EDS and POTS: Why These Two Conditions Often Overlap

EDS and POTS often overlap because the connective tissue problem in Ehlers-Danlos syndrome, especially hypermobile EDS (hEDS), lets blood vessels stretch instead of tightening when you stand, so blood pools in the legs and abdomen and the heart races to compensate. Studies report that 50 to 80% of people with hEDS meet criteria for postural orthostatic tachycardia syndrome (POTS) or another form of dysautonomia, according to research that includes De Wandele and colleagues (2014) [2].

Two Conditions, One Pattern

If you’ve been diagnosed with Ehlers-Danlos syndrome and you feel dizzy every time you stand up, your heart races when you take a shower, and you can barely get through a grocery store trip without feeling like you need to sit down, you’re not imagining things. You’re likely dealing with POTS on top of EDS.

POTS (postural orthostatic tachycardia syndrome) is defined as a sustained heart rate increase of 30 beats per minute or more (40 bpm for ages 12-19) within 10 minutes of standing, without a significant drop in blood pressure, accompanied by symptoms of orthostatic intolerance [1]. In the general population, POTS affects roughly 1-3 million Americans. In the hypermobile EDS population, the prevalence is strikingly higher.

Studies consistently show that 50-80% of patients with hypermobile EDS (hEDS) meet criteria for POTS or another form of dysautonomia [2]. That’s not a coincidence. These conditions share a biological link rooted in what collagen does in the cardiovascular system.

The link also runs in the other direction. The 2020 Canadian Cardiovascular Society position statement on POTS lists hypermobile EDS, hypermobility spectrum disorder and mast cell activation disorder among the conditions that commonly accompany POTS [12]. Anyone diagnosed with POTS first has good reason to ask about joint hypermobility, and anyone diagnosed with EDS first has good reason to ask about autonomic symptoms such as dizziness, racing heart and heat intolerance.

The Connective Tissue Hypothesis

Your blood vessels aren’t just hollow tubes. Their walls are composed of layers of connective tissue, including collagen and elastin, that give them the ability to actively constrict and relax. When you stand up from a lying or sitting position, gravity pulls about 500-700 mL of blood into your legs and abdomen. Your autonomic nervous system detects this shift and triggers blood vessels in the lower body to constrict, pushing blood back toward the heart and brain.

In EDS, the collagen in blood vessel walls is structurally different. Vessel walls are more compliant, meaning they stretch more easily than they should. When they’re supposed to constrict in response to standing, they don’t tighten sufficiently. The result: excessive blood pooling in the lower body, reduced blood return to the heart, and a compensatory spike in heart rate as the heart tries to maintain adequate cardiac output [3].

This isn’t just theory. Researchers have measured increased venous distensibility (stretchiness) in EDS patients compared to controls. An echocardiographic study of 144 patients with hEDS or hypermobility spectrum disorder found smaller cardiac chamber sizes in those with dysautonomia, consistent with reduced blood return to the heart and with earlier findings in POTS [4]. The authors, Ruiz Maya and colleagues at Mount Sinai, published the cohort in 2021 and linked it to deconditioning after flares.

Think of it this way: a normal blood vessel is like a garden hose that maintains its shape and pressure. An EDS blood vessel is more like a thin plastic bag that expands under pressure instead of maintaining tension. The pump (heart) is fine. The plumbing is just too stretchy.

Is vessel laxity the whole explanation?

Vessel laxity is the leading explanation, not the only one. Researchers also point to small fiber neuropathy affecting the nerves that control blood vessels, low blood volume, a small deconditioned heart and, in some patients, mast cell mediators that dilate vessels. Many people likely have several at once, which is why treatment is layered.

Which Types of EDS Are Linked to POTS?

Hypermobile EDS is the type most strongly linked to POTS. The 2017 international classification led by Malfait and colleagues recognizes 13 subtypes of Ehlers-Danlos syndrome, and hEDS is the most common and the only one of the 13 with no identified gene, so it is diagnosed on clinical criteria rather than a genetic test [11]. Hypermobility spectrum disorder (HSD), the label for symptomatic joint hypermobility that does not meet full hEDS criteria, shows a similar autonomic picture. Older papers, including Gazit and colleagues (2003), use the earlier term joint hypermobility syndrome (JHS) for much of the same group [3].

