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The importance of reducing SFA to limit CHD

Published online by Cambridge University Press:  12 September 2011

Jan I. Pedersen*
Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, POB 1046 Blindern, 0316Oslo, Norway
Philip T. James
London School of Hygiene and Tropical Medicine, London, UK
Ingeborg A. Brouwer
Department of Health Sciences, VU University, 1081 HVAmsterdam, The Netherlands
Robert Clarke
Clinical Trial Service Unit, University of Oxford, Oxford, UK
Ibrahim Elmadfa
Institute of Nutritional Sciences, University of Vienna, 1090Vienna, Austria
Martijn B. Katan
Department of Health Sciences, VU University, 1081 HVAmsterdam, The Netherlands
Penny M. Kris-Etherton
Department of Nutritional Sciences, Penn State University, University Park, PA16802, USA
Daan Kromhout
Division of Human Nutrition, Wageningen University, 6700EV, Wageningen, The Netherlands
Barrie M. Margetts
Faculty of Medicine, University of Southampton, Southampton General Hospital, Southampton, UK
Ronald P. Mensink
Department Human Biology, School for Nutrition, Toxicology and Metabolism, Maastricht University, Maastricht, The Netherlands
Kaare R. Norum
Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, POB 1046 Blindern, 0316Oslo, Norway
Mike Rayner
British Heart Foundation Health Promotion Research Group, Department of Public Health, University of Oxford, Oxford, UK
Matti Uusitupa
Institute of Public Health and Clinical Nutrition, Clinical Nutrition, Kuopio Campus, University of Eastern Finland, Kuopio, Finland
*Corresponding author: Dr J. I. Pedersen, email
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Guest Editorial
Copyright © The Authors 2011

Uncertainty has recently been expressed as to the role of SFA for the development of atherosclerosis and CHD(Reference Siri-Tarino, Sun and Hu1). This confusion, created primarily by interpretation of results from prospective cohort studies(Reference Siri-Tarino, Sun and Hu2), was recently thoroughly discussed with strong emphasis on the shortcomings of such studies(Reference Kromhout, Geleijnse and Menotti3). The seriousness of the problem makes it desirable to broaden the scope of this discussion with a main focus on the public health implications.

Confusion in the scientific literature on these issues may easily be misused by the food industry to promote their interests. More serious, however, is the potential damage this uncertainty may cause to public health strategies and the priority given to saturated fat and serum LDL-cholesterol reduction in the prevention of CHD. Thus, an important report on non-communicable diseases (NCD) recently published as an input to the forthcoming UN High-Level Meeting (UN HLM) in September 2011 listed tobacco control and salt reduction as its top priorities among the well-known risk factors for NCD(Reference Beaglehole, Bonita and Adams4). Furthermore, at the recent conference of Global Health Ministers in Moscow, the WHO listed smoking cessation, alcohol controls and dietary salt reduction as particularly cost-effective interventions to reduce the risk of NCD while also giving special attention to the promotion of healthy diets (low in SFA, trans-fatty acids (TFA), salt and sugar, and high in fruit and vegetables)(5). In the draft outcome document of the HLM on the prevention and control of NCD, cost-effective measures to reduce risk factors mentioned are: tobacco and alcohol control; reducing salt and sugar intake; replacing trans-fats in foods with polyunsaturated fats; promoting public awareness about diet; and physical activity(6). Thus, among risk factors, the role of SFA reduction and serum LDL-cholesterol reduction are listed but not specifically mentioned as priority tasks.

We agree with these reports in their emphasis on the multiple risk factors and urgency for action. Our main concern, however, is to emphasise the importance of lowering SFA intakes to reduce blood LDL-cholesterol levels at a time when there are tendencies to downplay the importance of SFA(Reference Siri-Tarino, Sun and Hu1, Reference Micha and Mozaffarian7, Reference Astrup, Dyerberg and Elwood8). There have been substantial reductions in mortality from CVD in North America, Western Europe and Australasia over the last 30 years that reflect successful national public health policies to reduce the intakes of SFA, in addition to promoting smoking cessation and controlling blood pressure. Nevertheless, excessive intakes of SFA remain a major public health problem not only in affluent countries but are also now a major and increasing problem in low- and middle-income countries where 80 % of cardiovascular deaths occur.

