Prostaglandins, Leukotrienes and Essential Fatty Acids., 2010, Volume 83; Pages 45 – 54.

Elevated plasma fibrinogen caused by inadequate a-linolenic acid intake can be reduced by replacing fat with canola-type rapeseed oil.

Seppanen-Laakso, T. Laakso, I. Lehtimaki, T. Rontu, R. Moilanen, E. Solakivi, T. Seppo, L et al.

Key Findings:

Hemostasis entails the ability of the body to degrade blood clots. In prothrombotic and proinflammatory situations, fibrinogen is the main protein in coagulation processes and elevated levels are correlated with CHD, strokes, diabetes, Alzheimer disease and dementia. Here canola (rapeseed) oil substitution for saturated fats produced only small effects on serum cholesterol levels. The small levels of ALA in canola (about 10%) inhibited the formation of arachidonate (AA, 20:4n-6) from linoleic acid. Lower levels of ALA in phospholipids were correlated with elevated fibrinogen levels. Reductions in fibrinogen with ALA were associated with a competitive inhibition of LA conversion to AA. DHA increased 3-fold in the canola oil group. ALA conversion to DHA was reduced when fibrinogen concentrations were elevated. This study did show that the competitive effects of ALA on n-6 PUFA metabolism can favorably 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.

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,16–62 years) replaced fat with RSO for 6 weeks in a parallel design. The average cholesterol and fibrinogen concentrations were 5.0 mmol/l and2.6g/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 (2.6–3.9g/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. (Author’s abstract)

 

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