Written By | Health News Agencies
One in five people with high blood pressure may be carrying a hormone disorder that can be cured.
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BRISTOL, England
It is about the size of a mobile phone. It clips onto a waistband. It does not hurt, it does not beep, and it does not involve a single needle.
And it may be about to overturn the way doctors hunt for one of the most common — and most quietly devastating — causes of high blood pressure on the planet.
For twenty-four hours, sixty patients in Bristol, Bergen, Stockholm and Athens wore one. They went to work. They ate dinner. They argued with the television. They went to bed. And all the while, every twenty minutes, the device drew a microscopic sample of the fluid sitting just beneath their skin and measured the hormones swimming in it.
What it recorded while those patients were asleep is the reason specialists across Europe spent the weekend rereading a paper in the journal Science Translational Medicine — and quietly wondering how many patients they have sent home over the years with a clean result and a condition they actually had all along.
THE DISEASE HIDING INSIDE THE DIAGNOSIS
The condition is called primary aldosteronism. If you have never heard of it, you are in enormous company — and that is precisely the problem.
It happens when one or both of the adrenal glands, the small triangular organs perched on top of the kidneys, start churning out too much of a hormone called aldosterone. Aldosterone is the body's salt-and-water foreman. It tells the kidneys to hold on to sodium and let go of potassium. Too much of it, and the body retains fluid, the volume in the blood vessels rises, and the pressure climbs.
Crucially, this is not ordinary high blood pressure. It is high blood pressure with a cause — and often a cause that can be removed.
The numbers attached to it are genuinely startling. The new research describes primary aldosteronism as a disorder that may affect up to one in five people living with high blood pressure. Estimates from primary care put the figure at 5 to 14 per cent of hypertensive patients, rising to as high as 30 per cent among those referred on to specialist clinics.
Now set that against the global picture. The World Health Organization counts roughly 1.4 billion adults aged 30 to 79 living with hypertension. Around 600 million of them — some 44 per cent — do not know they have it. High systolic blood pressure is the single biggest risk factor for early death on Earth, implicated in an estimated 10.8 million avoidable deaths every year. Even a modest slice of that mountain represents an enormous number of people carrying a treatable hormone problem that nobody has gone looking for.
And people with primary aldosteronism are not simply at the same risk as everyone else with high readings. The excess aldosterone appears to damage the heart, blood vessels and kidneys directly, over and above the effect of the pressure itself. It is associated with a raised risk of heart disease, stroke, diabetes and other serious complications.
Which makes the next part of the story rather difficult to read.
WHY THE BLOOD TEST KEEPS MISSING IT
The standard way to look for primary aldosteronism is to take a blood sample, measure aldosterone and a second hormone called renin, and calculate the ratio between them. It is cheap, it is available, and — critically — it is a snapshot. One moment, one tube, one number.
The team behind the new work, led by researchers at the University of Bristol and the University of Manchester in the UK and the University of Bergen in Norway, with collaborators in Stockholm and Athens, suspected that a snapshot might be the wrong instrument for a moving target.
So they built a film instead.
Using a wearable sampling device developed at Bristol and known as U-RHYTHM, they measured hormone levels in their sixty patients every twenty minutes across a full twenty-four-hour cycle. Because the device samples from the tissue fluid beneath the skin rather than drawing blood from a vein, participants could carry on with normal life — including, and this turned out to be the decisive detail, sleeping through the night undisturbed.
Alongside aldosterone itself, the team tracked two closely related hormones, 18-hydroxycortisol and 18-oxocortisol, and ran the resulting profiles through computational analysis.
The results did not show what the textbook picture would predict. Aldosterone in these patients was not simply parked at a permanently high level. Instead, it came in repeated bursts — and the overall day-night rhythm of hormone activity remained intact underneath them.