Recent critics of the role of SFA have questioned the rigour of the early dietary trials of CVD prevention and questioned current public health policy on limiting the intake of SFA(Reference Astrup, Dyerberg and Elwood8); they suggest that more attention should be paid to increased intake of PUFA(Reference Mozaffarian, Micha and Wallace9). The trials demonstrate unequivocally that replacing SFA, largely from dairy and meat fats (but in the Leren trial also with some TFA), by PUFA reduces serum cholesterol levels and CHD risk(Reference Mozaffarian, Micha and Wallace9). That replacement of SFA by a variety of carbohydrate-containing foods also reduces CHD risk may be inferred from ecological studies, e.g. in Finland. CHD was also almost non-existent in rural China when mean cholesterol levels were approximately 3·5 mmol/l (1350 mg/l), with total fat intakes only about 15 % of energy and extremely low intakes of SFA(Reference Campbell, Parpia and Chen10, Reference Campbell and Chen11). These observations, replicated in many other countries, should not be ignored even if meta-analyses of prospective cohort studies suggest no independent associations of SFA intake with CHD risk(Reference Siri-Tarino, Sun and Hu2). The null results of the latter studies(Reference Siri-Tarino, Sun and Hu2) probably reflect measurement error, residual confounding, over-adjustment by covariates on the causal pathway and large variations in plasma cholesterol compared to variations in intake of dietary fat(Reference Kromhout, Geleijnse and Menotti3, Reference Stamler12Reference Fewell, Davey Smith and Sterne15). The role of SFA risks may also be overlooked, given the strong emphasis on TFA(Reference Mozaffarian, Aro and Willett16) and the incorrect proposition that the CHD epidemic in affluent societies has been primarily linked to a high consumption of TFA(Reference Stender and Dyerberg17).

Atherosclerosis is the pathological basis of CHD and other CVD. Extensive research over the last century has established that atherosclerosis is a complex process in which disturbed lipoprotein metabolism plays a critical role. Elevated levels of apo B containing cholesterol-rich lipoprotein particles drive the development of atherosclerosis in humans and in experimental animals, even in the absence of other known risk factors(Reference Glass and Witztum18). Accumulation of these LDL particles in the intima and binding of apo B to the extracellular proteoglycans appear to be the initial step in atherosclerosis(Reference Tabas, Williams and Borén19) with further triggering of inflammatory reactions(Reference Kaptoge and Di Angelantonio20). The amount and type of dietary fat to a large extent determines the number of circulating LDL particles and blood levels of total cholesterol. Moreover, SFA with 12–16 carbon atoms are the most potent LDL- or total-cholesterol-raising fatty acids(Reference Mensink, Zock and Kester21).

Recently, several studies have quantified the proportion of the decline in CHD mortality that is explained by changes in risk factors and treatment. Ford & Capewell estimated that almost half to three-quarters of the lower CHD mortality in the USA may be explained by risk factor reduction, with the remainder being attributed to more effective treatment for dyslipidaemia and hypertension(Reference Ford and Capewell22). Further studies in European populations also suggest that reduction in CVD risk factors is more important than improvements in treatment. The relative importance of the different risk factors in different populations will of course depend on the magnitude of change. In the USA, 24 % of the decline in CHD mortality has been ascribed to a reduction in total cholesterol(Reference Ford and Capewell22). However, in the Nordic countries where national preventive programmes have been conducted since the early 1960s, dietary changes with a reduction in population mean total cholesterol explain a far greater proportion of the decline in CHD mortality.