Vascular EDS matters here even though it is uncommon. Features such as thin translucent skin, easy bruising, a family history of sudden arterial events or early aneurysm should prompt genetic testing before a POTS treatment plan includes heavy exertion or invasive procedures.

The EDS-POTS-MCAS Triad

Over the past decade, clinicians working with EDS patients have identified a pattern that appears frequently enough to be recognized as a clinical entity: the triad of hypermobile EDS, POTS, and mast cell activation syndrome (MCAS). A deeper look at the overlap is in our article on the MCAS, POTS and EDS triad.

MCAS is a condition where mast cells (immune cells found throughout connective tissue) release their chemical mediators inappropriately. Symptoms include flushing, hives, abdominal cramping, diarrhea, brain fog, headaches, and episodes of anaphylaxis-like reactions. When all three conditions are present, they create a feedback loop [5]:

• EDS provides the structural abnormality: Lax connective tissue throughout the body, including blood vessel walls and the tissue surrounding mast cells.
• POTS creates the hemodynamic instability: Blood pooling, tachycardia, and poor perfusion of the brain and other organs.
• MCAS drives inflammation and reactivity: Mast cell mediators like histamine cause vasodilation (which worsens POTS), increase GI motility (contributing to EDS-related GI symptoms), and can directly trigger tachycardia.

Each condition makes the others worse. Histamine from MCAS causes blood vessels to dilate, worsening POTS. POTS-related physiologic stress can trigger mast cell degranulation. And the structural laxity of EDS provides the tissue environment where both POTS and MCAS thrive.

Not every EDS patient has all three conditions. But if you have one, it’s worth screening for the others. The treatment approach changes significantly when multiple conditions are at play.

The triad is a clinical observation more than a settled mechanism. Much of the data comes from specialist clinics that see the most complex patients, and MCAS criteria vary between research groups, so estimates of how often all three co-occur differ widely.

Shared Symptoms and Diagnostic Confusion

One reason EDS and POTS go undiagnosed for so long is that their symptoms overlap heavily, and both can mimic other conditions:

Many patients are told they have anxiety, panic disorder, chronic fatigue syndrome, fibromyalgia, or conversion disorder before either EDS or POTS is identified. One study found that POTS patients see an average of seven physicians over four years before receiving a correct diagnosis [6]. Add EDS to the mix, and the timeline stretches even longer.

Some of those labels can coexist with EDS and POTS rather than replace them. Orthostatic intolerance is common in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), widespread pain overlaps with fibromyalgia, and new-onset POTS has been reported after viral illness, including in people with long COVID. A hypermobility screen and an orthostatic heart rate check are quick ways to see whether EDS and POTS belong on the list too.

Signs that point to both conditions

The combination is more likely when joint symptoms and upright symptoms show up together. Common clues include:

• Joints that dislocate or partially dislocate (subluxate) easily, plus dizziness or a pounding heart on standing.
• Soft, stretchy or fragile skin with slow-healing scars, plus symptoms that worsen in heat, after meals or in hot showers.
• Childhood “double-jointedness” or flexibility that later turned into chronic pain, plus fatigue that improves when lying down.

For a fuller checklist, see our overview of POTS symptoms and how they show up day to day.

How to Get Properly Evaluated

POTS Testing

The gold standard for POTS diagnosis is a tilt table test. You lie flat on a motorized table that tilts you to a 70-degree angle while your heart rate and blood pressure are continuously monitored. The test lasts 10-45 minutes and captures the hemodynamic response to positional change in a controlled setting.

If a tilt table test isn’t accessible, an active standing test can provide the same information with lower cost and complexity:

1. Lie flat for 5-10 minutes. Record resting heart rate and blood pressure.
2. Stand up and remain still (no walking or fidgeting).
3. Record heart rate and blood pressure at 2, 5, and 10 minutes.
4. A sustained heart rate increase of 30+ bpm (or absolute heart rate above 120 bpm) with orthostatic symptoms meets POTS criteria.

