The Cholesterol Heart Disease Connection

There is no clear scientifically proven explanation as to exactly how a diet high in saturated fat can be the cause of rising cholesterol in the blood. We also do not know exactly how cholesterol can contribute to heart disease. But there is a very plausible theory that has a large following in the scientific community.

The LDL connection

It begins with a high level of LDL cholesterol. Excess levels of LDL cholesterol often cause some of the excess cholesterol to move to the artery walls. The higher the LDL levels, the more cholesterol moves out of the blood and into the blood vessel walls. Rigidity of the artery walls may determine how much cholesterol may adhere to the artery walls. Smoking, high blood pressure, diabetes, and other influences like stress may constrict artery walls. This can cause a disruption in the flow of blood and the pressure. When this happens, artery walls can weaken or become scarred in the first layer of the lining allowing LDL to further embed into the artery walls.

The role of inflammation

This sets off a chain reaction where the body effectively sabotages itself. Inflammation flares up in the affected area causing White blood cells or macrophages to rush to the scene. The macrophages ingest the cholesterol and become engorged further blocking the blood vessels. These cells continue to call for even more reinforcements resulting in even more congestion for the flow of blood. The macrophages are designed to kill off infectious microbes and then disappear are fighting Lipids which by their very nature are being continually reproduced. A never ending battle rages. This leads to a steady and continuing state of inflammation in the artery wall. At some point the overloaded macrophage is killed and all the cholesterol and inflammatory substances are released into the artery wall.

At some point the body forms a cap of sorts over the inflamed wall section. This cap forms plaque which begins the state of atherosclerosis and the shrinking of the artery opening and resultant constriction in the blood flow. Should this occur in an artery that leads to the heart, it can impede the flow of blood to the heart. This restriction however is not usually causes a heart attack. Plaque deposits are loaded with inflammation and LDL. Immune cells, T-lymphocytes and macrophages, are the most severe in terms of containing inflammatory cells. If the plaque deposit has a thin cap, it is more likely to rupture.

Ruptures are the most common cause of heart attacks.

Should a plaque cap rupture, blood will seep into the artery wall. The typical wound response mechanism begins and clotting agents are sent to the area. Platelets enter the wound to form a scab that inside an artery wall is life threatening. This scab or clot inside an artery is called a thrombus. It can cut off blood flow and oxygen to the heart muscle. The section of the heart that is deprived of oxygen rich blood begins to die. This is how heart attacks occur. The medical term is a myocardial infarction.