Ehlers-Danlos Syndrome Symptoms: What to Watch For

The main symptoms of Ehlers-Danlos syndrome (EDS) are joint hypermobility with chronic joint pain and recurrent subluxations, soft stretchy skin that bruises and scars easily, and fatigue that rest does not fix, often joined by POTS, gut problems and mast cell symptoms. Hypermobile EDS (hEDS), the most common of the 13 subtypes in the 2017 international classification [1], has no genetic test, and the average time from first symptoms to diagnosis is 10 to 12 years.

What Is Ehlers-Danlos Syndrome?

Ehlers-Danlos syndrome (EDS) is a group of inherited connective tissue disorders caused by defects in collagen or the proteins that interact with collagen. Since collagen is the most abundant protein in the human body, found in skin, joints, blood vessels, organs, and the GI tract, problems with it can cause symptoms almost everywhere [1].

There are 13 recognized subtypes of EDS, but three account for the vast majority of diagnoses:

• Hypermobile EDS (hEDS): The most common type. Primarily affects joints and soft tissue. No identified genetic mutation yet, which makes genetic testing impossible for this subtype.
• Classical EDS (cEDS): Marked by extremely stretchy, fragile skin that bruises easily and heals with characteristic “cigarette paper” scars. Caused by mutations in COL5A1 or COL5A2 genes.
• Vascular EDS (vEDS): The most dangerous subtype. Affects blood vessels and organs, raising the risk of arterial rupture and organ perforation. Caused by COL3A1 mutations. Estimated prevalence is 1 in 50,000 to 1 in 200,000 [2].

Most of the symptom sections below focus on hEDS because it’s what most patients and practitioners will encounter. Knowing the other subtypes still matters, because some carry serious medical risks that require different management.

Older names still appear in medical records. Hypermobile EDS was previously called EDS type III or EDS hypermobility type, and vascular EDS was called EDS type IV [10]. Joint hypermobility syndrome (JHS), an older diagnosis, is now mostly folded into hypermobility spectrum disorder (HSD) [3].

What Are the Most Common EDS Symptoms?

The most common EDS symptoms are joint hypermobility, chronic joint and muscle pain, joint instability with subluxations, skin that is soft, stretchy or easily bruised, and persistent fatigue. Many people with hEDS also have dizziness on standing, digestive symptoms and poor sleep. No single symptom makes the diagnosis; the pattern across body systems does.

The table below groups the symptoms covered in the sections that follow, with the subtypes where each is most prominent.

Joint Hypermobility: The Hallmark Symptom

The Beighton Score

The Beighton score is a 9-point screening tool used to assess generalized joint hypermobility. You get points for:

1. Passively extending each pinky finger beyond 90 degrees (1 point per hand)
2. Bending each thumb to touch the forearm (1 point per hand)
3. Hyperextending each elbow beyond 10 degrees (1 point per arm)
4. Hyperextending each knee beyond 10 degrees (1 point per leg)
5. Placing palms flat on the floor with knees straight (1 point)

A score of 5 or higher in adults (4 or higher if over age 50) suggests generalized hypermobility [3]. The 2017 criteria set a higher bar of 6 or more for children and adolescents who have not gone through puberty [1]. A high Beighton score alone does not mean you have EDS. Roughly 10-20% of the general population is hypermobile, and most of these people will never develop problems from it.

The score also misses people. Joints stiffen with age, injury and surgery, so an adult who was very flexible as a child can score low today. Clinicians often add a five-part questionnaire about past flexibility, such as whether you could once do the splits or bend your thumb to your forearm, to catch this [3].

