The Cholesterol Heart Disease Connection
There is no clear scientifically proven explanation as to precisely 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. There is however 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 often 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 bloodstream and into the blood vessel walls. Rigidity of the artery walls may determine how much cholesterol might adhere to the artery walls. Smoking, high blood pressure, diabetes, and other influences like stress might constrict artery walls. This could result in a disruption in the flow of blood and pressure. When this happens, artery walls can 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 chain reaction where the body effectively sabotages itself. Swelling flares up in the affected area causing White blood cells or macrophages to rush to the scene. The macrophages ingest the cholesterol and get engorged further blocking the arteries. These cells continue to demand even more reinforcements resulting in even more congestion for the flow of blood. The macrophages are designed to kill off 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 stable and continuing state of inflammation 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.
Eventually 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 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 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 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 normal wound response mechanism begins and clotting agents are transported 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 could cut off blood flow and oxygen to the heart muscle. The section of the heart which is deprived of oxygen rich blood begins to die. This is the way cardiac arrest occur. The scientific term is known as a myocardial infarction.
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