Journal of Gerontological Nursing

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Hyperlipidemia Research Results Reported

Abstract

Excess dietary fat, including choles- terol, is to blame for clogging arteries, which is responsible for high rates of heart and blood vessel disease. Researchers at a symposium on "Coronary Artery Heart Disease: Hyperlipidemia and its Management" outlined the mechanisms that contribute to hyperlipidemia and hypercholesterolemia and their management by drugs and diet.

Low density lipoprotein (LDL), which transports two-thirds of blood cholesterol, is increased by the intake of fat and cholesterol. This results in hardening of the arteries. When excessive amounts of fat (45% of total caloric intake in research animals) are taken in, a different type of cholesterol-carrying lipoprotein - beta-very low density lipoprotein (beta-VLDL) - appears. This aberrant fat vehicle shows a strong affinity to macrophages (removers of foreign and toxic substances) that lie underneath and along artery linings and travels to receptors in the macrophage membranes to dump cholesterol and produce "foam cells" - so called because they look fat and foamy under a microscope.

High density lipoprotein (HDL), believed to have a protective effect against cardiovascular disease because of its actions, must then remove the excess cholesterol from the tissues and deposit it in the liver. The liver then excretes the fat and cholesterol in bile. The system responds to unusually heavy loads of tissue and macrophage cholesterol by producing a new type of HDL - HDLc - to help with the overload, but even that is overwhelmed by a continued high-fat diet. Since the fat is removed by bile salts, and since bowel cancer is associated with high turnover of these salts, excess cholesterol is even more dangerous in populations at risk for bowel cancer.

Although the "garden variety" hypercholesterolemia is caused by too much fat in the diet and could be lowered by the reduction of that fat, "familial" hypercholesterolemia is a genetic disorder. This condition is rare and has been found, through research with a special strain of rabbits, to be caused by a gene that is missing or not functioning.

This strain of rabbits has blood cholesterol levels of 800-900 mg/dl (the normal level is 30 mg/dl) and shows clear-cut atherosclerosis by three months and drastic arterial disease by three years. This is similar to human hypercholesterolemia, in which a child may have a heart attack by 10 years of age and normally does not live past 30 years of age.

The missing (or dysfunctional) gene is one that controls macrophage receptors to which LDL normally attaches. Thus, LDL and cholesterol are not removed fast enough and high blood cholesterol levels accumulate. In the homozygous condition of the disorder, the gene pair is missing - this is extremely rare. In the heterozygous condition, only one gene is missing. This affects one in 500 people, in whom blood cholesterol levels rise to 300-400 mg/dl, leaving them at risk for heart attack by early middle age.

It is suggested that an individual aim at a cholesterol level of less than 150 mg/dl, although the ideal probably is less than 100 mg/dl. The American Heart Association recommends keeping dietary fat intake to 30-35% of caloric intake, but researchers suggest limiting fat intake to 25% of total calories - reducing animal (saturated) fat to 10% and increasing vegetable (unsaturated) fat to 10%. Current diets for Americans now averages 35-40% fat, with 15% saturated.

A typical, low-cholesterol diet would cut meat intake to 3-4 oz per day, using lean meat and poultry, and substituting fish for meat as often as possible. Other meals could consist of vegetable and cereal products. It is best to avoid coconut and palm oils - saturated fats of a vegetable origin…

Excess dietary fat, including choles- terol, is to blame for clogging arteries, which is responsible for high rates of heart and blood vessel disease. Researchers at a symposium on "Coronary Artery Heart Disease: Hyperlipidemia and its Management" outlined the mechanisms that contribute to hyperlipidemia and hypercholesterolemia and their management by drugs and diet.

Low density lipoprotein (LDL), which transports two-thirds of blood cholesterol, is increased by the intake of fat and cholesterol. This results in hardening of the arteries. When excessive amounts of fat (45% of total caloric intake in research animals) are taken in, a different type of cholesterol-carrying lipoprotein - beta-very low density lipoprotein (beta-VLDL) - appears. This aberrant fat vehicle shows a strong affinity to macrophages (removers of foreign and toxic substances) that lie underneath and along artery linings and travels to receptors in the macrophage membranes to dump cholesterol and produce "foam cells" - so called because they look fat and foamy under a microscope.

