The replacement of dietary saturated fat with polyunsaturated fat has been the mainstay of our dietary guidelines for reducing the risk of coronary heart disease (CHD) for over 30 years.1 However, the validity of these guidelines has now been challenged by the outcome of meta-analyses that could find no evidence for a direct relationship between the intake of saturated fat and CHD.2-4 These findings have fueled a backlash of claims that current recommendations to reduce intake of saturated fat are overstated3 or should never have been introduced.4
So what or who should we believe? Have we been over-estimating the importance of saturated fatty acids (SFA) and polyunsaturated fatty acids (PUFA) to cardiovascular health, or have these meta-analyses produced an erroneous outcome that is leading consumers away from dietary guidelines that should be reinforced, rather than ignored? The answers to these questions are of vital importance to nutrition practitioners who have a duty to deliver the correct information to their patients and clients, and the general public, who are the ultimate benefactors of evidence-based dietary guidelines.
Two of the most recent and controversial studies to raise doubt over the validity of replacing saturated fat with polyunsaturated fat to improve cardiovascular health are the Sydney Heart Study,5 and a meta-analysis from the Cambridge Epidemiology Unit in the UK.3 The Sydney Heart Study was a randomly controlled intervention trial with high PUFA safflower oil and margarines in men with existing CHD that was originally conducted between 1966 and 1973, but revisited and reported in 2013.5 While the re-analysis showed a highly significant increase in risk of CHD in the group who replaced dietary SFA with PUFA, it had two major flaws. First, it failed to control for the intake of trans fatty acids, which are known to raise serum LDL, lower HDL, and have been unequivocally associated with increased CHD risk.6,7 It is highly likely that these fatty acids were consumed in the test spreads and background diet in the late 1960s. Second, the intake of dietary PUFA in the intervention group increased from 6% at baseline to 15.4% of energy, a level of intake that exceeds previous and current recommendations for these dietary fatty acids in Europe and the US. The more recent meta-analysis from Cambridge also concluded that their evidence did not clearly support guidelines to encourage high consumption of dietary PUFA and low consumption of total SFA.3 Nevertheless, exclusion of the Sydney Heart Study from their analysis produced a beneficial 20% reduction in CHD risk in response to the removal of dietary SFA.8
Further insight into the discrepant findings of recent meta-analyses can be gained by placing these secondary forms of analyses in perspective of the totality of existing evidence from primary sources for the impact of saturated fat on CHD. These sources include epidemiological, prospective cohort and randomly controlled trials, all of which are consistent in showing that a high intake of saturated fat is related to an increased morbidity and mortality of CHD.9 What is critical to appreciate is that this relationship is not direct, but mediated to a large extent through the capacity of certain SFA to raise serum LDL cholesterol,7,10 an established risk factor that is directly involved in the development and endpoints of the disease.11 This provides one major explanation for why meta-analyses can find no direct relationship between SFA and CHD for two reasons. First, the effects of SFA on serum LDL cholesterol are complex and determined by many factors, including macronutrient substitution, variable effects of specific SFAs, and food source, none of which have been fully accounted for in meta-analyses. Second, raised serum LDL cholesterol is a single risk factor influencing a disease (CHD) with multi-factorial origins.
The effects of dietary saturated fat on serum LDL cholesterol are usually described in relative rather than absolute terms. In other words, the effect of removing dietary SFA on serum LDL cholesterol depends, to a large extent, on what macronutrient takes its place. The addition of dietary PUFA, chiefly from linoleic acid from plant sources (soy, safflower, sunflower and corn oils), has been proven to be the most effective substitute for SFA in terms of lowering both LDL cholesterol and CHD risk (1% reduction in energy from SFA equates with ≥2-3% reduction CHD risk).1, 6-8 In contrast, replacing SFA with monounsaturates or carbohydrates produces a relatively small effect in lowering LDL cholesterol, with little or no benefit to CHD risk. Importantly, if the carbohydrate that replaces SFA is unrefined and high in free sugars, it may exert adverse effects on CHD risk by increasing energy intake and body weight, and/or through the distinct metabolic effects of sugar.12 Failure of prospective cohort studies to take account of macronutrient substitution over time, may have contributed to the negative outcomes of meta-analyses, as the adverse effects of replacing SFA with unrefined carbohydrates and sugar, counter the beneficial effects of replacing SFA with PUFA.
