If you have hypermobile Ehlers-Danlos syndrome (hEDS), you may have heard an explanation that sounds like this:

“The connective tissue is too stretchy, so the veins stretch too much. Blood pools in the legs, the vein valves stop working properly, venous insufficiency develops, and this causes POTS.”

It sounds logical.

Parts of this idea may be possible.

But scientists have not proved this whole chain of events.

What do we know?

Research shows that people with hEDS and hypermobility spectrum disorders (HSD) seem to have higher rates of orthostatic intolerance and POTS.

Research also shows that some people with POTS have more blood collecting in their lower legs when they stand.

And we know that chronic venous disease can involve changes in vein walls, vein valves, collagen and elastin.

But there is still an important missing piece:

We do not currently have strong evidence showing that hEDS or HSD directly causes abnormal superficial vein reflux because the veins are unusually weak or stretchy.

That difference matters because venous pooling, POTS and venous reflux are not the same condition.

First, some important definitions

Joint hypermobility

Joint hypermobility means that one or more joints move farther than usual.

Some people are naturally flexible and have no health problems because of it.

Joint hypermobility can affect one joint, several joints or many joints throughout the body.

So:

Being hypermobile does not automatically mean you have Ehlers-Danlos syndrome.

What is HSD?

HSD stands for hypermobility spectrum disorder.

People with HSD have joint hypermobility that causes symptoms or health problems, but they do not meet the full current criteria for hEDS or another condition that explains their hypermobility.

What is hEDS?

hEDS stands for hypermobile Ehlers-Danlos syndrome.

It is diagnosed using a combination of findings that can include:

• generalised joint hypermobility;

• certain body-wide connective-tissue features;

• musculoskeletal problems;

• family history in some cases;

• and the exclusion of other possible conditions.

At present, there is no established genetic or blood test that can confirm hEDS in routine medical care.

Researchers have found some signs of abnormal connective-tissue biology in both hEDS and HSD.

For example, a 2025 study found unusual fragments of fibronectin and type-I collagen in the blood of people with hEDS and HSD.

That finding is interesting.

But it does not prove that the veins in the legs are abnormally weak, that their valves fail, or that venous reflux is more common in hEDS or HSD.

Vascular EDS is different from hEDS

This is especially important.

Vascular Ehlers-Danlos syndrome, or vEDS, is not the same disease as hEDS.

vEDS is usually caused by a harmful change in the COL3A1 gene, which affects type III collagen.

People with vEDS can have serious tissue and blood-vessel fragility.

Important complications can include:

• arterial tears or rupture;

• bowel rupture;

• and uterine rupture.

Because of these risks, vEDS has a very different medical risk profile from hEDS and HSD.

Early varicose veins can sometimes be seen in people with vEDS.

However, ordinary varicose veins are common in the general population.

Having varicose veins, haemorrhoids or easy bruising does not by itself mean someone has vEDS.

A diagnosis of vEDS depends on the whole clinical picture and genetic testing.

For this reason, research about fragile blood vessels in vEDS should not automatically be applied to people with hEDS or HSD.

What is venous insufficiency?

To understand the research, it helps to understand how veins normally work.

Veins carry blood back toward the heart.

They are naturally able to stretch and hold a large amount of blood.

When we stand, several systems help push blood back upward.

These include:

• valves inside the veins;

• the calf-muscle pump;

• breathing;

• pressure changes in the veins;

• and signals from the nervous system that control blood vessels.

So veins being able to stretch and hold blood is normal.

It does not automatically mean someone has venous disease.

What is venous reflux?

Veins in the legs contain valves.

These valves are supposed to help blood move toward the heart and prevent too much blood from flowing backwards.

When doctors suspect abnormal venous reflux, they usually use a duplex ultrasound.

The test can measure whether blood is flowing backwards through a vein when it should not be.

Current vascular guidelines define abnormal reflux in major superficial leg veins as reversed flow lasting more than about 500 milliseconds, although different limits can be used for some deeper veins.

This is very different from simply saying:

“There seems to be more blood in the legs when someone stands.”

Venous pooling is not the same as venous reflux

This is probably the most important point in the whole discussion.

Venous pooling means that more blood collects in the lower part of the body while someone is upright.

