Saturated Fat
Friend, foe, or simply neutral?
Abstract
There is widespread belief that saturated fat (SF) is adversely associated with coronary heart disease (CHD) and cardiovascular disease (CVD). This hypothesis has been incorporated into practice and nutritional guidelines. Specific targets for maximum amounts of SF as a percentage of dietary energy are also a common aspect of guidelines. Historically total fat was viewed as the culprit, but when evidence was not forthcoming, the focus shifted to SF. Central to this subject is the syllogism, i.e. SF elevates LDL cholesterol, LDL cholesterol causes heart disease and therefore SF causes heart disease. This syllogism falls apart when one examines its two critical components. First, there is a remarkably poor correlation between SF intake and LDL cholesterol, especially in the range of low intake to that common in North America. As regards the second component of the syllogism, LDL cholesterol levels are not related to the prevalence of adult coronary atherosclerosis, independent of age, gender or ethnicity. For asymptomatic individuals, cholesterol
is not a significant CHD/CVD risk factor for women, the elderly, or men over about 50 years of age. For younger men, the association may be seriously confounded by issues associated with blood pressure reactivity and stress. Lowering LDL with statin drugs in asymptomatic individuals has a near negligible effect on acute event risk (approximately 1% absolute risk reduction) which may be due to pleiotropic effects, and no impact on mortality. Finally, the association between SF and CHD or CVD has come under intense attack in the past two years. The overall conclusion is that there is no significant evidence for concluding that dietary SF is associated with the risk of CHD or CVD. This conclusion was already evident in 1998 but ignored. In addition, many studies find that SF does not appear to be a risk factor for several common cancers, nor with the risk of type2 diabetes, and if there is a weak association with insulin resistance, it does not appear to carry over to type 2 diabetes risk.
The original suggestion that there was a connection between saturated fat (SF) consumption and the risk of coronary heart disease was made on the basis of ecological studies. Such studies are notoriously prone to pointing in the wrong direction. This was followed by the observation that it was possible to elevate cholesterol and LDL cholesterol by feeding individuals excess saturated fat. Thus the syllogism: SF raises LDL, LDL causes heart disease, and therefore SF causes heart disease. In a comment in 2001 on an article in the journal Science titled “The Soft Science of Dietary Fat” (Taubes 2001), Scott Grundy, a high profile academic advocate of the diet-cholesterol-heart disease hypothesis, stated that, contrary to Taubes’ critical view, SFs are the main dietary cause of coronary heart disease (CHD) (Grundy 2001). This is still the conventional wisdom today with a number of guidelines recommending low SF consumption, typically ≤ 7% of total energy intake, although as will be discussed, there are a growing number of sceptics and a remarkable lack of evidence.
Keeping SF intake low was part of the low-fat diet movement, which started some 30-40 years ago. With the backing of governments, professional nutritional and medical associations and the media, fat was demonized and there was a significant move to lower intake. Low-fat products appeared on the supermarket shelves in ever increasing numbers. The calorie deficit was, for most followers of the new path, made up by carbohydrates and the carbohydrates turned out to be mostly the rapidly digestible, high glycemic variety. It is now generally recognized that this mass hysteria over fat had unintended consequences. Excess carbohydrate stimulated excess insulin production and fat storage, obesity, insulin resistance and the risk of diabetes. It is also ironic that in order to avoid a minor elevation in LDL of debatable clinical significance, those following the low-fat philosophy raised their triglycerides and lowered their HDL, in fact to an extent that was vastly more risky than the danger attributed to the minor elevation in LDL.
It is also important to recognize that nutritional studies which address the question of the association between dietary fat and various disorders present fundamental difficulties. If one macronutrient is decreased, then either it must be replaced by another macronutrient to maintain the same energy intake or the decrease in energy intake must be taken into account as a confounder. Either way, two critical variables are changed simultaneously. If the intake of A is reduced and B increased and benefit is observed with regard to, for example, the incidence of heart disease, this does not prove that the decrease in A was responsible or that A is a risk factor. In addition, randomized interventional nutrition studies, which are relied upon to produce definitive guidance, are frequently accompanied by failure to achieve the desired intakes, have poor long-term adherence to the study plan and frequently there is a convergence of the control and the intervention groups toward a common diet leading to non-significant results.
Hypotheses survive until falsified (to paraphrase Karl Popper). One is reminded of the famous black swan example. The hypothesis that saturated fat causes heart disease is now coming under scrutiny due to a number of studies which appear to directly falsify it, followed by several new meta-analysis which simply add confirmation. Recent research will be reviewed in this article along with related issues such as the connection between saturated fat and other diseases. In fact, the so-called Great Fat Debate is heating up (Zelman 2011). A number of black swans have been sighted.