Important note: hydration status significantly affects results. Being dehydrated can produce a false positive. Being over-hydrated can produce a false negative. Test under normal conditions and avoid caffeine beforehand [1].

A diagnosis also requires ruling out other causes of a fast upright heart rate, such as dehydration, anemia, an overactive thyroid, medication effects or prolonged bed rest. Cardiologists and autonomic neurologists usually pair the standing or tilt test with basic blood work and an ECG, and sometimes a Holter monitor or echocardiogram. Our POTS diagnosis walkthrough covers each of these tests in more detail.

EDS Evaluation

If you already have a POTS diagnosis, screening for hypermobile EDS involves the 2017 diagnostic criteria, which include:

• Criterion 1: Generalized joint hypermobility (Beighton score of 5+ for adults, with age-adjusted thresholds)
• Criterion 2: Two or more of three features: systemic manifestations of connective tissue disorder, positive family history, and musculoskeletal complications
• Criterion 3: Exclusion of other diagnoses that could explain the findings

A geneticist or rheumatologist experienced with connective tissue disorders is the best person to perform this evaluation. For a detailed breakdown of symptoms to watch for, see our EDS symptoms guide.

The Beighton score is a 9-point exam of the little fingers, thumbs, elbows, knees and the ability to place both palms flat on the floor. The 2017 criteria, published by Malfait and colleagues for the International Consortium on EDS, lower the adult cutoff with age because joints stiffen over time [11]. The step-by-step process is in our guide to how EDS is diagnosed.

MCAS Screening

If you have both EDS and POTS, ask your doctor about MCAS if you experience:

• Flushing episodes (face, chest, or neck turning red)
• Hives or skin reactions without clear allergic triggers
• GI symptoms that fluctuate unpredictably
• Reactions to medications, foods, fragrances, or temperature changes that seem out of proportion
• Episodes resembling allergic reactions without identifiable allergens

MCAS testing involves measuring serum tryptase, 24-hour urine for N-methylhistamine and prostaglandin D2 metabolites, ideally collected during or shortly after a symptomatic episode [5].

An allergist or immunologist usually orders and interprets these tests. Many give patients a standing lab order so samples can be collected within hours of a flare.

Who does what in an EDS and POTS workup

Treatment Strategies That Address Both Conditions

The most effective approach treats EDS and POTS as an integrated problem rather than managing each one in isolation. Many interventions help both conditions simultaneously.

The plan starts with non-drug measures that raise blood volume, adding medication only when those are not enough. The Heart Rhythm Society (2015) and the Canadian Cardiovascular Society (2020) both put fluids, salt, compression and exercise first [1][12]. For a broader view of the options, see the POTS treatment guide and the companion dysautonomia treatment overview.

Salt and Fluid Loading

This is the simplest and often the quickest strategy to ease POTS symptoms. Increasing blood volume compensates for the excessive blood pooling caused by lax vessels.

• Fluid intake: 2-3 liters of water per day, spread throughout the day. Front-loading fluids in the morning is particularly helpful since POTS symptoms tend to be worst in the first few hours after waking.
• Sodium intake: 3-5 grams of supplemental sodium per day (in addition to dietary sodium). Salt tablets, electrolyte drinks, or adding salt to food can all contribute. Some patients use oral rehydration solutions (like WHO rehydration formula) for more efficient absorption [7].
• Avoid alcohol and large meals: Both cause peripheral vasodilation and worsen blood pooling. Smaller, more frequent meals reduce the postprandial blood pressure drop that’s common in POTS.

Sodium and salt are not the same number. Table salt (sodium chloride) is about 40% sodium by weight, so a gram of salt supplies roughly 0.4 grams of sodium, and labels on salt tablets and electrolyte mixes use both units. People with high blood pressure, kidney disease or heart failure should agree a target with their clinician before salt loading. Food-based approaches are covered in our POTS diet article.

Compression Garments

Compression works by externally supporting the lax blood vessels that can’t constrict effectively on their own. This reduces blood pooling and improves venous return to the heart.

