Scientists have identified a natural compound produced by the body after consuming certain foods that may enhance heart relaxation and improve function in a particularly difficult-to-treat type of heart failure. In laboratory studies, this compound boosted some measures of cardiac performance by as much as 80%. The substance, known as urolithin A, is generated when gut bacteria break down nutrients found in foods like pomegranates, walnuts, and some berries.
Researchers at King’s College London explored whether urolithin A could benefit individuals with heart failure with preserved ejection fraction (HFpEF). Their findings are set to be published in Science Advances. It’s important to understand that in HFpEF, the heart doesn’t necessarily weaken or stop pumping, but instead becomes stiff and struggles to relax between beats. This stiffness hinders the heart’s ability to fill with blood properly, which can lead to reduced blood flow during physical activity despite the heart’s normal pumping capacity.
Individuals with HFpEF often experience symptoms like shortness of breath, fatigue, swelling, and limited exercise tolerance. These issues can significantly impair daily life and increase the risk of repeated hospital stays. The condition is increasingly common among aging populations, often linked to high blood pressure, obesity, diabetes, and other chronic health conditions that cause the heart muscle to become rigid.
Treating HFpEF has historically been challenging due to its complex causes. While some newer medications can lower hospitalization rates and improve certain outcomes, there remains a pressing need for treatments that directly enhance the heart muscle’s ability to relax.
In their recent study, the King’s College London team examined how urolithin A affects heart function. They found that the compound activates a specific protein pathway critical for maintaining normal cardiac and blood vessel function. Activation of this pathway appeared to improve heart muscle relaxation and decrease fibrosis — the formation of stiff scar tissue that diminishes heart flexibility. Additionally, urolithin A helped reduce abnormal enlargement of heart muscle cells, a change that often results from prolonged high blood pressure or stress.
In animal models of HFpEF, treatment with urolithin A led to up to an 80% improvement in some heart function metrics compared to untreated subjects. The researchers also observed less scarring and other detrimental alterations in the hearts of treated animals. Further tests on human heart tissue grown from stem cells revealed that urolithin A notably enhanced the tissue’s capacity to relax, suggesting that the compound’s effects could extend to humans.
An added benefit is that urolithin A has been studied previously in humans for other conditions and has generally demonstrated a favorable safety profile. Nevertheless, this does not confirm its safety or effectiveness as a treatment for heart failure. Senior author Dr. Joseph Burgoyne emphasized that the study uncovers a novel pathway that could be targeted in future treatments for HFpEF and that urolithin A warrants further research.
It’s important to note that consuming large amounts of pomegranates, walnuts, or berries won’t necessarily treat heart failure, as individuals vary greatly in their ability to produce urolithin A depending on their gut bacteria. Moreover, the current findings are preliminary; benefits observed in animals and lab-grown human tissues need to be confirmed through clinical trials involving patients to evaluate actual improvements in symptoms, hospitalization rates, or survival.
Overall, this research offers an optimistic new avenue for tackling a challenging form of heart failure. The promising biological results support moving forward with human studies, but it remains too early to consider urolithin A an established treatment.