THE SYLLOGISM: QUESTIONS
Earlier articles by the author which have appeared in this publication (Ware 2011a, Ware 2011b) presented strong evidence that LDL is not a risk factor for the prevalence or progression of coronary atherosclerosis in either diabetics or non-diabetics, and is a weak or for many individuals a non-existent risk factor for acute cardiac events. Lowering LDL with drugs in asymptomatic individuals carries an absolute risk reduction of only around 1% for acute events and no impact on cardiac related mortality, and the number needed to treat to prevent one non-fatal event is about 100. This small impact may also be a pleiotropic effect and have no connection with lipid lowering. Thus, the above chain of reasoning that leads from SF to LDL elevation to heart disease risk appears seriously weakened for these reasons alone.
Critical to the case against SF is its alleged ability to elevate cholesterol and LDL to an extent that is clinically significant. Based on a meta-analysis of metabolic ward studies, when 10% of energy intake from saturated fat was replaced by carbohydrates while keeping calorie intake constant, there was a decrease in LDL by 0.36 mmol/L (14 mg/dL) (Clarke 1997). Another meta-analysis, where 1% of energy from carbohydrates was replaced by various individual saturated fats keeping the total energy intake constant, found changes in LDL that ranged from 0.05 to -0.004 mmol/L (1.9 to -0.16 mg/dL) (Mensink 2003). But using these numbers, even a 5% or 10% change in energy from SFs produces an LDL change that is of the same size as the normal variation of LDL levels in any given individual seen over short periods of time (Hegsted 1987). Furthermore, this ignores the huge individual variations. Thus one can question the clinical significance of these small changes. Furthermore, the above studies are inconsistent with more recent studies.
In a 2008 paper (Volek 2008), the authors present a scatter plot (Fig. 5) from a frequently cited paper used to support the claim that saturated fat intake increases serum cholesterol (Clarke 1997). If one examines just the part of the plot ranging from 5% to 25% saturated fat intake as a percentage of total energy, a range that encompasses the intake of a majority of North Americans who on average consume about 14% of energy as SF, the correlation between SF intake and cholesterol is almost impossible to see, and if one looks at the range from 15% to 7%, approximately the change recommended by the current guidelines, the scatter is so great that this decrease in SF intake appears equally likely to raise as to lower total cholesterol. Volek and coauthors conclude that total cholesterol is not a strong predictor and find it hard to consider the cited figure as evidence of substantial benefit for reducing SF across the board.
These results alone are enough to generate justified skepticism, but they are strongly reinforced by two recent studies which also addressed the question of correlation between SF intake and LDL levels and found no association (Mirmiran 2009, Wood 2011). Thus the syllogism presented above appears to have fatal flaws.
OBSERVATIONAL AND INTERVENTION STUDIES. SATURATED FAT AND CHD/CVD
Already in 1998 a lengthy and comprehensive systematic review appeared in the Journal of Clinical Epidemiology which examined the evidence for and against the hypothesis that SF intake was related to either CVD incidence or mortality (Ravnskov 1998). A very large number of ecological (population) studies, as well as cross-sectional (snapshot), case-control and cohort follow-up studies were examined. In addition autopsy studies that examined the relationship between saturated fat (animal fat) intake and the extent of atherosclerosis were reviewed. Ravnskov did not find any convincing evidence up to 1998 for the association. The overall picture that emerged was one of inconsistency with more studies falsifying the hpothesis than supporting it, even when studies of comparable quality were compared in detail.
In 2005 a 20-year update on the famous Nurses’ Health Study also looked at the association between dietary fat intake and CHD (Oh 2005). When the results of this prospective cohort study were corrected for confounding, there was no significant relation between the relative risk of coronary heart disease and saturated fat intake when the lowest vs. the highest quintile were compared. The same was true for total fat intake, but polyunsaturated fat was found to be significantly protective and trans fats significantly harmful. This study involved the analysis of data from a lengthy follow-up study of over 78,000 female nurses.
A recent meta-analysis of 21 prospective epidemiologic studies and a pooled analysis of 11 cohort studies have recently appeared which have fueled the SF-heart disease debate. The pooled analysis (Jakobsen 2009) examined the impact on coronary events or CHD-related mortality associated with the various combinations of substitution of monounsaturated fatty acids (MUFAs), polyunsaturated fatty acids (PUFAs) or carbohydrates in place of SF. PUFA substitution was found to decrease the risk of both endpoints whereas carbohydrates were found to significantly increase the risk for coronary events but not mortality. MUFA substitution for SF was not associated with CHD risk. There was no effect modification by gender or age.
