In epidemiological studies, dairy food consumption has been associated with minimal effect or decreased risk of some cardiometabolic diseases (CMD). However, current methods of dietary assessment do not provide objective and accurate measures of food intakes. Thus, the identification of valid and reliable biomarkers of dairy product intake is an important challenge to best determine the relationship between dairy consumption and health status. This review investigated potential biomarkers of dairy fat consumption, such as odd-chain, trans- and branched-chain fatty acids (FA), which may improve the assessment of full-fat dairy product consumption. Overall, the current use of serum/plasma FA as biomarkers of dairy fat consumption is mostly based on observational evidence, with a lack of well-controlled, dose–response intervention studies to accurately assess the strength of the relationship. Circulating odd-chain SFA and trans-palmitoleic acid are increasingly studied in relation to CMD risk and seem to be consistently associated with a reduced risk of type 2 diabetes in prospective cohort studies. However, associations with CVD are less clear. Overall, adding less studied FA such as vaccenic and phytanic acids to the current available evidence may provide a more complete assessment of dairy fat intake and minimise potential confounding from endogenous synthesis. Finally, the current evidence base on the direct effect of dairy fatty acids on established biomarkers of CMD risk (e.g. fasting lipid profiles and markers of glycaemic control) mostly derives from cross-sectional, animal and in vitro studies and should be strengthened by well-controlled human intervention studies.

Dairy fat is rich in SFA such as palmitic acid (16:0) but low in linoleic acid (18:2n-6). The natural carbon 13 enrichment (δ13C) of 16:0 is higher in dairy fat than in most of the food supply. In adults, serum levels of pentadecanoic acid (15:0) and heptadecanoic acid (17:0) are recognised as biomarkers of dairy intake. In adolescents, no study has evaluated serum fatty acid levels or δ13C in response to chronic dairy consumption. The objectives of this study were to evaluate whether increased dairy product consumption can modulate (1) serum fatty acid levels and (2) 16:0 δ13C in adolescents with overweight/obesity who followed a 12-week weight management programme. This secondary analysis of a randomised control trial included two groups of adolescent females: recommended dairy (RDa; n 23) and low dairy (LDa; n 23). The RDa group was given 4 servings/d of dairy products while the LDa group maintained dairy intakes at ≤ 2 servings/d. Blood was sampled before and after the intervention. Lipids were extracted and separated, and fatty acids were quantified by GC. Isotope ratio MS was used to assess 16:0 δ13C. There were no group differences on serum changes of 15:0 or 17:0. Within TAG, 18:2n-6 was lowered by 7·4 % only in the RDa group (P = 0·040). The difference in delta 16:0 δ13C between the LDa and RDa groups did not reach statistical significance (P = 0·070). Reductions in serum 18:2n-6 by dairy consumption could have positive health implications, but more studies are needed to confirm this assertion.

Milk fat is high in saturated fatty acids (SFA) and high intakes of SFA are associated with cardiovascular diseases. The aim of the present study was to prospectively evaluate the potential risk of a first-ever acute myocardial infarction (AMI) in relation to the estimated milk-fat intake, reflected as the proportions of pentadecanoic acid (15:0) and heptadecanoic acid (17:0) in serum lipid esters. This was evaluated in a study population selected within the Västerbotten Intervention Program and the northern Sweden ‘Monitoring of Trends and Determinants in Cardiovascular disease’ survey populations. A prospective case–control design was used. The proportions of the biomarkers were lower in the cases (n78) than in the controls (n156), who were matched for age, sex, sampling time and geographical region. The standardised odds ratios of becoming an AMI case were between 0·7 and 0·8 for the biomarkers. The proportions of 15:0 and 17:0 in serum phospholipids were significantly and negatively correlated to serum concentrations of plasminogen activator inhibitor-1, tissue-type plasminogen activator, triacylglycerols, insulin, specific insulin, pro-insulin and leptin (all P<0·0001), suggesting a negative relationship to the insulin-resistance syndrome and the risk of CHD. Adjustment for BMI did not materially change the relationships. Although there seems to be a negative association between milk-fat intake as mirrored by the proportions of 15:0 and 17:0 in serum lipid esters and a first-ever AMI, adjustment for clinical risk factors removed this relationship.