Comparison of the effects of two low fat diets with different alpha-linolenic: linoleic acid ratios on coagulation and fibrinolysis.
Comparison of the effects of two low fat diets with different alpha-linolenic: linoleic acid ratios on coagulation and fibrinolysis.
Year: 1999
Authors: M A Allman-Farinell, D Hall, K Kingham, D Pang, P Petocz, E J Favaloro.
Publication Name: Atherosclerosis.
Publication Details: Volume 142; Number 1; Page 159.
Abstract:
Fish oils rich in very long chain n-3 polyunsaturated fatty acids (PUFAs) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHAA) lower the concentrations of the compound fibrinogen, which is considered desirable for vascular disease. However, EPA and DHA may lower concentrations and activities of tissue plasminogen activator and increase plasminogen activator inhibitor which has been found to be negative with regard to vascular disease. The 18 carbon precursor of very long chain n-3 PUFAs, alpha-linolenic acid (ALA) may exert similar effects independently or as a result of conversion to EPA and DHA. The objective of this study was to compare the effects of two low saturated fat diets, one rich in ALA and the other in linoleic acid (LA) on coagulation factors and fibrinolysis. Twenty-nine healthy male subjects consumed a 2-week run-in diet with 39.5% total energy from fat and a fatty acid representative of a common Australian diet. This period was followed by random allocations to one of two test diet groups for six weeks. Test diets were lower in fat (31.5% energy) with approximately 7% energy from PUFA and an ALA:LA ration of either 1:1.2 (ALA-rich, flaxseed) or 1:21 (LA-rich, safflower oil, the more traditional Australian diet used for cholesterol lowering). Blood was collected at the beginning, middle and end of test diets and analyzed for Factor VIIc and VIIIc, fibrinogen, von Willebrand factor, activated protein C resistance (APC resistance), tissue plasminogen activator and plasminogen activator inhibitor type-1 activities and/or protein concentrations and platelet fatty acids. Comparison of the effects of ALA-rich versus LA-rich showed no significant differences in the blood parameters measured, except that the diet with the maximum ALA:LA ration tripled platelet phospholipid EPA. An increase in PL EPA is not unexpected and supports previous evidence of conversion of ALA to the long chain n-3 fatty acids, EPA and DHA. The APC ratio demonstrated significantly increased anticoagulant activity following the ALA-rich diet. The authors suggest that studies in patients with vascular pathologies are needed to verify the these findings. Higher ratios of ALA:LA, achievable only with greater amounts of PUFAs, may be necessary in order to produce effects similar to fish oil supplementation. The authors postulate that ALA-rich diets may not produce the same effects of fish oil supplementation because subjects consuming a normal Western style diet have low tissue concentrations of EPA/DHA and thus, the final percentage of EPA in PLs was lower than in other studies reporting changes in hemostasis. As well, the actual conversion to very long chain n-3 PUFA may be less than predicted from previous studies. With regard to coagulation and fibrinolysis, the consumption of a low saturated fat diet in combination with a high ratio of ALA:LA demonstrated little difference to the same diet high in LA:ALA ratio. The effects of ALA on patients with vascular diseases may be different than the results noted in this study which examined young healthy subjects.
