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Chronic dietary fat intake modifies the postprandial response of hemostatic markers to a single fatty test meal^1,2,3

¹ From the Lipids and Atherosclerosis Research Unit, Reina Sofía University Hospital, Córdoba, and Ciber Fisiopatología Obesidad y Nutrición (CB06/03) Instituto de Salud Carlos III, Spain

² Supported by Consejeria de Innovación, Proyectos de Investigación de Excelencia Junta de Andalucia (AGR 05/00922 to PP-M and P06-CTS-01425 to JL-M), and Ministerio de Educación y Ciencia (AGL-2006-01979/ALI to JL-M); the Lipids and Atherosclerosis Unit at Reina Sofia University Hospital is a partner of Ciber Fisiopatología Obesidad y Nutrición (CB06/03) Instituto de Salud Carlos III, Spain.

³ Reprints not available. Address correspondence to J López-Miranda, Servicio de Medicina Interna, Unidad de Lípidos y Arteriosclerosis, Hospital Universitario Reina Sofia, Edificio de Consultas Externas, 2 planta, 14004 Córdoba, Spain. E-mail: jlopezmir{at}uco.es.

	ABSTRACT

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS DISCUSSION REFERENCES

 
Background: Hemostasis is the result of a complex equilibrium between coagulation and fibrinolysis, and the influence of different dietary models on this equilibrium is not entirely known.

Objective: The objective was to compare the effects of the chronic intake of different dietary models on postprandial hemostasis.

Design: In a randomized crossover design, 20 healthy men consumed for 28 d each diets rich in monounsaturated fatty acids (MUFAs), saturated fatty acids (SFAs), and carbohydrates plus n–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 B₂) were measured; meal tests for the postprandial measures were based on butter, virgin olive oil, and walnuts for the SFA, MUFA, and CHO/N3 diets, respectively.

Results: There were no differences in the fasting variables after the dietary periods. After the 3 fatty meals were consumed, we observed an increase in thromboxane B₂ and D-dimer and a reduction in tissue plasminogen activator, irrespective of the dietary model. The MUFA or CHO/N3 meals lowered postprandial concentrations of factor VII coagulant activity, although the reduction was greater after the MUFA-enriched meal. The concentration of plasminogen activator inhibitor-1 was greater after the SFA meal than after the other 2 meals.

Conclusions: The administration of a fatty meal induces a postprandial procoagulant tendency, irrespective of the type of fat consumed. However, the use of a dietary model rich in SFA creates a more procoagulant environment than does a model that includes MUFA or CHO/N3 as the source of fatty acids.

Key Words: Hemostasis • postprandial state • olive oil • monounsaturated fatty acids • saturated fatty acids • n–3 fatty acids

	INTRODUCTION

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Hemostasis is the process that ensures the integrity of the vascular system. Because of the longevity of human, a strict balance is needed to avoid the appearance in the course of life of diseases due to a lack of (hemorrhage) or an excess of (thrombosis, embolism) coagulation. Many factors can affect hemostasis. We can broadly separate them into intrinsic factors, mainly genetic or sex factors, and extrinsic factors because of the external processes, mainly environmental. Of the extrinsic factors, diet is one of the most important determinants of hemostasis. A prothrombotic state is the predominant situation of Western populations because of their dietary patterns rich in SFAs. In the search for healthier diets, interest has focused on Mediterranean (rich in MUFAs) or n–3-enriched diets. The lower incidence of cardiovascular disease death associated with adherence to these diets has led to the study of the underlying causes. Although the lipoprotein profile has long been widely studied, the modifications that nutritional patterns (whether of the background diet or of an isolated meal) can induce in the hemostatic system are currently a field of interest. 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 (1–8). However, and although SFAs seem to promote a poorer hemostatic profile, 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 fully set out (9, 10). On this basis, we performed a 2-stage study in which we submitted 20 healthy young men to a chronic (4-wk) dietary intervention with 3 dietary models and measured the effects of this intervention on fasting coagulation markers. 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.

	SUBJECTS AND METHODS

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Participants
A group of healthy young adults were recruited from among the students at the University of Cordoba. The subjects (n = 20) were 23.31 ± 2.17 y of age ( ± SD). Informed consent was obtained from all participants. All subjects underwent a comprehensive medical history, physical examination, and clinical chemistry analysis before enrollment. Subjects showed no evidence of any chronic disease (hepatic, renal, thyroid, or cardiac dysfunction) or obesity, nor were they involved in unusually high levels of physical activity (eg, sports training). None of the subjects had a family history of premature coronary artery disease or had taken medications or vitamin supplements in the 6 mo before the study. Physical activity and diet, including alcohol consumption, were recorded in a personal log for 1 wk, and the data were used to calculate individual energy requirements. The mean (±SD) body mass index (BMI; in kg/m²) was 24.63 ± 2.87 at the onset of the study and remained constant throughout the experimental period. Subjects were requested to maintain their regular physical activity and lifestyle and were asked to record in a diary any event that could affect the outcome of the study, such as stress, change in smoking habits and alcohol consumption, or intake of foods not included in the experimental design. The study protocol was approved by the Human Investigation Review Committee at the Reina Sofia University Hospital in Cordoba.