The second study, a meta-analysis of prospective studies (Siri-Tarino 2010a) examined the relationship between SF and cardiovascular disease (CVD). It was found that there was no significant evidence for concluding that dietary SF is associated with increased risk of CHD or CVD. The researchers comment that more data are needed to elucidate the question of CVD risks being associated with specific nutrients used to replace SF. Some would be satisfied at this point with the picture that has emerged.
In the introduction of the meta-analysis of Siri-Tarino et al, the authors point out that there are only a limited number of randomized clinical intervention trials that have examined the issue of saturated fat and CVD or CHD. The results have been inconsistent with some showing benefit, others none. Those what showed beneficial effects associated with reducing saturated fat intake replaced it with PUFAs. These positive results could have been due to simply an increase in PUFAs. The pooling study discussed above supports this conjecture.
THE ASSOCIATION OF SATURATED FAT WITH OTHER DISORDERS
Cancer. Interest in the potential association between cancer and dietary fat in general and saturated fat in particular has extended over more than two decades. Interest has focused on breast, prostate and colorectal cancer. For breast cancer, two recent very large meta-analyses did not support a positive independent association with either total fat or animal fat (Alexander 2010, Turner 2011). Meta-analyses for colorectal cancer were also negative (Alexander 2009, Liu 2011). Prospective studies failed to find a consistent association between fat and prostate cancer, but the risks associated with saturated fat are unclear (Dennis 2004). Reduction of consumption of processed meat may in general decrease cancer risk. However, here the issue appears to be carcinogens rather than fat (Kushi 2002).
Diabetes and Insulin resistance.
In the Nurses’ Health Study, total, saturated and monounsaturated fat were not associated with the risk of type 2 diabetes. Furthermore, polyunsaturated fat was protective and trans-fats increased risk (Salmeron 2001). In the Health Professionals Follow-up, saturated fat was not associated with the risk of type 2 diabetes in men once the results were adjusted for BMI (van Dam 2002). As regards fat type and insulin resistance, if fat intake was high, no fat-type dependence was found. No changes in insulin resistance were found when fat composition was kept constant but total intake varied between 20% and 40% of energy. However, if fat intake is low there is some evidence that saturated fat may decrease insulin sensitivity, but this does not carry over to increased incidence of diabetes (Siri-Tarino 2010b).
Decades ago, the traditional diet for diabetics involved severe carbohydrate restriction. As the 20th century progressed this became less popular and then with the advent of the highly successful anti-fat campaign, diabetic patients were warned of the extreme dangers of substituting fat for carbohydrates. Dr. Robert Atkins was brought before a U.S. congressional committee to defend the accusation that by promoting a low-carbohydrate (and therefore elevated fat) diet, he was seriously endangering public health, an accusation proven false by a number of studies over the past decade. Today there are calls for a return to this traditional approach of treating type 2 diabetes, and the merits of carbohydrate restriction in the context of diabetes prevention and therapy have been pointed out repeatedly in the past few years (Accurso 2008, Volek 2005a, Volek 2005b, Volek 2008, Volek 2009). The success achieved by Richard K. Bernstein using carbohydrate restriction and carefully selected carbohydrates matched to the individual’s metabolism is now documented in several editions of his book Dr. Bernstein’s Diabetes Solution (Bernstein 2011). The HbA1c levels he achieves are vastly better than anything conventional medicine appears able to achieve, and this is accomplished with diet. Drugs or insulin are used only when absolutely necessary. Taken together, the journal literature and the evidence in this book should give cause for reflection among diabetologists.
CONCLUSIONS
The fat-is-bad notion is alive and well as evidenced by the recent move by Denmark to place a special tax, thought to be the world’s first ever, on foods high in saturated fat. Health authorities in Denmark claim it will save countless lives. The scientists advising the government presumably refused to give any weight to the contrary evidence, in fact the lack of evidence, in the literature and the associated numerous commentaries, and in addition, to studies regarding the danger of substituting high glycemic index carbohydrates for fat. Yet the natural human tendency is to do just that and in particular to increase refined carbohydrates. The saturated fat saga is an excellent example of the tendency among professionals to ignore vast amounts of literature that disagree with their long-held beliefs. Hypotheses that appear to have been conclusively falsified have a remarkably long lifetime and vitality.
A reasonable approach to the dietary fat issue is perhaps simply to avoid all trans-fats (Aronis 2011), severely limit processed meats (Micha 2010), make sure of an adequate intake of omega-3 fatty acids and in particular, the long-chain fatty acids found in fish (Mozaffarian 2007), use general calorie restriction rather than specific macronutrient restriction when trying to lose weight and consider carbohydrate restriction when attempting to control blood sugar levels (Feinman 2008, Omodei 2011).
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