Ehlers-Danlos Syndrome: Diagnostic Criteria, Types, and What the 2026 Updates Mean for You

Medically reviewed by Regenerated.com Team · Updated March 2026 · 12 min read

Ehlers-Danlos syndrome (EDS) is diagnosed with genetic testing for 12 of its 13 types, while hypermobile EDS (hEDS), the most common type, is still diagnosed clinically: under the 2017 International Classification, a patient must meet all three criteria, which are generalized joint hypermobility on an age-adjusted Beighton score, at least two of three supporting features, and exclusion of other conditions. The Ehlers-Danlos Society says updated criteria from the International Consortium on EDS and HSD are scheduled for publication in early December 2026, and a 2025 study found a fibronectin fragment in the blood of every hEDS and hypermobility spectrum disorder (HSD) patient tested, which could become the first blood test for the condition.

If you have spent years hearing that you are “just flexible,” that your pain is “probably anxiety,” or that nothing is really wrong because your labs keep coming back normal, you are in the right place. The experience of living in a body that dislocates, aches, and refuses to cooperate while doctors shrug their shoulders is not imaginary. It is not anxiety. And you are not alone. Ehlers-Danlos Syndrome, particularly the hypermobile type, remains one of the most underdiagnosed connective tissue disorders in medicine, with patients waiting an average of 12 years before receiving a correct diagnosis. But the field is finally shifting. The sections below cover the current diagnostic criteria, the tests involved, the research breakthroughs reshaping the field, and what the 2026 updates could mean for your journey toward answers.

What Is Ehlers-Danlos Syndrome?

Ehlers-Danlos Syndrome (EDS) is a group of heritable connective tissue disorders caused by defects in collagen and other structural proteins that hold the body together. Connective tissue is everywhere: in your skin, joints, blood vessels, organs, and gut lining. When that tissue is structurally compromised, the effects ripple across every system in the body.

The 2017 International Classification recognizes 13 subtypes of EDS, each with distinct genetic causes and clinical presentations. These include classical EDS (cEDS), vascular EDS (vEDS), kyphoscoliotic EDS, and others. Most subtypes have identified genetic markers and can be confirmed through genetic testing. The glaring exception is hypermobile EDS (hEDS), the most common subtype, which remains a clinical diagnosis with no confirmed genetic test.

This is the cruel irony of hEDS. It is the type most people have, the type that causes widespread pain and dysfunction, and the type that is hardest to prove. No single lab value. No definitive imaging finding. Just a clinical evaluation that many doctors have never been trained to perform.

What are the 13 types of Ehlers-Danlos syndrome?

The 13 types of Ehlers-Danlos syndrome are defined by the 2017 International Classification published by Malfait and colleagues in the American Journal of Medical Genetics Part C. Twelve are linked to known genes and are confirmed by genetic testing. Hypermobile EDS, once called EDS type III or the hypermobility type, is the only type without a known gene, which is why it relies on a clinical checklist.

Vascular EDS matters most to rule out early, because fragile arteries, bowel and uterus carry a risk of rupture that changes how surgery, pregnancy and imaging are planned. Classical EDS is marked by very stretchy skin and wide, thin scars. The rarer recessive types usually show up in infancy or childhood with features such as severe muscle weakness, progressive scoliosis or fragile corneas. For a wider look at how each type presents, see our overview of common EDS symptoms by body system.

The 2017 Diagnostic Criteria for Hypermobile EDS

The current diagnostic framework for hEDS was established by the International EDS Consortium in 2017 and described in detail by Tinkle and colleagues in the American Journal of Medical Genetics Part C (2017). To receive an hEDS diagnosis, a patient must satisfy all three of the following criteria.

Criterion 1: Generalized Joint Hypermobility

The Beighton Score is a standardized screening tool that measures joint hypermobility on a 9-point scale. It evaluates five specific maneuvers: bending each pinky finger back beyond 90 degrees (2 points), bending each thumb to touch the forearm (2 points), hyperextending each elbow beyond 10 degrees (2 points), hyperextending each knee beyond 10 degrees (2 points), and placing both palms flat on the floor with knees straight (1 point).