When Flexibility Becomes a Problem

The line between “benign” hypermobility and EDS gets crossed when joint looseness starts causing actual damage. In EDS, hypermobility leads to:

• Chronic joint pain: Not the occasional ache after exercise. This is daily, persistent joint pain that worsens with activity and doesn’t respond well to standard treatments. It often starts in childhood or adolescence.
• Recurrent subluxations and dislocations: Joints slip partially or fully out of place during normal activities. Shoulders, kneecaps, fingers, and jaws are frequent offenders. Some patients report subluxations from sneezing, reaching for something on a shelf, or rolling over in bed.
• Joint instability: A constant feeling that joints are “loose” or might give out. Many patients describe their joints as feeling like they’re held together by rubber bands instead of ligaments.
• Early osteoarthritis: Unstable joints wear down cartilage faster. It’s not unusual to see degenerative changes in the 20s and 30s in EDS patients [4]. Our osteoarthritis condition page covers how that wear pattern is usually managed.

Pain in EDS is often widespread rather than limited to loose joints. Rombaut and colleagues (2011) found that women with EDS reported pain and functional impairment comparable to women with fibromyalgia and rheumatoid arthritis [4]. That overlap is one reason hEDS is sometimes misread as fibromyalgia.

Skin Symptoms

Skin involvement varies by subtype, but even in hEDS, you’ll often see some of the following:

• Hyperextensibility: Skin stretches beyond what’s normal for the body site. In classical EDS, skin can be pulled several centimeters away from the body. In hEDS, it may be subtler but still noticeable.
• Easy bruising: Bruises appear with minimal or no recalled trauma. Some patients wake up with new bruises regularly.
• Delayed wound healing: Cuts and surgical incisions take longer to close and are more prone to widening over time.
• Atrophic scarring: Scars that are thin, widened, and often described as looking like “tissue paper.” Most prominent in classical EDS.
• Soft, velvety skin texture: Described by clinicians as having a “doughy” quality. This is actually a clinical finding that can help point toward an EDS diagnosis.
• Stretch marks (striae): Appearing at a young age and in unusual locations, not just from rapid weight change or pregnancy.

Two other skin findings appear in the 2017 hEDS checklist: piezogenic papules, small soft bumps on the heels that show when you stand, and abdominal hernias or recurrent hernias at a young age [1]. Dermatologists and geneticists look for these because they are easy to see and rarely asked about.

Fatigue: The Symptom Nobody Expects

If you ask EDS patients what symptom affects their quality of life the most, many won’t say joint pain. They’ll say fatigue.

The fatigue in EDS is not ordinary tiredness. It’s a bone-deep exhaustion that doesn’t fully resolve with rest or sleep. Voermans and colleagues (2010) found that fatigue severity in EDS is comparable to what’s seen in chronic fatigue syndrome and multiple sclerosis [5]. Several factors contribute:

• Muscle overwork: When ligaments can’t stabilize joints properly, muscles have to work overtime to compensate. This creates constant low-grade muscle fatigue.
• Poor sleep quality: Joint pain, difficulty finding comfortable positions, and frequent waking all disrupt sleep architecture.
• Autonomic dysfunction: Many EDS patients have dysautonomia (especially POTS), which causes blood pressure and heart rate instability. The body expends enormous energy just trying to maintain basic cardiovascular regulation.
• Chronic pain itself: Pain is neurologically exhausting. The central nervous system processing required to manage constant pain signals drains energy reserves.
• Mast cell activation: A significant subset of EDS patients have concurrent mast cell activation syndrome (MCAS), which causes inflammatory mediator release and its own fatigue burden.

Because the causes are layered, fatigue in EDS rarely has one fix. Clinicians usually look for treatable contributors first, such as orthostatic intolerance, sleep disruption, low iron or vitamin D, and medication side effects, before treating the fatigue itself.

Dysautonomia and Cardiovascular Symptoms

Up to 80% of hEDS patients meet criteria for some form of dysautonomia, and POTS is the most common presentation [6]. The connection makes anatomical sense: if your blood vessel walls contain faulty collagen, they’re more compliant (stretchy) than they should be. Blood pools in the legs and abdomen when you stand up, your heart rate spikes to compensate, and you feel dizzy, lightheaded, or like you might pass out.