It may cause symptoms or signs such as:

• purple or reddish feet;

• leg heaviness;

• swelling;

• or worsening symptoms while standing.

But pooling does not tell us why the blood is collecting there.

And pooling does not prove that the vein valves are faulty.

A person can therefore have:

• venous pooling without superficial venous reflux;

• superficial venous reflux without POTS;

• both;

• or neither.

What does the newest POTS research show?

A useful 2026 study compared 14 women with POTS with 15 women without POTS.

When the participants stood up, the POTS group had about 29% more calf venous blood volume.

Their veins also took longer to fill.

This gives us good evidence that unusual blood distribution in the legs can happen in POTS.

But there are some very important limits.

The study did not show that these people had:

• great saphenous vein reflux;

• small saphenous vein reflux;

• faulty vein valves;

• or hEDS.

In fact, the POTS group had higher central arterial stiffness, not lower stiffness.

So this study does not support the simple idea that all blood vessels in POTS are unusually “loose” or “stretchy”.

Does POTS pooling happen because veins are too stretchy?

Not necessarily.

A much older but still useful study from 2002 tested this question directly.

Researchers studied young people with POTS or orthostatic intolerance.

They found that their venous compliance was not different from healthy controls.

In other words, their veins did not appear to stretch more than normal.

Instead, the researchers found evidence that some patients were not tightening their smaller blood vessels enough when upright.

That could allow more blood to move into the veins of the legs.

So the key lesson is:

More blood in the legs does not automatically mean the veins are too stretchy, and it does not prove the vein valves are leaking.

How strong is the link between hEDS, HSD and POTS?

This link has much better evidence.

A large 2026 systematic review looked at 30 studies involving more than 8,000 people with EDS and nearly 13,000 people with POTS.

The studies repeatedly found that EDS and POTS occur together.

However, the reported numbers varied a lot.

Different studies found POTS in anywhere from 17.5% to 92.7% of people with EDS.

They also found EDS in around 17.9% to 50% of people with POTS.

That is a very wide range.

It tells us that the association appears real, but we still do not know the exact percentage of people affected.

A separate 2026 review focused on hEDS and HSD.

Across the included studies, researchers estimated that around 35.9% had some form of orthostatic intolerance and around 21.9% had POTS.

But the researchers also warned that the quality of the evidence was low and the studies were very different from one another.

So we can say:

hEDS/HSD and POTS are associated.

But we cannot yet say:

hEDS causes POTS because the veins are too stretchy.

That mechanism is still a theory.

Do people with hEDS have abnormal autonomic function?

There is evidence that some do.

A 2025 study looked at 270 people with hEDS who had been referred for specialist autonomic testing.

About 33% met POTS criteria during tilt-table testing.

Researchers also found other abnormalities involving blood flow to the brain, autonomic function and small nerve fibres.

But these patients were already being seen in a specialist clinic.

That means we cannot assume that 33% of all people with hEDS have POTS.

People sent for specialist testing are more likely to have symptoms in the first place.

Does joint hypermobility increase the risk of varicose veins?

There is some evidence, but it is weak.

One of the most relevant studies was published in 2015.

Researchers followed 718 young male soldiers.

Of these, 211 had generalised joint hypermobility.

The soldiers spent long periods standing during military training.

The hypermobile group developed more visible small-vein changes than the non-hypermobile group.

That sounds important.

But the details matter.

The men were around 20 years old.

The study lasted only three months.

And the researchers did not use standard duplex ultrasound to show abnormal venous reflux.

The venous changes were also classified as CEAP C1.

C1 means small visible veins such as spider veins or reticular veins.

True varicose veins are classified as C2.

So this study suggests that joint hypermobility might make some people more likely to develop early visible vein changes during long periods of standing.

But it does not prove that hypermobility causes chronic venous insufficiency or saphenous vein reflux.

What about the connective tissue inside vein walls?

This is where the theory becomes biologically interesting.

Vein walls contain:

• collagen;

• elastin;

• smooth muscle;

• fibroblasts;

• and endothelial cells.

All of these help determine how a vein behaves.

Because hEDS and HSD involve connective tissue, it is reasonable to ask whether the vein wall might also be affected.

That is a good scientific question.