The 2017 criteria introduced age-adjusted cutoffs because joint mobility naturally decreases with age:

• Children and adolescents: minimum 6 out of 9
• Adults up to age 50: minimum 5 out of 9
• Adults over age 50: minimum 4 out of 9

If you score one point below the cutoff for your age group, you can still meet Criterion 1 if you answer yes to at least two historical questions. These include things like, “As a child, could you contort your body into unusual shapes or do the splits?” and “Do you consider yourself double-jointed?” This is important because many patients lose measurable hypermobility over time due to injury, muscle guarding, or age, even though the underlying connective tissue disorder remains.

These questions come from the five-part questionnaire developed by Hakim and Grahame (2003) in the International Journal of Clinical Practice. The other three ask whether you can place your hands flat on the floor without bending your knees now or could in the past, whether you can now or could ever bend your thumb to touch your forearm, and whether your kneecap or shoulder dislocated on more than one occasion as a child or teenager.

Criterion 2: Two or More of Three Features (A, B, or C)

To meet Criterion 2, you must have at least two of the following three features.

Feature A: Systemic manifestations of a connective tissue disorder (five or more required). This checklist includes unusually soft or velvety skin, unexplained stretch marks (particularly in adolescents or young men, or women who have never been pregnant), widened atrophic scars at two or more sites, pelvic floor or rectal prolapse, dental crowding combined with a high or narrow palate, arachnodactyly (unusually long fingers), arm span-to-height ratio of 1.05 or greater, mitral valve prolapse, and other signs.

The full Feature A list in the 2017 checklist has 12 items, and five must be present:

1. Unusually soft or velvety skin.
2. Mild skin hyperextensibility.
3. Unexplained stretch marks (striae) on the back, groin, thighs, breasts or abdomen, without a history of significant weight gain or loss.
4. Piezogenic papules on both heels, which are small fat bumps that appear when standing.
5. Recurrent or multiple abdominal hernias.
6. Atrophic scarring at two or more sites, without the very thin, paper-like scars typical of classical EDS.
7. Pelvic floor, rectal or uterine prolapse in children, men or women who have never given birth, without another predisposing cause.
8. Dental crowding together with a high or narrow palate.
9. Arachnodactyly, shown by a positive wrist sign (Walker sign) or thumb sign (Steinberg sign) on both sides.
10. An arm span-to-height ratio of 1.05 or greater.
11. Mitral valve prolapse, mild or greater, on strict echocardiographic criteria.
12. Aortic root dilatation with a Z-score above +2.

Feature B: Positive family history. One or more first-degree relatives independently meet the diagnostic criteria for hEDS. Since hEDS is hereditary, a family pattern of hypermobility, chronic pain, joint dislocations, and related symptoms strongly supports the diagnosis.

Feature C: Musculoskeletal complications. This requires at least one of the following: musculoskeletal pain in two or more limbs recurring daily for at least three months, chronic widespread pain for at least three months, or recurrent joint dislocations (three or more in the same joint without trauma, or dislocations in two or more different joints).

Criterion 3: Exclusion of Other Conditions

Before an hEDS diagnosis can be made, other connective tissue disorders must be ruled out. This includes other EDS subtypes (particularly classical and vascular, which have genetic tests), Marfan syndrome, Loeys-Dietz syndrome, and autoimmune conditions like lupus or rheumatoid arthritis that could explain joint symptoms. This criterion exists to ensure diagnostic accuracy, but it also means that reaching a diagnosis often requires referrals to genetics, rheumatology, or both.

Unusual skin fragility is itself a reason to look for another EDS type, because hEDS skin is soft but not easily torn. The checklist also asks clinicians to consider neuromuscular disorders, such as Bethlem myopathy, and skeletal dysplasias, such as osteogenesis imperfecta. When a person has an acquired autoimmune condition such as lupus or rheumatoid arthritis, the 2017 checklist allows an additional hEDS diagnosis only when both Feature A and Feature B are met, because joint pain alone cannot be credited to hEDS in that setting.

