What is heart disease? Well, there are many conditions associated with the cardiovascular system as well as the heart specifically. The term heart disease is commonly used to refer to atherosclerosis, which is a disease of the blood vessels (not actually the heart). Atherosclerosis is also known as “clogged arteries,” an advanced-stage feature of a narrowing of the arterial canal, which has become clogged by clotted blood cells and debris. Many people think that the accumulation of plaque on the vascular walls is what causes the narrowing—and that the plaque is accumulating due to “thick and sticky” saturated fat and “bad” cholesterol building up on the inner wall of the vessel. However, this concept is a flat-out myth. Keep reading to learn the truth about clogged arteries, including the scientific explanation, the causes, and the role of cholesterol.
What Are Clogged Arteries?
The vessel has a wall composed of three layers: the inner, outer, and intermediate layers. Each layer contains many cells, and each has a different function. In the case of clogged arteries, it is important to understand that the plaque is not actually on the inside of the vessel wall. Rather, it is within the vessel wall itself (illustrated diagram available here). The plaque builds up between the inner layer and the lining of the vessel’s inner wall as a result of cell dysfunction. The vascular cells are not acting appropriately; the metabolism of the cells is altered, and their metabolic byproducts create a toxic environment. The fat and cholesterol alone are not creating the plaque produced within the vessel’s tissue—damaged blood cells, fibrotic connective tissue, and old cell debris is also accumulating.1
The cholesterol and lipoproteins (which are delivering the cholesterol to aid in repair) are damaged by a toxic environment within the vessel’s walls. This toxic environment is created by an imbalance of cell function, and perpetuated by damaged materials such as cellular debris and oxidized fats. This is why oxidized lipids are one of the most general risk factors for heart disease.2-4 The dangerous plaque associated with heart attack and other traumatic vascular events contains much more polyunsaturated fat which has become oxidized. This is a sign that the toxic environment causes the damage of unstable molecules, such as the polyunsaturated fats, which in turn further destabilize the tissue integrity. The more of this unstable material present, the more advanced and likely to become life-threatening the condition.
The Role of Cholesterol and the Immune System
When the cells of the vessel are dying and the debris needs to be cleaned up, the immune system steps in. However, the immune system also needs to be in an environment that provides good working conditions. When the accumulation of damaged materials and calcium has altered the tissue quality such that it is not allowing the vessel to heal, the immune cells that go there to clean up begin creating more damage in the process.5-7 Then even more cholesterol is delivered to help rebuild the tissue, and even more immune cells arrive, creating even more damage. In the process, a large deposit of waste begins to build up within the vascular wall, eventually causing damage to the red blood cells trying to deliver blood. This can lead to a rupture of the rigid and over-stretched inner wall. The debris and aggregated platelets and red blood cells will begin pouring into the canal due to the plaque building up within it. And this is where the clot and “clog” emerges, leading to clogged arteries.
Check out my previous post What Is Bad Cholesterol Good for Anyway? to learn more about “bad” cholesterol and the essential role of cholesterol in the body.
What Can You Do to Prevent Atherosclerosis?
To prevent the cell dysfunction that leads to atherosclerosis (a.k.a. clogged arteries) and other forms of heart disease, eat a diet that is low in polyunsaturated fatty acids (PUFAs). For better heart health, avoid fried foods and vegetable oils, eat a diet high in fruit and whole foods, and trade your fish oil supplements for coconut oil.
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- Ashley EA, Niebauer J. “Coronary heart disease” in Cardiology Explained. London: Remedica (2004). http://www.ncbi.nlm.nih.gov/books/NBK2216/
- Tsimikas S. Brilakis ES, Miller ER, et al. Oxidized phospholipids, Lp(a) lipoprotein, and coronary artery disease. N Engl J Med 353 (Jul 2005): 46-57. http://www.nejm.org/doi/full/10.1056/NEJMoa043175
- Ishigaki Y. Katagiri H, Gao J, et al. Impact of plasma oxidized low-density lipoprotein removal on atherosclerosis. Circulation 118, No. 1 (Jul 2008): 75-83. http://www.ncbi.nlm.nih.gov/pubmed/18559699
- Bochkav VN, Oskolkova OV, Birukov KG, et al. Generation and biological activities of oxidized phospholipids. Antioxid Redox Signal 12, No. 8 (Apr 2010): 1009-1059. http://www.ncbi.nlm.nih.gov/pubmed/19686040
- Boyle JJ. Macrophage activation in atherosclerosis: pathogenesis and pharmacology of plaque rupture. Curr Vasc Pharmacol 3, No. 1 (Jan 2005): 63-68. http://www.ncbi.nlm.nih.gov/pubmed/15638783
- Stary HC, Chandler AB, Dinsmore RE, et al. A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Arterioscler Thromb Vasc Biol 15, No. 9 (Sep 1995): 1512-1531. http://www.ncbi.nlm.nih.gov/pubmed/7670967
- Kushiyama A, Okubo H, Sakoda H, et al. Xanthine oxidoreductase is involved in macrophage foam cell formation and atherosclerosis development. Arterioscler Thromb Vasc Biol 32, No. 2 (Feb 2012): 291-298. http://www.ncbi.nlm.nih.gov/pubmed/22095983