How Can an Osteopath Help With Ehlers-Danlos Syndrome (EDS)?

By Dr. Anthony Dileo (Osteopath)

Understanding Ehlers-Danlos Syndrome

Ehlers-Danlos syndrome (EDS) is not a single condition, but a group of inherited connective tissue disorders that can affect the body in very different ways.

For some people, symptoms may be relatively mild and mainly involve joint hypermobility, recurrent sprains, or persistent muscular pain. For others, EDS can have a much broader impact involving fatigue, autonomic dysfunction, digestive symptoms, skin fragility, chronic pain, headaches, or cardiovascular involvement.

There are currently multiple recognised subtypes of EDS, including:

• Hypermobile EDS (hEDS),

• Classical EDS,

• Vascular EDS,

• Kyphoscoliotic EDS,

• Arthrochalasia EDS,

• and several rarer genetic forms.

By far the most commonly encountered presentation clinically is hypermobile EDS (hEDS) and related Hypermobility Spectrum Disorder (HSD).

Importantly, every person’s experience is different. Two people with the same diagnosis may present completely differently, which is why management needs to be individualised rather than protocol-driven.

As an osteopath with postgraduate study in hypermobility-related disorders and a member of the The Ehlers-Danlos Society, my approach is focused not simply on joints, but on understanding how connective tissue disorders interact with the nervous system, autonomic system, movement patterns, fatigue, pain sensitivity, recovery capacity, and day-to-day function.

In clinical practice, I commonly see overlap with:

• Postural Orthostatic Tachycardia Syndrome (POTS),

• mast cell activation symptoms,

• chronic fatigue presentations,

• migraines,

• gastrointestinal symptoms,

• anxiety,

• and increasingly, neurodivergence including ADHD.

There is emerging research supporting associations between hypermobility and ADHD, autonomic dysfunction, and anxiety-related conditions. Clinically, recognising these overlaps can be incredibly important because they often influence pacing, sensory load, exercise tolerance, fatigue management, and recovery.

What’s My Clinical View on Osteopathy and EDS?

EDS is incredibly individual. Two people with the same diagnosis can present very differently, and that’s one of the most important things to understand when discussing treatment.

I see osteopathy as one part of a broader, multimodal management approach. Manual therapy can help reduce pain, improve body awareness, calm protective muscle guarding, and help patients tolerate movement more comfortably — but it is rarely the entire answer on its own.

In my experience, the best long-term outcomes usually occur when treatment combines:

• education,

• pacing,

• strength and conditioning within tolerance,

• autonomic nervous system management,

• load modification,

• sleep and recovery strategies,

• appropriate referral pathways,

• and carefully selected hands-on treatment.

I’m also cautious about over-pathologising normal movement variability in EDS. Many patients have spent years being told things are constantly “out” or “misaligned,” which can create fear and hypervigilance around movement.

In certain patients I may avoid or modify high velocity techniques, particularly where there is significant cervical instability, autonomic sensitivity, severe pain sensitisation, or a history of poor tolerance to forceful treatment.

The goal is not to aggressively “correct” the body. It is to support function, confidence, and capacity over time.

What Type of EDS Patients Do I Commonly See?

Most of the patients I see fall somewhere within:

• hypermobile EDS (hEDS),

• hypermobility spectrum disorder,

• or individuals with significant hypermobility-related symptoms who are still navigating diagnosis.

Many have spent years trying to understand why they experience:

• recurrent injuries,

• chronic pain,

• fatigue,

• headaches,

• dizziness,

• digestive symptoms,

• jaw pain,

• or exercise intolerance.

I also commonly see patients who were previously very active — dancers, gymnasts, runners, athletes — who suddenly find their body no longer tolerates load in the same way.

One of the most important parts of treatment is recognising that EDS rarely exists in isolation. Exploring associated presentations such as POTS, mast cell activation symptoms, sleep disturbance, fatigue, or ADHD can sometimes help explain why patients are struggling beyond what would be expected from “joint hypermobility” alone.

What Have I Personally Found Works Best?

The biggest thing I’ve learned is that management needs to be individualised and sustainable.

Patients often improve most when we stop chasing perfection and instead focus on building tolerance gradually.

Some of the most effective strategies I’ve found include:

• graded strengthening,

• improving movement confidence,

• reducing boom-bust cycles,

• pacing activity more effectively,

• improving sleep and recovery,

• breathing and ribcage mechanics,

• autonomic nervous system support,

• and helping patients understand what their body is doing without catastrophising every symptom.

Exercise within a tolerable range is often one of the most important long-term tools — but dosage matters enormously.

Too little movement can worsen deconditioning and instability. Too much, too quickly, can trigger flares that last days or weeks. Finding the “middle ground” is often the challenge.

Supportive options such as:

• compression leggings,

• taping,

• braces,

• orthotics,

• or mobility aids

These can absolutely help in the right context. However, choosing when and how to use them is important. For some patients they can reduce fatigue, improve proprioception, or help during flares. In other situations, over-reliance may unintentionally reduce confidence or muscular conditioning over time.

Again, there is rarely a one-size-fits-all answer.

What Are the Biggest Misconceptions About EDS?

