What is atherosclerosis?

What is atherosclerosis? Is cholesterol to blame?

Pawel Malczewski
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Short summary

Without cholesterol there would be no atherosclerosis, but also there would be no life.

There are a number of factors causing atherosclerosis. Cholesterol, however, is not a cause, but only a building material used in atherosclerotic plaque formation.

One of the causing factors, with which cholesterol is often confused, are the low-density lipoproteins (LDL) that actually carry that building material. If the amount of this particle is controlled and the atherosclerotic risk factors reduced, cholesterol is not able to reach the damaged area of the artery and, therefore, cannot be used to build the plaque. For a quick answer click here.

Explanation

To understand why cholesterol is not causing the atherosclerotic plaque it is important to understand the process of plaque formation.

There are various causes of atherosclerosis and cardiovascular disease (CVD) but for the purpose of this article I want to focus on the process of how does cholesterol become a part of the plaque. The risk factors are listed below.

What is atherosclerosis

Atherosclerosis is a disease of the arteries which can lead to heart attack, stroke and death. The function of arteries is to deliver oxygenated blood to the heart and other parts of the body. In the case of atherosclerosis, a plaque is formed inside the artery wall which, with time, hardens and narrows the artery making the blood flow more difficult. This plaque is built from various substances found in blood such as cholesterol, fat molecules, calcium and macrophages.

The process of plaque build-up in arteries

In summary, for the atherosclerotic plaque build-up to occur, the artery wall needs to be damaged through some sort of stress and the building material (cholesterol and other ) needs to be delivered and deposited through the compromised arterial wall. Stress to arterial wall can be caused by various factors, but the delivery of building material is done by lipoproteins, specifically LDL cholesterol transporters of the small, dense type. (1)Davidson MH, Toth PP, Maki KC. Therapeutic Lipidology (Contemporary Cardiology). Humana Press. Edition 2007. Available here.
Atherosclerosis doesn’t occur without the above risk factors, even in the presence of a higher than “normal” total cholesterol level.

The process of forming atherosclerotic plaque starts with the irritation of the inner layer of the artery called endothelium. The irritation can be caused by various factors, such as smoking or high blood pressure.

The body’s immune system reacts to this irritation by sending white blood cells to clean-up and remove the irritants and heal the area. Inflammation is a necessary part of the healing process.

The injury caused by the irritation may be a one-time occurrence and the issue may go away. But if the irritation occurs on regular basis, the inflammation of the arterial walls becomes chronic and the body’s defense system starts to behave uncontrollably and may act against the heart’s health.

Since the endothelium is irritated and inflamed, it is easier for certain particles to penetrate their walls. This is where the well-known LDL particle starts its plaque formation process. But it is not any LDL lipoprotein, but a small, dense LDL type.

Small dense LDL particles have low antioxidant levels, so when these small particles get between the layers of an inflamed artery wall, they are easily oxidized and broken down by other chemical processes.

The presence of oxidized LDL and their components cause the release of more white blood cells (macrophages). These macrophages are like vacuum cleaners. They “swallow” the remnants of LDLs. Macrophages are, however, unable to destroy/eliminate cholesterol and fat molecules that are swallowed, so they become large and foamy. Eventually, macrophages cannot continue to clean-up, die and release toxic substances. These substances contribute to breaking up the plaque, increasing the danger of blocking arteries and heart attack (when part of the heart muscle dies) which may result in death.

The irritated cells in the artery lining produce molecules that attract special cells released by the defence system. Those molecules act like sticky tapes and become a seedbed for the plaques that get formed from the collection of fluffy macrophages, cholesterol, remnants of the damaged cells and chemicals released in the process.

The build-up of this material is strengthened by a fibrous cap created in the process.

The build-up of the plaque continues blocking the blood flow.

Plaques may be stable with a large amount of fibrous tissue that have a little risk to rupture and they can be unstable such as those younger plaques loaded with cholesterol and covered by a proportionally small amount of fibrous layer.

To reduce a risk of the heart disease one needs to reduce or eliminate risk factors. Some of these risk factors (such as cholesterol amounts vs lipoprotein count) are still misunderstood by many health professionals.

