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Americans have made substantial progress in reducing cholesterol consumption. The average cholesterol consumed by men and women respectively in 1960 was 704 mg/day and 493 mg/day. By 1994,
How LDL cholesterol contributes to coronary artery disease is not completely understood, but the "lipid oxidation theory" appears to have the support of the scientific community. According to this theory, LDLs do not latch on to the artery linings, depositing the cholesterol that eventually forms plaque. Instead, high circulating levels of LDL in the blood stimulate the cells beneath the artery lining to transport the LDLs into the artery wall. This process is facilitated when artery linings are damaged by any one or a combination of the following: cigarette smoking, high blood pressure, diabetes mellitus, viruses, and other toxic substances.
After infiltrating the artery wall, LDLs are oxidized, or converted to harmful forms that are toxic to endothelial and smooth muscle cells, thus further damaging the artery lining. This process triggers the body's immune system, which responds by sending white blood cells, called monocytes, that also penetrate into the inner layer of the artery. The monocytes turn into macrophages, which engulf oxidized LDLs in an effort to protect the artery from further damage. The macrophages become bloated from gobbling up LDLs, and in this condition they eventually develop into foam cells. Foam cells in turn stimulate the smooth muscle cells in the affected arteries to grow in size and number. This adds to the thickness of the artery walls. Concurrently, blood platelets congregate at the sites of disease, further adding to the thickening process. The culmination of these events results in the development of fatty streaks in the arteries. This is an initial sign of coronary artery disease. Some of these streaks develop into atherosclerotic plaques, which are the lesions that define diseased coronary arteries.
In some instances the cells lining the artery flake off or retract, exposing the foam cells lying beneath. Once again, the body attempts to repair the damage, but the restoration process causes the wounded artery to scar down as a fibrous plaque. This represents a later-stage lesion in the development of atherosclerotic plaque.
Lesions grow over time by accumulating fibrous tissue, cholesterol, and other debris from the blood stream. Concomitantly, the channel narrows severely, diminishing blood flow to the myocardium. At this point the lesion has progressed to a mature plaque. Finally, further damage to the artery wall may cause either a blood clot to develop or bleeding to occur into the core of the plaque, or the artery may go into spasm. Any of these events can abruptly interrupt or block the flow of blood to a portion of the heart muscle, resulting in a heart attack.
Heart attacks are rare when LDL values in the blood are below 100 mg/dl. A national panel of experts has developed guidelines for safe and unsafe levels of LDL. A high circulating level of LDL cholesterol is positively related to cardiovascular disease. Weight loss, a diet low in saturated fat and total fat, exercise, and medication (if needed) will lower LDL levels in the blood.
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Americans have made substantial progress in reducing cholesterol consumption. The average cholesterol consumed by men and women respectively in 1960 was 704 mg/day and 493 mg/day. By 1994,
How LDL cholesterol contributes to coronary artery disease is not completely understood, but the "lipid oxidation theory" appears to have the support of the scientific community. According to this theory, LDLs do not latch on to the artery linings, depositing the cholesterol that eventually forms plaque. Instead, high circulating levels of LDL in the blood stimulate the cells beneath the artery lining to transport the LDLs into the artery wall. This process is facilitated when artery linings are damaged by any one or a combination of the following: cigarette smoking, high blood pressure, diabetes mellitus, viruses, and other toxic substances.
After infiltrating the artery wall, LDLs are oxidized, or converted to harmful forms that are toxic to endothelial and smooth muscle cells, thus further damaging the artery lining. This process triggers the body's immune system, which responds by sending white blood cells, called monocytes, that also penetrate into the inner layer of the artery. The monocytes turn into macrophages, which engulf oxidized LDLs in an effort to protect the artery from further damage. The macrophages become bloated from gobbling up LDLs, and in this condition they eventually develop into foam cells. Foam cells in turn stimulate the smooth muscle cells in the affected arteries to grow in size and number. This adds to the thickness of the artery walls. Concurrently, blood platelets congregate at the sites of disease, further adding to the thickening process. The culmination of these events results in the development of fatty streaks in the arteries. This is an initial sign of coronary artery disease. Some of these streaks develop into atherosclerotic plaques, which are the lesions that define diseased coronary arteries.
In some instances the cells lining the artery flake off or retract, exposing the foam cells lying beneath. Once again, the body attempts to repair the damage, but the restoration process causes the wounded artery to scar down as a fibrous plaque. This represents a later-stage lesion in the development of atherosclerotic plaque.
Lesions grow over time by accumulating fibrous tissue, cholesterol, and other debris from the blood stream. Concomitantly, the channel narrows severely, diminishing blood flow to the myocardium. At this point the lesion has progressed to a mature plaque. Finally, further damage to the artery wall may cause either a blood clot to develop or bleeding to occur into the core of the plaque, or the artery may go into spasm. Any of these events can abruptly interrupt or block the flow of blood to a portion of the heart muscle, resulting in a heart attack.
Heart attacks are rare when LDL values in the blood are below 100 mg/dl. A national panel of experts has developed guidelines for safe and unsafe levels of LDL. A high circulating level of LDL cholesterol is positively related to cardiovascular disease. Weight loss, a diet low in saturated fat and total fat, exercise, and medication (if needed) will lower LDL levels in the blood.
Cancer - The Problem and the Solution:
* Discover The Truth About Cancer And How To Eliminate Sickness And Disease Naturally. More details
* Cancer: From Diagnosis To All Clear In 11 Months. More details
* Treating Prostate Cancer Naturally. More details
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