Diets
Participants were randomly assigned to receive, in a crossover design, three diets for 28-d periods each (Table 1). The 3 diets were as follows: 1) SFA-rich diet, with 15% of energy as protein, 47% of energy as carbohydrate, and 38% of energy as fat [22% as SFA, 12% as monounsaturated fatty acids (MUFAs), and 4% as polyunsaturated fatty acids (PUFAs), of which 0.4% was -linolenic n–3 fatty acid]; 2) MUFA-rich diet, with 15% of energy as protein, 47% of energy as carbohydrate, and 38% of energy as fat (24% as MUFAs, <10% as SFAs, and 4% as PUFAs, of which 0.4% was -linolenic n–3 fatty acid); and 3) CHO/N3-rich diet, with 15% of energy as protein, 55% of energy as carbohydrate, and <30% of energy as fat (<10% as SFAs, 12% as MUFAs, and 8% as PUFAs, of which 2% was -linolenic n–3 fatty acid).

The composition of the experimental diets was calculated by using the US Department of Agriculture (11) food tables and Spanish food-composition tables for local foodstuffs (12). All of the meals were prepared in the hospital kitchen and were supervised by a dietitian. Lunch and dinner were eaten in the hospital dining room, and breakfast and an afternoon snack were eaten in the medical school cafeteria. Menus (n = 14) were prepared with regular solid foods and rotated during the experimental period. Duplicate samples from each menu were collected, homogenized, and stored at –70 °C. The protein, fat, and carbohydrate contents of the diet were analyzed by using standard methods. Dietary compliance was verified by analyzing the fatty acids in plasma LDL cholesterol esters at the end of each dietary period (13). Additional measurements of total, LDL, and HDL cholesterol were made at the end of each dietary period to test whether the dietary design was adequate to provoke a change in these fractions. After the completion of each dietary period, the participants underwent 3 postprandial lipemia studies in which they consumed meals with the same fat content (1 g fat/kg body wt, 7 mg cholesterol/kg, and 40 retinol equivalents/kg body wt) but with different fatty acid compositions following a random administration order. After fasting for 12 h, at time 0, the subjects were given a fatty meal consisting of 50–66% of their daily normal intake of calories. The meals consisted of 60% fat, 15% protein, and 25% carbohydrate. The fat composition of the test meals used in the postprandial lipemia studies was as follows: fatty meal rich in MUFAs, based on extra virgin olive oil (olive oil meal: 22% SFAs, 38% MUFAs, 4% PUFAs, and 0.7% -linoleic acid); fatty meal rich in SFAs, based on butter (butter meal: 35% SFAs, 22% MUFAs, 4% PUFAs, and 0.7% -linoleic acid); and fatty meal rich in n–3 fatty acids, based on walnuts (Junglans regia L. walnut meal: 20% SFAs, 24% MUFAs, 16% PUFAs, and 4% -linoleic acid).

Each fat meal was matched with the type of diet received in the 3 previous weeks. Venous blood samples were collected at time 0 (before the meal) and 4 h after fat food intake. Other results from the same population were published elsewhere (14).

Determination of cholesterol fractions
Total cholesterol and triacylglycerols were assayed by enzymatic procedures. HDL-cholesterol was measured after precipitation with phosphotungstic acid. LDL-cholesterol concentrations were estimated by using the Friedewald formula based on the cholesterol, triacylglycerol, and HDL-cholesterol values (15).

Determination of coagulation markers
t-PA was determined by a commercial enzyme immunoassay (Asserachrom tPA; Diagnostica Stago, Minneapolis, MN). Plasminogen activator inhibitor-1 (PAI-1) was quantified by a 2-stage, indirect enzymatic assay (Spectrolyse PL PAI-1; Biopool, Trinity Biotech, Ireland). D-Dimer was assessed with a commercial enzyme immunoassay (Tintelize-D-Dimer, strip-well format; Biopool, Trinity Biotech). Factor VII coagulant activity (FVIIc) was determined with a chromogenic kit in 2 stages (COASET FVII; Chromogenix AB, Mölndal, Sweden). Thromboxane B₂ was quantified with a commercial enzyme immunoassay (thromboxane B₂ immunoassay; R&D Systems Inc, Minneapolis, MN).

