The Cholesterol Coronary Disease Connection

There isn't any clear scientifically proven explanation as to precisely how a diet high in saturated fat could be the cause of rising cholesterol levels in the blood. We also do not know exactly how cholesterol can 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 an increased level of LDL cholesterol. Excess levels of LDL cholesterol usually result in 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 might determine how much cholesterol may stay on the artery walls. Smoking, high blood pressure levels, diabetic issues, and also other influences such as stress may constrict artery walls. This can 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 swelling

This sets off a sequence of events where 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 ingest the cholesterol and get engorged further blocking the bloodstream. These cells continue to demand even more reinforcements causing far more congestion for the flow of blood. The macrophages are designed to kill off infectious bacterias and then disappear are fighting Lipids which by their very nature are being constantly reproduced. A never ending battle rages. This leads to a stable and continuing state of swelling inside the artery wall. Gradually 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 swollen wall section. This cap forms plaque which starts the state of atherosclerosis as well as the shrinking of the artery opening and resultant constriction in the blood circulation. 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 loaded with 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 likely to rupture.

Ruptures are the common cause of cardiac arrest.

If a plaque cap rupture, blood will seep into the artery wall. The normal wound response mechanism starts 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 may block blood circulation and oxygen to the heart muscle. The section of the heart which is lacking oxygen rich blood begins to die. This is how heart attacks occur. The scientific term is a myocardial infarction.

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