Why These Criteria Are Controversial

The 2017 criteria were designed to increase diagnostic specificity, and they succeeded at that. But many clinicians and researchers have criticized them as overly restrictive. Patients who clearly have symptomatic hypermobility, chronic pain, and systemic features may still fall short of the formal hEDS threshold. These patients are typically placed under the umbrella of Hypermobility Spectrum Disorder (HSD), a category that, while clinically valid, often carries less weight in medical settings and may not be recognized by insurance systems in many countries.

The Beighton score also has known blind spots. It tests fingers, thumbs, elbows, knees and the spine, but not the shoulders, hips, jaw or feet, which are frequent sites of instability in people with hEDS. A person whose hypermobility sits mainly in those joints can score low and still be living with daily subluxations.

Hypermobility Spectrum Disorder vs. hEDS: Are They the Same Condition?

This is one of the most actively debated questions in the connective tissue disorder community. HSD was introduced alongside the 2017 hEDS criteria as a diagnostic category for people with symptomatic hypermobility who do not meet the full hEDS checklist. It is further divided into subtypes: Generalized HSD, Peripheral HSD, Localized HSD, and Historical HSD.

The original intent was to position HSD as a less severe condition than hEDS. But the evidence has not supported that assumption. Research consistently shows that patients with HSD can experience pain, fatigue, and disability just as severe as those with hEDS. Management approaches are identical. Long-term outcomes after coordinated physical therapy are similar.

A 2025 study from the Mayo Clinic examined over 2,600 patients and found that those with localized and historical HSD reported symptoms and comorbidities that closely resembled generalized HSD and hEDS. The 2025 biomarker research (discussed below) found the same fibronectin fragment pattern in both hEDS and HSD patients, further suggesting a shared molecular mechanism.

The emerging consensus leans toward viewing these conditions as existing on a spectrum rather than as fundamentally different diseases. If the 2026 criteria update reflects this view, it could mean fewer patients falling through diagnostic gaps, and more people gaining access to the recognition and care they need.

What Tests Are Used to Diagnose EDS?

No single test diagnoses hypermobile EDS. A diagnosis rests on a physical exam, a detailed personal and family history, and targeted tests that rule out other types of EDS and look for complications. The tests a clinician orders depend on which EDS type looks most likely.

A normal genetic panel does not rule out hEDS. Because no gene is yet confirmed for the hypermobile type, a negative result mainly tells the clinician that the monogenic types on the panel are unlikely. Skin biopsy and collagen studies are now rarely used for diagnosis, since gene testing has largely replaced them for the types with known causes.

The Road to 2026: What Is Changing?

The Ehlers-Danlos Society launched the “Road to 2026” initiative to produce the first major update to EDS classification since 2017. The work is being led by the International Consortium on EDS and HSD, bringing together researchers, clinicians, and patient advocates. According to the Ehlers-Danlos Society, the updated classification for all types of EDS and HSD is scheduled for publication in the American Journal of Medical Genetics in early December 2026, with practical assessment and care guidance for clinicians to follow in March 2027. Here are the key developments shaping that update.

The Society describes the update as built on a systematic literature review, Delphi consensus methodology and peer review, and states that the new framework will replace previously published criteria once it appears. It also states that a diagnosis made under the 2017 criteria does not need to be repeated. The details of the new hEDS checklist are not public until publication, so the changes below are the areas under review rather than final rules.

A Potential Blood Test for hEDS and HSD

In 2025, a landmark study published in the American Journal of Medical Genetics Part A identified what may become the first blood-based biomarker for hEDS and HSD. Researchers analyzed blood samples from 466 adults and discovered that all patients with hEDS or HSD carried a specific 52-kilodalton fragment of fibronectin in their plasma. This fragment was completely absent in healthy controls and in patients with classical EDS, vascular EDS, rheumatoid arthritis, psoriatic arthritis, and osteoarthritis.

