title: Treatment of common lipoprotein disorders.
abstract: The pathogenesis of arteriosclerosis is not yet fully understood. The growing body of scientific information strongly indicates that the plasma lipoproteins are playing a crucial role in the development of this disease. We now have conclusive information that dietary cholesterol can produce arteriosclerosis in animals and its removal from the diet can result in regression of these lesions. Most importantly, we know that reducing plasma cholesterol in humans will prevent mortality and morbidity related to the clinical sequelae of arteriosclerosis. A diet can be prescribed that can produce profound reductions in lipoprotein levels in many individuals. The rate of success in achieving modifications that reduce plasma cholesterol is very high. Most patients over time find a diet with reduced cholesterol and saturated fat to be quite palatable. As food suppliers become more active in emphasizing low fat, low cholesterol products, and as restaurants see a demand for healthier entrees, the task for the physician and nutritionist will become much easier. Achieving sustained weight reduction is a much more difficult problem, but this too can be accomplished in many patients if the health professionals maintain a hopeful supportive approach. Ultimately, it is the patient's responsibility to bring about these lifestyle changes. It is the physician's and nutritionist's job to monitor the process and provide sound information and encouragement. For individuals with severe lipoprotein disorders such as familial hypercholesterolemia where diet therapy is helpful but not adequate, the use of medications is now indicated (bile acid binding resins and nicotinic acid). Other medications that promise additional effectiveness and safety are under development (Compactin, Mevinolin). It is our belief that control of coronary heart disease and stroke requires appropriate treatment of lipoprotein disorders and the methods for a strong beginning in this endeavor are at hand.
mesh_terms: D000328:Adult; D000368:Aged; D045930:Anabolic Agents / Q000627:therapeutic use; D001647:Bile Acids and Salts / Q000378:metabolism; D002648:Child; D002792:Cholestyramine Resin / Q000627:therapeutic use; D002994:Clofibrate / Q000031:analogs & derivatives / Q000627:therapeutic use; D003084:Colestipol / Q000627:therapeutic use; D003918:Dextrothyroxine / Q000627:therapeutic use; D004040:Dietary Carbohydrates / Q000008:administration & dosage; D004041:Dietary Fats / Q000008:administration & dosage; D004043:Dietary Fiber / Q000008:administration & dosage; D004044:Dietary Proteins / Q000008:administration & dosage; D004359:Drug Therapy, Combination; D002149:Energy Intake; D004967:Estrogens / Q000627:therapeutic use; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D006937:Hypercholesterolemia / Q000178:diet therapy / Q000628:therapy; D006951:Hyperlipoproteinemias / Q000178:diet therapy / Q000188:drug therapy / Q000628:therapy*; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D008077:Lipoproteins, LDL / Q000097:blood; D008079:Lipoproteins, VLDL / Q000097:blood; D008297:Male; D008875:Middle Aged; D009355:Neomycin / Q000627:therapeutic use; D009525:Niacin / Q000627:therapeutic use; D011341:Probucol / Q000627:therapeutic use; D011372:Progestins / Q000627:therapeutic use; D014280:Triglycerides / Q000097:blood
chemical_list: D045930:Anabolic Agents; D001647:Bile Acids and Salts; D004040:Dietary Carbohydrates; D004041:Dietary Fats; D004043:Dietary Fiber; D004044:Dietary Proteins; D004967:Estrogens; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D000960:Hypolipidemic Agents; D008077:Lipoproteins, LDL; D008079:Lipoproteins, VLDL; D011372:Progestins; D014280:Triglycerides; D002792:Cholestyramine Resin; D009525:Niacin; D003918:Dextrothyroxine; D002994:Clofibrate; D009355:Neomycin; D003084:Colestipol; D011341:Probucol