The Heart Failure Breakthrough That Starts With Pomegranates

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Researchers at King’s College London have identified a compound called urolithin A, produced naturally in the gut after eating foods like pomegranates, walnuts and berries, as a potential new avenue for treating heart failure with preserved ejection fraction, a form of heart failure that affects roughly half of all people diagnosed with the condition and currently has limited treatment options.

What exactly is HFpEF, and why is it hard to treat?

HFpEF occurs when the heart’s pumping strength stays relatively normal, but the heart muscle becomes stiff and struggles to relax and refill with blood between beats. That stiffness leads to symptoms like fatigue and breathlessness, and it has proven notoriously difficult to treat, with major clinical trials targeting related biological pathways largely failing to improve patient outcomes in the past. HFpEF accounts for roughly half of all heart failure cases and carries significant health risks, according to the British Heart Foundation, which funded the new research.

What did the researchers actually find?

The study, led by Dr. Joseph Burgoyne and published in Science Advances, identified urolithin A as a compound capable of activating a protein called PKGIα, which plays a central role in helping heart muscle and blood vessels relax. The team pinpointed a specific site on that protein, a location known as Cys42, as the target urolithin A engages to trigger this effect, representing what researchers describe as a genuinely new therapeutic target for HFpEF rather than a variation on existing approaches. In animal models of the condition, treatment with urolithin A improved measures of heart function by as much as 80% compared to untreated animals, and in engineered human heart tissue grown from stem cells, the compound significantly improved the tissue’s ability to relax.

Does this mean pomegranates can treat heart failure?

No, and the researchers have been direct about that distinction. Burgoyne has said there isn’t enough evidence to suggest people should eat pomegranates specifically to treat heart failure, since urolithin A isn’t consumed directly from the fruit itself. Instead, gut bacteria convert compounds called ellagitannins, found in pomegranates, walnuts and certain berries, into urolithin A after digestion. How efficiently someone’s body performs that conversion varies significantly based on individual gut bacteria composition, meaning dietary intake alone doesn’t guarantee meaningful urolithin A production.

What has to happen before this could become an actual treatment?

Quite a lot. The findings so far come entirely from animal models and lab-grown human heart tissue, not from actual patients. Cardiologists not involved in the study, including Dr. Kevin Shah, have emphasized that clinical trials in humans are the necessary next step to determine whether these benefits translate into real improvements in symptoms, hospitalizations or survival. Urolithin A has already been tested in some human studies for other purposes, including muscle function in older adults, and has shown a generally favorable safety profile, which may help support future heart-specific trials, but no such trial for HFpEF has been conducted yet.

What should someone actually do with this information right now?

Registered dietitian Monique Richard has pointed to practical ways to incorporate ellagitannin-rich foods into a normal diet, such as adding berries to oatmeal or yogurt, topping grain bowls with pomegranate arils, mixing walnuts into salads, or drinking pomegranate juice on its own or in herbal iced tea. These are reasonable additions to a generally heart-healthy eating pattern, but experts are clear that no single food or compound replaces prescribed medications, regular physical activity, adequate sleep or the broader dietary habits already linked to cardiovascular health.

What’s the bigger picture here?

This research opens a new biological pathway that scientists can now study specifically for HFpEF treatment, which matters given how few effective options currently exist for the condition. Whether urolithin A itself, or a therapy built around the same target, eventually reaches patients will depend entirely on how it performs in the human clinical trials that still need to happen.

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