Atherosclerosis and CVD risk factors

There are well known risk factors of developing atherosclerosis and cardiovascular diseases (2)Better Health Channel. Heart disease – risk factors. Available here.:

  • An elevated number of small, compact LDL particles able to penetrate the artery inner wall.NOTE: a high total cholesterol level has been blamed for many years. However, recent studies show that it is not the cholesterol itself but these specific cholesterol carrying particles that are to blame. The harmfully high numbers of these small dense LDL particles are associated with a diet rich in carbohydrates, especially fructose (read more..).Diets rich in fat (including saturated fat) on the other hand, are associated with an increase in the ratio of the larger fluffy LDLs (not responsible for oxidisation and accumulation on the artery walls). (read more..)
  • A low number of HDL particles – associated with increased risk of atherosclerosis and cardiovascular disease. HDL particles remove cholesterol from the blood, cells and the arterial walls and dump it into the liver for breakdown and removal.
  • Smoking – reduces the amount of oxygen in the blood, causing it to become stickier and clump together, slowing down the blood flow. The artery walls turn sticky and, eventually, get damaged.
  • High blood pressure – overloads the heart and the coronary arteries and places stress on the inner arterial layers, damaging them. High blood pressure speeds up the artery-clogging process. Prolonged high blood pressure also weakens the heart muscle and may eventually result in a heart failure. Click here to see how you can reduce the high blood pressure.
  • Being overweight and obese. Intra-abdominal fat increases the blood pressure, blood lipid levels and insulin resistance, which may lead to the development of diabetes, which are all risk factors of atherosclerosis and cardiovascular diseases.
  • Diabetes is associated with a higher risk of heart attack, angina and stroke.
  • Depression, stress and anxiety are related with the development and progression of cardiovascular diseases. (3)Liu YL, Szklo M, Davidson KW, Bathon JM, Giles JT. Differential Association of Psychosocial Comorbidities With Subclinical Atherosclerosis in Rheumatoid Arthritis. Arthritis Care & Research. Volume 67, Issue 10, pages 1335–1344, October 2015. Available here. (4)Vural M, Satiroglu O, Akbas NB, Goksel I, Karabay O. Association between Depression and Anxiety Symptoms and Major Atherosclerosis Risk Factors in Patients with Chest Pain. The Tohoku Journal of Experimental Medicine (Impact Factor: 1.35). 07/2007; 212(2):169-75. Available here.
  • Physical inactivity – being physically active reduces morbidity and mortality related to atherosclerosis through both direct changes to the cardiovascular system and indirect reduction of other risk factors. It regulates weight, modulates blood pressure, reduces insulin resistance, improves lipid and glucose metabolism, increases the amount of HDL, reduces the number of triglycerides and LDL, improves general health of the blood vessels, and reduces inflammation. (5)Goldberg AP. Aerobic and resistive exercise modify risk factors for coronary heart disease. Medicine and Science in Sports and Exercise [1989, 21(6):669-674]. Available here.

Conclusion

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Cholesterol does not cause atherosclerosis or heart disease. Cholesterol is essential for our survival and has many important functions in the body. It is used as a building material in an atherosclerotic plaque only if it is delivered to the damaged arterial wall by small, dense lipoproteins.

Eliminating or reducing the risk factors that lead to the damage of arterial walls and controlling the production of small, dense LDLs through the proper diet will reduce the risk of cholesterol being deposited in the artery walls and atherosclerosis.

References   [ + ]

1. Davidson MH, Toth PP, Maki KC. Therapeutic Lipidology (Contemporary Cardiology). Humana Press. Edition 2007. Available here.
2. Better Health Channel. Heart disease – risk factors. Available here.
3. Liu YL, Szklo M, Davidson KW, Bathon JM, Giles JT. Differential Association of Psychosocial Comorbidities With Subclinical Atherosclerosis in Rheumatoid Arthritis. Arthritis Care & Research. Volume 67, Issue 10, pages 1335–1344, October 2015. Available here.
4. Vural M, Satiroglu O, Akbas NB, Goksel I, Karabay O. Association between Depression and Anxiety Symptoms and Major Atherosclerosis Risk Factors in Patients with Chest Pain. The Tohoku Journal of Experimental Medicine (Impact Factor: 1.35). 07/2007; 212(2):169-75. Available here.
5. Goldberg AP. Aerobic and resistive exercise modify risk factors for coronary heart disease. Medicine and Science in Sports and Exercise [1989, 21(6):669-674]. Available here.

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