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

Abstract

There are still many open questions regarding the modulation of 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]. Amongst dietary fats, extra-virgin olive oil (EVOO) is a key 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 established whether meals rich in EVOO could favourably affect 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 compounds on postprandial markers related to thrombogenesis and fibrinolysis, and triglycerides (TG) in healthy subjects. ROO was obtained by physical refining of EVOO and had no detected minor compounds with antioxidant activity, whereas the contents (in mg kg−1) of carotenoids, tocopherols and polyphenols in EVOO were 22, 350 and 1125, respectively. The fatty acid composition and TG molecular species were identical for EVOO and ROO. Fourteen healthy male non-smokers [age (mean ± SD) 27.41 ± 7.20 years; BMI (kg m−2) 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, within-subject 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−2 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 long- and 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 activation of extrinsic coagulation pathway and attenuation of profibrinolytic processes associated with increased postprandial lipemia, which is probably modulated by the nature of dietary fatty acids [1]. Here, we show that the postprandial hemostatic system can also be modulated by non-fatty acid compounds with antioxidant activity from EVOO. Oxidative stress, which appears to be common during postprandial lipemia [2], is a result of the release of reactive oxygen species that activate several intracellular responses, including the nuclear factor kappa B (NFκB) with the subsequent upregulation of target genes. Notably, EVOO does not elicit postprandial activation of NFκB in human monocytes as do other fats [8]. The present study is the first to establish a role for antioxidant minor compounds from EVOO in the regulation of the postprandial hemostatic system. These novel effects of EVOO mediated by antioxidant minor compounds complement the role of oleic acid in terms of cardioprotective effects. We conclude that the consumption of EVOO could postprandially improve states of hypercoagulability. J. Villar (Service of Internal Medicine, Hospitales Universitarios Virgen del Rocío, Seville, Spain) should be considered as an equal author participating as a clinical investigator. This study was supported by grants from MCYT (AGL2001-0584 and AGL2004-04958).