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Nutrition and Atherosclerosis

Atherosclerosis results from a gene-environmental interaction mediated by a multicellular process in the arterial wall in which monocytes internalize oxidized cholesterol through the actions of a scavenger receptor. Cholesterol bound to lipoproteins moves freely through the vascular wall from the circulation, and if oxidized, is taken up by monocytes which ultimately become foam cells. These cells burst leading to the formation of a cholesterol plaque in the vessel wall. Smooth muscle cell hyperplasia, cholesterol crystal accumulation and calcification with the formation of bone cells in the vessel wall all contribute to narrowing of the vessel lumen.

Most heart attacks occur in individuals where there is less than 50% blockage of the vessel lumen and unstable plaques burst, triggering formation of an intraluminal clot. A number of nutritional factors including obesity, increased fat intake, reduced fiber intake, and reduced intake of fruits and vegetables have all been associated with an increased risk of heart disease. In fact, many of these factors have occurred together in modern diets making it difficult to separately evaluate each of these nutritional entities separately. It is clear that cholesterol intake, when considered separately from high fat foods, has a lesser effect on cholesterol levels than dietary fat and calories.

Cholesterol levels correlate with risk of heart disease, with two fold increase in risk between patients with cholesterol levels <180 mg/dl compared to individuals with cholesterol levels > 240 mg/dl. There are 37 million Americans with cholesterol > 240 mg/dl, and 56 million individuals with cholesterol levels greater than 200 mg/dl. Only 3 to 4 million individuals are taking cholesterol-lowering drugs, and debates on the cost-effectiveness of medication for primary prevention continue.

Despite the important effects of obesity and high fat diets, there are individuals who exercise and eat a low fat, high fiber diet, who still have cholesterol levels in a moderately elevated range (200 to 240 mg/dl). A number of nutritional factors, including phytosterols, soy protein, naturally occurring inhibitors of cholesterol synthesis, and some classes of lipids (such as conjugated linoleic acid), have been shown to affect cholesterol levels. Appropriate use of dietary supplements together with diet and exercise offer an alternative approach to medications for the reduction of heart disease risk. The combination of population studies, experimental studies, and intervention trials suggest that nutrition plays a major role in determining the incidence of and mortality from heart disease resulting from atherosclerosis.

 

 

 

 

 

 
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