, has walked this path herself.
Diagnosed with hypermobile EDS in her thirties after years of navigating the many co-morbidities commonly seen in hEDS, she understands firsthand the complexity, the frustration, and the sense of not being heard or understood.
Having rebuilt her own health and now thriving, she knows that meaningful improvement is possible. Even if you have struggled for a long time, it is possible to feel better, function better, and rebuild trust in your body again.
