The Cholesterol Cardiovascular Disease Connection

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

The LDL connection

It starts with a high level of LDL cholesterol. Excess levels of LDL cholesterol usually cause some of the excess cholesterol to move towards the artery walls. The more the LDL levels, the more cholesterol moves out of the bloodstream and into the blood vessel walls. Rigidity of the artery walls may determine how much cholesterol may stay on the artery walls. Smoking, high blood pressure levels, diabetic issues, and also other influences like stress may constrict artery walls. This could cause a disruption in the blood circulation and pressure. When this occurs, artery walls may weaken or become scarred in the first layer of the lining allowing LDL to even further embed into the artery walls.

The role of inflammation

This sets off a sequence of events in which the body effectively sabotages itself. Inflammation flares up in the affected area resulting in White blood cells or macrophages to rush to the scene. The macrophages absorb the cholesterol and get engorged further blocking the bloodstream. These cells continue to demand even more reinforcements resulting in far more congestion for the blood circulation. The macrophages are designed to destroy infectious bacterias and then vanish 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 swelling in the artery wall. At some point the overloaded macrophage is destroyed 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 as well as the shrinking of the artery opening and resultant constriction in the blood flow. If this occur in an artery that leads to the heart, it may impede the flow of blood to the heart. This restriction however does not usually cause a heart attack. Plaque deposits are full of inflammation and LDL. Immune cells, T-lymphocytes and macrophages, are the most severe when it comes to containing inflammatory cells. If the plaque deposit has a thin cap, it is more certain to rupture.

Ruptures are the common cause of heart attacks.

If 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 deadly. This scab or clot inside an artery is called a thrombus. It can block blood circulation and oxygen to the heart muscle. The section of the heart which is deprived of oxygen rich blood starts to die. This is how heart attacks occur. The medical term is a myocardial infarction.