Elevated plasma fibrinogen caused by inadequate a-linolenic acid intake can be reduced by replacing fat with canola-type rapeseed oil
Elevated plasma fibrinogen caused by inadequate a-linolenic acid intake can be reduced by replacing fat with canola-type rapeseed oil
Year: 2010
Authors: Seppanen-Laakso, T. Laakso, I. Lehtimaki, T. Rontu, R. Moilanen, E. Solakivi, T. Seppo, L. et. al.
Publication Name: Prostaglandins, Leukotrienes and Essential Fatty Acids
Publication Details: Volume 83; Pages 45 ? 54.
Abstract:
The effects of canola-type rapeseed oil (RSO) on serum lipids, plasma fibrinogen, lipid oxidation and fatty acids were studied in three groups of subjects, two of which had not been consuming fish in their habitual diets. Forty-two volunteers(35 women, 7men,16 to 62 years) replaced fat with RSO for 6 weeks in a parallel design. The average cholesterol and fibrinogen concentrations were 5.0 mmol/l and 2.6g/l, respectively. The intake of alpha-linolenic acid (a-LLA) was doubled. Efficient competitive inhibition by a-LLA was seen as a decrease in long-chain (LC) n-6 PUFA at 3 weeks. Elevated fibrinogen (2.6 to 3.9g/l) decreased by 0.95g/l at 6 weeks. Docosahexaenoic acid (22:6n-3) in plasma phospholipids increased at low fibrinogen levels only. The associations and changes in plasma C18 and LCPUFA followed the competitive and metabolic principles of the body, and especially in the case of n-3 PUFA according to the recycling pathway. (Authors abstract)
A balanced n-6/n-3 PUFA intake is of importance in hemostasis, which is a complex system of factors that normally form and degrade blood clots. Fibrinogen is the main protein in coagulation processes and elevated levels, found in prothrombotic and proinflammatory states, are associated with a higher risk of CHD, strokes, diabetes, and Alzheimer disease and dementia. Dietary prevention of type 2 diabetes should be directed at lowering trans fatty acids and balancing the unsaturated/saturated fat ratio [In this study, the effects of canola/RSO substitution (for saturated fats) on serum lipids, plasma fibrinogen levels, lipid oxidation and fatty acid composition were assessed. The aim was also to study ALA metabolism to LCn-3PUFA in subjects that do not consume fish in their habitual diets. The results showed only modest effects on serum cholesterol levels. However consumption of ALA inhibited the formation of arachidonate (AA,20:4n-6) from LA,. Lower levels of PL ALA were associated with elevated fibrinogen levels. During fat substitution, both ALA and LCn-6PUFA were also involved in the decreases in fibrinogen. A substantial reduction of elevated plasma fibrinogen concentrations of 30% was associated with a marked increase in ALA intake from RSO and a decrease in the LA/ALA ratio. Reductions in fibrinogen, initiated at 3 weeks by ALA through strong competitive inhibition of LA conversion to LCn-6 AA. This study shows that ALA is effective in inhibiting the formation of n-6 eicosanoid precursors from LA. An increase in DHA was about 3-fold in the high ALA group. The decrease in LA enhances the increase in DHA. This study also showed that ALA conversion to DHA could be interrupted by elevated fibrinogen concentrations. The authors speculate that impaired LCn-3 PUFA patterns may be indicative of elevated fibrinogen caused by an ALA-deficient diet and a lack of effective inhibition of LCn-6 PUFA. The role of a long-term, deficient ALA intake in the development of a number of diseases characterized by impaired n-3 PUFA metabolism remains to be studied. The authors state that dietary fat changes must be aimed at lowering elevated fibrinogen, which may prevent the development of prothrombotic and proinflammatory conditions. The unique competitive functions of ALA with regard to n-6 PUFA metabolism can favourably affect hemostasis by reducing fibrinogen. The authors conclude that ALA should be the first omega-3 to be used in correcting n-6/n-3 PUFA imbalances in the body. (Editors comments)
A balanced n-6/n-3 PUFA intake is of importance in hemostasis, which is a complex system of factors that normally form and degrade blood clots. Fibrinogen is the main protein in coagulation processes and elevated levels, found in prothrombotic and proinflammatory states, are associated with a higher risk of CHD, strokes, diabetes, and Alzheimer disease and dementia. Dietary prevention of type 2 diabetes should be directed at lowering trans fatty acids and balancing the unsaturated/saturated fat ratio [In this study, the effects of canola/RSO substitution (for saturated fats) on serum lipids, plasma fibrinogen levels, lipid oxidation and fatty acid composition were assessed. The aim was also to study ALA metabolism to LCn-3PUFA in subjects that do not consume fish in their habitual diets. The results showed only modest effects on serum cholesterol levels. However consumption of ALA inhibited the formation of arachidonate (AA,20:4n-6) from LA,. Lower levels of PL ALA were associated with elevated fibrinogen levels. During fat substitution, both ALA and LCn-6PUFA were also involved in the decreases in fibrinogen. A substantial reduction of elevated plasma fibrinogen concentrations of 30% was associated with a marked increase in ALA intake from RSO and a decrease in the LA/ALA ratio. Reductions in fibrinogen, initiated at 3 weeks by ALA through strong competitive inhibition of LA conversion to LCn-6 AA. This study shows that ALA is effective in inhibiting the formation of n-6 eicosanoid precursors from LA. An increase in DHA was about 3-fold in the high ALA group. The decrease in LA enhances the increase in DHA. This study also showed that ALA conversion to DHA could be interrupted by elevated fibrinogen concentrations. The authors speculate that impaired LCn-3 PUFA patterns may be indicative of elevated fibrinogen caused by an ALA-deficient diet and a lack of effective inhibition of LCn-6 PUFA. The role of a long-term, deficient ALA intake in the development of a number of diseases characterized by impaired n-3 PUFA metabolism remains to be studied. The authors state that dietary fat changes must be aimed at lowering elevated fibrinogen, which may prevent the development of prothrombotic and proinflammatory conditions. The unique competitive functions of ALA with regard to n-6 PUFA metabolism can favourably affect hemostasis by reducing fibrinogen. The authors conclude that ALA should be the first omega-3 to be used in correcting n-6/n-3 PUFA imbalances in the body. (Editors comments)