For maximum benefit:

• Waist-high compression stockings (20-30 mmHg or higher): Thigh-high or knee-high stockings are less effective because a significant amount of blood pools in the abdominal and pelvic vasculature, not just the legs [8].
• Abdominal binders: An abdominal compression garment (or even a firm waistband) can be as effective as lower extremity compression because the splanchnic (abdominal organ) blood vessels are a major pooling site.
• Put them on before standing: Compression works best when applied before blood has already pooled. Put stockings on while still lying in bed in the morning.

Compression also provides the proprioceptive input that EDS joints benefit from. Compression sleeves on knees and ankles can simultaneously stabilize joints and improve blood flow.

The strongest data come from a randomized crossover trial by Bourne and colleagues (2021) in the Journal of the American College of Cardiology, which found that lower body and abdominal compression reduced upright heart rate and symptoms in POTS patients [8]. That trial was not limited to people with EDS, so the benefit in EDS-POTS is inferred rather than measured directly.

Exercise Reconditioning

This is where EDS and POTS treatment overlap most productively. Exercise improves POTS by increasing blood volume, improving cardiac stroke volume, and enhancing autonomic function. It improves EDS by building the muscular support system around unstable joints.

The Levine Protocol (also called the Dallas protocol, with a widely used CHOP modification from Children’s Hospital of Philadelphia) is the most studied exercise program for POTS. It was originally designed for deconditioned POTS patients and is commonly adapted for EDS-POTS patients with joint-protecting modifications [9].

In the study behind the protocol, Fu, Levine and colleagues (2010) used cardiac MRI to show that hearts in POTS patients were about 16% smaller than in sedentary controls, and three months of training increased heart size and blood volume [9]. Exercise ideas that respect lax joints are collected in our POTS exercises article. A typical EDS-adapted progression runs in three phases:

Month 1-2: Base building (recumbent only)

• Recumbent bike, swimming, or rowing (exercises where you’re not upright)
• Start with 15-20 minutes, 3-4 times per week
• Keep heart rate at a comfortable conversational pace
• For EDS: focus on controlled form; avoid locking joints on the bike or rower

Month 3-4: Introduce upright exercise

• Gradually add short periods of upright exercise (walking, elliptical)
• Continue recumbent exercise as the primary modality
• Begin adding lower extremity strengthening (leg press, wall sits, calf raises)
• For EDS: mid-range motion only; avoid full knee lockout

Month 5-6: Progress intensity

• Increase upright exercise duration
• Add interval training if tolerated
• Expand strength training to include upper body and core
• For EDS: higher reps, controlled tempo, avoid end-range positions

The key principle: progress slowly and don’t push through crashes. A day or two of increased symptoms after exercise means you did too much. Scale back and progress more gradually. Some patients take 6-12 months to work through the full protocol, and that’s completely fine.

Medications

When lifestyle measures aren’t sufficient, several medications can help:

• Fludrocortisone (0.1-0.2 mg daily): A mineralocorticoid that promotes sodium and water retention, increasing blood volume. Particularly useful for patients who can’t consume enough salt orally. Monitor potassium levels.
• Midodrine (2.5-10 mg, 3 times daily): An alpha-1 agonist that directly constricts blood vessels. Helpful for the lax vasculature in EDS-related POTS. Don’t take within 4 hours of bedtime (can cause supine hypertension).
• Ivabradine (2.5-7.5 mg, twice daily): Selectively slows heart rate without affecting blood pressure. Particularly useful when the primary complaint is tachycardia and palpitations. Does not cause the fatigue that beta-blockers often do [10].
• Beta-blockers (low-dose propranolol 10-20 mg): Can reduce heart rate and tremor. Start at very low doses since EDS-POTS patients often have lower baseline blood pressure and are sensitive to hypotensive effects. Some patients find beta-blockers worsen fatigue.
• Pyridostigmine (30-60 mg, 2-3 times daily): An acetylcholinesterase inhibitor that enhances autonomic ganglionic transmission. Can improve both heart rate control and GI motility, making it useful when both POTS and gastroparesis are present.

