New Drug Could Cut Heart Disease Risk by Harnessing the Power of Gut Bacteria, Study Suggests

Scientists have developed a new class of drug which could reduce the risk of cardiovascular disease by harnessing our gut bacteria.

The compound, developed by scientists at Cleveland Clinic, can stop gut microbes from making a molecule which has been linked to heart disease without harming them.

The research is the latest to investigate the role of the microbiome on our overall physical health. This is the genetic makeup of the bacteria which populate the inside and outside of our bodies and outnumber our own cells by 10 to 1.

Dr. Stanley Hazen of the Cleveland Clinic department of cardiovascular medicine, who was an author of the study published in the journal Nature Medicine, said in a statement: "To our knowledge, this is the most potent therapy to date for 'drugging' the microbiome to alter a disease process."

A new class of drug could decrease the risk of cardiovascular disease by targeting a specific microbial pathway in the gut. Getty Images

To develop the drug, researchers carried out experiments in mice. They found the compound they'd created made platelets (cell fragments in the blood which help with clotting) less overly responsive and also prevented excessive blood clots, thus diminishing the risk of cardiovascular disease.

The drug achieved this by reducing levels of trimethylamine N-oxide (TMAO), a byproduct of digestion, in the blood.

Previous studies headed by the same team indicated that high levels of TMAO in the blood could be a way to predict if a person will suffer a heart attack or stroke.

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When the gut digests nutrients present in animal products such red meat, egg yolks, and high-fat dairy products, it release TMAO. This in turn can affect how platelets behave, and raises the risk of thrombosis, which can cause heart attacks and stroke.

One dose of the drug cut the levels of TMAO in the blood for up to three days. It also returned platelets to their normal levels of responsiveness, and made clots less likely to form after damage to the arteries. The drug lingered in the gut but did not harm important bacteria, meaning it would not put patients at risk of antibiotic resistance.

Hazen said, "Gut bacteria are altered [by the drug] but not killed by this drug, and there were no observable toxic side effects. The approach developed could potentially be used to target other gut microbial pathways."