Atherosclerosis - Causes

Causes

Although the atherosclerotic process is not fully understood, atherosclerosis is initiated by inflammatory processes in the vessel wall in response to retained low-density lipoprotein (LDL) molecules. Once inside the vessel wall, LDL molecules become susceptible to oxidation by free radicals, and become toxic to the cells. The damage caused by the oxidized LDL molecules triggers a cascade of immune responses which over time can produce an atheroma. The LDL molecule is globular shaped with a hollow core to carry cholesterol throughout the body.

The body's immune system responds to the damage to the artery wall caused by oxidized LDL by sending specialized white blood cells (macrophages and T-lymphocytes) to absorb the oxidized-LDL forming specialized foam cells. These white blood cells are not able to process the oxidized-LDL, and ultimately grow then rupture, depositing a greater amount of oxidized cholesterol into the artery wall. This triggers more white blood cells, continuing the cycle.

Eventually, the artery becomes inflamed. The cholesterol plaque causes the muscle cells to enlarge and form a hard cover over the affected area. This hard cover is what causes a narrowing of the artery, reduces the blood flow and increases blood pressure.

Some researchers believe that atherosclerosis may be caused by an infection of the vascular smooth muscle cells; chickens, for example, develop atherosclerosis when infected with the Marek's disease herpesvirus. Herpesvirus infection of arterial smooth muscle cells has been shown to cause cholesteryl ester (CE) accumulation. Cholesteryl ester accumulation is associated with atherosclerosis.

Also, cytomegalovirus (CMV) infection is associated with cardiovascular diseases.

Linus Pauling's and Matthias Rath's extended theory states that deaths from scurvy in humans during the ice age, when vitamin C (an antioxidant) was scarce, selected for individuals who could repair arteries with a layer of cholesterol provided by lipoprotein(a), a lipoprotein found in vitamin C-deficient species (higher primates and guinea pigs). Pauling and Rath hypothesized that, although eventually harmful, lipoprotein deposition on artery walls was beneficial to the human species and a "surrogate for ascorbate" in that it kept individuals alive until access to vitamin C allowed arterial damage to be repaired. Atherosclerosis is from this viewpoint, hypothesized as a vitamin-C-deficiency disease, and while there is some evidence to suggest an inverse correlation between blood levels of vitamin C and incidence of atherosclerosis in some populations, there is mixed evidence for supplementation of vitamin C as a method to reduce incidence of cardiovascular disease.