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Public health

Saturated fat: guidelines to reduce coronary heart disease risk are still valid

On the balance of evidence from a wide range of research, it is clear that the consumption of saturated fat should be limited to protect cardiovascular health.

Current dietary guidelines issued by Public Health England (Department of Health) to lower risk of coronary heart disease (CHD) by eating less saturated fat have once again come under attack. But evidence still stands: its consumption should be limited


Current dietary guidelines issued by Public Health England (PHE) to lower risk of coronary heart disease (CHD) by eating less saturated fat have once again come under attack. This is largely because a recent meta-analysis failed to demonstrate a direct relationship between saturated fat and death from heart disease. This has led to accusations that recommendations to restrict intake of saturated fat to improve heart health have been overstated[1], or worse, should never have been introduced[2].

Understandably, this has raised concerns among healthcare professionals who, as end users of this information, could deliver dietary advice that is potentially inappropriate for cardiovascular health. In defence of existing guidelines[3] from PHE, it is imperative to interpret the negative outcome of secondary meta-analyses in relation to the totality of evidence for the impact of saturated fatty acids (SFAs) on CHD from primary studies. The outcomes of meta-analyses should also be viewed in perspective of the limitations of these primary studies, which include follow-up studies in populations (prospective cohort trials) and randomised controlled trials (RCTs) of dietary intervention.

Analysing the studies

The totality of evidence to link saturated fats with heart disease comes from a wide range of different types of research study over the past 60 years. This has included studies in animal models, observational epidemiology, metabolic ward studies, prospective cohort and randomly controlled trials, and systematic reviews and meta-analyses of the latter. The collective weight of evidence from this breadth of research is consistent in showing that replacement of dietary SFAs, with a chain length of between 12–16 carbons, with polyunsaturated fatty acids (PUFAs), reduces serum low-density lipoprotein cholesterol and CHD risk in a dose-dependent manner.

On the other hand, although replacement of SFAs with either monounsaturated fatty acids (MUFAs) or carbohydrates also lowers serum low density lipoprotein (LDL) cholesterol, it produces less or no measurable effect on CHD risk, respectively[4]. There is also evidence to suggest that if the replacement of SFAs with carbohydrates delivers excess energy as free sugars, this can exacerbate cardiometabolic risk factors associated with central obesity and diabetes. The impact of this evidence on dietary guidelines for the prevention of CHD has been substantial, partly because it comes from studies in different populations who are the main recipients of dietary advice to prevent CHD. This evidence has also provided significant insight into the relative effects of exchanging SFAs with other macronutrients on serum LDL cholesterol, risk of CHD and the pathology of coronary atherosclerosis, through mechanisms unrelated to serum cholesterol, such as inflammation, blood clotting and dysfunction of blood vessels.

Scrutinising the evidence

A major limitation of applying meta-analyses to dietary studies lies in the inherent weaknesses in the design of the individual primary studies. Prospective cohort studies involve the assessment of dietary intake in a population, then following up the development of disease in that population over a period of several years, and establishing associations between dietary intake at the beginning, with the outcomes of disease at the end, such as fatal or non-fatal cardiovascular events.

Although this study design has been used extensively to provide evidence for associations to support dietary guidelines, dietary intake can change over the follow-up period, especially when an individual has been diagnosed with a life-threatening disease. This problem can be further confounded by changes in other dietary and lifestyle factors that can influence the disease. These problems will not be resolved by combining data from primary studies in a secondary meta-analysis.

The gold standard for producing evidence for a causal effect of an intervention on the outcome or biomarker of disease is an RCT in which patients or healthy subjects are randomly assigned to either an intervention or a control treatment. However, RCTs were primarily designed to demonstrate the efficacy of drugs and not the impact of a single nutrient such as SFAs, within a complex diet, on a multi-factorial disease. Dietary RCTs fail to account for the critical effects of what replaces SFAs (PUFAs, MUFAs, or carbohydrates) and, in many cases, have been trials of fat supplementation rather than replacement, in which oils of modified fatty acid composition are superimposed on top of an existing diet.

Prime examples of such RCTs formed the basis of a meta-analysis that examined six trials between 1977 and 1983[2]. It failed to demonstrate a significant relationship between dietary SFAs and CHD mortality, and so concluded that the guidelines to reduce intake of SFAs that were introduced in the United States and Europe in 1983 were unfounded and should never have been introduced.

Close scrutiny of the trials under investigation in this meta-analysis reveals that several studies involved the addition of an oil, such as corn oil, olive oil or soya bean oil, to the existing diets of patients with CHD. In many cases, the oil supplement produced extreme changes in the intake of dietary fatty acids in patients, some of whom had suffered a heart attack just four weeks before commencing a trial. In all these studies, removal of dietary SFAs resulted in reduction in serum cholesterol, but since there was no significant effect on CHD mortality, it was claimed that serum cholesterol was inadequate as a biomarker of disease.

