Nutrition in coronary heart disease prevention: a program for the 1980s.
Within a quarter century the convergence of geographical and prospective epidemiology, clinical research, and laboratory investigation has provided strongly attested theories of coronary heart disease (CHD) etiology. Evidence that application of these theories will reduce CHD incidence is incomplete but adequate to justify their use at clinical and population levels. Additional etiological hypotheses (HDL, hyperinsulinism, personality type) are persuasive but await comparable investigation. Risk-benefit considerations require ongoing scrutiny: current evidence, however, does not give cause for concern that attainable reduction of plasma cholesterol has deleterious effects. To minimize lipoprotein-mediated CHD risk it may be necessary to attain population mean plasma cholesterol levels of less than 200 mg/dl, a target which is probably feasible by dietary modifications directed to lipid, fiber, and energy intake. A substantial obstacle to CHD prevention is the irresponsible rearguard action by small segments of the food industry and the medical profession, permitting inertia on the false grounds that scientific opinion is seriously divided.
D000328:Adult; D001161:Arteriosclerosis / Q000517:prevention & control; D002784:Cholesterol / Q000097:blood; D003327:Coronary Disease / Q000517:prevention & control*; D006801:Humans; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D008875:Middle Aged; D009369:Neoplasms / Q000401:mortality; D009747:Nutritional Physiological Phenomena
D008077:Lipoproteins, LDL; D002784:Cholesterol