Linolenic acid in rapeseed oil partly compensates for the effect of fish restriction on plasma long chain n-3 fatty acids.

January 1, 1996 Human Health and Nutrition Data 0 Comments

Linolenic acid in rapeseed oil partly compensates for the effect of fish restriction on plasma long chain n-3 fatty acids.

Year: 1996
Authors: L Valsta, I Salminen, A Aro, M Mutanen.
Publication Name: European Journal of Clinical Nutrition
Publication Details: Volume 50; Page 229.


The consumption of the long chain n-3 PUFAs, EPA and DHA, has been correlated with a decrease in CHD risk principally through alterations in the synthesis of eicosanoids which are involved in thrombogenesis. ALA from flaxseed oil is elongated in humans to EPA and DHA and has also been reported to have positive effects on platelet aggregation. This study was conducted to examine plasma fatty acid compositions following the feeding of ALA in low erucic acid rapeseed oil – CO, in combination with a restriction in dietary fish intake. The study comprised two 6 week periods in crossover randomized design. Subjects were 40 healthy women and men (age 20-46 years). Subjects consumed their regular diets but replaced fats and fatty foods with experimental oils and products. They were assigned to 2 fish restricted diets including a CO diet and high oleic acid sunflower oil (TriSun oil – SO) diet. The CO and SO diets comprised similar proportions of SFA:MUFA:PUFA (11.5:17.5:8.5% of total energy), but differed in their ALA content (2.2 and 0.3%, respectively) and n-6:n-3 ratio (3:1 and 23:1, respectively). The fatty acid compositions of plasma TG, cholesterol esters (CE) and phospholipids (PL) were analyzed by gas chromatography. Dietary intake was evaluated based on 3- to 7-day food records. The authors reported that the proportion of ALA in TG and CE decreased significantly on the SO diet (from 1.6 to 0.9% and from 0.9 to 0.4%, respectively) and significantly increased on the CO diet (from 1.7 to 3.4% and from 0.9 to 1.3%, respectively) compared to baseline. The proportion of EPA in all 3 plasma fractions decreased on the SO but not on the CO diet. There was no difference in DHA levels in CE between the diets. DPA and DHA in PL remained at a significantly higher level on the CO diet compared to the TSO diet. These findings indicate that ALA from CO is effectively elongated and desaturated to EPA in humans. A small proportion of this EPA can be further elongated to DPA which is desaturated to DHA. The authors speculated that the lower levels of DHA may be due to a degree of retroconversion to EPA. In addition, levels of DHA in other tissues not measured in this study may have increased to a more significant extent. LA levels were significantly increased following the SO diet in both TG and CE fatty acids. AA increased slightly in the PL fraction with the SO diet. The results indicated that ALA is metabolized to EPA in humans to a significant extent. ALA consumption from CO is recommended as, unlike flaxseed oil, the ALA levels present would not interfere to a significant extent with n-6 PUFA metabolism. Extrapolating from their data, the authors estimated that the consumption of approximately 50 g/day of CO affects the proportion of EPA in plasma fatty acids similar to the effect of a weekly intake of approximately 50 – 100 g/day of fatty fish or up to 50 –150g/day of lean fish. The authors concluded that this is an important finding especially for those individuals who avoid the consumption of fish in their diet.

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