High density lipoprotein (HDL), believed to have a protective effect against cardiovascular disease because of its actions, must then remove the excess cholesterol from the tissues and deposit it in the liver. The liver then excretes the fat and cholesterol in bile. The system responds to unusually heavy loads of tissue and macrophage cholesterol by producing a new type of HDL - HDLc - to help with the overload, but even that is overwhelmed by a continued high-fat diet. Since the fat is removed by bile salts, and since bowel cancer is associated with high turnover of these salts, excess cholesterol is even more dangerous in populations at risk for bowel cancer.

Although the "garden variety" hypercholesterolemia is caused by too much fat in the diet and could be lowered by the reduction of that fat, "familial" hypercholesterolemia is a genetic disorder. This condition is rare and has been found, through research with a special strain of rabbits, to be caused by a gene that is missing or not functioning.

This strain of rabbits has blood cholesterol levels of 800-900 mg/dl (the normal level is 30 mg/dl) and shows clear-cut atherosclerosis by three months and drastic arterial disease by three years. This is similar to human hypercholesterolemia, in which a child may have a heart attack by 10 years of age and normally does not live past 30 years of age.

The missing (or dysfunctional) gene is one that controls macrophage receptors to which LDL normally attaches. Thus, LDL and cholesterol are not removed fast enough and high blood cholesterol levels accumulate. In the homozygous condition of the disorder, the gene pair is missing - this is extremely rare. In the heterozygous condition, only one gene is missing. This affects one in 500 people, in whom blood cholesterol levels rise to 300-400 mg/dl, leaving them at risk for heart attack by early middle age.

It is suggested that an individual aim at a cholesterol level of less than 150 mg/dl, although the ideal probably is less than 100 mg/dl. The American Heart Association recommends keeping dietary fat intake to 30-35% of caloric intake, but researchers suggest limiting fat intake to 25% of total calories - reducing animal (saturated) fat to 10% and increasing vegetable (unsaturated) fat to 10%. Current diets for Americans now averages 35-40% fat, with 15% saturated.

A typical, low-cholesterol diet would cut meat intake to 3-4 oz per day, using lean meat and poultry, and substituting fish for meat as often as possible. Other meals could consist of vegetable and cereal products. It is best to avoid coconut and palm oils - saturated fats of a vegetable origin - that are used in many packaged foods to retain long shelf life. The New York Heart Association currently is compiling a cooking course package consisting df manuals, slides, and posters illustrating dietary principles.

Although diet therapy is the mainstay of treatment for hyperlipidemia, lowering of cholesterol levels often is more efficient with the use of medications or combinations of medications. These drugs inhibit the production of LDL and possibly increase the numbers of LDL receptors.

A cholesterol level of 200-260 mg% signifies mild hyperlipidemia and may be treated by diet alone. Intermediate hyperlipidemia, 275-300 mg%, has been treated with cholestyramine (a bileacid-binding resin that lowers cholesterol quickly) or probucal (which is tolerated better). Familial hypercholesterolemia can be fought with a combination of cholestyramine and nicotinic acid, probucal alone, or a combination of probucol and cholestyramine. In hypercholesterolemia associated with high triglyceride levels, and where weight loss does not help, Clofibrate, a Clofibrate derivative, or nicotinic acid is indicated.

Anyone over the age of 30 should be screened for elevated blood fats and high cholesterol. Those with a history of heart disease, smoking, high blood pressure, elevated blood sugar, and other risk factors should be checked even earlier. Family history and concurrent medical problems such as obesity, underactive thyroid, diabetes, and kidney, liver, or blood disease should be taken into account when deciding on a treatment course - diet or medications and diet. Investigators suggest that any individual at risk for coronary artery disease because of a factor other than high cholesterol should keep his/her cholesterol level under that considered normal to offset the other risk factor(s).

Researchers admit that lowering blood cholesterol levels 10-15% may not reduce significantly the risk of heart disease in individuals whose levels are high, but a similar change for the population as a whole would have a profound effect. Current research by the Lipid Research Clinic under the auspices of the National Institutes of Health involves 4,000 men at 12 university medical centers. It is aimed at showing that a significant drop in heart disease follows lowering of the LDL blood levels

10.3928/0098-9134-19820701-13

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