A collagen I fragment was also found in all hEDS and HSD patients, though this marker was less specific because it also appeared in rheumatoid arthritis patients. The combination of both markers creates a distinctive signature that appears unique to hEDS and HSD.

If larger validation studies confirm these findings, a simple blood test could replace or supplement the lengthy clinical evaluation process. For someone who has spent a decade trying to get a diagnosis, this is potentially transformative. The Ehlers-Danlos Society is sponsoring additional studies to validate these biomarkers in larger and more diverse populations.

For now, the test is a research tool. The Ehlers-Danlos Society states in its Road to 2026 materials that no reliable laboratory test yet confirms or rules out hEDS or HSD, so diagnosis still depends on clinical evaluation. A lab or clinic offering a commercial “hEDS blood test” today is offering something that has not been validated for diagnosis.

New Genes Identified: The Kallikrein Discovery

For years, hEDS was the only EDS subtype without a known genetic cause. That began to change in 2024 when researchers from the Norris Lab at the Medical University of South Carolina identified variants in the Kallikrein gene family (specifically KLK15) that appear to play a role in hEDS. Whole-exome sequencing of 200 patients with hEDS revealed rare variants in 14 of the 15 Kallikrein genes, including a recurring KLK15 variant that segregated with disease in multiple families.

Mouse models engineered with the KLK15 variant displayed connective tissue defects across multiple organ systems, consistent with the clinical picture of hEDS. The mouse work was published by Gensemer and colleagues in iScience (2025). Importantly, Kallikrein genes also play roles in blood pressure regulation and immune cell function, which may help explain why conditions like POTS and MCAS so frequently accompany hEDS.

This does not mean a single genetic test for hEDS is imminent. The genetics of hEDS are likely polygenic, involving multiple genes. But the Kallikrein findings represent the most significant genetic advance in hEDS research to date and will inform the 2026 criteria update.

Other Anticipated Changes

• Beighton Score revisions: The committee is reviewing whether to modify the Beighton scale to include commonly affected joints like hips and shoulders, which the current scale does not assess.
• New subtypes: hEDS may be split into additional subtypes based on symptom clusters and emerging genetic markers, recognizing that the current “hEDS” category likely encompasses multiple distinct presentations.
• Integration of systemic symptoms: Comorbidities like dysautonomia, mast cell activation, gastrointestinal dysfunction, and brain fog may be formally incorporated into diagnostic criteria rather than treated as secondary associations.
• HSD reclassification: The diagnostic relationship between HSD and hEDS is expected to be clarified, with the possibility that they will be recognized as points on the same spectrum rather than separate entities.

Will I need to be re-diagnosed under the 2026 criteria?

A diagnosis made under the 2017 criteria remains valid, according to the Ehlers-Danlos Society, which has said existing patients do not need to be reassessed. The label in your chart may change over time if the hEDS and HSD categories are redrawn, but your symptoms, history and care needs stay the same. People still waiting for an evaluation may find their clinician applies the new framework once it is published.

The MCAS-POTS-EDS Triad

If you have hEDS, there is a significant chance you also deal with Postural Orthostatic Tachycardia Syndrome (POTS), Mast Cell Activation Syndrome (MCAS), or both. This cluster is so common that it has earned its own name: the trifecta. We cover this overlap in depth in our article on the MCAS, POTS, and EDS triad, but here is a brief summary of why these conditions travel together.

The connective tissue defects in EDS affect blood vessel walls, making them overly compliant. When you stand, blood pools in the lower body because the vessels stretch too easily. The autonomic nervous system compensates by dramatically increasing heart rate, producing the hallmark symptoms of POTS: dizziness, racing heart, brain fog, and exercise intolerance. This autonomic dysfunction also connects to broader patterns of nervous system dysregulation and vagus nerve involvement.