Common dysautonomia symptoms in EDS include:

• Dizziness or lightheadedness when standing
• Heart palpitations and racing heart rate
• Exercise intolerance that seems out of proportion to fitness level
• Heat intolerance and excessive sweating (or inability to sweat normally)
• Difficulty regulating body temperature
• Brain fog and difficulty concentrating
• Pre-syncope (feeling like you’re about to faint) or actual fainting

If you’ve been told you have anxiety but your “panic attacks” happen when you stand up, start with a tilt table test or a simple active stand test before accepting a psychiatric diagnosis. Learn more in our guide to EDS and POTS overlap.

POTS is defined by a sustained, excessive rise in heart rate within minutes of standing, without a drop in blood pressure, along with symptoms that last for months. A cardiologist or autonomic specialist usually confirms it, and our dysautonomia treatment guide explains the usual first steps.

Mast cell activation symptoms

Mast cell activation syndrome (MCAS) causes flushing, hives, itching, wheezing, nasal congestion, abdominal cramping and reactions to foods, heat or fragrances. Clinicians have described a frequent overlap of hEDS, POTS and MCAS, sometimes called the triad, although the size of that overlap is still debated and the research is mostly small clinic samples. Our post on the MCAS, POTS and EDS triad walks through how the three interact.

GI Symptoms: The Gut Connection

Gastrointestinal problems are reported by 50-75% of EDS patients, yet this is one of the most under-recognized parts of the condition. The GI tract is essentially a tube made of connective tissue and smooth muscle, so it makes sense that collagen defects would affect gut function [7].

Common GI manifestations include:

• Gastroparesis (delayed stomach emptying): Food sits in the stomach longer than normal, causing nausea, early fullness, bloating, and sometimes vomiting. Some EDS patients are misdiagnosed with eating disorders because of their inability to eat normal portions.
• Functional dyspepsia: Chronic upper abdominal pain, burning, or discomfort without an identifiable structural cause on endoscopy.
• IBS-like symptoms: Alternating constipation and diarrhea, abdominal cramping, and bloating. Many EDS patients carry an irritable bowel syndrome diagnosis for years before the underlying connective tissue disorder is identified.
• Gastroesophageal reflux (GERD): A lax lower esophageal sphincter allows acid to reflux more easily. Some EDS patients also have hiatal hernias at young ages.
• Rectal prolapse and pelvic floor dysfunction: Lax connective tissue in the pelvic floor can lead to organ prolapse, difficulty with bowel movements, and urinary issues.

If you’re being treated for IBS that isn’t responding to standard therapy, and you also have joint flexibility or chronic pain, bring up the possibility of an underlying connective tissue disorder with your gastroenterologist.

Fikree and colleagues (2017), writing for the international EDS consortium, note that much of the GI evidence comes from referral clinics, so it may overstate how common severe gut symptoms are in everyone with hEDS [7]. Dizziness and gut symptoms also feed each other: poor blood flow on standing can slow digestion, and nausea makes it harder to keep up the fluids and salt that POTS care relies on.

Other Symptoms You Might Not Connect to EDS

EDS is genuinely a whole-body condition. Symptoms that patients and doctors frequently overlook include:

• TMJ dysfunction: The temporomandibular joint is particularly susceptible to instability in EDS. Jaw clicking, locking, and pain are common. Some patients can sublux their jaw while yawning or eating. See our page on temporomandibular joint disorder for how jaw instability is assessed.
• Dental crowding and high-arched palate: Connective tissue abnormalities affect craniofacial development.
• Myopia (nearsightedness): The sclera (white of the eye) is made of collagen. Lax scleral tissue can change the shape of the eye.
• Chronic headaches: A combination of cervical instability, TMJ dysfunction, and muscle tension. Some EDS patients also develop intracranial hypertension or CSF leak headaches.
• Easy muscle tears and tendinopathy: Tendons and muscles are more injury-prone.
• Anxiety and panic attacks: While there may be a true neurological component, many patients diagnosed with anxiety actually have unrecognized POTS or mast cell activation. The physical symptoms (racing heart, breathlessness, dizziness) get mislabeled [8].
• Proprioception deficits: Reduced awareness of where joints are in space. This contributes to clumsiness, frequent tripping, and difficulty with balance.
• Bladder and pelvic symptoms: Urinary urgency, recurrent prolapse and painful periods are reported more often in women with hEDS, and they are easy to treat as separate problems.
• Local anesthetic resistance: Some people with hEDS report that dental or skin numbing wears off quickly or barely works. The reason is not settled, but it is worth telling a dentist or surgeon in advance.

