The Cholesterol Heart Disease Connection

The Cholesterol Heart 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 cardiovascular disease. However, there is a very plausible theory that has a large following in the scientific community.

The LDL connection

It begins with an increased level of LDL cholesterol. Excess levels of LDL cholesterol often result in some of the excess cholesterol to move to the artery walls. The more 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 might stay on the artery walls. Smoking, high blood pressure levels, diabetic issues, as well as other influences like stress may constrict artery walls. This may result in a disruption in the blood circulation as well as pressure. When this happens, 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. Swelling flares up in the affected region causing White blood cells or macrophages to rush to the scene. The macrophages ingest the cholesterol and become engorged further blocking the arteries. These cells continue to demand even more reinforcements resulting in far more congestion for the blood circulation. The macrophages are created to kill off infectious microbes 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 in 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 inflamed wall section. This cap forms plaque that begins the state of atherosclerosis as well as 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 may impede the flow of blood to the heart. This restriction however does not usually cause a cardiac arrest. Plaque deposits are full of 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 certain to rupture.

Ruptures are the common cause of heart attacks.

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 create a scab that inside an artery wall is deadly. This scab or clot inside an artery is known as thrombus. It may block blood circulation and oxygen to the heart muscle. The section of the heart that is lacking oxygen rich blood begins to die. This is the way cardiac arrest occur. The scientific term is known as a myocardial infarction.