Gut Microbiome and Heart Disease
So how does one’s gut health affect cardiovascular health? The gut microbiota plays crucial roles in digestion, immune function, and the production of various chemicals that can profoundly impact our cardiovascular health. The balance and diversity of microbes within our gut can also determine whether we are at risk of developing certain cardiovascular diseases. Hypertension, for example, has been associated with gut dysbiosis and poor gut diversity. This is often characterized by an over-abundance of Prevotella, Klebsiella, and Enterobacter bacteria groups. In contrast, there seems to be a drastic reduction of beneficial bacteria such as Roseburia, Blautia, Ruminococcus, and Bifidobacteria.
In 2011, Dr. Stanley Hazen and his colleagues at the Cleveland Clinic made a groundbreaking discovery on the gut-heart alliance. Their research revealed that certain gut bacteria can metabolize choline and carnitine, abundant in foods like eggs, red meat, and dairy, to produce a compound in the liver known as trimethylamine-N-oxide (TMAO). Elevated levels of TMAO damage blood vessels and cause inflammation and clotting, all of which contribute to an increased risk of heart disease. Gut bacteria known to be involved in the production of TMAO include Clostridium, Peptostreptococcus, and Desulfovibrio. Conversely, Neisseria, Veillonella, and Fusobacterium can generate nitric oxide (NO) from nitrate in green leafy vegetables and beetroot. Nitric oxide is known to dilate our blood vessels and help reduce blood pressure.
Short-chain fatty acids (SCFAs), which are compounds predominantly produced by keystone gut bacteria, e.g., Faecalibacterium, Roseburia (produce butyrate), Bacteriodetes (produce propionate), Enterococcus (produce acetate), have also been shown to play crucial roles in cardiovascular health. SCFAs are important for enhancing the function of cells lining our blood vessels, reducing cholesterol levels, and helping regulate blood sugar. Interestingly, hypertension occurrence seems to be inversely related to SCFA production. There are several ways SCFAs have been proposed to regulate hypertension. One of them is that they can directly bind to G-protein coupled receptors in vascular smooth muscles to regulate hypertension. Similarly, butyrate regulates hypertension development through an immune response. It is well known that excessive inflammation plays a role in the development of hypertension. Butyrate has been shown to clinically reduce increased levels of proinflammatory cells such as Th17 and IL-17 in hypertension patients.