How Do EDS Symptoms Change Across Life?

EDS symptoms change with age, hormones and activity level, which is part of why the condition is hard to spot. The same person can look like a flexible, clumsy child, a teenager with sports injuries, and an adult with chronic pain and fatigue.

Children and teenagers

Early signs in children include marked flexibility, frequent sprains, “growing pains” that persist, late or clumsy motor milestones, easy bruising and constipation. Many people first notice real pain and dislocations in adolescence, when growth, sport and hormonal change all load the joints at once.

Hormones, pregnancy and menopause

Hypermobile EDS is diagnosed far more often in women than in men, and many women notice symptoms flaring around periods, during pregnancy and after childbirth. Joint pain and instability can also change around menopause. Research on why hormones affect connective tissue in EDS is limited, so these patterns come mostly from patient reports and clinic experience.

Later adulthood

With age, joints often stiffen and the Beighton score falls, while pain, osteoarthritis and fatigue may rise. Tinkle and colleagues (2017) describe hEDS as moving through phases, from hypermobility in childhood toward pain and stiffness later in life [10].

The Other EDS Subtypes: A Brief Overview

While hEDS dominates the conversation, other subtypes carry their own distinct symptom profiles:

• Classical EDS: Extreme skin extensibility, severe scarring, generalized hypermobility. The skin involvement is what sets it apart from hEDS.
• Vascular EDS: Thin, translucent skin (veins visible through the skin), characteristic facial features, and risk of spontaneous arterial or organ rupture. This subtype requires specialized monitoring because of life-threatening complications. Median life expectancy was historically around 50 years, though improving with surveillance [2].
• Kyphoscoliotic EDS: Severe muscle weakness at birth, progressive scoliosis, and ocular fragility.
• Arthrochalasia and dermatosparaxis EDS: Extremely rare subtypes with severe skin or joint involvement.

If you have signs of classical or vascular EDS, genetic testing is available and recommended. These subtypes have identified gene mutations and confirmed genetic tests.

Vascular EDS warning signs that need emergency care

Sudden, severe pain in the chest, abdomen, flank or head in someone with known or suspected vascular EDS can mean an arterial dissection, arterial rupture or bowel perforation, and it needs emergency care. Pepin and colleagues (2000) reported that most major complications in vascular EDS were arterial, followed by bowel rupture and, in pregnancy, uterine rupture [2]. People with confirmed vEDS often carry an emergency letter or card that names the diagnosis.

Why Diagnosis Takes So Long

The average time from symptom onset to EDS diagnosis is 10 to 12 years. Some patients wait two decades or more. This delay isn’t just frustrating; it’s harmful. Years of improper treatment, unnecessary surgeries, and psychological damage from being told “nothing is wrong” take a real toll [9].

Several factors contribute to the diagnostic delay:

• Symptom fragmentation: Patients see a rheumatologist for joint pain, a gastroenterologist for GI symptoms, a cardiologist for palpitations, a dermatologist for bruising, and a psychiatrist for “anxiety.” No single specialist sees the full picture.
• Medical education gaps: EDS gets about five minutes of coverage in most medical school curricula. Many physicians have never diagnosed it and may not recognize it.
• The “you look fine” problem: EDS patients typically don’t look sick. They’re often young women (the most common demographic) who appear healthy and active. Invisible illness is easy to dismiss.
• Diagnostic criteria complexity: The 2017 international criteria for hEDS are rigorous and involve a three-part checklist that many clinicians aren’t familiar with. Unlike other subtypes, there’s no blood test or genetic test for hEDS [3].
• Normalization of symptoms: Patients who’ve been hypermobile since childhood often don’t realize their experience is abnormal. They assume everyone’s joints hurt. They think dislocating a shoulder during gym class is just bad luck.

