Effects on Cardiovascular Disease
Overall SFA Intake
Recent systematic reviews on prospective cohort studies have questioned the relationship between dietary SFA and CVD.[78,79] Coronary heart disease (CHD) has also not been directly associated with SFA intake, although is associated with a western dietary pattern, high in SFA-rich foods. A western dietary pattern (highest quartile of intake) has also been associated with an increased odds ratio for myocardial infarction (MI) in a large case–control study. In addition, observational studies indicate that overall SFA intake does not increase the risk for stroke. Overall, epidemiological evidence for a link between SFA and CVD is surprisingly weak, possibly indicating that in a western diet reductions in overall SFA intake may be accompanied by increases in refined carbohydrates, which could thus obscure these relationships. By contrast, the results from the North Karelia study demonstrate that dietary change (i.e., reduction in SFA), mainly by replacing butter with margarine, was the main explanation for the decrease in serum cholesterol and seemingly a significant part of the substantial reduction of CVD during the same time period.
Replacing SFA with PUFA
In a pooled analysis of prospective cohort studies, where not only SFA intakes but also the replacement nutrients were considered, replacement with PUFA was associated with decreased CHD risk, and there is some recent evidence to suggest that for replacement with carbohydrate, the type of carbohydrate is of high importance.[83,84] Although few RCTs of sufficient size and duration have been performed, eight eligible trials were recently included in a meta-analysis, with concordant results (i.e., exchanging SFA with PUFA lowers risk of MI and cardiovascular mortality). Interestingly, this is also perfectly in line with the predicted effects from change in TC:HDL-C (Figure 3). Taken together, there is rather convincing evidence for decreased CHD risk when replacing SFA (as a group) with PUFA.
Effect on coronary heart disease risk when 5% of energy intake of saturated fatty acids is replaced with polyunsaturated fatty acids.
RCT: Randomized controlled trial.
Data taken from [50,82,85].
Individual SFA: Observational Data
Owing to strong intercorrelations between SFA, it is difficult to differentiate individual SFA in cohort studies with disease end points. In the large Nurses' Health Study of 80,082 healthy women this was, however, attempted with available data from FFQs. In this cohort, intakes of 12:0–18:0 were collectively and separately (12:0 and 14:0 were combined due to small amounts and similar food sources) associated with CHD risk after 14 years. There was no evidence that 18:0 was less associated with CHD risk than other LC SFA. Indeed, the relative risk for 18:0 was increased by 30% at 4% of energy intake. In this population, LC SFA were predominantly consumed from meat and dairy food sources. The SC and MC SFA 4:0–10:0 (mostly from dairy) were not associated with increased risk when considered jointly.
Some prospective cohort studies have investigated associations between circulating or tissue SFA and CVD. In a Swedish cohort, 14:0 and 16:0 in serum cholesterol esters independently predicted cardiovascular and all-cause mortality over 33 years. For 14:0, this could reflect dairy intake. For 16:0, this was likely associated with SFA intake, as a low-fat/high-carbohydrate diet was unusual in this population. No increase in CVD incidence, CVD mortality or total mortality was observed for 18:0. In a Finnish cohort, both dietary and serum SFA:PUFA ratio was associated with cardiovascular and all-cause mortality, but results on individual SFA were not reported.
Clin Lipidology. 2011;6(2):209-223. © 2011 Future Medicine Ltd.