POTS and EDS: Why They Show Up Together

How Often Do POTS and EDS Overlap?

EDS is a group of connective tissue conditions, and the hypermobile type (hEDS) is the type diagnosed without a gene test. Hypermobility spectrum disorders (HSD) share the loose joints without meeting the full hEDS criteria.

The link shows up in both directions. A 2026 systematic review of 30 studies covered 8,421 people with EDS and 12,983 people with POTS. Its abstract gives a range in each direction, "depending on the population," shown in the figure below. The authors conclude that the 2 conditions "frequently co-occur" and that the proportions depend on the population evaluated (Kwok, 2026).

Why Do the Numbers Vary So Much?

2 things move the numbers: which patients a study draws from, and which definition it uses. A single center showed how much the definition alone can do. In a retrospective review of 100 young patients at that center who met POTS criteria, drawn from 392 records of orthostatic intolerance, the abstract reports that joint hypermobility disorders ranged from 13% under the strict criteria for hypermobile EDS (hEDS) to 34% under the broader criteria for hypermobility spectrum disorders (Yao, 2025). The patients were the same, and only the rulebook changed.

The authors warn that strict cutoffs can miss people who need care: "Using overly strict criteria to diagnose conditions which have a high prevalence of co-occurrence misses opportunities for potential therapeutic strategies" (Yao, 2025). In our team's experience, a person who falls just short of the hEDS cutoff can still have the loose joints, the fatigue and the racing heart.

That line is drawn on exam and history, because hEDS is diagnosed clinically. The 2017 international classification revised the clinical criteria for the hypermobile type to separate it from other joint hypermobility disorders (Malfait, 2017), and where a study sets that line shifts who counts.

Does EDS Cause POTS?

The studies above show that the 2 conditions travel together, and none of them was built to test whether either causes the other. Reviews offer several explanations for the overlap. A 2026 review names connective tissue laxity, altered baroreflex function, small fiber neuropathy and mast cell activation as mechanisms that may be involved (Johnson, 2026). That's a review's summary of the field, so our team treats each as a working idea to test in the person in front of us.

When hEDS comes with small fiber neuropathy, it looks different from small fiber neuropathy with no known cause. In 35 people with hEDS and small fiber neuropathy compared with 38 people with small fiber neuropathy of unknown cause, the abstract reports higher autonomic symptom scores in the hEDS group, "particularly in orthostatic intolerance, gastrointestinal, and urinary domains" (Dell'Aversana, 2026). That study compared the groups at 1 point in time, so it can't say what caused the difference. How these nerves drive dysautonomia is covered in small fiber neuropathy and POTS.

Mast cell activation syndrome (MCAS) is diagnosed in some of the same patients, and its measured frequency swings even more than hypermobility does. In the same 100-patient POTS cohort, the abstract reports MCAS in 2% under the first consensus criteria, 37% under conservative second-consensus criteria and 87% under broader clinical criteria (Yao, 2025). The mast cell side has its own page: MCAS and dysautonomia.

How Does Our Team Read the Overlap?

Our team starts from posture. In our team's view, the reflexes that hold you upright against gravity and the reflexes that tighten your blood vessels when you stand work from the same control system, so when posture control falls short, the squeeze on your vessels can too. Your vessels tighten on standing and relax a little when you lie down, the same way your leg and trunk muscles fire automatically when you tip backward.

When that vessel reflex falls behind, brain blood flow is harder to hold on standing, and our team sees the fast heart rate in POTS as the heart speeding up to rescue it. POTS is the rescue succeeding, and orthostatic hypotension, where blood pressure falls on standing, is the rescue failing. A 2026 review of POTS in general, not only with EDS, makes a related argument: in many patients, it says, the dominant physiology is compensatory activation in response to orthostatic stressors such as low central blood volume, venous pooling, impaired vasoconstriction or deconditioning (Chopra, 2026). That review is built around a hypothesis, so treat it as an argument that fits ours.

Falling behind Keeping up

Replay

That shared control is why our team checks muscle tone in anyone labeled hypermobile. On exam, our team finds that some people who seem hypermobile have low muscle tone, called hypotonia, instead. That's our team's clinical observation, and we know of no study that measures it. Joints can move too far because the ligaments have extra play, because the brain's signal to the surrounding muscles runs low, or both. Some of our patients with low tone describe feeling clumsy, learning complex movements slowly or rolling an ankle easily. The difference matters to us because muscle tone is a nervous system output, and our team works on it with training.

How Does the Clinic Evaluate POTS With Hypermobility?

The clinic's chiropractic neurologists look at how the body handles gravity. At the bedside, our team checks muscle tone and postural reflexes, then tracks heart rate, blood pressure and breathing from lying to standing to see how the vessels are keeping up as the person sits up, stands, moves, turns their head or relies on their inner ear and eyes for balance. Heart rate, blood pressure and breathing are tracked through the change from lying to standing, so the team can see which part of the system is falling behind. The joint history and the hEDS criteria still matter, and since hEDS is diagnosed clinically and has no gene test, the history and exam decide it.

The plan comes from those findings. Our team works on sensory input, motor control and postural reflexes, using loading and movement that feed the brain better information about where the body is in space. As those reflexes improve, the goal is for the vessels to do more of the work of getting blood to the brain, so the heart rate has less to compensate for. For a picture of what that looked like in practice, read 1 patient's case with EDS and POTS. It's a single case, and it doesn't predict anyone else's result.

Where Do Medications Fit?

Medications that expand blood volume, tighten blood vessels or slow the heart can ease symptoms, and they can be a useful bridge. In our team's view, their ceiling is that they help while they're being taken without changing how well the postural reflexes do their job, so the compensation underneath is still there. Our team's chiropractic neurologists don't prescribe, so we leave existing medications alone and don't advise changes, which is the prescriber's call. Alongside them, our team works on the reflexes the heart rate is covering for.

POTS and EDS: FAQ