Gut microbiota: the secret to heart health

In recent years, the gut microbiota has increasingly become central to maintaining good health and preventing inflammatory, neurological and heart disease. Indeed, certain molecules contained in red meat are transformed by intestinal bacteria into TMAO, a substance that increases the risk of heart disease. A recent study, however, suggests that adopting a Mediterranean-type diet could block this transformation and thus reduce the risk of heart attack and stroke.

It is now clearly established that the high consumption of animal products, in particular red meats, is associated with a substantial increase in the risk of heart disease such as heart attack or stroke. Although it was once thought that this link was due to the high content of these foods in saturated fat, we now know that the negative impact of these fats is relatively low and that other factors associated with meat consumption are involved. .

Studies have shown that the hundreds of billions of bacteria that populate our digestive system, known as the gut microbiota, play an important role in this increased risk of heart disease. These bacteria metabolize certain molecules contained in foods of animal origin (phosphatidylcholine, choline and carnitine) to obtain the carbon atoms necessary for their survival. Unfortunately for us, this metabolism generates in parallel triethylamine (TMA), a metabolic “waste” which is transported to the liver where it is transformed into TMA N-oxide (TMAO).

Double the risk of heart disease

Several studies indicate that TMAO may be the main culprit in the rise in heart disease caused by foods of animal origin. For example, a recent study showed that the production of TMAO by the gut microbiota increased the reactivity of blood platelets and the potential for blood clot formation. Thus, high levels of TMAO in the blood are associated with an almost twice as high risk of heart attack or stroke within three years.

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It is therefore no coincidence that vegetarians are less at risk of being affected by heart disease than carnivores: by not eating meat, their intestinal bacteria do not generate TMAO, which spares the cardiovascular system .

Red wine and olive oil: the Mediterranean diet protects the heart

Without necessarily encouraging people to become vegetarians, a recent study indicates that it would also be possible to block the formation of TMAO by directly interfering with the metabolism of bacteria. A team of scientists in California (UCLA) has indeed shown that a molecule with a structure similar to choline, 3,3-dimethyl-1-butanol (DMB), acts as a very powerful inhibitor of the production of TMAO. by different strains of bacteria. The therapeutic potential of this molecule seems high, because it blocks the formation of atherosclerotic lesions, without toxicity.

The most important thing for us is that we can now take advantage of this positive effect of DMB: this natural substance is found in appreciable quantities in certain foods such as red wine and olive oil, two pillars of the Mediterranean diet that have been repeatedly associated with a significant reduction in the risk of heart disease.

The intestinal microbiota, a way forward to protect the heart

In addition to the positive impact of the Mediterranean diet on HDL-cholesterol levels and inflammation, it is therefore possible that the cardiovascular protection offered by this diet also involves a reduction in the production of TMAO. by intestinal bacteria. The possibility of attacking cardiovascular pathologies by targeting these bacteria could therefore represent a future strategy for the treatment of these diseases.

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  • Micha R. et al. Red and processed meat consumption and risk of incident coronary heart disease, stroke, and diabetes mellitus: a systematic review and meta-analysis. Traffic; 121: 2271-83.
  • Zhu W et al. Gut microbial metabolite TMAO enhances platelet hyperreactivity and thrombosis risk. Cell 2016; 165: 1-14.
  • Wang Z et al. Non-lethal inhibition of gut microbial trimethylamine production for the treatment of atherosclerosis. Cell 2015; 163: 1585-95.


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