Finland has experienced an over-80 % fall in CHD mortality due to a large extent to the reduction in total cholesterol(Reference Laatikainen, Critchley and Vartiainen23); lower blood pressure and less smoking in men amplify this cholesterol-lowering benefit(Reference Laatikainen, Critchley and Vartiainen23, Reference Vartiainen, Laatikainen and Peltonen24). In Finland, a reduced SFA intake was the main reason for the fall in blood cholesterol caused by a massive decline in dairy fat consumption(Reference Valsta, Tapanainen and Sundvall25). The intake of TFA from partially hydrogenated oils has always been low in Finland; so its removal cannot explain either the reduction in blood cholesterol or the impressive fall in CHD mortality(Reference Valsta, Tapanainen and Sundvall25). By contrast, in Norway, the consumption of TFA was high and its removal may explain part of the decline in national cholesterol levels. However, the major part of the reduction was explained by reduced SFA intake(Reference Pedersen, Tverdal and Kirkhus26). Similar analyses have recently been reported for Iceland where lowering of cholesterol accounted for 32 % of the CHD mortality reduction(Reference Aspelund, Gudnason and Magnusdottir27). In all these Nordic populations, a modest initial increase in PUFA intake (which has, however, been stable for the last 25 years at 5–6 % of energy) may have contributed to the early but not the later fall in blood cholesterol.

These examples illustrate the substantial benefits of reducing intake of SFA. While we would strongly endorse the high priority given to smoking and salt reduction made elsewhere(Reference Beaglehole, Bonita and Adams4), we would consider the evidence for a reduction in intake of SFA by reducing intake of animal- and high-SFA-containing vegetable fat sources to be even stronger than when this policy was introduced by the WHO in the early 1980s. It should therefore also be included in the highest priority category. We approve of the relatively simple and cost-effective measures for the food industry, highlighted by the reports proposing removing salt and most TFA from the food supply. However, TFA removal must not sidetrack us from the very substantial quantitative importance of reducing SFA from the food supply.

SFA reduction has proven exceptionally cost-effective; so governments should not be distracted by industrial pressure or problematic new analyses of prospective studies to change dietary policies which in affluent societies have been remarkably successful in limiting CVD before the role of TFA became clear. The WHO should continue to support the member states based on its earlier successful policy about saturated fats in order to combat the burden of CVD now arising in poorer countries as saturated fat intakes escalate.


J. I. P. is member of the scientific advisory board of the food company Mills ASA, Oslo, Norway. I. E. is the current president of the International Union of Nutritional Sciences (IUNS); IUNS has signed a time-limited agreement on scientific cooperation with Unilever. M. R. receives funding for his research group including his own salary from the British Heart Foundation. P. M. K. E. is a member of the Scientific Advisory Board for Unilever, California Walnut Commission, MonaVie, Campbell Soup Company, Abunda and receives research support from The Peanut Institute, General Mills, Almond Board of California, Hershey Foods, National Cattleman's Beef Association and Hass Avocado Board. R. P. M. received unrestricted research grants from the Dutch Dairy Association, Raisio Nutrition Limited, Malaysian Palm Oil Board, from the TIFN (Top Institute for Food and Nutrition) and Sime Darby Research Sdn Bhd for studies on dietary effects on risk markers related to the metabolic syndrome. All other authors declare that they have no conflicts of interest. The first two authors drafted the manuscript. All co-authors criticised and commented on the content and contributed to the final version.


