This review reappraises dietary advice to reduce and replace SFA for the prevention of CVD. In the 1970s, SFA accounted for about 18% UK food energy, by 2001 it had fallen to 13% and continues to be above the <11% target. Compared with carbohydrates, C₁₂–C₁₆ SFA raise serum total cholesterol (TC), LDL-cholesterol (LDL-C) and HDL-cholesterol (HDL-C) without affecting the TC:HDL-C ratio; other SFA have neutral effects on the fasting lipid profile. Replacing 3% dietary SFA with MUFA or PUFA lowers LDL-C by 2% and TC:HDL-C ratio by 0·03. No other specific adverse effects of SFA compared with MUFA on risk CVD factors have been proven. Meta-analyses of prospective cohort studies report the relative risks (95% CI) of high v. low intakes of SFA to be 1·07 (0·96, 1·19) for CHD, 0·81 (0·62, 1·05) for stroke and 1·00 (0·89, 1·11) for CVD mortality and were not statistically significant. Exchanging 5% energy SFA for PUFA or carbohydrates found hazard ratios (95% CI) for CHD death to be 26% (−23, −3) and 4% (−18, 12; NS) lower, respectively. Meta-analysis of randomised controlled trials with clinical endpoints reports mean reductions (95% CI) of 14% (4, 23) in CHD incidence and 6% (−25, 4; NS) in mortality in trials, where SFA was lowered by decreasing and/or modifying dietary fat. In conclusion, SFA intakes are now close to guideline amounts and further reductions may only have a minor impact on CVD.