Urolithin A, made by the body from pomegranates, improved heart function up to 80% in animals

A compound the human gut makes after a meal of pomegranates, walnuts or certain berries has just been credited with a striking result in the lab: urolithin A improved heart function by up to 80% in animal models of a stubborn form of heart failure. The finding comes from a team at King’s College London, and the researchers themselves are careful to say it does not amount to a diet prescription.

The work was published in August in the journal Science Advances and covered by outlets including ScienceDaily as recently as late September, which is why it may look newer than it is. What it shows, and what it leaves untested, is worth laying out plainly, because the word “pomegranate” invites conclusions the data do not support.

A compound the body makes, not the fruit itself

Urolithin A is not found in pomegranates in any meaningful amount. It is a postbiotic, produced when bacteria in the gut break down ellagitannins, plant compounds abundant in pomegranates, walnuts and some berries. Whether a given person makes much of it depends on their gut microbiome, so eating the fruit and having the compound circulate are not the same thing.

That distinction shapes how the King’s team framed the work. According to the university’s own announcement dated August 20, urolithin A is the substance produced after those foods are eaten, which is the compound the study examines rather than the fruit itself.

The 80% figure: which measure, and which animals

The target was heart failure with preserved ejection fraction, known as HFpEF. In this condition the heart pumps out a normal share of its blood with each beat but is too stiff to relax and fill properly in between. The university says about half a million people in the UK have it and that it accounts for roughly half of all heart failure cases. Treatment options are limited because the disease is so varied from patient to patient.

The experiments used mice with diet- and hormone-induced HFpEF, according to a summary of the paper on Sci.News. A week of urolithin A treatment improved measures of diastolic function, meaning how well the heart muscle relaxes, reduced heart enlargement and fibrosis, and increased how much the animals ran. The university reported heart function improved by up to 80% compared with untreated controls. The paper appears as Science Advances volume 12, issue 34, with the identifier 10.1126/sciadv.aec8088.

The phrase “up to” matters. It describes the best-performing measure, not an average across every outcome, and the researchers’ summaries do not say that all the readouts moved by that much.

A switch on one protein

Lead author Dr. Joseph Burgoyne and colleagues traced the effect to a protein called PKGIα, which the team says plays an important role in both blood vessel function and heart muscle relaxation. Urolithin A appears to act on a specific amino acid site on that protein, called Cys42, and in doing so switches on a beneficial pathway. In genetically modified mice lacking a working Cys42 site, the benefits disappeared, which is the strongest evidence in the study that the compound works through that route rather than by some general effect.

The team also tested the compound in heart tissue engineered from human stem cells, where it improved contraction and relaxation speed. Burgoyne told the university that the findings “identify a completely new therapeutic target” for a disease in which, in his words reported by the university, “this type of heart failure remains one of the most challenging forms of heart disease to treat.” The work was funded by the British Heart Foundation, a News-Medical report of the release notes.

The authors’ own warning against eating pomegranates for heart failure

The obvious question is whether pomegranate consumption could reproduce any of this in people, and the authors answer it themselves. “While there isn’t enough evidence to suggest that people should eat pomegranates to treat heart failure,” Burgoyne said, according to the ScienceDaily version of the release, “these findings raise the possibility that dietary approaches that enhance urolithin A production may help alleviate this condition.”

Professor James Leiper of the British Heart Foundation was more direct: “No single food can prevent or treat heart disease on its own.” He also pointed out that the benefits so far come from animals and engineered tissue, so clinical trials involving people are needed to test whether the approach works for patients.

Mice are a limited stand-in for a disease that mostly affects older people with several coexisting conditions, and a week of treatment says little about long-term safety or dose. Whether a drug or supplement built around urolithin A could ever reach a human trial, and whether raising the compound’s levels through diet is even feasible for people who make little of it, remains an open question that the King’s team has not yet answered.

This article was produced with the assistance of AI and reviewed by Morning Overview editors prior to publication.

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