What Are EDS and HSD? A Guide to Understanding Hypermobility

Oct 13, 2024

10 min read

If you have found this page, you are likely searching for answers. You may have been told you are simply "double jointed." Or a doctor mentioned Ehlers-Danlos syndrome (EDS) or Hypermobility Spectrum Disorder (HSD), but the explanation was confusing, rushed, or left you with more questions than answers.

Here is why that happens. EDS is not one condition. It is a group of conditions. The name refers to a shared pattern of how connective tissue behaves in the body, not a single disease. Some types are rare and genetically defined. Others, like hypermobile EDS (hEDS), are far more common but have no known genetic marker yet. The labels overlap in ways that are not clearly explained, the diagnostic criteria have changed over time and will change again, and most guides do not walk you through how to make sense of any of it.

This guide will give you a clear map: what these terms actually mean, where the confusion comes from, and how to think about your own body without getting lost in technical details.

What Is Ehlers-Danlos Syndrome?

Ehlers-Danlos Syndrome (EDS) refers to a group of conditions that affect the body's connective tissue. Connective tissue is not just "glue." It provides structure, transmits force, and helps your body sense where it is in space. When connective tissue behaves differently, it affects your skin, joints, blood vessels, and internal organs.

The syndrome is named after two physicians, Edvard Ehlers and Henri Danlos, who described a similar pattern in patients more than a century ago. However, serious research into the full body impact of these conditions is very recent. Many of the insights we discuss in this guide were not widely known even five years ago.

The Different Types of EDS: A Quick Orientation

There are currently 13 recognized types of EDS. (Some sources mention up to 14 clinical types; this reflects ongoing refinement of the classification, not disagreement.) They are not all the same. Some are primarily structural, affecting skin and joints. Others involve significant vascular or organ risk. Each type has different genetic causes and different management priorities.

The most common by far is hypermobile EDS (hEDS). The rare subtypes are individually very uncommon, and hEDS accounts for the majority of clinically diagnosed cases. Other types you may hear about include:

Classical EDS (cEDS) – often presents with very stretchy, fragile skin and easy bruising.
Vascular EDS (vEDS) – rarer, with higher risk for blood vessel and organ fragility.

For a complete, detailed list of all 13 (or 14) types of EDS, the best resource is the Ehlers-Danlos Society website. This guide focuses on hEDS and HSD because they represent the vast majority of symptomatic hypermobility cases and are where most confusion exists.

Genetics: What We Know (And What We Don't)

For almost all rare EDS subtypes, doctors can identify a specific gene mutation. These are the genetically defined types.

Hypermobile EDS (hEDS) is the major exception. There is no single known genetic marker for it. You cannot get a blood test to confirm or rule it out. Diagnosis is based on a clinical checklist.

Why does this matter? Because hEDS does not fit neatly into the "rare genetic disease" model. Current research strongly suggests that hEDS is polygenic (involving multiple genes) and likely involves multiple interacting pathways. This is one reason the classification of hEDS and HSD is likely to change over time.

The Big Shift in Thinking: More Than Just Collagen

For years, hEDS was described mainly as a collagen disorder. More recent research suggests the picture is broader and likely involves immune, nervous system, inflammatory, and pain regulation pathways as well.

Recent proteomics and genetic studies have identified differences in immune signaling, autonomic regulation, and neuroimmune pathways in people with hEDS. Researchers also found genetic overlap between hEDS and conditions such as ME/CFS, fibromyalgia, migraine, anxiety, ADHD, autism, and gastrointestinal disorders.

This research is still evolving, but it supports a growing view of hEDS as a complex multisystem condition rather than a purely structural connective tissue disorder.

Where Hypermobility Spectrum Disorder (HSD) Fits In

HSD is diagnosed when someone has symptomatic joint hypermobility but does not meet the full 2017 criteria for hEDS. However, HSD is not a single, uniform diagnosis. The 2017 classification describes four distinct subtypes based solely on the anatomical pattern of joint hypermobility.

Type	Pattern of Hypermobility	Location
Generalized HSD (G-HSD)	Generalized joint hypermobility	Throughout the body
Peripheral HSD (P-HSD)	Peripheral joint hypermobility	Hands and/or feet
Localized HSD (L-HSD)	Localized joint hypermobility	A single joint or group of joints in the same area
Historical HSD (H-HSD)	History of generalized joint hypermobility	Past (may no longer be present on exam)

Generalized HSD (G-HSD) resembles hEDS most closely in its widespread joint involvement. The Beighton score is typically positive, and individuals often experience musculoskeletal symptoms across multiple body areas.