If MCAS is also present, adding H1 and H2 antihistamines (cetirizine and famotidine) and potentially a mast cell stabilizer (cromolyn sodium) should be considered. Controlling mast cell mediator release can independently improve both POTS and GI symptoms.

None of these drugs is FDA approved specifically for POTS, so every one of them is prescribed off label for this use. Midodrine is approved for symptomatic orthostatic hypotension, and ivabradine for certain types of heart failure. The ivabradine evidence comes from a small randomized, placebo-controlled crossover trial by Taub and colleagues (2021) in hyperadrenergic POTS [10]. The prescribing cardiologist or neurologist sets the actual dose.

What about IV fluids?

Intravenous saline is sometimes used to rescue severe POTS flares, for example during illness, heat waves or before surgery. The 2015 Heart Rhythm Society consensus statement describes IV saline as an option for short-term use during decompensation rather than routine ongoing therapy [1], and specialists generally avoid long-term central lines for it because of infection and clot risk. Outpatient clinics that offer IV hydration therapy vary in how closely they coordinate with a patient’s cardiologist, so ask before booking.

Day-to-Day Management Tips

Beyond formal treatment, small daily habits can make a meaningful difference:

• Stand up slowly: Sit on the edge of the bed for 30-60 seconds before standing. Flex your calf muscles and cross your legs before going fully upright.
• Counter-maneuvers: When you feel symptomatic while standing, crossing your legs, tensing your thigh muscles, or shifting your weight from foot to foot can push blood back toward the heart.
• Shower modifications: Use a shower chair. Keep water temperature lukewarm (heat causes vasodilation). If showers are a major trigger, try bathing instead.
• Timing matters: Symptoms are often worst in the morning and after meals. Schedule demanding activities for your best time of day.
• Portable salt: Keep salt packets, electrolyte tablets, or a water bottle with electrolytes with you at all times. If you start feeling symptomatic, drinking a salty fluid while sitting or lying down can help within 15-20 minutes.
• Cooling strategies: Cooling vests, handheld fans, and cold water can help when heat triggers POTS flares.

Joint protection belongs in the same routine. Supportive pillows that keep hips and shoulders in mid-range at night, and chores paced so standing tasks alternate with seated ones, reduce both subluxations and upright symptoms. A symptom diary of fluids, salt, sleep and activity shows which change helped.

What the Evidence Shows and Where It Is Thin

The EDS-POTS link is well documented, but treatment evidence specific to people with both conditions is limited. Most trials enroll POTS patients in general, and few report results separately for hEDS. The table summarizes how solid each part of the picture is.

Two gaps matter for patients. There is no blood test or gene test for hEDS, so diagnosis depends on a careful clinical exam. And there is no FDA-approved drug for POTS, so medication choices rest on smaller studies and clinician experience.

When to See a Specialist

Primary care can manage mild EDS-POTS with salt, fluids, compression, and exercise guidance. But consider referral to a specialist if:

• Symptoms are severe enough to limit daily function (unable to work, attend school, or maintain basic activities)
• You’re fainting regularly
• First-line treatments haven’t produced meaningful improvement after 3-6 months
• You suspect the MCAS triad is at play
• You need help differentiating EDS subtypes (especially ruling out vascular EDS)

Specialists to consider: autonomic neurologists, cardiologists with dysautonomia expertise, geneticists with connective tissue disorder experience, or multidisciplinary clinics that specialize in EDS-POTS-MCAS. The Dysautonomia International and Ehlers-Danlos Society websites maintain provider directories.

The outlook is encouraging for many people: a large share of EDS-POTS patients improve meaningfully with proper, targeted treatment. It takes patience and often some trial-and-error with medications and exercise programs, and progress tends to come in small steps over months rather than weeks.

Fainting with injury, chest pain, a heart rate that stays high while lying down, or sudden severe headache are not typical POTS symptoms and call for prompt medical evaluation rather than a wait for a specialist appointment.

