Dietary Strategies to Improve Cardiovascular Health: Focus on Increasing High-Density Lipoprotein Functionality

Abstract

Cardiovascular disease is one of the leading causes of morbidity and mortality worldwide, with increasing incidence. A cornerstone of cardiovascular disease prevention is lifestyle modification through dietary changes to influence various risk factors such as obesity, hypertension and diabetes. The effects of diet on cardiovascular health are complex. Some dietary components and metabolites directly affect the composition and structure of high-density lipoproteins (HDL) and increase anti-inflammatory and vasoprotective properties. HDLs are composed of distinct subpopulations of particles of varying size and composition that have several dynamic and context-dependent functions. The identification of potential dietary components that improve HDL functionality is currently an important research goal. One of the best-studied diets for cardiovascular health is the Mediterranean diet, consisting of fish, olive oil, fruits, vegetables, whole grains, legumes/nuts, and moderate consumption of alcohol, most commonly red wine. The Mediterranean diet, especially when supplemented with extra virgin olive oil rich in phenolic compounds, has been shown to markedly improve metrics of HDL functionality and reduce the burden, or even prevent the development of cardiovascular disease. Particularly, the phenolic compounds of extra virgin olive oil seem to exert the significant positive effects on HDL function. Moreover, supplementation of anthocyanins as well as antioxidants such as lycopene or the omega-3 fatty acid eicosapentaenoic acid improve parameters of HDL function. In this review, we aim to highlight recent discoveries on beneficial dietary patterns as well as nutritional components and their effects on cardiovascular health, focusing on HDL function.

Keywords: HDL composition; Mediterranean diet; cholesterol efflux capacity; paraoxonase1; polyphenols.

Figure 1

Schematic representation of HDL biosynthesis and maturation. HDL biosynthesis starts with the production and secretion of apolipoprotein A-I (apoA-I) by the liver and intestine. Lipid-poor apoA-I interacts with ATP-binding cassette A1 (ABCA1) to acquire lipids, resulting in pre-β HDL formation. Through lecithin-cholesterol-acyl transferase (LCAT), the ingested free cholesterol on the surface of HDL is esterified to cholesteryl-ester forming larger particles. ABCA1 preferentially interacts with pre-β HDL or small HDL3 particles, while ATP binding cassette G1 (ABCG1) stimulates cholesterol transfer to larger HDL2 particles. Cholesterol is delivered to the liver via scavenger receptor BI (SR-BI) or transferred to very low-density lipoproteins (VLDL) by cholesteryl-ester transfer protein (CETP). HDL-associated triglycerides and phospholipids are mainly hydrolyzed by endothelial lipase (EL) and hepatic lipase (HL).

Figure 2

HDL composition and HDL-mediated protective mechanisms in cardiovascular disease. Apo, apolipoprotein; PON1, paraoxonase1.

Figure 3

Effects of the Mediterranean diet on composition and metrics of HDL function.