Mast cells are immune cells embedded within connective tissue throughout the body. When connective tissue is structurally abnormal, the mechanical environment around mast cells changes. Research suggests this may contribute to inappropriate mast cell activation, leading to symptoms like flushing, hives, gastrointestinal distress, and anaphylactoid reactions. The relationship also appears to flow in the other direction: mast cell-derived enzymes may further degrade already-vulnerable connective tissue, creating a feedback loop.

The Kallikrein gene discovery adds another dimension. Kallikreins are involved in both blood pressure regulation and immune cell function, which could provide a genetic explanation for why EDS, POTS, and MCAS cluster together so reliably.

Each condition in the triad is diagnosed separately. POTS is usually confirmed with a tilt table or active stand test, as described in our guide to how POTS is diagnosed, while MCAS testing relies on mast cell mediators such as serum tryptase measured during a flare, covered in our MCAS diagnosis guide. Getting each one named in your record helps specialists coordinate care and supports the systemic picture in an EDS evaluation.

How to Get Diagnosed

Getting an EDS diagnosis requires seeing the right specialist with the right information. This is not a condition most primary care doctors are trained to identify. Here is a practical roadmap.

1. Ask your primary care clinician to record your Beighton score and your history of dislocations, pain and systemic symptoms.
2. Request a referral to medical genetics, or to a rheumatologist with hypermobility experience if genetics waitlists are long.
3. Complete the printable hEDS checklist from the Ehlers-Danlos Society and gather family history before the visit.
4. Expect genetic testing and an echocardiogram to rule out other EDS types and check the heart valves and aortic root.
5. Ask for separate evaluation of POTS, MCAS, gastrointestinal symptoms or small fiber neuropathy if they are present.

Which Specialists to See

• Geneticist or genetic counselor: This is the gold standard for EDS diagnosis. A medical geneticist can perform a detailed connective tissue evaluation, order genetic testing to rule out other EDS subtypes, and formally apply the hEDS diagnostic criteria.
• Rheumatologist: Some rheumatologists are experienced with hypermobility disorders and can perform the clinical assessment. However, EDS awareness varies widely among rheumatologists, so it is worth confirming the provider has experience with connective tissue disorders specifically.
• Neurologist or cardiologist: If you have symptoms of POTS or small fiber neuropathy, a specialist in dysautonomia can evaluate and treat these comorbidities while supporting the broader diagnostic picture.
• Physical therapist: A PT experienced with hypermobility can provide both functional assessment and treatment. While they cannot formally diagnose EDS, their evaluation of joint instability and movement patterns can generate valuable documentation for your medical record.
• Allergist or immunologist: When flushing, hives, food reactions or unexplained gastrointestinal symptoms suggest mast cell activation, an allergist or immunologist can order mediator testing and guide MCAS care.

What to Bring to Your Appointment

• A symptom timeline: Document when symptoms started, how they have progressed, and what body systems are affected. Include joint dislocations or subluxations, chronic pain patterns, skin changes, gastrointestinal issues, and any autonomic symptoms.
• Family medical history: Note any relatives with hypermobility, chronic pain, early-onset arthritis, heart conditions (especially mitral valve prolapse), or unexplained multisystem symptoms. Family history of these conditions strengthens the case for a connective tissue disorder.
• Photos and documentation: Photographs of skin hyperextensibility, unusual scarring, joint hyperextension, or bruising can be helpful. Bring any prior imaging, genetic test results, or specialist reports.
• The diagnostic checklist: The Ehlers-Danlos Society publishes a printable hEDS diagnostic criteria checklist. Filling this out before your appointment and bringing it with you can help ensure nothing is overlooked, especially if your provider is less familiar with the condition.

What If You Do Not Meet the Criteria for hEDS?

If you have symptomatic hypermobility but do not meet the full hEDS criteria, you may receive an HSD diagnosis. This is not a lesser diagnosis. It acknowledges that your connective tissue is causing real symptoms that require real management. The treatment approach is the same. And as the 2026 criteria update approaches, the diagnostic field may shift in ways that better capture the full spectrum of hypermobility-related conditions.

