Fat quantity versus quality: importance of the ratio of n-6:n-3 polyunsaturated fatty acids
The underlying principle for a reduction in total fat intake is to reduce energy intake from the consump-tion of the most energy-dense macronutrient in order to prevent weight gain and ultimately obesity. The current recommendation for the UK is to reduce energy derived from fat to 35% or less. Since weight gain is associated with raised plasma TAGs and abnor-malities in circulating lipoproteins, reducing total fat intake should, in theory, reduce blood lipids. However, in practice there is little evidence to support such an effect within populations. Metaanalyses have revealed that little benefit is to be gained, at least in terms of changes in blood lipids, by reducing total fat without altering the composition of dietary fatty acids. Metaanalyses have also helped to resolve the issue of what represents the most appropriate replacement nutrient for SFAs. Since PUFAs, and specifically lin-oleic acid, were shown to counter the actions of SFAs and were abundant in natural sources such as sun-flower and corn oils, they were an obvious first choice. The alternative was to substitute fat with dietary car-bohydrate. There have been problems associated with both of these approaches. First, increasing dietary lin-oleic acid excludes the lesser abundant, but more met-abolically active, n-3 PUFA, and especially the longer chain (C20–C22) members of this series derived from marine oils [C20:5 (eicosapentaenoic acid) and C22:6 (docosahexaenoic acid)]. Overemphasis on linoleic acid in the food industry, together with a widespread resistance to the consumption of fish, has increased the ratio of n-6 to n-3 PUFAs in northern Europe and the USA since the 1970s. This situation has major implications for the development of abnormalities in circulating lipoproteins, since deficiency in eicosapen-taenoic acid and docosahexaenoic acid could help to promote an increase in plasma TAG. This could occur through an overproduction of endogenous TAG (VLDL) in the liver and intolerance to dietary (exoge-nous) fat, and lead to the development of dyslipidemia known as an ALP. The frequency of this dyslipidemia is believed to be very rare in Mediterranean countries that have a high intake of dietary n-3 PUFA and an n-6:n-3 ratio closer to 1. High-carbohydrate diets have been shown to increase plasma TAG. Carbohydrate-induced hypertriacylglyc-erolemia is not, as was originally thought, a short-term adaptive response in the liver, as it changes its pattern of oxidation from fat to carbohydrate, but a real phenomenon associated with the overconsump-tion of the non-milk extrinsic sugars, sucrose and fructose, most notably in individuals with insulin-resistant dyslipidemia. There is evidence to suggest that this effect can be avoided by limiting the intake of sucrose and increasing the intake of slowly absorbed carbohydrate with a low impact on blood glucose.
The results of several metaanalyses of dietary inter-vention trials support dietary MUFAs as the most favored substitute for dietary saturated fatty acids, and even linoleic acid in areas of high intake.
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