ABSTRACT
The proposition that dietary SFAs should be restricted to the maximal extent possible (e.g., to achieve approximately half of current consumption) is based primarily on observational and clinical trial data that are interpreted as indicating a benefit of such limitation on cardiovascular disease (CVD) risk. Further support is believed to derive from the capacity of SFAs to raise LDL cholesterol, and the evidence that LDL-cholesterol lowering reduces CVD incidence. Despite their apparent merit, these arguments are flawed. In fact, although it is possible that dietary intake of SFAs has a causal role in CVD, the evidence to support this contention is inconclusive. Moreover, other considerations argue against a guideline focused primarily on limiting SFA intake, including the heterogeneity of individual SFAs, the likelihood of clinically meaningful interindividual variation in response to SFA reduction, the potential for unintended health consequences of population-wide promotion of severe restriction, and the critical differences in health impacts among individual SFA-containing foods.
Public health guidelines should recommend reducing saturated fat consumption as much as possible: NO