Most significantly of all, the bursts clustered at night. The researchers uncovered a pattern of nocturnal aldosterone secretion that no routine clinic could ever have seen, for the simple and rather obvious reason that almost nobody gets their blood drawn at three in the morning.
Then came the finding that should give every clinician pause. Even in some of the most severe cases in the study, hormone levels at certain moments dropped below the minimum thresholds normally used to make the diagnosis. In other words, a patient with unmistakable primary aldosteronism could, at the wrong moment, produce a blood result that looks entirely reassuring.
A single test at a single point in time can land squarely in one of those troughs. The patient goes home. The disease does not.
THE EVIDENCE THAT SEALED IT
Correlation is cheap; researchers know it and reviewers hunt for it. So the team looked for something harder.
They found that the nighttime hormone spikes originated in the adrenal glands, and that they were especially pronounced in patients whose disease came from a problem affecting only one adrenal gland rather than both — the so-called unilateral form, which is the type most likely to be surgically curable.
Then they watched what happened when the affected gland was removed.
The abnormal patterns disappeared.
That is about as close to a causal fingerprint as this kind of study can get. Take out the gland, and the strange overnight bursts vanish with it — strong evidence that the bursts were not background noise or an artefact of the device, but a direct signature of the disease itself.
WHAT THE SCIENTISTS SAY
Dr Thomas Upton, Clinical Research Fellow at the University of Bristol and Senior Clinical Fellow at Bristol Hospitals NHS Foundation Trust, and a co-lead author of the study, was blunt about the scale of what is being missed.
"Primary aldosteronism is an important cause of high blood pressure and the most common cause of secondary hypertension we see in our blood pressure clinic," he said. "It could be affecting millions of people in the UK. However, due to the way hormones change during the day and the current complexity of the diagnostic process, diagnosis is often delayed or never made at all."
He described the value of watching patients in their own lives rather than in a hospital bay. "In our study, patients were monitored at home during normal activity, and this allowed us to see how hormones changed over time in realistic settings. This approach could potentially revolutionise how we diagnose hypertension and ultimately reduce cardiovascular disease — particularly heart disease and strokes — that could have been prevented."
Dr Eder Zavala, a UKRI Future Leader Fellow at the University of Manchester and the study's senior author, framed the discovery as a shift from measuring a number to reading a rhythm.
"By continuously monitoring hormones over 24 hours, we were able to reveal a previously hidden pattern of nocturnal hormone bursts," he said. "This gives us a much clearer understanding of the disease and could ultimately help doctors detect it earlier and treat patients more effectively."
He went further, suggesting the same approach might pick up the disease in its earliest stages, long before conventional tests would flag anything. "A more detailed mathematical and computational analysis of daily hormonal profiles could eventually also help uncover earlier and more subtle forms of the disease, opening new opportunities to improve outcomes for patients living with high blood pressure."
Professor Stafford Lightman of the University of Bristol, the inventor of the U-RHYTHM technology, went straight for the implication clinicians will find hardest to swallow.
"The findings suggest that clinicians may need to rethink how they look for the disorder," he said, noting that Endocrine Society clinical practice guidelines now recommend that primary aldosteronism be considered in all people with hypertension.
"Future diagnosis could move away from single time point blood tests and towards tracking the body's hormone rhythms over time, particularly the overnight patterns that appear to hold crucial clues to disease. Further research is needed to define the best clinical pathways, using dynamic hormone measurement, to ensure early diagnosis of this common and potentially curable cause of high blood pressure."
THE GUIDELINE NOBODY IS FOLLOWING
Professor Lightman's reference to the Endocrine Society is not a throwaway line. In 2025 the Society published an updated clinical practice guideline that advised clinicians to test every patient with hypertension for primary aldosteronism by measuring aldosterone and renin — and, helpfully, confirmed that patients do not need to come off their blood pressure medication to be screened.
