Nutritional and Lifestyle Factors and High-Density Lipoprotein Metabolism

Abstract

The purpose of this chapter is to review our knowledge of the effects of nutritional and lifestyle factors on high-density lipoprotein (HDL) metabolism. Alcohol intake increases HDL apolipoprotein (apo) A-I by increasing its production, and is the topic of a chapter by Dr. Brinton. Dietary cholesterol increases HDL apolipoprotein (apo) A-I by increasing its secretion, probably due to a greater need for enhanced reverse cholesterol transport. Diets high in polyunsaturated fatty acids relative to saturated fatty acids and monounsaturated fatty acids (oleic acid), as well as high carbohydrate, low-fat diets, lower HDL apoA-I by enhancing its fractional clearance, due to upregulation of hepatic scavenger receptor B1 (SR-B1) activity. Omega-3 fatty acids have little effect on HDL cholesterol or apoA-I levels, but decrease both apoA-I production as well as its fractional catabolism; but they do increase large beneficial HDL particles. Trans fatty acids lower HDL apoA-I, by modestly enhancing its fractional clearance. Dietary carbohydrate, especially refined carbohydrate high in sugar or high-fructose corn syrup, when replacing fat in the diet, lowers HDL apoA-I by enhancing its fractional clearance. Alterations in dietary protein have little effect on HDL metabolism. Weight loss via caloric restriction and increased exercise decrease TRL levels, resulting in less transfer of cholesteryl ester from HDL to TRL in exchange for triglyceride, and delayed fractional clearance of HDL apoA-I. Weight loss, exercise, and restriction of sugars are the most effective way to raise HDL cholesterol. In intervention studies, replacement of animal fat with vegetable oil and increasing n3 fatty acids in the diet have been associated with significant heart disease risk reduction.