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Treatment guidelines and population-based recommendations evolve from research vetted by the scientific community. Healthcare providers require practice guidelines resulting from rigorous review of the totality of evidence. Open discussion/debate among experts is fundamental and encouraged, but blatant disregard for scientific process can lead to confusion and public distrust. A recent example is the controversy among scientists, healthcare professionals and the public about dietary saturated fat (SFA) recommendations to lower risk of cardiovascular disease (CVD).
Dietary recommendations for SFA from authoritative organisations
More than 60 years ago (in 1957), the American Heart Association (AHA) proposed that modifying dietary fat could reduce the incidence of coronary heart disease (CHD). This was based on research, including controlled feeding studies, and endpoint measures of blood lipids and blood pressure.1 In 1980, the first Dietary Guidelines for Americans recommended ‘avoiding too much SFA’.2 For decades, research has substantiated this consistent dietary recommendation from authoritative organisations to decrease SFA to reduce CVD risk.3–6 Current dietary guidelines for SFA and evidence ratings are summarised in table 1. While the strong evidence to reduce SFA specifically targets decreasing low-density lipoprotein (LDL)-cholesterol, it is very much germane to CVD risk reduction.
Challenging practice guidelines and population-based recommendations: the SFA SAGA
In 2010, a meta-analysis of 21 prospective epidemiological studies totalling 347 747 subjects reported that higher intake of SFA was not associated with an increased risk of CHD, stroke or CVD.7 Aspects of this methodology were widely criticised,8–10 most notably the failure to account for the proportional differences in dietary macronutrient composition with varying SFA intake.8 10 Using similar meta-analytic methods, and again without considering the macronutrient composition of diets differing in SFA, Chowdhury et al and also de Souza et al further concluded that SFA was not associated with CHD or CVD or CHD mortality.11 12 Additional analyses of prospective cohort studies and randomised controlled trials that carefully evaluated both the dietary nutrient profile and SFA intake have consistently demonstrated a lower risk of CHD when polyunsaturated fatty acids (PUFAs) are consumed instead of SFA.13 14 More recently,15 findings from the Nurses' Health Study (NHS) (1980–2010) and Health Professionals Follow-up Study (1986–2010) suggested that lowering energy from SFA by 5% and proportionally increasing PUFA, monounsaturated fatty acids (MUFAs) or carbohydrates from whole grains was associated with a 25%, 15% and 9% lower risk of CHD, respectively (PUFAs: HR: 0.75, 95% CI 0.67 to 0.84; p<0.0001; MUFAs: HR: 0.85, 95% CI 0.74 to 0.97; p=0.02; carbohydrates from whole grains: HR: 0.91, 95% CI 0.85 to 0.98; p=0.01).15 Similarly, lower intake of predominant long-chain SFA in favour of other macronutrients and plant proteins reduced risk of CHD in the NHS and the Health Professionals Follow-up Study.16 Consumption of 1% of energy from plant proteins instead of C12:0–C18:0 SFA decreased CHD risk (HR: 0.93, 95% CI 0.89 to 0.97; p=0.001).
The clinical trial evidence has focused on evaluating replacement of SFA with PUFA. Based on three recent meta-analyses of clinical studies,17–19 the debate continues. The first two papers concluded that the evidence does not support current recommendations to replace SFA with PUFA since there was no effect on CHD mortality and total/all-cause mortality.17 18 Hamley18 also reported no effect on major CHD events and total CHD events. In contrast, the recent AHA Presidential Advisory on dietary fats and CVD19 concluded that ‘lowering intake of SFA and replacing it with unsaturated fats, especially PUFAs, will lower the incidence of CVD’. This conclusion was based on both epidemiological evidence as well as a meta-analysis of four well-controlled clinical trials, the latter of which demonstrated a 29% reduction in CHD events when SFA was replaced with PUFA. This disagreement reflects the studies included in the meta-analyses. Harcombe et al 17 and Hamley18 included studies that were excluded by Sacks et al 19 due to methodological concerns (discussed in the AHA Presidential Advisory). Since this debate still continues, it is important to recognise the robust literature that demonstrates that lowering SFA reduces LDL-cholesterol (table 2), an established causal factor in the development of atherosclerosis.20
The need for rigorous dietary research: learning from the SFA debate
Dietary patterns are comprised of foods and nutrients, and this inter-relationship must be acknowledged in dietary research.21 A reductionist approach has plagued SFA research and demonstrates the hazards of isolating a single nutrient and failing to account for the overall nutrient composition. This leads to confusion and unintended deleterious consequences (eg, a reduction in fat intake and an increase in refined carbohydrates) and impedes accurate translation of nutrition research. Future epidemiological research requires a more holistic approach to account for macronutrient substitutions. This translational approach favors support of healthy eating patterns and reduces unforeseen adverse effects more common when single nutrient recommendations are issued. Clinical research likewise benefits from dietary interventions that address the total dietary pattern including the influence of replacement foods and nutrients on the outcomes assessed.
Summary and perspective
Although there is no biological requirement for SFA, a healthy diet will provide some SFA by virtue of meeting food-based dietary guidelines. A diet that limits SFA to <7% of calories accommodates a modest intake while achieving the recognised benefits of unsaturated fatty acids.
Observational studies show cardiovascular benefits associated with lowering SFA and proportionally increasing PUFA, MUFA, whole grains and plant proteins.
Epidemiological research that ignores nutrient differences in diets across the spectrum of SFA intake demonstrates no association of SFA with CVD risk. SFA intake is typically lowered and proportional increases in refined carbohydrates occur. Thus, the appropriate conclusion is that SFA and refined carbohydrates are equally deleterious on CVD risk. The controversy about the clinical trial evidence stems from studies with methodological problems and inclusion of these studies in meta-analyses.
Recommendations to decrease SFA for CVD risk reduction are supported by robust evidence of a CVD benefit. The consensus of many scientists is to focus on a replacement message22 23 that SFA be replaced with PUFA, MUFA, whole grains and plant proteins. This can be achieved with many healthy dietary patterns.
Nutrition research must consider dietary patterns and the complex inter-relationship between dietary components to ensure translation into meaningful and health-promoting dietary recommendations.
Contributors All authors contributed to conceptualising and writing the manuscript.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent Not required.
Provenance and peer review Commissioned; externally peer reviewed.