Peripheral HSD (P-HSD) describes hypermobility limited to the hands and feet. A person with P-HSD may have a negative Beighton score because the Beighton test does not assess the feet directly, yet they still experience significant symptoms in those areas.

Localized HSD (L-HSD) involves hypermobility restricted to a single joint or a specific group of joints in one region of the body, such as the shoulder, jaw (temporomandibular joint), or ankle. The Beighton score is typically negative, but the affected joint or region causes real, measurable symptoms.

Historical HSD (H-HSD) applies to individuals who previously had generalized joint hypermobility but, due to aging, injury, surgery, or joint stiffening, no longer demonstrate it on physical examination. Their Beighton score may now be negative, but they continue to experience musculoskeletal symptoms stemming from their history of hypermobility.

A critical limitation of this classification

The classification above is based only on joint hypermobility. It does not account for systemic symptoms, comorbidities, autonomic dysfunction, pain patterns, fatigue, skin involvement, or any of the other multisystemic features that make up your full experience.

This means two people with the same HSD subtype can have completely different realities. One person with G-HSD might have severe POTS, MCAS, and widespread pain, while another person with G-HSD might have only joint instability with no other symptoms. A person with peripheral HSD can still experience debilitating fatigue, migraines, and dysautonomia – even though their hypermobility is "only" in their hands and feet.

Do not assume that your systemic symptoms are less real or less severe just because your HSD subtype is peripheral or localized.

Why the distinction between hEDS and HSD remains unstable

On paper, the four HSD subtypes create a clear framework. In real life, the boundary between hEDS and HSD is still unstable for the same reasons we have discussed:

hEDS has no confirmed genetic marker, so the boundary is based on a clinical checklist, not biology.
The 2017 criteria were designed for research consistency, not to capture every real world presentation.
hEDS is far more common than other EDS subtypes, making it an outlier within the rare disease framework.
Many researchers now believe hEDS and HSD exist on a continuum of the same underlying condition.
The new diagnostic criteria scheduled for December 2026 are expected to revise this framework.

If you have an HSD diagnosis, your experience is just as valid as an hEDS diagnosis. The label is a starting point, not a measure of severity, and not the whole story. The real work is understanding your own body's patterns – which may include systemic symptoms regardless of which HSD subtype you were assigned.

The Diagnostic Criteria for hEDS (Beyond Joints)

A diagnosis of hEDS is not made by the Beighton score alone. The 2017 international criteria require meeting all three of the following conditions simultaneously.

Criterion 1: Generalized Joint Hypermobility (GJH)

GJH is measured using the Beighton score, a 9-point scale that assesses five specific movements: bending forward to put palms flat on the floor, hyperextending each elbow and knee beyond 10 degrees, bending each thumb back to touch the forearm, and bending each pinky finger back past 90 degrees.

The required Beighton score depends on age and puberty status:

Adults over age 50: score of 4 or more out of 9
Adults and adolescents after puberty up to age 50: score of 5 or more
Pre-pubertal children and adolescents: score of 6 or more

If a person scores one point below the required cutoff, a "yes" answer to two or more questions on the five-point questionnaire (which asks about past or present joint pain, dislocations, or ability to perform certain movements) can still qualify as meeting this criterion.

Important limitations of the Beighton score

The Beighton score remains the most widely used clinical tool for assessing GJH, but it has significant limitations that are increasingly recognized. It focuses predominantly on upper limb joints (fingers, thumbs, elbows, and spine) and may fail to identify hypermobility when it is present at excluded sites such as the shoulders, hips, or temporomandibular joints (jaw). The score is sensitive to age, sex, and ethnicity: joint laxity tends to diminish with age and is more pronounced in females and certain ethnic groups. Beighton scores also do not always reflect the severity of connective tissue involvement.

For these reasons, the Beighton score should not be the sole tool to confirm or exclude GJH. Clinicians are encouraged to incorporate broader phenotypic assessments and historical data.

Criterion 2: Two or more of the following features (A, B, or C) must be present

Feature A (systemic manifestations): a total of five must be present from a list that includes unusually soft or velvety skin, mild skin hyperextensibility, unexplained stretch marks, bilateral piezogenic papules of the heel, recurrent abdominal hernias, atrophic scarring, pelvic prolapse, dental crowding, arachnodactyly, mitral valve prolapse, or aortic root dilatation.

Feature B: a positive family history, meaning one or more first-degree relatives independently meet the current diagnostic criteria for hEDS.

