Dietary MUFA

Interest in the potential health benefits of dietary MUFA originated from the use of olive oil in the Mediterranean diet. Whilst substitution of SFA with MUFA is less effective in lowering LDL cholesterol than n-6 PUFA, there is evidence to suggest that this substitution may be more effective in preventing the decrease in HDL-C that accompanies the removal of SFA (Schwingshackl and Hoffmann 2012). This finding is supported by data to show that MUFA is relatively less effective in stimulating cholesteryl ester transfer protein (CETP), and thus the remodelling and increased clearance of HDL from serum, than either SFA or n-6 PUFA (Groener et al. 1991; Lagrost et al. 1999). This finding is in accord with data from a recent study which concluded that dietary MUFA reduced the catabolic rate of the principal apolipoprotein (apo) in HDL, apo A-I (Labonte et al. 2013).

n-3 Polyunsaturated Fatty Acids

The principal essential fatty acid of the n-3 series, α-linolenic acid (18:2) is the most abundant fatty acid on earth, but is consumed in significantly less quantity by humans than linoleic acid (18:2 n-6) (National Diet and Nutrition Survey. Department of Health 2011). When fed in physiologically relevant amounts, α-linolenic acid has been shown to be equivalent to linoleic acid as a substitute for SFA in lowering LDL cholesterol (Harris 1997). However, even though a recent metaanalysis indicated a benefit of α-linolenic acid intake on CVD risk (Pan et al. 2012), human interventions with α-linolenic acid-enriched diets have shown variable effects on serum HDL-C (Harper et al. 2006; Goyens and Mensink 2006; Kaul et al. 2008; Griffin et al. 2006). The longer-chain derivatives of α-linolenic acid, chiefly eicosapentaenoic and docosahexaenoic acids (EPA, DHA), which in humans are mainly obtained directly from oily fish, exert only a moderate elevating effect on HDL-C (Harris 1989). This is perhaps surprising given the potent TAG-lowering effect of these long-chain fatty acids.

Carbohydrate and Extrinsic Sugars

The replacement of dietary fat with carbohydrate in low-fat, high-carbohydrate diets has long been associated with a reduction in serum HDL-C that may be linked to the carbohydrate-induced increase in TAG (Katan et al. 1997). The latter is known to promote lipid exchanges between HDLand TAG-rich lipoproteins that remodel HDL into smaller and denser particles with an increased catabolic rate and thus reduced residence time in serum. Adverse effects of carbohydrate on HDL-C in the longer term may also be mediated through increased body weight and the accumulation of body fat (Stanhope et al. 2013). Whilst the reduction in HDL-C has been attributed to diets with a high glycaemic index (Frost et al. 1999), there is now little doubt that the extrinsic sugars, sucrose and fructose make a major contribution to this effect (Lustig 2010). The findings of a recent meta-analysis which concluded that a very high intake of fructose (>100 g/d) increases serum LDL cholesterol, but has no significant effects on HDL-C, are somewhat surprising in both respects (Zhang et al. 2013) and in contrast to the outcome of dietary interventions with beverages sweetened with fructose. One example of the latter showed marked increases in cardiometabolic risk factors, including significant reductions in serum HDL-C, relative to glucose-sweetened beverages (Stanhope et al. 2009). A vital question to be answered is whether populations are consuming amounts of extrinsic sugars which are sufficient to elicit these adverse changes in HDL in the long term. Dietary intakes in the United Kingdom (National Diet and Nutrition Survey. Department of Health 2011) indicate that the upper 2.5th percentile of the population may be approaching intakes of extrinsic sugars which have the potential to induce adverse effects on metabolism and increase body weight. The overconsumption of sweetened beverages in adolescents is of particular concern in promoting premature obesity and lowering of HDL-C, as shown in a recent Australian study (Ambrosini et al. 2013).

Effects of Dietary Fatty Acids and Cholesterol on HDL Function

HDL-C is a surrogate marker of HDL particle size and number and may convey little or no information about the anti-atherosclerotic properties of HDL in the process of reverse cholesterol. There is evidence to suggest that paradoxical increase in HDL-C induced by dietary SFA and cholesterol in mice (Escola-Gil et al. 2011) and in egg-fed humans (Andersen et al. 2013) results in a beneficial increase in cholesterol efflux capacity. Beneficial effects of dietary fatty acids on cholesterol efflux capacity have also been described for EPA and DHA supplementation in hamsters (Kasbi Chadli et al. 2013) and MUFA-rich extra-virgin olive oil consumption in humans (Helal et al. 2013). Conversely, several intervention studies in humans showed no effect on cholesterol efflux capacity of replacing of SFA with either PUFA (Kralova Lesna et al. 2008) or carbohydrate (De Vries et al. 2005), or differences between diets enriched with trans fatty acids (8.3 % energy), SFA (13.2 % energy) and PUFA (14.6 %) elicited by either total plasma HDL or HDL subfractions (Buonacorso et al. 2007).

In conclusion, evidence from meta-analyses to support the relative effects of dietary fatty acids on HDL-C may be statistically incontrovertible, but they do not necessarily translate directly to the effects of complex foods and diets on HDL-C and CVD risk. Reduction in HDL-C induced by the overconsumption of dietary extrinsic sugars in sugar-sweetened beverages may have major implications for cardiometabolic health, especially in adolescents. Finally, evidence for the effects of dietary components on the anti-atherogenic, functional properties of HDL is inconclusive and warrants further study.

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