Role of Different Dietary Saturated Fatty Acids for Cardiometabolic Risk

David Iggman; Ulf Risérus

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

Biomarkers of SFA Intake

Dietary assessments (e.g., food frequency questionnaires [FFQ]), 24-h recalls, and food records all have limitations and both prospective cohort studies and randomized controlled trials (RCTs) often benefit from utilizing biomarkers as an alternative, or as a validation of dietary compliance. For total SFA, the associations between tissue or circulating fatty acids and dietary intake are diverse and often weak,^[1,2] possibly reflecting endogenous metabolism. Nevertheless, pentadecanoic (15:0) and margaric (17:0) acid, which cannot be synthesized in humans, have been considered to be valid biomarkers for dairy intake^[1,2] but 15:0 and 17:0 are also present in lamb, beef, venison and fatty fish. Thus, 17:0 in plasma phospholipids may also be a marker of a healthy diet including fish consumption since these 'milk fat biomarkers' are correlated with fish intake at an ecological level.^[3] Additional support for this possibility was derived from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort where high intake of dairy products was strongly associated with eicosapentaenoic acid plasma levels.^[3] Thus, the link between dairy fat, plasma fatty acid markers (i.e., 15:0 and 17:0) and cardiometabolic disease risk clearly requires more study to understand the associations observed in epidemiological studies.

Adipose tissue 14:0 has also been considered a valid biomarker for long-term dairy intake,^[4,5] although it can be synthesized endogenously as well.^[6] Plasma 16:0 levels increase with dietary intake of SFA, although not as much as expected and not in a dose–response manner, probably partly due to conversion of 16:0 to 16:1 by steaoryl-CoA-desaturase (SCD).^[7] Thus, the ratio of 16:1 to 16:0 may be used as a marker of dietary 16:0 intake.^[8] It should be noted that LC SFA levels may also be determined by the individuals' rate of de novo lipogenesis, desaturation and elongation processes, independent of dietary macronutrients. Thus, metabolic and/or genetic factors may explain some associations with metabolic risk. However, as circulating and tissue levels of 14:0, 16:0 and 18:0 can be affected by high intakes of carbohydrate or alcohol, for example, the relationships with dietary SFA intake are less clear-cut than for 15:0 and 17:0.^[1]

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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.