Conditions that can look like hEDS

Several conditions share widespread pain, fatigue or loose joints with hEDS, and clinicians weigh them during Criterion 3. Fibromyalgia causes widespread pain without the joint hypermobility and skin signs of EDS, though the two can coexist. Inflammatory diseases such as rheumatoid arthritis and lupus show up on blood work and imaging. Chronic fatigue syndrome, Marfan syndrome and Loeys-Dietz syndrome each have their own criteria or genetic tests that help separate them.

Living with EDS: Management Approaches

No treatment currently corrects the underlying connective tissue defect in EDS. Management focuses on reducing symptoms, preventing injury, and improving quality of life. Because EDS affects multiple body systems, effective care is almost always multidisciplinary. Our EDS treatment overview goes deeper on each option below.

Physical Therapy

This is the cornerstone of EDS management. The goal is to build muscular stability around hypermobile joints without triggering flares. Traditional physical therapy can be harmful if the therapist pushes range of motion rather than focusing on neuromuscular control. Look for a PT who understands hypermobility and emphasizes proprioceptive training, isometric strengthening, and joint stabilization. Low-impact activities like swimming, Pilates (modified for hypermobility), and walking are often well-tolerated.

Bracing and Joint Support

Custom or over-the-counter braces, ring splints for fingers, ankle supports, and kinesiology tape can help stabilize vulnerable joints during daily activities. The goal is supportive stabilization, not immobilization, since restricting movement entirely can lead to deconditioning and worsen long-term outcomes.

Pain Management

Pain in EDS is complex. It may be mechanical (from joint instability), neuropathic (from nerve compression or small fiber neuropathy), or inflammatory (from tissue damage and mast cell activation). Effective pain management often combines physical therapy, medications (such as low-dose naltrexone, gabapentin, or topical treatments), and sometimes interventional procedures. Many EDS patients also report benefits from addressing brain fog and sleep disruption, which can amplify pain perception.

A review of pain management in the Ehlers-Danlos syndromes by Chopra and colleagues (2017) describes this layered approach in detail. Low-dose naltrexone is used off label for EDS pain, as covered in our low-dose naltrexone overview. For a broader look at non-surgical options for persistent chronic pain, see our chronic pain treatment guide.

Regenerative injections for unstable joints

Some people with hEDS explore injection treatments such as platelet-rich plasma (PRP) and prolotherapy for loose or painful joints, tendons and ligaments. The evidence for these injections in hypermobility is thin: most published studies involve people without EDS, and neither treatment is a recognized EDS therapy. Both are usually cash pay. Our prolotherapy guide and platelet-rich plasma guide explain how each works, and the national directory of PRP clinics lists providers by city. Listing order there is not paid ranking, Featured slots are labeled and capped, Verified means credential checks rather than spend, and the directory is free for patients; inclusion is not an endorsement, so ask any clinic about its experience with hypermobile joints.

Managing Comorbidities

For many people with EDS, the comorbidities are more disabling than the joint symptoms. POTS may require salt loading, compression garments, and medications to manage blood pressure and heart rate. MCAS often responds to a combination of antihistamines, mast cell stabilizers, and trigger avoidance. Gastrointestinal dysfunction may need targeted dietary approaches and motility support. Each of these areas benefits from specialist involvement and a coordinated care plan.

Our POTS treatment guide and dysautonomia treatment overview cover the options for the autonomic side, and our article on how EDS and POTS interact explains why the two so often appear together.

Autonomic and Nervous System Support

Given the high prevalence of dysautonomia in EDS, strategies that support autonomic regulation can be valuable. Vagus nerve stimulation techniques, graded exercise protocols, and nervous system regulation practices may help manage the autonomic dysfunction that drives many of the most disabling symptoms.