The guideline also set out what happens when the condition is found. For patients whose disease is confined to one adrenal gland and who are fit for an operation, removing that gland is the preferred route, and can amount to a cure. For those with disease in both glands, or who are not surgical candidates, mineralocorticoid receptor antagonists are the mainstay — with spironolactone suggested first, on the grounds that it is cheap and available almost everywhere.
So the treatments exist. The guideline exists. The problem is the step before all of it.
Study after study has found that screening simply is not happening. One population-based analysis found that among patients who had both hypertension and low potassium — a combination that practically shouts primary aldosteronism — only 1.6 per cent were screened for it. In a cohort of patients with chronic kidney disease, 39 per cent had a clear indication for testing under Endocrine Society criteria; just 14 per cent of those were actually tested.
The new research adds an uncomfortable second layer to that picture. It is not only that too few people are being tested. It is that some of the people who are being tested may be getting a falsely reassuring answer.
WHAT THIS MEANS FOR YOU
Let us be clear about what this study does not say. It does not say your blood pressure tablets are wrong. It does not say your GP has missed something. And it certainly does not say you should stop any medication.
What it does say is that there are questions worth asking.
If your blood pressure is stubbornly high despite taking three or more medications, that is a recognised flag. If blood tests have ever shown your potassium running low, that is another. If you were diagnosed with high blood pressure unusually young, or if there is a family history of early strokes or heart disease, those are worth mentioning too. And if you have never had aldosterone and renin measured at all — which, statistically, is overwhelmingly likely — that is a reasonable thing to raise at your next appointment.
The prize here is not a better pill. It is the possibility of stopping altogether. Primary aldosteronism is one of the rare cases in cardiovascular medicine where the phrase "potentially curable" genuinely applies. A patient with unilateral disease who has the affected gland removed can, in the best cases, walk away from their blood pressure medication for good.
The cost of missing it is measured in the same currency as the cost of missing high blood pressure itself: heart attacks, strokes, kidney failure, and years that did not have to be lost.
WHAT THE STUDY CANNOT YET TELL US
Sixty patients is sixty patients. The authors describe this as a proof-of-concept study, and the phrase is doing real work. It demonstrates that continuous hormone monitoring can reveal a pattern that conventional testing misses; it does not yet establish how that pattern should be measured, scored, or turned into a diagnosis in an ordinary clinic.
There is no new diagnostic threshold on offer here. There is no trial showing that patients diagnosed this way do better over five or ten years than patients diagnosed the old way. There is no health economics analysis telling a cash-strapped health service whether it can afford to put a wearable sampler on every difficult hypertension patient who walks through the door.
The device itself is also not something you can buy. U-RHYTHM emerged from academic research at Bristol and was taken up and developed further by the spinout company Dynamic Therapeutics in 2023. It remains a research tool.
The researchers themselves say plainly that further work is needed to define the best clinical pathways. Funding for the study came from a long list of public and charitable bodies including EU Horizon 2020, the Trond Mohn Foundation, the UK's BBSRC and Medical Research Council, University Hospitals Bristol and Weston NHS Foundation, the Swedish Medical Research Council and the Knut and Alice Wallenberg Foundation.
THE BIGGER IDEA
Strip away the hormone names and the acronyms, and what this study really challenges is a habit of mind that runs through almost all of modern medicine: the assumption that a single measurement, taken at a convenient hour, tells you the truth about a body that never stops moving.
Blood pressure itself made this journey decades ago. Doctors once measured it once, in a clinic, and called it a day — until it became clear that some patients spike only at the surgery and others only at home, and 24-hour monitoring became standard.
Hormones have not made that journey yet, largely because until recently there was no practical way to follow them around. Now there is.
"The findings suggest that clinicians may need to rethink how they look for the disorder," Professor Lightman said — a sentence delivered with characteristic academic restraint about a result that, if it holds up in larger studies, means a great many people currently labelled with plain old high blood pressure have been carrying something else entirely. Something with a name. Something with a cause. And, for some of them, something with an ending.
