Nutrients other than fat play an important role in preventing or promoting atherosclerosis by changing blood levels of cholesterol, HDL and triglycerides. These include:
Calcium in large amounts lowers the cholesterol and triglyceride level.
Carbohydrates, especially simple sugars in large quantities tend to cause excessive manufacture of triglycerides and increase the risk in susceptible individuals of forming atherosclerotic plaque.
Chromium may have a protective role against plaque formation. When chromium is supplemented HDL levels increase and total cholesterol levels drop.
Copper deficiency has been shown to increase serum cholesterol levels in rats. Although the evidence is inconclusive, copper may protect against plaque formation.
Soluble dietary fibre has been documented to reduce cholesterol levels.
Severe deficiency of iron increase blood lipid levels but moderate anemia lowers blood lipid levels.
Experiments showed that zinc in large quantities reduces HDL levels. Evidence suggests that large amounts of zinc increases the risk of the disease.
Omega 3 fatty acids, Eicosapentanoic acid (EPA) and docosahexaenoic acid (DHA) have been found to reduce platelet aggregation and thus reduce thrombus formation. They also decrease the formation of LDL and have anti inflammatory effects.
Thus it is seen that many nutrients and not just fat affect the formation of atherosclerotic plaque and the diet as a whole should be considered to control or prevent atherosclerosis.
Myocardial infarction or heart attack occurs when the blood supply to the heart is cut off. The portion of the heart muscle serviced by the blocked artery is deprived of oxygen and nutrients and slowly dies. The area of necrosis in the heart muscle is called a myocardial infart. The functioning of the heart muscle is reduced to this extent. Thus if a large portion of the heart becomes unfunctional, death results. Acute damage to the heart muscle due to myocardial infarction leads to an increase in levels of certain enzymes and an enzyme assay helps in diagnosing myocardial infarction. The enzymes from the damaged heart muscle escape into the intestitium; some of them are denatured but others reach the circulation.
Participants