Extra‐virgin vs. refined olive oil on postprandial hemostatic markers in healthy subjects

There are stillmanyopenquestions regarding themodulationof the hemostatic system by dietary fats in the postprandial state [1]. However, rapidly accumulating evidence links the ingestion of a high-fat meal to oxidative stress [2], which has also recently emerged as a determinant for thrombogenesis and fibrinolysis [3,4]. Amongstdietary fats, extra-virginoliveoil (EVOO) isakey contributor to the cardiovascular and thrombotic disease preventive properties attributed to the Mediterranean diet [5]. As antioxidants are common in EVOO, it remains to be establishedwhethermeals rich inEVOOcould favourablyaffect the postprandial hemostatic system, independently of the effects usually associated with dietary fatty acids. The aim of this study was to evaluate the effects of olive oil with (EVOO) and without (refined olive oil, ROO) antioxidant minor compoundsonpostprandialmarkers related to thrombogenesis and fibrinolysis, and triglycerides (TG) in healthy subjects. ROOwas obtained by physical refining of EVOO and had no detected minor compounds with antioxidant activity, whereas the contents (in mg kg) of carotenoids, tocopherols and polyphenols in EVOOwere 22, 350 and 1125, respectively. The fatty acid composition and TG molecular species were identical for EVOO and ROO. Fourteen healthy male nonsmokers [age (mean ± SD) 27.41 ± 7.20 years; BMI (kg m) 23.92 ± 1.91] were recruited by advertising. Subjects were required to have no evidence of established coronary heart disease, renal impairment, hypothyroidism or liver dysfunction. Prior to the study, all subjects provided informed consent using Human Clinic Commission and Ethic Committee approved protocols. The design of the study was, randomized, withinsubject crossover and blinded investigators. Subjects had an adaptation 1-week lead-in period that consisted of a NCEP Step I diet with the corresponding fat (EVOO or ROO), which supplied 9623 kJ daily and identical distribution of carbohydrates (49%), proteins (13%), fats (38%), cholesterol (184 mg) and fibers (23 g). Subjects were then sampled after a 12-h overnight fast (baseline values), immediately, they were administered a fat-rich meal consisting of the corresponding dietary fat (EVOO or ROO, 50 g m body surface area) mixed with one portion of plain pasta (50 g), one slice of brown bread (28 g) and one skimmed yogurt. Blood samples were drawn every 1 h for a total of 8 h (postprandial values). Plasma levels of TG, tissue factor, fibrinogen, tissue-type plasminogen activator (t-PA) antigen and plasminogen activator inhibitor-1 (PAI-1) antigen were measured. For all parameters, mean and standard deviations were calculated. Differences were evaluated using one-factor repeated-measures ANOVA. A Bonferroni correction was used for the post hoc detection of significant pairwise differences. The net incremental area under the curve (netAUC) was calculated by the trapezoidal method. All P-values are two-sided, and the designated level of significance was P < 0.05. Our findings are depicted in Table 1. We found that, after 1-week lead-in dietary period, EVOO and ROO did not change fasting plasma levels of TG, TF, fibrinogen, t-PA and PAI-1. The TG postprandial responses to EVOO and ROO meals were also similar. However, the netAUC for hemostatic markers were significantly lower after the EVOO meal compared with the ROO meal. Our data are in line with longand short-term and postprandial studies showing cardiovascular benefits and protection of endogenous antioxidant defences by EVOO [5– 7]. In the postprandial state, TG-rich lipoproteins support the