Humans lack the Δ15-destaurase enzyme necessary for the conversion of linoleic acid (LA, C18:2 (n-6)) to α-linolenic acid (ALA, C18:3 (n-3)). However, plants possess Δ15-destaurase and some plant foods are therefore good sources of ALA. In humans, plant derived ALA is metabolised to eicosapentanoic acid (EPA, C20:5 (n-3)) and docosahexanoic acid (DHA, C22:6 (n-3)) which are subsequently converted to important signal molecules required for correct cellular function. The traditional view was that plant sources of ALA should be consumed to allow production of these signal molecules. However, the fatty acids EPA and DHA are both present in fatty fish and so health can be maintained without the need for ALA if adequate fatty fish is consumed. In fact, recent evidence suggests that the conversion of ALA to EPA and DHA is poor and that consumption of preformed EPA and DHA may be necessary to maintain health.
The pathways of long-chain fatty acid metabolism are complex and not fully understood. However, a picture is emerging that ALA cannot substitute for EPA and DHA in human nutrition despite being linked by a common metabolic pathway. In fact, ALA appears on merit to be functionless in human metabolism with its sole function being to serve as a precursor to the longer and more unsaturated EPA and DHA. Research suggests that ALA does not readily accumulate in cell membranes, unlike EPA and DHA, but the reason for this is not understood. Some evidence suggests that this is related to the fact that ALA is a preferential substrate for oxidation. The obvious question that emerges from this is why would an essential precursor molecule be oxidised as fuel if this risks preventing the formation of useful metabolites? The answer to this is not clear.
Because the conversion of ALA to EPA is not efficient, high intakes of ALA produce relatively low levels of EPA in cell membranes when compared to supplementation with EPA. This is due to low activity of the rate limiting enzyme Δ5-desturase. Within tissues EPA and DHA can be inter-converted, but the low synthesis of EPA from dietary ALA results in even lower synthesis of DHA. While both EPA and DHA supplements have been shown to favourably effect a number of biomarkers for cardiovascular disease, high intakes of dietary ALA do not cause the same changes. This suggest that plant sources of ALA are not as beneficial as fish sources of EPA and DHA in providing the necessary n-3 fatty acids for health. Some research studies have found some benefits for ALA, but when compared directly to both DHA and EPA from fish, ALA performs very poorly.
Differences exist between the tissues in which EPA and DHA accumulate. For example, EPA is readily taken-up by phosphatidylethanolamine and phosphatidylcholine, and the liver, kidney, platelets and erythrocytes tend to accumulate EPA to a greater degree than DHA. For example in rat liver, DHA is readily retro-converted to EPA, preventing DHA accumulation. In contrast in neuronal tissue, EPA is readily converted to DHA, which subsequently accumulates. While EPA and DHA both vary in their accumulation in tissues, ALA is reluctant to accumulate at all. Dietary sources of EPA and DHA are superior at causing accumulation of n-3 fatty acids when compared to dietary sources of ALA. The fact that dietary ALA performs badly when compared to dietary EPA and DHA has raised doubts about its benefits. Based on the evidence in the literature, the viewpoint that it provides the same benefits as n-3 fatty acids from fish oils is unfounded.
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