A more realistic and plausible explanation for the lack of positive outcome is that the size of cohorts in this meta-analysis was too small (needs to be in the order of several hundred participants), and the duration of the trials too short (months to years instead of weeks to months) to show a statistically significant relationship between SFA intake and CHD mortality. Remarkably, one of the supplementation trials with corn and olive oil from 1965 was terminated prematurely because half of the patients had died. This highlights the limited translational value of findings in patients with existing CHD to dietary guidelines for the prevention of CHD in healthy populations.

A further complication with the interpretation of these trials is that not all dietary SFAs exert the same effect on serum LDL cholesterol. For example, stearic acid, which is a common constituent of many foods, has no effect on LDL cholesterol. The effects of dietary SFAs on LDL cholesterol have also been shown to depend on the type and composition of food in which the SFAs are consumed. Butter and cheese are prime examples of SFA-rich foods, but the SFAs in butter have a greater effect on raising serum LDL cholesterol than the SFAs in cheese, even when the amount of SFA in both foods are identical.

There are a few notable exceptions of RCTs of dietary intervention that have been large enough and long enough to show substantial benefits in reducing risk factors and clinical endpoints of cardiovascular disease, but these trials have involved the modification of whole diets and not individual nutrients (e.g. ‘DASH ’, ‘PREDIMED’[5],[6]). It is reasonable to expect that a disease with multi-factorial aetiology such as CHD will be more responsive to multiple dietary changes that are achieved by modifying the overall pattern of food intake, rather than a single nutrient.

It is also reasonable to question whether it is correct to base a guideline for the reduction of dietary SFAs on the strength of their effects on a single biomarker of CHD risk, such as serum LDL cholesterol. Moreover, it is highly unlikely there will ever be an RCT of a scale and duration that has sufficient power to demonstrate a statistically significant link between the intake of dietary SFAs and dying from coronary disease.

Saturated fat is still bad

The totality of existing evidence to link dietary SFAs with CHD, primarily through their effect on serum LDL cholesterol, is still sufficiently robust to uphold current UK guidelines to reduce SFA intake to no more than 10% of total energy intake. It is also reassuring to know that this guideline has been endorsed recently in draft recommendations from the Dietary Guidelines Advisory Committee (DGAC) in the United States[7].

Healthcare professionals have a duty to help dispel confusion and put exaggerated news headlines into perspective. After all, there will be many people enquiring whether, for example, butter is “back in fashion”. Despite recent studies suggesting no link between saturated fat and CHD, once you scrutinise the evidence, there is no question that too much saturated fat is bad for your health. Of course, a balanced nutritious diet remains the best way to prevent CHD and metabolic diseases.

Bruce A Griffin is professor of nutritional metabolism at the University of Surrey.

Citation: The Pharmaceutical Journal DOI: 10.1211/PJ.2015.20068191

Readers' comments (2)

  • It is strange to read the conclusions at the end of Professor Griffin's very well-informed article after reading, in the article itself, how weak is the evidence linking saturated fat consumption and CHD. Professor Griffin argues that meta-analysis is a crude tool, and RCTs may not last long enough or have enough participants for results to show.
    However, if you were to look at a meta-analysis of red meat and colorectal cancer, or of processed meat and cardiovascular disease, you would see a significant correlation. A small one, and possibly exaggerated by the fact that health-conscious people of the fortunate classes have long minimized intake of these foods, but it is there to be seen, which makes it all the more curious that saturated fat, which health conscious people have also long avoided, is still not associated with the outcome most often attributed to it.
    DASH and the faux-Mediterranean diet are healthy diet patterns that are low in saturated fat, but this does not mean that there are no healthy diet patterns that are higher in saturated fat than the guidelines recommend. It just means that, due perhaps to over-reliance on the cholesterol test as a measure of health, only diet patterns that are low in saturated fat have received the funding and approval they required to be tested for cardiovascular outcomes. At least one of these multifactoral interventions, the DART study, did not result in lower CHD outcomes when SFA was limited.(1)
    Does the argument to retain the guidelines amount to much more than the fact that there are no other guidelines to replace them, and may never be?
    One thing that seems to be clear is that the evidence around the various SFAs, and that around the various PUFAs, are actually separate , and that previous attempts to combine the two into a single formula, as the guidelines do, is becoming hard to justify.
    While there is evidence of increased benefit from higher PUFA intakes (around 5-7%E) in epidemiological studies, if not in RCTs, it does not matter whether this replaces saturated fat or carbohydrate (nor, indeed, monounsaturated fat) in sub-group analysis, and the difference has no association with all-cause mortality.
    Perhaps this is the sort of thing the guidelines should empathize in regard to fats; as well as the evidence that certain fatty foods - olive oil, nuts, and full-fat dairy - are associated with reduced CVD risk, despite their different fat compositions.

    (1) M.L. Burr, J.F. Gilbert, R.M. Holliday, et al. EFFECTS OF CHANGES IN FAT, FISH, AND FIBRE INTAKES ON DEATH AND MYOCARDIAL REINFARCTION: DIET AND REINFARCTION TRIAL (DART). The Lancet Volume 334, Issue 8666, 30 September 1989, Pages 757–76

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  • Graham Phillips

    I agree, George. For those interested in this debate, its worth googling Gary Taub (Why we get fat) and Petter Attia. Here's a good place to start:

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