Demmler and colleagues (2019) used national health records from Wales and found that diagnosed EDS and HSD were more common than older estimates suggested, which supports the view that many cases go unrecognized for years [9].

The Diagnostic Criteria Debate

The 2017 criteria for hEDS were intended to create more consistent diagnosis, but they’ve generated controversy. Some clinicians argue the criteria are too restrictive, missing patients with significant symptoms who fall just short of meeting threshold. Others say they’re necessary to prevent over-diagnosis [10].

The reality is that many patients fall into a gray zone called “hypermobility spectrum disorder” (HSD). HSD shares many symptoms with hEDS but doesn’t meet the full 2017 criteria. Importantly, HSD can be just as disabling as hEDS and requires the same treatment approach. Whether you technically meet hEDS criteria or fall under HSD shouldn’t change how your symptoms are managed.

How Is Hypermobile EDS Diagnosed?

Hypermobile EDS is diagnosed by a clinical exam and history using the 2017 criteria, because no gene for hEDS has been found. A clinician must confirm all three of the following, as set out by Malfait and colleagues (2017) [1]:

1. Generalized joint hypermobility, judged by the Beighton score with age-adjusted cutoffs and, where needed, a history of past flexibility.
2. At least two of three features: signs of a systemic connective tissue problem (five of a list of twelve, such as soft skin, unusual stretch marks, piezogenic papules, hernias, atrophic scars, pelvic floor prolapse, dental crowding and heart valve findings), a first-degree relative who meets the criteria, or musculoskeletal complications such as daily pain in two or more limbs for at least three months, widespread pain, or recurrent dislocations.
3. Exclusion of other explanations, including unusual skin fragility that points to another EDS subtype, other heritable connective tissue disorders such as Marfan syndrome, and autoimmune rheumatologic conditions such as lupus or rheumatoid arthritis.

For suspected classical, vascular or rarer subtypes, a geneticist orders a gene panel. For hEDS, blood tests and imaging are used to rule out other conditions rather than to confirm EDS. Our post on how Ehlers-Danlos syndrome is diagnosed covers the appointment itself in more detail.

When to Seek Evaluation

Consider pursuing an EDS evaluation if you have a combination of:

• Generalized joint hypermobility (Beighton score of 5+ or a history of flexibility)
• Chronic musculoskeletal pain that started before age 30
• Recurrent joint subluxations or dislocations
• Unusual skin features (hyperextensibility, easy bruising, atrophic scars)
• A first-degree relative with confirmed or suspected EDS
• Unexplained fatigue, GI dysfunction, or dysautonomia symptoms
• Multiple seemingly unrelated diagnoses across different specialties

Good starting points for evaluation are a geneticist with connective tissue expertise or a rheumatologist familiar with EDS. The Ehlers-Danlos Society maintains a provider directory that can help you find someone experienced with these conditions.

Which doctors are involved in EDS care?

A geneticist or rheumatologist usually makes the diagnosis, and a primary care physician often coordinates care afterward. Depending on symptoms, the team can include a cardiologist or autonomic specialist for POTS, a gastroenterologist, a physical medicine and rehabilitation physician (physiatrist), a pain specialist, and a physical therapist who has worked with hypermobile patients. Bring a written timeline of symptoms, injuries and family history to the first appointment.

How Are EDS Symptoms Managed?

No treatment changes the underlying collagen problem in hEDS, so care focuses on each symptom and on protecting joints. Physical therapy that builds muscle strength, joint stability and proprioception is the foundation for most people. POTS is managed with fluids, salt, compression garments, gradual reconditioning and, when needed, medication, as our POTS treatment guide describes.