Where Integrative and Regenerative Clinics Fit

Core EDS and POTS care comes from cardiologists, neurologists, geneticists and physical therapists. Some patients also look for clinics offering IV hydration or integrative support for fatigue. Those services are usually cash pay, the evidence for them in EDS-POTS is limited, and they work best as an add-on to a plan your specialist knows about, not a replacement for it.

If you want to compare options, the national list of clinics offering IV hydration shows providers by state and city, and the broader IV therapy clinic directory covers clinics that also offer vitamin and nutrient infusions.

Regenerated.com is free for patients, and listing order is not paid ranking. Featured slots are clearly labeled and capped. Verified means a clinic completed credential checks, not that it paid more. Inclusion in the directory is not an endorsement, and our explainer on Featured, Verified and organic listings sets out how each label works.

Before booking IV or integrative care for EDS-POTS, these questions help separate a well run clinic from a risky one:

1. Will a physician or nurse practitioner review my POTS diagnosis and current medications before treatment?
2. Do you use peripheral IV lines only, and what is your protocol if a line problem or reaction occurs?
3. Will you send visit notes to my cardiologist or primary care physician?
4. What is the total cost per visit, and is any part billable to insurance?
5. What published evidence do you rely on for this treatment in POTS or EDS?

Frequently asked questions

Does EDS cause POTS?

EDS is a major contributor to POTS, but it does not lead to POTS in everyone. In hypermobile EDS, the altered collagen in vein walls lets blood pool in the legs and abdomen on standing, and the heart speeds up to compensate. Studies by Gazit (2003) and De Wandele (2014) found dysautonomia in a large share of hypermobile patients, but many people with EDS never develop POTS, and POTS also occurs without EDS.

What percentage of people with EDS have POTS?

Studies report that roughly 50 to 80% of people with hypermobile EDS meet criteria for POTS or another form of dysautonomia. The range is wide because studies use different diagnostic criteria and often recruit from specialist clinics that see more severe cases. The Ruiz Maya 2021 cohort at Mount Sinai, for example, found dysautonomia in 65% of women and 44% of men with hEDS or hypermobility spectrum disorder.

What kind of doctor treats EDS and POTS together?

Care is usually shared across several clinicians. A cardiologist or autonomic neurologist diagnoses and treats POTS, a geneticist or rheumatologist confirms the EDS subtype, an allergist evaluates possible MCAS, and a physical therapist runs a joint-safe reconditioning program. A primary care physician often coordinates the plan. Dysautonomia International and the Ehlers-Danlos Society both maintain directories of clinicians familiar with these conditions.

Can POTS caused by EDS go away?

POTS linked to EDS often improves substantially, even though the underlying connective tissue difference is lifelong. Raising blood volume with fluids and salt, wearing waist-high or abdominal compression, and completing a graded program such as the Levine protocol can reduce symptoms over several months. Some people reach near-normal daily function, while others manage a long-term condition with flares during heat, illness or hormonal changes.

Should people with POTS be checked for Ehlers-Danlos syndrome?

Yes, a hypermobility screen is reasonable for anyone diagnosed with POTS. The 2020 Canadian Cardiovascular Society position statement lists hypermobile EDS and hypermobility spectrum disorder among the conditions that commonly accompany POTS. A clinician can check the Beighton score in a few minutes, and a positive screen leads to a full assessment against the 2017 hEDS criteria, plus genetic testing if vascular or classical EDS is possible.

Do IV fluids help EDS and POTS?

IV saline can relieve symptoms for a short time, especially during dehydration, illness or a severe flare. The 2015 Heart Rhythm Society consensus treats it as a short-term option rather than routine therapy, and long-term central lines carry infection and clot risk. Oral fluids, salt, compression and exercise remain the foundation, and outpatient IV hydration is usually cash pay with limited evidence specific to EDS-POTS.

Related Reading

• Ehlers-Danlos Syndrome: The Complete Guide
• EDS Symptoms: What to Watch For
• EDS Treatment: Managing Hypermobility and Pain
• POTS Treatment: Managing Postural Orthostatic Tachycardia Syndrome
• Dysautonomia Symptoms: Recognizing Autonomic Dysfunction

Sources

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