Data analysis
Statistical analyses were carried out by using SPSS statistical software (version 13.0; SPSS Inc, Chicago, IL). Analysis of variance (ANOVA) for repeated measures was used to analyze the differences in the hemostatic factors and in the different cholesterol fractions. One-factor ANOVA was used to assess differences in the postprandial changes of the variables from fasting among the diets. When statistically significant effects were found, Bonferroni's post hoc comparison test was used to identify group differences. Differences were considered significant when P was <0.05. The tPA/PAI-1 ratio was defined as the result of the mathematical division of tPA concentration by that of PAI-1.

	RESULTS

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Fasting state
Consumption of the different model diets did not produce any differences in the fasting concentrations of the coagulation markers analyzed (Table 2). Data about cholesterol fractions after the different diets was published elsewhere (14). Total cholesterol was higher after the SFA-rich diet than after the CHO/N3 (148 ± 21 compared with 137 ± 24 mg/dL; P = 0.032) and MUFA (148 ± 21 compared with 138 ± 21 mg/dL; P = 0.041) diets. LDL cholesterol was also higher after the SFA-rich diet than after the CHO/N3-rich diet (87 ± 20 compared with 79 ± 22 mg/dL; P = 0.043) and the MUFA-rich diet (87 ± 20 compared with 78 ± 18 mg/dL; P = 0.031). We found no differences in HDL between the end of the SFA period (45.2 ± 8.0 mg/dL) and the other 2 diets, but it was lower after the CHO/N3-rich period than after the MUFA-rich period (43.1 ± 8 compared with 45.3 ± 7 mg/dL; P = 0.046).

Evaluating the differences between the fasting and postprandial states (effect of extraction time) within each dietary model, we found that the MUFA-rich meal was followed by a decrease in the concentrations of FVIIc (37 ± 19% compared with 25 ± 16%; P = 0.003) and PAI-1 (18 ± 8 compared with 13 ± 6 ng/mL; P = 0.028), whereas the CHO/N3-enriched meal reduced FVIIc (38 ± 22% compared with 31 ± 16%; P = 0.050). We observed a time effect for postprandial decreases in tPA (P = 0.001) and tPA/PAI-1 (P = 0013) and increases in thromboxane B₂ (P = 0.001) and D-dimer (P = 0.014) without finding any interaction with the different diets, which accounts for a variation of these markers in the postprandial state, irrespective of the diet consumed.

Changes from fasting to postprandial states among the different diets
The amount of change between the fasting and the postprandial values of the different hemostatic factors among the different diets was tested by one-factor ANOVA (Figure 1). The postprandial change in FVII compared with the fasting concentration was significantly different between diets (P = 0.037). Post hoc comparisons showed differences between the MUFA-rich diet and the SFA-rich diet (–12 ± 4 compared with –0.2 ± 3 ng/mL; P = 0.033) diets. PAI-1 was also different between the diets (P = 0.046). In the post hoc analysis, the means of the changes between the fasting and the postprandial measures differed from MUFA-rich diet and SFA-rich diet (–4 ± 2 compared with 3 ± 2 ng/mL; P = 0.041). There were no other significant differences in the other hemostatic factors.

View larger version (10K): [in this window] [in a new window]   FIGURE 1.. Mean (±SE) postprandial changes from fasting in factor VIIc (FVIIc) and plasminogen activator inhibitor-1 (PAI-1) after the diets rich in monounsaturated fatty acids (MUFA diet), saturated fatty acids (SFA diet), and carbohydrates plus n–3 fatty acids (CHO/N3 diet). n = 20. One-factor ANOVA was used for the statistical analysis.

	DISCUSSION

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There is a growing interest in the changes that occur in the hemostatic system during the postprandial phase. This is understandable if we bear in mind that coagulation factors are important protagonists in the development of atherothrombosis and that the postprandial state is the normal state of human beings in society today. A rise in triacylglycerols is sufficient to activate FVII, because this molecule adheres to the surface of large triacylglycerol-rich lipoprotein (TRL) particles (16, 17). Moreover, during the postprandial phase, there is an increase in nuclear factor B (NF-B), which in turn promotes the transcription of proinflammatory products. The start of this response, in conjunction with the procoagulant state resulting from the activation of the intrinsic cascade of coagulation, produces an obviously procoagulant and proinflammatory environment, to which is added an increase in platelet aggregation mediated by membrane markers (basically thromboxanes). Recent studies have confirmed this scenario, showing a postprandial rise in intravascular fibrin concentrations in both healthy subjects and coronary patients (18).

