I. The Magnitude of the Problem
II. Historical and Clinical Trials
III. Causes of Hypercholesterolemia
IV. Types of Cholesterol
V. Blood Tests
VI. Coronary Artery Disease Risk
VII. Diets and Cholesterol
VIII. Cholesterol-Lowering Drugs
GLOSSARY
angina chest pain caused by temporary lack of blood to an area of the heart muscle cells, usually caused by severe obstruction of the artery supplying blood to the segment of cells.
atheroma same as atherosclerosis, raised plaques filled with cholesterol, calcium, and other substances on the inner wall of arteries that obstruct the lumen and the flow of blood; the plaque of atheroma hardens the artery, hence the term atherosclerosis (sclerosis ¼ hardening).
coronary heart disease obstruction of the coronary arteries with symptoms such as chest pain, angina, or heart attacks.
dyslipidemia the same as hypercholesterolemia, elevated blood cholesterol, LDL cholesterol, triglycerides, or low HDL cholesterol.
myocardial infarction death of an area of heart muscle due to blockage of a coronary artery by blood clot and atheroma, medical term for a heart attack or coronary thrombosis. of scientific evidence proving that lowering elevated blood cholesterol in humans prevents fatal or nonfatal heart attacks was missing.

• I. THE MAGNITUDE OF THE PROBLEM
  If cholesterol is the major cause of atheroma that obstructs the flow of blood in arteries of the heart and brain, significant morbidity and mortality from cardiovascular disease would be prevented by the aggressive lowering of total serum cholesterol and low-density lipoprotein (LDL) cholesterol. The complete occlusion of a coronary artery or cerebral artery is virtually always caused by a combination of atheromatous obstruction of the artery and subse¬quent rupture of the plaque of atheroma with thrombus formation on the ruptured material. Thus, the term atherothrombosis (see the chapter, Atherosclerosis/Athero-thrombosis).
• II. HISTORICAL AND CLINICAL TRIALS A. 1900–1983
  Few physicians believed that cholesterol was a major factor in the development of atherothrombosis. Supportive evidence was based mainly on investigations in choles-terolfed, hypercholesterolemic rabbits that showed the development and progression of atheroma formation relative to the elevation in blood cholesterol. Anecdotal reports and small clinical studies supported this notion.
• III. CAUSES OF HYPERCHOLESTEROLEMIA
  A. Familial Hypercholesterolemia
• IV. TYPES OF CHOLESTEROL
  Cholesterol is a member of a class of naturally occurring compounds called sterols. It is an essential part of the fatty sheath that insulates nerves and the outer membrane of all animal cells, and is a component of chemicals that include steroids (cortisone) and sex hormones such as androgens and estrogens. Cholesterol acts as a precursor of bile acids and occurs in high concentrations in the brain, nerves, and adrenal glands; cholesterol concentra¬tion is greater than 3 g per 100 g in the brain. Body cells satisfy their cholesterol requirements for maintenance and growth by intracellular synthesis of cholesterol and the receptor-mediated uptake from the external medium of cholesterol-rich LDL particles.
• V. BLOOD TESTS
  A. Total Cholesterol
• VI. CORONARY ARTERY DISEASE RISK
  A. Based on LDL Cholesterol
• VII. DIETS AND CHOLESTEROL A. Saturated Fats and Cholesterol
  All animal fat is saturated and solid at normal room temperatures. The degree of hydrogenation of a fat determines how solid and saturated it is. Saturated fats are broken down in the body and increase blood cho¬lesterol. Therefore, the most effective dietary method of lowering blood cholesterol is to reduce intake of saturated fats. High-cholesterol foods are few, therefore, we do not use the term low-cholesterol diet.
• VIII. CHOLESTEROL-LOWERING DRUGS
  A. HMC-CoA Reductase Inhibitors (Statins)
• BIBLIOGRAPHY
  Ashley, F. W., and Kannel, W. B., Relation of weight change to changes in atherogenic traits. The Framingham study. J. Chronic Dis., 27:103–14, 1974.