Looking Ahead

For people living with undiagnosed hypermobility, the next few years hold genuine reason for hope. The combination of plasma biomarker research, the Kallikrein gene discoveries, and the full 2026 criteria update could fundamentally change how EDS and HSD are identified and validated. A future where a blood test can support what patients have known about their own bodies for years is no longer theoretical. It is being actively built.

Until then, the 2017 checklist remains the standard: generalized joint hypermobility on the Beighton score, two of the three supporting features, and exclusion of other conditions, applied by a geneticist or an experienced rheumatologist.

In the meantime, your symptoms are real. Your pain deserves to be taken seriously. And a 12-year diagnostic journey is not a reflection of the complexity of your body. It is a reflection of a medical system that is still catching up to connective tissue science.

Frequently asked questions

How is Ehlers-Danlos syndrome diagnosed?

Ehlers-Danlos syndrome is diagnosed with a physical exam, personal and family history, and genetic testing. Twelve of the 13 types have known genes that a genetic panel can confirm. Hypermobile EDS has no known gene, so it is diagnosed clinically with the 2017 checklist: generalized joint hypermobility on an age-adjusted Beighton score, at least two of three supporting features, and exclusion of other conditions. A medical geneticist or experienced rheumatologist usually makes the diagnosis.

Is there a blood test for hypermobile EDS?

There is no validated blood test for hypermobile EDS yet. A 2025 study in the American Journal of Medical Genetics Part A found a 52-kilodalton fibronectin fragment in the plasma of every adult with hEDS or HSD it tested and in none of the healthy controls. Larger validation studies are underway, and the Ehlers-Danlos Society says diagnosis still relies on clinical evaluation until a test is shown to be reliable.

What Beighton score do you need for hEDS?

The 2017 hEDS criteria require a Beighton score of at least 6 of 9 in children and adolescents, 5 of 9 in adults up to age 50, and 4 of 9 in adults over 50. If you score one point below your cutoff, you can still meet the hypermobility criterion by answering yes to at least two of the five Hakim and Grahame history questions, such as whether you could do the splits as a child.

What kind of doctor diagnoses Ehlers-Danlos syndrome?

A medical geneticist is the specialist most often responsible for diagnosing Ehlers-Danlos syndrome, because they can order genetic testing and apply the hEDS checklist. Rheumatologists with hypermobility experience also diagnose hEDS and HSD. Cardiologists and neurologists evaluate POTS and small fiber neuropathy, allergists assess mast cell activation, and physical therapists document joint instability that supports the clinical picture.

When will the new EDS diagnostic criteria be published?

The updated classification for all types of EDS and HSD is scheduled for publication in the American Journal of Medical Genetics in early December 2026, according to the Ehlers-Danlos Society. A second publication with assessment and care guidance for clinicians is planned for March 2027. The Society says a diagnosis made under the 2017 criteria remains valid, so existing patients do not need to be re-diagnosed.

What is the difference between hEDS and HSD?

Hypermobility spectrum disorder (HSD) is diagnosed when a person has symptomatic joint hypermobility but does not meet every part of the 2017 hEDS checklist. Research, including a 2025 Mayo Clinic study of over 2,600 patients, shows HSD symptoms and comorbidities closely resemble hEDS, and management is the same. The 2026 update is expected to clarify whether the two are best treated as points on one spectrum.

Related Reading

• The MCAS, POTS, and EDS Triad: Understanding the Connection
• Vagus Nerve and Autoimmune Conditions
• Brain Fog: Causes, Mechanisms, and What Actually Helps
• Nervous System Dysregulation: What It Is and How to Address It
• Small Fiber Neuropathy: Symptoms, Diagnosis, and Treatment

Medical Disclaimer: This article is for informational purposes only and does not constitute medical advice. The content is based on published research and clinical guidelines available as of March 2026. Ehlers-Danlos Syndrome is a complex condition that requires individualized evaluation by qualified healthcare providers. Always consult with a medical professional before making decisions about your diagnosis or treatment. Regenerated Health does not diagnose, treat, or provide medical consultations.