Natural compound in fruits and nuts reverses damage caused by heart condition suffered by 4 million Americans, study suggests

A natural compound found in fruits and nuts may help reverse heart damage linked to a severe form of heart failure. 

Urolithin A is a compound produced when bacteria in the gut break down plant polyphenols in foods such as pomegranates, walnuts and berries.

It promotes cell health by clearing away damaged parts of cells and can support muscle function and overall healthy aging. It is commonly sold as a supplement in pill form. 

However, you don’t need to spend $100 on a bottle to reap its benefits. 

Pomegranates are the richest dietary source of the polyphenols that the gut breaks down into urolithin A, and walnuts, pecans, raspberries, strawberries and blackberries are also top sources. 

Now, scientists believe the compound could help treat an especially hard-to-manage form of heart failure.

Nearly 6.7 million Americans 20 years and older have heart failure, and about half of all heart failure cases are a condition called heart failure with preserved ejection fraction (HFpEF).

HFpEF occurs when the heart contracts normally but doesn’t relax properly between beats. When the heart remains stiff between beats, it has trouble filling with blood.

This causes shortness of breath and fatigue and is associated with substantial illness and death – though exact numbers are unknown – and there are limited treatment options. 

In a recent study in mice published in the journal Science Advances, researchers discovered that urolithin A switches on a heart protein involved in helping the heart relax between beats.

That relaxation is especially important for people with HFpEF, whose hearts become stiff and struggle to fill properly with blood. 

By activating this pathway, urolithin A appeared to improve the heart’s flexibility and reduce some of the damage associated with prolonged stiffness. 

Researchers traced the effect to cysteine 42, a specific site on the heart’s PKGIα protein, which helps regulate how the heart and blood vessels relax.

Additionally, urolithin A was able to reverse several key features of HFpEF in mice that were experimentally given the condition. 

Following the mice study, researchers conducted similar experiments in engineered human heart tissue grown from stem cells in a lab.

The treated tissue contracted and relaxed more efficiently, suggesting the compound’s benefits may extend beyond mice. 

Historically, HFpEF has been difficult to treat because most heart failure drugs are designed to improve the heart’s pumping ability. In HFpEF, however, the heart can usually pump normally. The problem is that it becomes too stiff to relax and fill efficiently. 

While the findings are still limited to animal models and lab-grown human tissue, they point to a potential new treatment approach that targets the underlying biology of HFpEF rather than simply managing symptoms. 

If future studies in humans produce similar results, the compound could offer hope to millions of people living with the condition.