1 Siri-Tarino, PW, Sun, Q, Hu, FB, et al. (2010) Saturated fat, carbohydrate, and cardiovascular disease. Am J Clin Nutr 91, 502509.Google Scholar
2 Siri-Tarino, PW, Sun, Q, Hu, FB, et al. (2010) Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr 91, 535546.Google Scholar
3 Kromhout, D, Geleijnse, JM, Menotti, A, et al. (2011) The confusion about dietary fatty acids recommendations for CHD prevention. Br J Nutr 106, 627632.Google Scholar
4 Beaglehole, R, Bonita, R, Adams, C, et al. (2011) Priority actions for the non-communicable disease crisis. Lancet 378, 566567.Google Scholar
7 Micha, R & Mozaffarian, D (2010) Saturated fat and cardiometabolic risk factors, coronary heart disease, stroke, and diabetes: a fresh look at the evidence. Lipids 45, 893905.Google Scholar
8 Astrup, A, Dyerberg, J, Elwood, P, et al. (2010) The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010? Am J Clin Nutr 93, 684688.Google Scholar
9 Mozaffarian, D, Micha, R & Wallace, S (2010) Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med 7, e1000252.Google Scholar
10 Campbell, TC, Parpia, B & Chen, J (1998) Diet, lifestyle, and the etiology of coronary artery disease: the Cornell China study. Am J Cardiol 82, 18T21T.Google Scholar
11 Campbell, TC & Chen, J (1999) Energy balance: interpretation of data from rural China. Toxicol Sci 52, Suppl. 2, 8794.Google Scholar
12 Stamler, J (2010) Diet-heart: a problematic revisit. Am J Clin Nutr 91, 497499.Google Scholar
13 Scarborough, P, Rayner, M, van Dis, I, et al. (2010) Meta-analysis of effect of saturated fat intake on cardiovascular disease: over adjustment obscures true associations. Am J Clin Nutr 92, 458459.Google Scholar
14 Katan, MB, Brouwer, IA, Clarke, R, et al. (2010) Saturated fat and heart disease. Am J Clin Nutr 92, 459460.Google Scholar
15 Fewell, Z, Davey Smith, G & Sterne, JA (2007) The impact of residual and unmeasured confounding in epidemiologic studies: a simulation study. Am J Epidemiol 166, 646655.Google Scholar
16 Mozaffarian, D, Aro, D & Willett, WC (2009) Health effects of trans-fatty acids: experimental and observational evidence. Eur J Clin Nutr 63, S5S21.Google Scholar
17 Stender, S & Dyerberg, J (2004) Influence of trans fatty acids on health. Ann Nutr Metab 48, 6166.Google Scholar
18 Glass, CK & Witztum, JL (2001) Atherosclerosis: the road ahead. Cell 104, 503516.Google Scholar
19 Tabas, I, Williams, KJ & Borén, J (2007) Subendothelial lipoprotein retention as the initiating process in atherosclerosis. Update and therapeutic implications. Circulation 116, 18321844.Google Scholar
20 Emerging Risk Factors Collaboration Kaptoge, S, Di Angelantonio, E, et al. (2010) C-reactive protein concentration and risk of coronary heart disease, stroke, and mortality: an individual participant meta-analysis. Lancet 375, 132140.Google Scholar
21 Mensink, RP, Zock, PL, Kester, ADM, et al. (2003) Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. Am J Clin Nutr 77, 11461155.Google Scholar
22 Ford, ES & Capewell, S (2011) Proportion of the decline in cardiovascular mortality disease due to prevention versus treatment: public health versus clinical care. Annu Rev Public Health 32, 522.Google Scholar
23 Laatikainen, T, Critchley, J, Vartiainen, E, et al. (2005) Explaining the decline in coronary heart disease mortality in Finland between 1982 and 1997. Am J Epidemiol 162, 764773.Google Scholar
24 Vartiainen, E, Laatikainen, T, Peltonen, M, et al. (2010) Thirty-five-year trends in cardiovascular risk factors in Finland. Int J Epidemiol 39, 504518.Google Scholar
25 Valsta, LM, Tapanainen, H, Sundvall, J, et al. (2010) Explaining the 25-year decline of serum cholesterol by dietary changes and use of lipid-lowering medication in Finland. Public Health Nutr 13, 932938.Google Scholar
26 Pedersen, JI, Tverdal, A & Kirkhus, B (2004) Diet changes and the rise and fall of cardiovascular disease mortality in Norway. Tidsskr Nor Laegeforen 124, 15321536.Google Scholar
27 Aspelund, T, Gudnason, V, Magnusdottir, BT, et al. (2010) Analysing the large decline in coronary heart disease mortality in the icelandic population aged 25–74 between the years 1981 and 2006. PLoS ONE 5, e13957.Google Scholar