In line with the aforegoing, this study has shown a procoagulant postprandial state after the administration of 3 different fatty food models, each of them given after 4 wk on a dietary regimen with an identical fat composition. After all the meals that we studied, there was a postprandial increase in thromboxane B₂ and a decrease in tPA (the principal natural fibrinolytic agent). However, there were clearly different effects in the wake of each of the meals. The meal based in olive oil (rich in MUFA) produced a decrease of as much as 34% in FVII concentrations 4 h after consumption, relative to fasting concentrations. Although there are inconsistent results concerning the effects of MUFAs on FVII, our findings agree with previous results (17, 19). Some earlier studies have found a larger increase in FVII after individual MUFA-rich meals than after meals containing other types of fat (20, 21), although when subjects had previously undergone a period on a diet rich in MUFA, the results were similar to ours (22, 23). Williams evaluated the effects of the type of fatty acid in the background diet on the postprandial response to a meal rich in saturated fatty acids and found a decrease of 18% in the postprandial increases in FVIIc and of 50% when her subjects had received a moderate or high amount of MUFAs during the previous 8 wk, relative to a standard Western diet rich in SFAs (17). 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 (17). It is known that factor VII binds to the protein fraction of TRLs, thus prolonging the length of stay of this factor in the bloodstream. By producing a smaller absolute increase in large TRL particles, the MUFA-rich diet produces less activation of FVII. Furthermore, the large TRLs, which are rich in MUFAs or n–3 fatty acids, are more easily cleared from the plasma than those derived from SFAs, thanks to their conformational structure (16). The SFAs are located primarily in position sn2 of the triacylglycerols, which interchange with much more difficulty from the surface of the chylomicrons than do those of the fatty acids in positions s1 and s3 of the triacylglycerols (those that are occupied preferentially by MUFAs and n–3 fatty acids). 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 that we 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. For its part, the walnut-enriched meal (rich in n–3 fatty acids) managed to reduce the postprandial concentration of FVIIc, a result that was similar to that of another recently published study (24), and possibly also mediated by the conformational structure of the n–3 fatty acids in the triacylglycerols transported by the TRLs (16).

On the other hand, the modulation of PAI-1 has multiple causes, but one of its principal determinants is the concentration of insulin in the blood. Our group previously showed that consumption of a MUFA-rich diet (rich in olive oil) improves sensitivity to insulin and reduces insulin and PAI-1 concentrations in comparison with SFA-rich diets (1, 5, 7, 25). The lower postprandial concentration of PAI-1 that we found after the MUFA-enriched meal than after the SFA-rich meal may thus reflect enhanced sensitivity to postprandial insulin secretion. This fact could also explain the differences in the changes from fasting between the MUFA-rich diet and the SFA-rich diet. In our study, the concentration of PAI-1 was also greater during the postprandial phase after the SFA-rich meal than after the CHO/N3-rich meal. This finding agrees with the findings of earlier studies in which SFAs produced increases in PAI-1 for up to 8 h after its consumption (26).

Some of the results we obtained may depend on minor components of the various foods we used rather than on the nature of their fats. Walnuts, for example, are a source of L-arginine, the original precursor of nitric oxide, so that an increase in nitric oxide might help to create a less proinflammatory and procoagulatory environment. For its part, virgin olive oil contains phenols in its nonsaponifiable part, and these have shown vasodilatory (27) and anticoagulant effects during the postprandial phase (28). The nomenclature of the different diets in the present study was chosen to make the article read easier, although we positively think that a more comprehensive name, such as the Mediterranean diet instead of a MUFA-rich diet, could also have been used and would probably make it easier to the reader to bear in mind that part of the effects showed after the consumption of this diet were not due to its fatty acid composition but to the minor compounds present in virgin olive oil.

The combination of biologically active compounds in virgin olive oil thus produces a milder activation of the mechanisms of inflammation and coagulation during the postprandial phase, a situation that leads to reduced postprandial activation of NF-B, an important cellular regulator that initiates the formation of procoagulant and proinflammatory signal peptides (14, 29).

One of the strong points of this study is the high degree of homogeneity of the sample, an aspect that permits us to exclude confusion factors such as age, sex, and BMI, which could be attributed to sample heterogeneity. Moreover, it forms an excellent point of departure for studies of larger populations that might evaluate different age groups.

Note that our results bring out 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 h/d.

The novelty of our work was the finding 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 virgin olive oil (rich in MUFAs) followed by a meal that is also rich in this ingredient produces anticoagulant effects on FVIIc in comparison with other dietary models that are rich in walnuts (rich in n–3 fatty acids) or butter (SFAs). The latter model also provokes 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. The results of this study indicate that virgin olive oil is a functional food with high anticoagulant potential.

	ACKNOWLEDGMENTS

 
The authors' responsibilities were as follows—JD-L: directed the fat test meals, performed the statistical analysis of the data, and wrote the article; BC, AL, RG-L, and MJG: performed the biochemical determinations and collaborated in the statistical analysis; RG-L and MJG: performed the biochemical determinations and helped with the logistics of the fat test meals; PP-M, PG, JC, and FF: helped design and collect the data; and FP-J and JL-M: contributed to the realization of the present article with significant advice and consultation. None of the authors declared any conflict of interests.

	REFERENCES

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS DISCUSSION REFERENCES

 

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