A natural compound found in fruits and nuts may help reverse heart damage linked to severe heart failure.
Urolithin A is a compound produced when bacteria in the intestines break down plant polyphenols in foods such as pomegranates, walnuts and berries.
It promotes cell health by clearing damaged areas of cells and can support muscle function and overall healthy aging. It is often sold as a supplement in pill form.
However, you don’t have to spend $100 on a bottle to reap the benefits.
Pomegranates are the richest dietary source of the polyphenols that are broken down by the intestines into urolithin A, and walnuts, pecans, raspberries, strawberries and blackberries are also top sources.
Now scientists believe the compound could help treat a special condition difficult-to-treat form of heart failure.
Nearly 6.7 million Americans age 20 and older have heart failure, and about half of all cases of heart failure are a condition called heart failure with preserved ejection fraction (HFpEF).
Urolithin A is a compound produced when bacteria in the intestines break down plant polyphenols in foods such as pomegranates, walnuts and berries
HFpEF occurs when the heart contracts normally, but does not relax properly between beats. When the heart remains stiff between beats, it has difficulty filling with blood.
This causes shortness of breath and fatigue and is associated with significant illness and death – although exact numbers are unknown – and there are limited treatment options.
In a recent study in mice published in the journal Scientific progressresearchers discovered that urolithin A turns on a heart protein involved in helping the heart relax between beats.
This relaxation is especially important for people with HFpEF, whose heart becomes stiff and has difficulty filling with blood properly.
By activating this pathway, urolithin A appeared to improve the heart’s flexibility and reduce some of the damage associated with long-term 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.
Furthermore, urolithin A was able to reverse several key features of HFpEF in mice experimentally given the condition.
After the mouse study, researchers conducted similar experiments using engineered human heart tissue grown from stem cells in a laboratory.
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 medications are designed to improve the heart’s pumping ability. However, in HFpEF the heart can usually pump normally. The problem is that it becomes too stiff to relax and fill efficiently.
Although the findings are still limited to animal models and laboratory-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 human studies yield similar results, the compound could offer hope to millions of people living with the condition.
