Journal Name:
Am. J. Clin. Nutr.
Article Title:
Chronic dietary fat intake modifies the postprandial response of hemostatic markers to a single fatty test meal.
Date Written:
2008
Volume:
87
Number:
2
Page:
317
Author(s):
Delgado-Lista, J.; Lopez-Miranda, J.; Cortés, B.; Perez-Martinez, P; Lozano, A.; Gomez-Luna, R.; Gomez, P.; Gomez, M.J.; Criado, J.; Fuentes, F.; Perez-Jimenez, F.
Article:
Hemostasis is the process that ensures the integrity of the vascular system. Many factors can affect hemostasis including intrinsic factors, mainly genetic, and extrinsic factors such as diet. A prothrombotic state is the predominant situation of Western populations because of their dietary patterns rich in saturated fats (SFAs). The lower incidence of cardiovascular disease death associated with adherence to diets which in monounsaturated (MUFA) and omega 3 fatty acids, such as found in canola oil, has led to the study of the underlying causes. It has been shown that during the hours after a fat-enriched meal, very important changes take place in the hemostatic system that turn it into a prothrombotic environment. However, the influence of various dietary patterns on both chronic and acute effects on hemostasis and the background effect of diet in postprandial activation have not been studied.
In this 2-stage study, 20 healthy young men were subjected to a chronic (4 week) dietary intervention with 3 dietary models and the effects on fasting coagulation markers were measured. This stage was followed by a fatty test meal with the same fat composition for the 3 dietary groups, with the aim of assessing postprandial effects on coagulation markers. The diets were rich in monounsaturated fatty acids (MUFAs), saturated fatty acids (SFAs), and carbohydrates plus omega 3 fatty acids (CHO/N3). Fasting and postprandial hemostatic factors (factor VII coagulant activity, plasminogen activator inhibitor-1, tissue-type plasminogen activator, d-dimer, and thromboxane B(2)) were measured. Test meals for the postprandial measures were based on butter, virgin olive oil, and walnuts for the SFA, MUFA, and CHO/N3 diets, respectively.
The results indicated that the consumption of a fatty meal produces a postprandial prothrombotic hemostatic state (increase in thromboxanes and D-dimer and decrease in tPA, irrespective of the type of fat ingested), although this phenomenon was attenuated if the fat was rich in olive oil (rich in MUFAs) or walnuts (rich in omega 3 fatty acids) rather than butter (rich in SFAs) (additional increase in PAI-1 and lack of reduction of FVIIc in the postprandial state). This study showed a procoagulant postprandial state after the administration of the different fats. After all the meals, there was a postprandial increase in thromboxane B2 and a decrease in tPA (the principal natural fibrinolytic agent). The meal based in olive oil (rich in MUFA) produced a decrease of as much as 34% in FVII concentrations 4 hours after consumption, relative to fasting concentrations.
It has been suggested that chronic exposure to a MUFA-rich diet increases the capacity of large TRLs to transport lipid particles during the postprandial phase, which reduces the number of TRL particles created. By producing a smaller absolute increase in large triacylglycerol (TRL) particles, the MUFA-rich diet produces less activation of FVII. Furthermore, the large TRLs, which are rich in MUFAs or omega 3 fatty acids, are more easily cleared from the plasma than those derived from SFAs. This combination of factors (a smaller number of large TRL particles and a shorter stay in the bloodstream than those of SFAs) might explain the lower concentration of FVII found after the MUFA-rich diet and meal as well as the difference between MUFA- and SFA-rich diets in the postprandial changes from fasting. The walnut-enriched meal (rich in omega 3 fatty acids) also reduced the postprandial concentration of FVIIc. The concentration of plasminogen activator inhibitor-1 was greater after the SFA meal than after the other 2 meals.
These results highlight the importance of studying the postprandial state as a reflector of the effects of the type of food on health, because this is the normal physiologic state of humans for most of the day, and during this state there are clearly different effects than during fasting, a state in which humans now spend no more than 4–6 hour/day. This study showed that during the postprandial state there exists a procoagulatory situation (an increase in thromboxanes and D-dimer and a decrease in tPA), but that the type of fat consumed, both in the acute meal itself and during the previous weeks, is a clear determinant of these changes. A basal diet rich in MUFAs (like canola oil) followed by a meal that is also rich in this ingredient produces anticoagulant effects on FVIIc. Diets rich in SFAs provoke an additional increase in the thrombophilic marker PAI-1. This suggests the creation of a more procoagulatory environment, which might encourage the appearance of acute thrombotic events.
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