Role of Different Dietary Saturated Fatty Acids for Cardiometabolic Risk

David Iggman; Ulf Risérus

Clin Lipidology. 2011;6(2):209-223.

Conclusion

It seems clear from clinical and recent observational data that replacing total SFA with PUFA could reduce the risk of CVD. The role of overall SFA intake for cardiometabolic risk has been recently questioned, mainly based on observational data from meta-analyses. Although caveats exist, finite amounts of SFA, when considered separately, may have some beneficial health effects. Healthy food choices can probably include modest amounts of SFA, and low-fat dairy products seem like a prudent food choice in this aspect. The role of high-fat dairy in cardiometabolic diseases is an interesting topic that needs further study in controlled interventions. To regard SFA as a single, homogenous group has probably been too much of an oversimplification, although differences in cardiometabolic risk appear greater between food groups and sources than between separate LC SFA. The current recommendations still appear sound and scientifically well grounded, not only because lowering LDL-C is one of the most established ways to lower cardiovascular risk, but also since the overall available data suggest a health benefit by limiting total SFA (in practice to limit excessive intakes of foodstuffs high in 16:0, 18:0, and 14:0) for replacement with vegetable MUFA and PUFA. SFA should not be replaced with refined (high-GI) carbohydrates. The different cardiometabolic effects of individual SFA are summarized in Figure 5. Based on the current available evidence, it is not possible to give dietary recommendations solely based on the content of individual SFA. Strictly controlled short-term and longer-term intervention studies are needed to test the various associations reported in observational studies.

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Figure 5.

Common food sources of, and possible cardiometabolic effects from, individual dietary saturated fatty acids: some evidence derived from biomarker studies.
(+): Weak evidence; +: Moderate evidence; ++: Clear evidence; CHD: Coronary heart disease; SFA: Saturated fatty acid.

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Executive Summary

Various metabolic effects of separate saturated fatty acids

Most dietary saturated fatty acids (SFA) are long chain 14:0–18:0.
Short-chain SFA may have a role in prevention of cancer and inflammation of the large intestine, medium-chain SFA may reduce adiposity, 12:0 may have antimicrobial properties, and 14:0 and 16:0 may have various regulatory functions in the cell via protein fatty acid acetylation.

Effects on cardiovascular risk factors

Long-chain SFA increase total cholesterol and LDL-C, except 18:0, which is neutral. Lauric acid (12:0) is the most potent SFA for raising cholesterol, but also reduces the total cholesterol:HDL-C ratio.
Some studies suggest an atherogenic and prothrombotic effect of 18:0, but not consistently. Whether 18:0 is preferable to 16:0 as a substitute for trans -fatty acids is not clear, but according to effects on blood lipids solely, this may be true.

Effects on cardiovascular disease

Overall, SFA consumption has not been clearly demonstrated to increase cardiovascular disease (CVD) in epidemiological studies using self-reported questionnaires, but the data may be weakened by reporting bias and residual confounding.
Exchanging SFA with polyunsaturated fatty acids decreases CVD risk and mortality.
Studies on individual SFA are limited but one large cohort study indicates an increased risk of coronary heart disease for 12:0, 14:0, 16:0 and 18:0, and biomarker studies suggest detrimental effects from circulating and tissue 16:0 content.

Effects on insulin resistance & diabetes

Long-chain SFA 16:0 and 14:0 seem detrimental to β-cell function in vitro and in animal experiments.
Biomarker studies have demonstrated associations between circulating 14:0, 16:0, and 18:0 and diabetes incidence, although this may only partly reflect dietary SFA intake.
Circulating 15:0 is inversely associated with diabetes incidence and may reflect dairy food intake, but also a 'healthy lifestyle', or other factors not captured due to residual confounding.

Dairy intake & cardiometabolic risk

High-fat dairy products raise LDL-C, and although controlled studies where dairy fat has been a major SFA source indicate increased CVD risk compared with polyunsaturated fatty acids, little epidemiological evidence exists for detrimental effects of dairy intake on disease end points, despite its SFA and trans -fatty acid content.
Milk fat biomarkers 15:0 and 17:0 have been inversely associated with insulin resistance and risk for myocardial infarction, but whether such relationships are explained by SFA-specific effects of dairy foods is unknown.
Long-term controlled intervention studies using high-fat dairy foods versus other types of fats are needed to confirm the epidemiological associations.
It will, however, be challenging to separate any potential health effect of dairy fat between the different individual SFA, as well as from other micronutrients and protein found in dairy products.