Effects of Substituting Dietary Saturated Fatty Acids

Serum HDL-C has been shown to be influenced by both the amount and quality of dietary fatty acids and carbohydrate. In the past, the relative effects of dietary fatty acids on HDL-C have been described in absolute terms, that is, SFA tends to raise HDL-C, whilst PUFA, trans fatty acids and carbohydrate, all tend to reduce HDL-C, with MUFA being relatively neutral (Grundy and Denke 1990). However, in reality the absolute effect of fatty acids, or any macronutrient, on HDL-C cannot be measured, as its addition or replacement may be counter-affected by whatever fatty acid or carbohydrate takes its place to maintain a feasible diet. This phenomenon of substitution limits the ability to interpret the impact of dietary macronutrients on HDL and CVD risk to 'relative', rather than 'absolute' effects. Meta-analyses of intervention studies have provided strong evidence to show that the iso-energetic replacement of SFA with PUFA, MUFA and carbohydrate decreases HDL-C, with carbohydrate exerting the greatest impact in lowering both HDL-C and the total cholesterol–HDL-C ratio (Mensink et al. 2003). In contrast, the iso-energetic replacement of carbohydrate with all dietary fatty acids, other than trans fatty acids, tends to raise HDL-C (Micha and Mozaffarian 2010). Estimates for the relative magnitude of change in the concentration of serum HDL-C in response to these dietary substitutions are directly proportional to the amount of energy being exchanged. An iso-energetic exchange of 5 % energy from carbohydrate to SFA, MUFA and PUFA is associated with increases in HDL-C of 0.05, 0.04 and 0.03 mmol/L, respectively, with trans fatty acids reducing HDL by 0.02 mmol/L. In addition, individual SFA is known to exert differential effects on serum HDL-C, so that replacing 5 % energy as carbohydrate with lauric, myristic, palmitic and stearic, increases HDL-C by 0.13, 0.09, 0.05 and <0.01 mmol/L, respectively. These associations between dietary fatty acids and serum HDL-C are statistically robust and have been used to formulate dietary guidelines. However, because they rely heavily upon data from measures of dietary intake, as estimated from dietary recall, food frequency questionnaires or diet diaries, this can limit their value in predicting the biological effects of complex foods on HDL (Astrup et al. 2011). In other words, foods are not single nutrients, but complex mixtures of nutrients within a food matrix, all of which interact together to produce a biological effect. Because a food is rich in one particular fatty acid, it does not mean that consumption of this food will result in an effect on HDL that is typical of that fatty acid.

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