Health Conditions

Cholesterol is a lipid - or fat - that is created from other nutrients in the liver, and is also obtained from animal products in the diet (red meats, dairy products, etc.). Because cholesterol is a fat, it does not dissolve in the blood. Instead, it connects with proteins to form small globules known as lipoproteins. There are four types of lipoproteins: they are chylomicrons (pronounced: ki-low-my-krons), very-low-density lipoprotein (VLDL), low-density lipoprotein (LDL), and high-density lipoprotein (HDL).

Chylomicrons are the lipoproteins that transport fats that have been broken down in the gut after a meal, to tissues in the body where they are used and stored. These fats are known as triglycerides. VLDL transports triglycerides and cholesterol to similar sites where they are either used or stored. When chylomicrons and VLDL reach tissues, an enzyme splits off the fatty acids and glycerol, leaving the cholesterol. The remains of the chylomicrons continue to circulate in the blood until they reach the liver, where they are broken down. At the same time, the remains of the VLDLs are converted into LDLs and are also cleared from the circulation by the liver. Liver cells that break down LDLs are equipped with special receptors that attract LDL, removing it from the bloodstream, and breaking it down for use in the cells. Variations in these receptors are believed to play a role in the ability of an individual to remove "bad" cholesterol from their bodies. It has been found, for example, that patients with familial hypercholesterolemia (high cholesterol that is hereditary or ?runs in the family?) have defective LDL receptors. If too few receptors are present or if they operate abnormally, LDL levels build up in the blood.

Researchers have also found that a high fat diet not only increases the amount of fat in the bloodstream, but also causes the liver to reduce the number of LDL receptors. With fewer receptors taking in the LDLs, the levels of LDLs and total cholesterol (TC) in the blood increase.

Receptors on cell walls attract LDL cholesterol, remove it from the bloodstream, and convert it for use by the cells. If there are not enough receptors or if they do not operate properly, LDLs build up in the blood.

While high blood triglyceride levels alone do not necessarily cause atherosclerosis, some lipoproteins that are rich in triglycerides also contain cholesterol. Furthermore, high triglycerides are often accompanied by other factors, like low HDL levels or a tendency toward diabetes. Therefore, high triglycerides may be a sign of a lipoprotein problem that contributes to heart disease.

HDL (sometimes referred to as the "good" cholesterol) plays a different role. It clears cholesterol from cells and helps transport it back to the liver. That is why low HDL levels are considered as important a risk factor for heart disease as high LDLs.

High levels of both LDLs and certain types of VLDLs increase the risk for coronary atherosclerosis. This is why LDL is called the "bad" cholesterol. Researchers believe that the reason these types of cholesterol play a role in building up plaque in the arteries is because of their size. These particular lipid globules are small, and when they come into contact with the cells lining the arteries, they are more easily trapped than larger globules. When cells in the artery wall absorb the cholesterol, they form a bump. This cholesterol-rich bump becomes covered by a hard-coated cap, creating what is called a plaque. Oxygenis also believed to be involved in this process. The LDL cholesterol globules are absorbed into the artery walls when they are oxidized. This is why some clinicians recommend the use of vitamins that prevent oxidation (antioxidants) to help decrease atherosclerosis, although the scientific evidence to support this is weak.

It appears that differences in the size of the LDL particles play an important part in predicting the risk of heart disease. In March, 1999, researchers at the University of Washington School of Public Health and Community Medicine reported studies showing that for every nanometer (a billionth of a meter, which is very, very tiny) decrease in low-density lipoprotein (LDL) particle diameter or size, heart disease risk increases from 30 to 230 percent, depending on the population studied.

Plaques come in various sizes and shapes. Doctors used to believe that the largest plaques were the most dangerous, and the ones most likely to cause total blockage of coronary arteries. In fact, these plaques are most likely responsible for causing angina (chest pain). This plaque buildup narrows the space in the coronary arteries through which blood can flow, decreasing the supply of oxygen and nutrients to the heart. If not enough oxygen-carrying blood can pass through the narrowed arteries to reach the heart muscle, the heart responds with the pain that is called angina. The pain usually happens with exercise or physical exertion when the heart needs more oxygen. It is typically felt in the chest or sometimes in other places like the left arm and shoulder. However, this same inadequate blood supply may cause no symptoms.

Small plaques, that block less than half of the artery opening, are often invisible on many of the tests doctors use to identify coronary heart disease. However, these small plaques are now thought to be very unstable and more likely to rupture or burst. The rough edge left over from this rupture attracts platelets and other clotting factors to the site of the plaque causing a blood clot to form. If the blood clot totally blocks the artery, it stops blood flow and a heart attack occurs. The muscle on the far side of the blood clot does not get enough oxygen and begins to die. The damage can be permanent and in some cases, deadly.