Another factor that may help to explain the discrepant findings of meta-analyses is that not all dietary SFA exert the same effect on serum LDL cholesterol. While the potential of dietary SFA to raise serum LDL cholesterol increases with a decreasing number of carbon atoms in the fatty acid chain--from 16 to 12 carbons (palmitic acid and lauric acid, respectively)--an exception is stearic acid (18 carbons), a common constituent of many foods, that has relatively little effect on LDL cholesterol.13 Similarly, not all SFA increase serum HDL to the same extent. In contrast to LDL, HDL is a cardio-protective lipoprotein, changes in which produce variable effects on the ratio of total to HDL cholesterol, a popular biomarker of CHD risk that is used in clinical practice. However, while a low TC:HDL-cholesterol ratio is indicative of a lower CHD risk, the true functional capacity of HDL to fulfil its physiological roles in protecting the artery walls from the development of CHD, is much more difficult to assess than simply measuring its cholesterol concentration in serum. This means there is no solid evidence, as yet, that lowering this ratio with foods high in SFA that raise HDL, will be beneficial in reducing CHD risk. Dietary fatty acids with medium chain length (6-10 carbons), as contained in medium chain triglycerides (MCTs), exert less of an effect on serum LDL cholesterol, primarily because they are removed rapidly from the blood circulation and oxidized to produce energy, before they can circulate in serum lipoproteins.13 Interestingly, while the high content of MCTs (~15%) in coconut oil, and its potentially favorable effects on the TC:HDL-C ratio have been used to support health messaging for this oil, there is no convincing evidence to suggest that these effects are operating, or if so, can off-set the adverse effect of coconut oil in raising serum LDL cholesterol.
The impact of dietary SFA on serum LDL cholesterol also depends on the type and composition of food in which the SFA is contained. Nutrients in foods are contained within a food matrix that can influence the absorption and bioavailability of nutrients. Foods also contain complex mixtures of components that can interact to alter the physiological properties of individual nutrients. The best example of this phenomenon in the context of dietary SFA and LDL cholesterol is provided by dairy foods, and specifically the relatively greater LDL cholesterol-raising effect of SFA in butter as compared to cheese.14 This finding has been attributed to the high calcium content of cheese, which can form insoluble salts with the SFA that cannot be absorbed in the gut and are excreted.15
In conclusion, the totality of existing evidence to link dietary SFA with CHD, primarily through its effect on serum LDL cholesterol, is sufficiently robust to uphold current guidelines to reduce SFA intake to no more than 10% of total energy intake, a recommendation that has been recently endorsed in the USA by the Dietary Guideline Advisory Panel.16 There is a well-documented portfolio of therapeutic diet and lifestyle changes for reducing elevated serum LDL cholesterol,17 which includes as a priority exchanging dietary SFA with PUFA as the most effective fatty acid substitute. But, how can this be achieved in practice?
The strongest existing evidence for the benefit of diet in reducing CHD risk and mortality comes from randomly controlled intervention trials of whole dietary patterns, the best examples of which are the DASH18 and Mediterranean diets.19 The effectiveness of these diets, which are inherently low in SFA and rich in PUFA from plant sources, is helping to shift emphasis away from the study of single nutrients like saturated fat, and towards the development of whole food-based dietary guidelines. It stands to reason, that the most effective dietary approach for reducing the risk and fatal outcome of a disease with multi-factorial origins like CHD, involves more than modifying the intake of dietary fat.
References:
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