But we do not yet have a clear answer.

What happens to vein walls in chronic venous disease?

In ordinary chronic venous disease, researchers have found changes involving:

• collagen;

• elastin;

• smooth muscle;

• inflammation;

• the extracellular matrix;

• vein dilation;

• and damage to vein valves.

These changes are well documented in people who already have chronic venous disease.

But this does not prove that people with hEDS or HSD start with the same changes.

It also does not prove that their connective-tissue disorder is what causes venous reflux.

That is an important difference.

But isn’t connective tissue abnormal in hEDS and HSD?

Yes, there is evidence of abnormal connective-tissue biology.

Researchers have found changes in cells called fibroblasts and have also found unusual collagen and fibronectin fragments in blood samples.

These findings make the idea of altered vein-wall behaviour possible.

But they do not tell us what is happening inside the great saphenous vein, small saphenous vein or their valves.

Scientists would need to study those veins directly before they could confidently say that hEDS or HSD causes abnormal venous reflux.

Are blood vessels in hEDS simply more stretchy?

The evidence does not support such a simple answer.

A 2020 study looked at arterial stiffness in 60 people with different types of EDS.

Their central arteries appeared more elastic than expected.

But greater elasticity was not linked to greater changes in heart rate or blood pressure when standing.

There were also important problems with the study.

The participants had different types of EDS, and the study did not include its own matched healthy control group.

Then, in the 2026 POTS study discussed earlier, people with POTS actually had higher arterial stiffness while also having more blood collect in their lower legs.

These results remind us that:

Arteries, veins, tiny blood vessels and vein valves are not all the same thing.

A finding in one part of the circulation does not prove that the same thing is happening everywhere else.

Could connective-tissue problems still affect veins?

Yes.

This remains possible.

For example, scientists could reasonably suggest that abnormal connective tissue might:

• change how much a vein stretches;

• affect how well valve leaflets meet;

• change how veins interact with the tissues around them;

• affect the calf-muscle pump if pain or joint problems reduce movement;

• or interact with autonomic problems that control blood-vessel tightening.

All of these ideas make biological sense.

But there is a difference between something being possible and something being proven.

Right now, researchers have not shown that these processes happen often enough in hEDS/HSD leg veins to explain chronic superficial venous reflux.

Why can POTS and venous insufficiency feel similar?

The symptoms can overlap.

Both conditions can involve symptoms such as:

• heavy legs;

• aching;

• swelling;

• colour changes;

• fatigue;

• and symptoms that become worse while standing.

That can make it difficult to tell what is happening based on symptoms alone.

The tests answer different questions.

Testing for POTS asks:

What happens to heart rate, blood pressure and symptoms when a person moves from lying down to standing?

Specialist tests may also look at blood flow to the brain and other parts of autonomic function.

Testing for venous reflux asks:

Does a standing duplex ultrasound show blood flowing backwards through a specific vein when it should not?

These are different problems.

That means purple feet or legs in someone with hEDS and POTS should not automatically be called chronic venous insufficiency.

And finding venous reflux in someone who has POTS does not automatically mean the reflux caused their POTS.

What does the evidence support in 2026?

These conclusions match the evidence grading in the original review.

What research do we still need?

There is one study that would answer many of these questions.

Researchers could compare three groups:

1. people with confirmed hEDS;

2. people with HSD;

3. people without hypermobility.

Everyone could then have the same standing duplex ultrasound.

Researchers could measure:

• reflux in the great saphenous vein;

• reflux in the small saphenous vein;

• deep-vein reflux;

• vein diameter;

• how long reflux lasts;

• and the severity of visible venous disease.

They could also measure how stretchy the veins are and perform POTS or autonomic testing in the same people.

That could help answer a much more useful question:

Do people with hEDS/HSD have abnormal vein valves, abnormal blood pooling, autonomic problems—or some combination of all three?

Right now, we do not have enough direct evidence to answer that confidently.

The bottom line

Here is what we can reasonably say in 2026.

hEDS and HSD are linked with a higher chance of having orthostatic symptoms and POTS.

Some people with POTS have more blood collecting in their lower legs while standing.

Joint hypermobility may be linked with early visible vein changes, but the evidence is limited.