One of the biggest misconceptions is that all hypermobility is dangerous or fragile. Many patients become understandably fearful of movement after years of injury, medical dismissal, or alarming information online. But avoiding movement completely can often worsen symptoms over time.

I also think social media can sometimes create an overly structural view of pain — where every symptom is explained by something being “out,” unstable, or damaged.

In reality, pain in EDS is often multifactorial. It may involve:

• connective tissue laxity,

• muscle fatigue,

• autonomic dysfunction,

• central sensitisation,

• poor sleep,

• stress physiology,

• deconditioning,

• inflammatory contributors,

• and nervous system overload.

Another misconception is that strengthening alone solves everything. Exercise is incredibly important, but it needs to be realistic, paced, and adaptable to the individual.

Some patients can tolerate gym-based programs early. Others may initially need very gentle exposure, hydrotherapy, breathing work, walking tolerance, or autonomic management before progressing further.

What Does an EDS Osteopathy Appointment Actually Look Like?

EDS appointments are usually far more detailed than a standard musculoskeletal consultation.

I’m interested not only in pain location, but also:

• fatigue patterns,

• recovery tolerance,

• dizziness,

• digestive symptoms,

• headaches,

• sleep,

• exercise response,

• injury history,

• autonomic symptoms,

• sensory overload,

• and how symptoms fluctuate over time.

I also spend time understanding what the patient has already tried and how their previous healthcare experiences have shaped their relationship with their body.

Treatment itself may include:

• hands-on therapy,

• movement assessment,

• pacing discussions,

• rehabilitation planning,

• autonomic management strategies,

• education,

• taping or support advice,

• and referral where appropriate.

Importantly, management is collaborative. The aim is not dependency on treatment, but helping patients build understanding, confidence, and long-term capacity.

Can an Osteopath Help Identify EDS?

One of the challenges with EDS — particularly hypermobile EDS — is that many patients spend years without a diagnosis or are told their symptoms are unrelated.

As part of an osteopathic assessment, I can perform hypermobility screening and assess whether a patient’s presentation may be consistent with hypermobility spectrum disorders or EDS.

This includes looking at:

• joint hypermobility,

• injury history,

• pain patterns,

• skin features,

• autonomic symptoms,

• family history,

• and broader systemic involvement.

Where appropriate, I may suggest further medical assessment or referral pathways.

Should You Pursue Genetic Testing?

For some forms of EDS, genetic testing can play an important role. Certain subtypes — particularly rarer forms such as vascular EDS — have known genetic markers and may require specialist medical management due to potentially serious complications.

However, hypermobile EDS (hEDS), which is the most common subtype, currently has no confirmed genetic test available in routine clinical practice. Diagnosis is instead based on clinical criteria.

Whether genetic testing is worthwhile depends on the individual presentation.

Potential reasons to pursue genetic testing may include:

• suspicion of rarer EDS subtypes,

• significant cardiovascular or vascular history,

• family history concerns,

• diagnostic clarification,

• reproductive planning,

• or accessing specialist services and supports.

On the other hand, genetic testing is not always necessary or helpful for every patient, particularly when symptoms clearly align with hypermobile EDS or hypermobility spectrum disorder and management would remain largely similar regardless of test results.

I think one of the most important things is ensuring patients receive balanced, evidence-informed guidance rather than feeling overwhelmed by worst-case scenarios online.

Real-World Examples From Clinical Practice

One patient I treated was a young athlete with recurrent ankle sprains, knee pain, and ongoing frustration around repeated injuries. They had been told they were simply “weak” and needed to strengthen more aggressively.

What became clear was that they were constantly cycling between overtraining and crashing. Management involved reducing flare cycles, improving pacing, introducing gradual strength exposure, improving recovery strategies, and modifying load rather than eliminating activity altogether.

Another patient presented with chronic neck pain, headaches, dizziness, fatigue, and significant anxiety around movement after years of being told their joints were “slipping out constantly.”

Treatment focused heavily on education, nervous system regulation, breathing strategies, graded exercise, and reducing fear around normal movement variability.

Their pain did not disappear overnight, but over time they became significantly more confident, active, and less consumed by symptom monitoring.

I’ve also worked with patients where exploring associated conditions such as POTS or mast cell activation symptoms became an important turning point because their presentation extended well beyond joint pain alone.

Often the breakthrough is not a single treatment. It’s helping patients make sense of a very complex presentation and creating a management plan that feels achievable long term.

Final Thoughts

EDS is complex, and I think patients deserve nuance rather than oversimplified advice.

Many people with EDS have spent years feeling dismissed, misunderstood, or caught between extremes. Some are told “nothing is wrong.” Others are exposed to very fear-based narratives that leave them terrified to move.

I believe the truth is usually somewhere in the middle.

EDS is real. Symptoms can be severe and genuinely life-altering. But many people can also improve function, reduce flare frequency, and build meaningful physical capacity with the right support and realistic expectations.

Not every click or pop is dangerous. Pain does not always equal damage. Perfection is not the goal.

The best outcomes usually come from consistent, manageable strategies over time rather than searching for a single fix.

Most importantly, every person’s experience with EDS is different, and management should reflect that individuality rather than forcing everyone into the same model of care.