Pain care usually combines physical therapy, pacing, sleep support and carefully chosen medication, and our chronic pain treatment guide covers the wider options. Jaw instability is often handled with conservative care first, which our TMJ treatment guide explains. For vascular EDS, a French trial led by Ong and colleagues (2010) studied the beta blocker celiprolol for preventing arterial events; it is not approved by the FDA, and US care centers on imaging surveillance and blood pressure control.

Where regenerative treatments fit

Some people with hEDS look into platelet-rich plasma (PRP) injections or prolotherapy for unstable or painful joints. These are cash-pay, off-label uses in EDS, and the evidence is thin: there are case reports and small studies, not controlled trials in people with EDS. If you consider them, ask any clinic how many patients with hypermobility it treats and how it adjusts for fragile tissue.

If you want to compare providers, you can browse PRP clinics in the Regenerated.com directory. 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 in the directory is not an endorsement. Our full post on EDS treatment options covers the rest of the care plan.

Frequently asked questions

What are the first signs of Ehlers-Danlos syndrome?

The first signs of Ehlers-Danlos syndrome are usually unusual flexibility, frequent sprains or dislocations, easy bruising and joint pain that starts in childhood or the teenage years. Soft or stretchy skin, slow wound healing and wide, thin scars are early clues in classical EDS. Many people only connect these signs later, when fatigue, dizziness on standing or gut problems join them, and a clinician sees the pattern across several body systems at once.

Can you have EDS without being very flexible?

Yes, an adult can have EDS with a low Beighton score, because joints stiffen with age, injury and surgery. The 2017 criteria lower the cutoff to 4 for people over 50 and allow clinicians to weigh a history of past flexibility. Someone who was very flexible as a child, and now has widespread pain, instability and other connective tissue signs, can still meet the criteria for hypermobile EDS or hypermobility spectrum disorder after a careful exam.

Is EDS the same as being double-jointed?

No, being double-jointed means having hypermobile joints, which is common and usually harmless, while EDS is an inherited connective tissue disorder that affects many body systems. Roughly 10 to 20 percent of people are hypermobile, and most never develop problems. EDS is considered when hypermobility comes with chronic pain, repeated dislocations, skin changes, fatigue or autonomic and gut symptoms, and when the 2017 criteria or a genetic test confirm it.

What does EDS pain feel like?

EDS pain is usually a daily, deep ache in several joints and muscles, often worse after activity, standing or sleeping in one position. Many people also describe sharp pain when a joint slips partly out of place, and burning or nerve-type pain over time. Rombaut and colleagues (2011) found that pain and disability in women with EDS were comparable to fibromyalgia and rheumatoid arthritis, which shows how much it can limit daily life.

Do EDS symptoms get worse with age?

EDS symptoms change with age rather than following one path. Flexibility often declines, while pain, stiffness, early osteoarthritis and fatigue can increase over the years, a pattern described in the natural history of hEDS by Tinkle and colleagues (2017). Hormonal shifts during puberty, pregnancy and menopause can also bring flares. Physical therapy, POTS care and joint protection help many people stay active, and outcomes differ widely from person to person.

What kind of doctor diagnoses Ehlers-Danlos syndrome?

A clinical geneticist or a rheumatologist with connective tissue experience usually diagnoses Ehlers-Danlos syndrome. Geneticists order gene panels for classical, vascular and rarer subtypes, while hypermobile EDS is diagnosed through an exam and history using the 2017 criteria. A primary care physician can start the referral, and specialists such as cardiologists, gastroenterologists and physical therapists usually join the care team afterward depending on which symptoms are most prominent.

Related Reading

• Ehlers-Danlos Syndrome: The Complete Guide
• EDS Treatment: Managing Hypermobility and Pain
• EDS and POTS: Why These Two Conditions Often Overlap
• Dysautonomia Symptoms: Recognizing Autonomic Dysfunction
• Chronic Fatigue Treatment: Evidence-Based Approaches
• POTS Symptoms: What Postural Tachycardia Feels Like

Sources

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