Chronic venous disease involves real changes in vein walls, connective tissue and valves.

But researchers have not yet shown that hEDS or HSD commonly causes superficial venous reflux because the veins are unusually weak or stretchy.

The most accurate way to describe the science is:

hEDS/HSD → orthostatic and autonomic problems: reasonably supported.

POTS → abnormal blood pooling in the lower body in some people: reasonably supported.

Joint hypermobility → early visible vein changes: possible, but evidence is limited.

hEDS/HSD → overly stretchy veins → valve failure → chronic venous reflux: biologically possible, but not proven.

That final difference is important.

A theory can make sense without yet being established as fact.

And when we are talking about Ehlers-Danlos syndrome, POTS and venous disease, keeping those two things separate gives patients the most accurate picture of what science currently knows.

Key academic references

1. Kwok CS, et al. The co-existence of Ehlers-Danlos syndrome and postural orthostatic tachycardia syndrome: A systematic review of the literature. Autonomic Neuroscience. 2026;267:103453.

2. Kulin D, et al. Meta-Analysis: Chronic Gastrointestinal Symptoms and Comorbidities in Hypermobile Ehlers-Danlos Syndrome and Hypermobility Spectrum Disorders. Alimentary Pharmacology & Therapeutics. 2026.

3. Lau DH, et al. Postural Orthostatic Tachycardia Syndrome: A State-of-the-Art Review. Heart, Lung and Circulation. 2026;35:171–185.

4. Pugh GE, Thomas KN, Fan J-L, Fisher JP. Central arterial stiffness, flow-mediated dilation, and venous function in postural orthostatic tachycardia syndrome. American Journal of Physiology–Heart and Circulatory Physiology. 2026;330:H89–H99.

5. Novak P, et al. Hypermobile Ehlers-Danlos Syndrome: Cerebrovascular, Autonomic and Neuropathic Features. American Journal of Medicine Open. 2025;14:100111.

6. Aziz Q, et al. AGA Clinical Practice Update on GI Manifestations and Autonomic or Immune Dysfunction in Hypermobile Ehlers-Danlos Syndrome: Expert Review. Clinical Gastroenterology and Hepatology. 2025;23:1291–1302.

7. Cohen JN, Au JS. The blueprint: contemporary venous physiology and measurement. American Journal of Physiology–Heart and Circulatory Physiology. 2025;329:H801–H814.

8. Nadasy GL, et al. Vicious Circle With Venous Hypertension, Irregular Flow, Pathological Venous Wall Remodeling, and Valve Destruction in Chronic Venous Disease: A Review. Angiology. 2026;77:271–295.

9. Kienzl P, Deinsberger J, Weber B. Chronic Venous Disease: Pathophysiological Aspects, Risk Factors, and Diagnosis. Hamostaseologie. 2024;44:277–286.

10. Gloviczki P, et al. Society for Vascular Surgery, American Venous Forum, and American Vein and Lymphatic Society clinical practice guidelines for management of varicose veins of the lower extremities. Journal of Vascular Surgery: Venous and Lymphatic Disorders. 2023–2024.

11. Ritelli M, et al. Bridging the Diagnostic Gap for Hypermobile Ehlers-Danlos Syndrome and Hypermobility Spectrum Disorders. American Journal of Medical Genetics Part A. 2025;197:e63857.

12. Demirdas S, et al. Vascular Ehlers-Danlos Syndrome: A Comprehensive Natural History Study in a Dutch National Cohort of 142 Patients. Circulation: Genomic and Precision Medicine. 2024.

13. Azma K, et al. Venous insufficiency after prolonged standing: Is joint hypermobility an important risk factor? Advanced Biomedical Research. 2015;4:98.

14. Miller AJ, et al. Arterial Elasticity in Ehlers-Danlos Syndromes. Genes. 2020;11:55.

15. Stewart JM. Pooling in chronic orthostatic intolerance: arterial vasoconstrictive but not venous compliance defects. Circulation. 2002;105:2274–2281.

16. Castori M, et al. A framework for the classification of joint hypermobility and related conditions. American Journal of Medical Genetics Part C. 2017;175:148–157.

This article is for education only and is not individual medical advice. It is based on the evidence reviewed in the original article, which was updated through August 2026.