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Written by: Irene Euodia
Medically reviewed by: Rob Philibert MD PhD

The gut microbiome is the middleman between diet and metabolic health. In particular, the gut biome moderates our risk of coronary heart disease, stroke, heart failure, and hypertension. Many recent studies suggest that the gut microbiome may be a potential target for the prevention and treatment of heart disease. This suggests an opportunity for each of us to prevent heart disease in ourselves by being more aware of our “gut health.”

The microbiome can release into the gut important metabolites such as Short-Chain Fatty Acids (SCFA), Bile acids, and Trimethylamine N-oxide (TMAO) that can significantly influence heart and metabolic functions. Each of these metabolites has a distinct role in moderating metabolic health.

SCFAs such as acetate, butyrate, and propionate are products of the fermentation of indigestible dietary fibers in the gut by the microbiota. One type of microbiota that is responsible for generating these compounds is Roseburia, a species that also has an anti-inflammatory role in the gut through its maintenance of the gut barrier. When these guardians of the intestinal barrier are depleted, the gut barrier is compromised, resulting in a “leaky gut”, which allows bacteria and toxins to enter the bloodstream and cause infection and inflammation in the other organs. SCFAs are absorbed through the gut and travel to the liver where they moderate lipid metabolism and glucose absorption. SCFA receptors are also found in the vascular endothelium, which directly affects systemic circulation and can cause hypertension when depleted. This depletion or low microbiome diversity is associated with low fiber intake in your diet. Therefore, try increasing your fiber intake with foods like avocado, berries, broccoli, lentils, beans, seeds, and oats.

Bile acids are crucial for emulsifying fats, vitamin absorption, and the elimination of cholesterol via excretion in the feces. This elimination pathway decreases serum cholesterol levels and helps prevent plaque build-ups. Bile acids are synthesized from cholesterol in the liver via multi-step processes involving several enzymes. These primary bile acids are secreted into the duodenum (the upper part of the small intestine) from the liver. Normally, these primary bile acids are modified to secondary bile acids before being reabsorbed and returned to the liver. When the enzymatic mechanisms affecting bile acid in the gut are altered, primary bile acid often is not converted to secondary bile acid, thus increasing plasma level of LDL (cholesterol) and risk for developing plaques (atherosclerosis). Fortunately, there are simple things you can do to prevent this condition. First, since low levels of bile acid may result from a lack of dietary fats, maintaining a well-balanced diet is critical. Second, because dark-leafy green vegetables, beetroot, artichokes, and pickles have important bile acid precursors, including these foods in your diet is a good way to promote bile acid production.

The breakdown of dietary substances rich in phosphatidylcholine, choline, or carnitine, which are commonly found in red meat, fish, or eggs forms trimethylamine (TMA), the precursor to TMAO. TMA is absorbed in the intestine and converted via the hepatic enzyme flavin-containing monooxygenase 3 to TMAO. TMAO is then released by the liver into the bloodstream and eventually cleared by the kidneys. At normal levels, TMAO is generally considered beneficial for the body for maintaining normal cholesterol levels, lipid metabolism, and gut physiology. But altered levels can have serious consequences. TMAO is eliminated through the kidneys with impaired renal function leading to high levels of TMAO. These elevated levels of TMAO can increase cholesterol deposition in arterial walls, resulting in plaque build-up, and increasing the risk of a heart attack. To lower the TMAO levels in your gut, try minimizing full-fat dairy products, such as cream cheese, full-fat milk, butter, and processed meat.

Food is not the only factor that affects the diversity of the gut microbiome. Medications like antibiotics can wipe out helpful species of microbiota in the gut. A way to restore microbiome diversity may be through probiotic administration. Some studies suggest that taking these supplements can reduce systemic inflammation. Other studies suggest that taking prebiotics promotes microbial fermentation of dietary fibers to SCFAs. Finally, some prebiotics, such as inulin, have the potential to counteract the harmful effects of antibiotics by promoting the diversity and functional capacity of the gut microbiota.

In summary, the gut microbiome can be our silent partner in maintaining our health. But there are other ways that a healthy gut can improve your quality of life besides lowering the risk of heart disease. Don’t forget to monitor meat and dairy intake to reduce TMAO production, consume high-fiber foods for healthier gut barriers and avoid high fat and/or high-sugar foods for better SCFA function. Contact your health care provider and nutritionist for more detailed health recommendations.

References:

  1. The Gut Microbiome and Cardiovascular Disease: Current Knowledge and Clinical Potential, https://journals.physiology.org/doi/full/10.1152/ajpheart.00376.2019
  2. The Gut Microbiome in Coronary Artery Disease and Heart Failure: Current Knowledge and Future Directions, https://www.thelancet.com/journals/ebiom/article/PIIS2352-3964(20)30024-4/full text
  3. Gut Microbiota in Cardiovascular Disease https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5390330/
  4. Gut Microbiota in Cardiovascular Disease: Opportunities and Challenges https://microbiomejournal.biomedcentral.com/articles/10.1186/s40168-020-00821-0
  5. Gut Microbes Role in Heart Failure Explored https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.119.043300
  6. Design of the GutHeart—targeting gut microbiota to treat heart failure—trial: a Phase II, randomized clinical trial https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6165929/
  7. Gut Microbiota and Cardiovascular Disease https://www.ahajournals.org/doi/full/10.1161/CIRCRESAHA.120.316242