Evidence is accumulating that alpha linolenic acid (ALA, C18:3 (n-3)) has different physiological effects to eicosapentanoic acid (EPA, C20:5 (n-3) and docosahexanoic acid (DHA, C22:6 (n-3). Alpha linolenic acid is an essential fatty acid because it is vital to health but humans do not possess the enzymes necessary for its synthesis. However, plants do possess the necessary enzymes and so ALA can be obtained in the diet from various vegetables, with flax seeds, walnuts and hemp being good sources. Humans convert dietary ALA into EPA via a series of desaturase and elongase reactions. Further elongation and desaturation and a final β-oxidation forms DHA. In addition, both EPA and DHA can be obtained directly from dietary intakes of fatty fish such as mackerel, tuna, salmon or trout. If EPA and DHA are present in the diet ALA is not needed, and so both EPA and DHA are conditionally essential.
Both EPA and DHA have been shown to have a number of beneficial effects and are thought to decrease the risk of developing cardiovascular disease. However, the levels shown to be beneficial to cardio health (0.85 g/d) are around 5 times higher than are consumed in the typical Western diet. For those vegetarians unable to eat the marine oils EPA and DHA, it is often recommended that intakes of ALA derived from plants such as flax are increased. In addition, ALA is often recommended to those who require high intakes of essential fatty acids, such as athletes. This advice is based on the assumption that ALA is converted to EPA and DHA is adequate amounts to allow metabolism to series 3 eicosanoids. However, research suggests that the conversion of ALA to EPA in humans is low and probably not more than 5% of ALA is metabolised to EPA.
Research1 has directly compared the physiological effects of dietary ALA with dietary EPA plus DHA in a placebo controlled parallel study involving 150 moderately hyperlipidaemic individuals. Subjects were randomly assigned to 5 different treatment groups that included supplementation with 0.8 or 1.7 g/d EPA and DHA as capsules and as margerine, 4.5 or 9.5 g/d of ALA in margarine or a n-6 rich margarine containing sunflower or safflower as a control. There was no difference in postprandial lipid levels, blood glucose, insulin concentrations or blood pressure between any of the n-3 fatty acid treatments and the n-6 control. In addition, α-tocopherol levels and antioxidant status did not change with any treatment. However, those subjects consuming the 1.7 g/d of EPA plus DHA had significantly lower triacylglycerol levels (-7.7%) compared to the 9.5 g/d ALA, and the susceptibility to ex vivo LDL oxidation was higher after the 1.7 g/d EPA plus DHA compared to the ALA treatment.
These results provide further evidence that dietary ALA does not provide the same physiological effects as the dietary marine oils DHA and EPA. Significant increases in phospholipids ALA concentrations were only apparent after consumption of the ALA treatments as would be expected. The 9.5 g/d intake of ALA caused a significant increase in EPA compared to the control, but did not cause a significant increase in DHA. This supports previous findings that suggests that dietary ALA is not effective at raising endogenous levels of DHA (here). Supplementation with the 1.7 g/d EPA and DHA caused a significant rise in phospholipids levels of EPA and DHA compared to the control. The increased susceptibility of EPA and DHA enriched LDL to ex vivo oxidation occurred despite addition of α-tocopherol to the margarine. However, the relevance of this assay to the oxidation potential in human plasma in vivo is questionable.
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