Atherosclerosis is characterized by an accumulation of fat on the walls of arteries, which can range from a simple narrowing to the complete obstruction of the blood vessel. New ideas for prevention are targeting diet and intestinal flora.
About this article
Atheromatous plaques, or lipid plaques consisting of cholesterol in particular, are very common; all adults have them. Their thickening can obstruct blood flow, meaning organs are no longer sufficiently supplied, which can lead to pain and changes in heart rate. A local inflammatory reaction can lead to plaque rupture. When plaques become unstable and break off, the results are dramatic: this is the cause of 80% of cases of sudden death. Plaque rupture can also cause myocardial infarction or stroke. Although there seems to be a genetic predisposition, risk factors have been identified: an excess of cholesterol and smoking.
Bacteria and diet in question
Intestinal microbiota may contribute to plaque vulnerability, and therefore to rupture. Some bacteria, as well as the components that they produce, could cause an inflammatory reaction that could eventually lead to atheromatous plaque rupture. Dysbiosis, an imbalance in the composition of the microbiota, might also increase the risk of atherosclerosis in cases of high lipid diets. Bacteria appear to play an important role, because it has even been shown that infections are risk factors for atherosclerosis--gum infections (periodontitis) in particular.
From prevention to probiotics
Prevention is crucial: diet, weight loss, stopping smoking, etc. However, some medications can have a beneficial effect in high-risk people with atherosclerosis. Studies are being conducted to find out if diet or probiotics could reduce the risk of atherosclerosis. The Mediterranean diet is also very beneficial. A new era of therapy could directly target the intestine in order to control the development of atheromatous plaques.
- Lievens D, Zernecke A, Seijkens T, et al. Platelet CD40L mediates thrombotic and inflammatory processes in atherosclerosis. Blood. 2010;116(20):4317-4327.
- Tang WH, Wang Z, Levison BS, et al. Intestinal microbial metabolism of phosphatidylcholine and cardiovascular risk. N Engl J Med. 2013;368(17):1575-1584.
- Wang Z, Klipfell E, Bennett BJ, et al. Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease. Nature. 2011;472(7341):57-63.
- Valtonen VV. Infection as a risk factor for infarction and atherosclerosis. Ann Med 1991; 23: 539-43.
- Zelkha SA, Freilich RW, Amar S. Periodontal innate immune mechanisms relevant to atherosclerosis and obesity. Periodontol 2000. 2010;54(1):207-221.
- Estruch R, Ros E, Salas-Salvadó J, et al. Retraction and Republication: Primary Prevention of Cardiovascular Disease with a Mediterranean Diet. N Engl J Med 2013;368:1279-90 [retraction of: N Engl J Med. 2013 Apr 4;368(14):1279-90]. N Engl J Med. 2018;378(25):2441-2442.
- Wong JM. Gut microbiota and cardiometabolic outcomes: influence of dietary patterns and their associated components. Am J Clin Nutr 2014; 100: 369S-77S.