Journal Name:
Eur. J. Clin. Investigation

Article Title:
Effects of dietary fat saturation on eicosanoid production, platelet aggregation and blood pressure.

Date Written:
1997

Volume:
27

Number:
9

Page:
780

Author(s):
Lahoz, C.; Alonso, R.; Ordovas, J.M.; Lopez Farre, A.; DeOya, M.; Mata, P.

Article:
Eicosaniods [prostaglandins (PG) and thromboxanes (TX) are synthesized from polyunsaturated fatty acids (PUFAs), mainly arachidonic acid (AA), and are involved in a number of physiological processes. The AA is derived from dietary omega 6 linoleic acid. Prostacyclin (PGI2), the main metabolite of AA in endothelial cells, is a vasodilator and inhibitor of platelet aggregation (PA) whereas thromboxane A (TXA2), a metabolite of AA in platelets, has the opposite effect. Both have a short half-life and are catabolised to stable metabolites, thromboxane B2 (TXB2) and 6-keto-protagladin in F1α (PGF1α) and excreted in the urine mainly as 2,3-donor-6-keto-prostaglandin f1α and 11-dehydro-thromboxane B2 respectively. The purpose of this study was to investigate the effect of regular diets differing in their fatty acid saturation on urinary eicosanoid excretion, platelet aggregation and blood pressure and to evaluate the interrelation among these variables.

Forty two healthy subjects consumed four consecutive diets differing in fat [saturated (SFA); monounsaturated (MUFA); polyunsaturated n-6 (PUFAn-6); and polyunsaturated n-6/n-3, (PUFA n-3)]. Each diet period lasted 5 weeks. The results showed that there were no differences in 24-hour 2,3-dinor-6-keto-prostaglandin F1α excretion among dietary periods. A significant effect in the excretion of 11-dehydro-thromboxane B2 was found. During the PUFA n-6 phase the excretion was significantly higher than during SFA and MUFA periods. Dietary fatty acid composition had a significant effect on ADP (1mmol/L) and collagen (2mg/L) induced platelet aggregation. Dietary fat had a significant effect on systolic and diastolic blood pressure. Both were significantly higher during SFA period than during the other three periods.

It is well established that changes in dietary n-3 fatty acids modify PA. For the most part, n-3 supplementation studies show a decrease in ADP- and collagen-induced platelet aggregation. In this study, no any differences in aggregation were seen between MUFA- and PUFA n-3-enriched diets. Some authors have found a dose-dependent relationship between n-3 ingestion and decrease in aggregation, whereas others did not. Differing doses of n-3 were noted between these studies as well as different proaggregant agents were used.

Epidemiological and clinical studies have reported an association between high consumption of MUFAs and lower BP, other studies have shown similar effects associated with a high intake of PUFA n-3.

In summary, in addition to their well-know effects on plasma lipoprotein concentrations and LDL oxidation, dietary fatty acids appear to have effects over other atherogenic factors such as eicosanoid production and platelet aggregation. Blood pressure was also significantly affected by dietary fat saturation, with the lowest systolic blood pressure being associated with the consumption of either MUFA- or PUFA n-3-enriched diets. The authors conclude that the substitution of MUFA for SFA appears to be a feasible alternative in order to lower the overall atherosclerosis risk in individuals.


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