Feature C (musculoskeletal complications): at least one of the following: musculoskeletal pain in two or more limbs recurring daily for at least three months, chronic widespread pain for three months or longer, or recurrent joint dislocations or instability in the absence of trauma.

Criterion 3: Exclusion of other diagnoses

A doctor must rule out other heritable and acquired connective tissue disorders, including other types of EDS, Marfan syndrome, Loeys-Dietz syndrome, osteogenesis imperfecta, and neuromuscular disorders. Alternative diagnoses that may also include joint hypermobility must be excluded before a diagnosis of hEDS can be confirmed.

Multisystemic Symptoms: How to Make Sense of a Full Body Experience

This is where most guides fail, and it is probably what you are living with. The symptoms of hEDS and HSD can affect nearly every system in your body.

A major 2025 global survey of people with hEDS reported an average of 24 comorbid conditions (self reported, so this reflects patient experience rather than clinical diagnosis for each item). The key is not the exact number but the pattern: symptoms do not happen in isolation.

Here are examples of where symptoms can show up:

System	Examples
Musculoskeletal	Chronic pain, joint instability, dislocations, early osteoarthritis, muscle fatigue
Gastrointestinal	Irritable bowel syndrome (IBS), gastroparesis, reflux
Nervous system	Migraines, nerve compressions (thoracic outlet syndrome, carpal tunnel), small fiber neuropathy
Autonomic nervous system	Dysautonomia, POTS (racing heart, dizziness upon standing)
Immune system	Higher rates of allergies, asthma, Mast Cell Activation Syndrome (MCAS)
Skin	Easy bruising, slow wound healing, soft or stretchy skin, abnormal scarring
Pelvic health	Pelvic organ prolapse, hernias, heavy menstrual bleeding
Neurodevelopmental	Higher co occurrence of ADHD, autism, anxiety

This list is not exhaustive. The important takeaway is: these are not random, separate conditions. They cluster in hEDS and HSD because they share underlying mechanisms: connective tissue differences (structure), nervous system dysregulation (regulation), and immune/inflammatory changes (signaling).

Note: These multisystemic patterns are most studied and most commonly reported in hEDS and HSD. The rarer, genetically defined EDS subtypes (like vascular or classical EDS) have their own characteristic features, which may include some of these symptoms but often with different frequencies and risks.

What This Means for You

The specific label (hEDS vs HSD) matters less than understanding the underlying pattern of your body.

Your connective tissue provides less passive stability than it should. That means your muscles and nervous system have to work overtime just to keep you upright, stable, and moving. Pain is often not a sign of injury but a signal of system overload – mechanical, neurological, or metabolic. Fatigue is not laziness or poor sleep; it is the cumulative cost of maintaining stability without built in support.

The label has value. It can help you access care, find community, and be taken seriously. But it is not the endpoint. The real work is understanding your own body's patterns.

From Understanding to Action: The ParaMotion Approach

Understanding your diagnosis, your comorbidities, and your body's patterns is the first step.

From there, the goal is to look at the bigger picture: how stability, fatigue, nervous system regulation, movement patterns, recovery, and daily load interact in your specific case.

The ParaMotion approach focuses on understanding those interactions and working through them systematically, from regulation and body awareness to stability, strength, and daily function.

The ParaMotion 7‑step framework:

Educate and identify: Understanding your specific patterns, triggers, and comorbidities.
Calm the foundation: Addressing immune (MCAS), circulatory (POTS), nutritional deficiencies, and sleep factors that create hidden load.
Regulate the nervous system: Shifting out of chronic protection states (fight, flight, freeze, shutdown).
Build body awareness: Restoring proprioception and interoception so you can feel what your body needs.
Stabilise, Gaining control over deep stabilising muscles before adding load.
Strengthen: Layering strength onto stable foundations, not compensation.
Functional integration: Bridging controlled exercises to real life: walking, carrying, reacting, living.

Each step is explained in detail in the main post here!

Final Thought: Keeping an Eye on What Comes Next

hEDS and HSD are still evolving fields of research, and the way these conditions are classified will likely continue to change over time.

But for many people, the most important shift happens earlier than that: when a long list of seemingly unrelated symptoms finally starts to form a coherent pattern.

The label itself is only one part of the picture. What matters more is understanding your own body's patterns, comorbidities, compensations, and responses to movement, stress, fatigue, and recovery, and learning how to work with them more effectively.

That understanding is often the beginning of a more structured and practical way forward.