Role of Different Dietary Saturated Fatty Acids for Cardiometabolic Risk

David Iggman; Ulf Risérus


Clin Lipidology. 2011;6(2):209-223. 

In This Article

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]