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Review
. 2015:35:517-43.
doi: 10.1146/annurev-nutr-071714-034449.

Saturated Fats Versus Polyunsaturated Fats Versus Carbohydrates for Cardiovascular Disease Prevention and Treatment

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Review

Saturated Fats Versus Polyunsaturated Fats Versus Carbohydrates for Cardiovascular Disease Prevention and Treatment

Patty W Siri-Tarino et al. Annu Rev Nutr. 2015.

Abstract

The effects of saturated fatty acids (SFAs) on cardiovascular disease (CVD) risk are modulated by the nutrients that replace them and their food matrices. Replacement of SFAs with polyunsaturated fatty acids has been associated with reduced CVD risk, although there is heterogeneity in both fatty acid categories. In contrast, replacement of SFAs with carbohydrates, particularly sugar, has been associated with no improvement or even a worsening of CVD risk, at least in part through effects on atherogenic dyslipidemia, a cluster of traits including small, dense low-density lipoprotein particles. The effects of dietary SFAs on insulin sensitivity, inflammation, vascular function, and thrombosis are less clear. There is growing evidence that SFAs in the context of dairy foods, particularly fermented dairy products, have neutral or inverse associations with CVD. Overall dietary patterns emphasizing vegetables, fish, nuts, and whole versus processed grains form the basis of heart-healthy eating and should supersede a focus on macronutrient composition.

Keywords: atherogenic dyslipidemia; diet; lipids; metabolism; sugar.

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Figures

Figure 1
Figure 1
Pathways of lipoprotein metabolism. Dietary carbohydrate increases hepatic TG that drives the secretion of very-low-density lipoproteins (VLDLs) that are larger and triglyceride (TG) enriched. These particles are rapidly lipolysed by lipoprotein lipase (LPL) to remnant lipoproteins that are then catabolized by hepatic lipase (HL) to small, dense low-density lipoprotein (LDL) particles that are less efficiently cleared from plasma, likely due to reduced LDL receptor affinity. Dietary saturated fat has been shown to preferentially increase plasma concentrations of larger LDL particles, likely by reducing their plasma clearance through suppression of LDL receptor activity, although increased hepatic secretion of their precursors may also play a role. Abbreviation: CETP, cholesteryl ester transfer protein.
Figure 2
Figure 2
Low-density lipoprotein (LDL) particles and atherogenesis. In the initial steps of atherogenesis, LDL particles circulating in the blood infiltrate the endothelial layer of arteries and are bound by proteoglycans and become oxidized. This triggers inflammatory processes and foam cell formation by responding macrophages. These lipid-laden foam cells form the core of the atherosclerotic plaque and can amplify local inflammation and promote thrombosis. Apolipoprotein CIII (apoCIII), an exchangeable apoprotein whose concentrations vary on apoB-containing particles, has been shown to play a direct role in some of these processes. Small, dense LDL is considered more atherogenic due to its longer plasma residence time, higher apoCIII content, greater arterial retention, and increased susceptibility to oxidation, triggering inflammatory and thrombotic processes. Abbreviation: oxLDL, oxidized LDL.
Figure 3
Figure 3
Dietary carbohydrate (CHO) and low-density lipoprotein (LDL) pattern B. Variation in dietary CHO is correlated with the prevalence of pattern B (R = 0.89; p < 0.0001) in metabolic feeding studies (92, 94, 105) (n = 833 men). Each data point is the summation of the response of at least 40 individuals to a dietary regimen that controlled for CHO and lasted three to six weeks. Abbreviation: E, energy.

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