title: The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010?
abstract: Current dietary recommendations advise reducing the intake of saturated fatty acids (SFAs) to reduce coronary heart disease (CHD) risk, but recent findings question the role of SFAs. This expert panel reviewed the evidence and reached the following conclusions: the evidence from epidemiologic, clinical, and mechanistic studies is consistent in finding that the risk of CHD is reduced when SFAs are replaced with polyunsaturated fatty acids (PUFAs). In populations who consume a Western diet, the replacement of 1% of energy from SFAs with PUFAs lowers LDL cholesterol and is likely to produce a reduction in CHD incidence of ≥2-3%. No clear benefit of substituting carbohydrates for SFAs has been shown, although there might be a benefit if the carbohydrate is unrefined and has a low glycemic index. Insufficient evidence exists to judge the effect on CHD risk of replacing SFAs with MUFAs. No clear association between SFA intake relative to refined carbohydrates and the risk of insulin resistance and diabetes has been shown. The effect of diet on a single biomarker is insufficient evidence to assess CHD risk. The combination of multiple biomarkers and the use of clinical endpoints could help substantiate the effects on CHD. Furthermore, the effect of particular foods on CHD cannot be predicted solely by their content of total SFAs because individual SFAs may have different cardiovascular effects and major SFA food sources contain other constituents that could influence CHD risk. Research is needed to clarify the role of SFAs compared with specific forms of carbohydrates in CHD risk and to compare specific foods with appropriate alternatives.
authors.affiliation: Department of Human Nutrition, Faculty of Life Sciences, University of Copenhagen, Denmark.
authors.forename: Arne
authors.initials: A
authors.lastname: Astrup
authors.forename: Jørn
authors.initials: J
authors.lastname: Dyerberg
authors.forename: Peter
authors.initials: P
authors.lastname: Elwood
authors.forename: Kjeld
authors.initials: K
authors.lastname: Hermansen
authors.forename: Frank B
authors.initials: FB
authors.lastname: Hu
authors.forename: Marianne Uhre
authors.initials: MU
authors.lastname: Jakobsen
authors.forename: Frans J
authors.initials: FJ
authors.lastname: Kok
authors.forename: Ronald M
authors.initials: RM
authors.lastname: Krauss
authors.forename: Jean Michel
authors.initials: JM
authors.lastname: Lecerf
authors.forename: Philippe
authors.initials: P
authors.lastname: LeGrand
authors.forename: Paul
authors.initials: P
authors.lastname: Nestel
authors.forename: Ulf
authors.initials: U
authors.lastname: Risérus
authors.forename: Tom
authors.initials: T
authors.lastname: Sanders
authors.forename: Andrew
authors.initials: A
authors.lastname: Sinclair
authors.forename: Steen
authors.initials: S
authors.lastname: Stender
authors.forename: Tine
authors.initials: T
authors.lastname: Tholstrup
authors.forename: Walter C
authors.initials: WC
authors.lastname: Willett
mesh_terms: D002784:Cholesterol / Q000097:blood; D003327:Coronary Disease / Q000097:blood / Q000209:etiology / Q000517:prevention & control*; D003920:Diabetes Mellitus; D004040:Dietary Carbohydrates / Q000494:pharmacology; D004041:Dietary Fats / Q000008:administration & dosage*; D005227:Fatty Acids / Q000009:adverse effects*; D005231:Fatty Acids, Unsaturated / Q000008:administration & dosage*; D006801:Humans; D007333:Insulin Resistance
chemical_list: D004040:Dietary Carbohydrates; D004041:Dietary Fats; D005227:Fatty Acids; D005231:Fatty Acids, Unsaturated; D002784:Cholesterol