Professor of Nutritional Immunology University of Southampton Southampton, United Kingdom
In the absence of significant intake of preformed EPA and DHA, endogenous synthesis from alpha-linolenic acid (ALA) becomes very important to maintain EPA status and to retain its benefits (DHA seems to be poorly synthesized). The conversion of ALA to EPA uses the same enzymes as the conversion of linoleic acid (LA) to arachidonic acid, so there is direct competition between the n-6 and n-3 PUFA pathways. A decrease in dietary LA intake, whilst keeping dietary ALA constant, resulted in marked increases in EPA in plasma and platelet phospholipids. Conversely, increased intake of ALA increases EPA (and DPAn-3) levels in blood and blood cells. These observations clearly demonstrate that the ratio of LA to ALA is a key determinant of endogenous EPA synthesis. In the absence of significant seafood consumption and use of “fish oil” supplements, the dietary LA to ALA ratio approximates the dietary n-6 to n-3 PUFA ratio, so both ratios have a very similar meaning. However, in other situations the use of the n-6 to n-3 PUFA ratio may not be warranted. If this is to be a true ratio of n-6 to n-3 PUFAs it should include all n-6 and all n-3 PUFAs. However, a ratio calculated in that way will no longer indicate the capacity to endogenously synthesize EPA. Furthermore, an n-6 to n-3 PUFA ratio carries with it some assumptions: firstly, that all n-6 PUFAs are “bad”, that all n-3 PUFAs are “good” and that all n-3 PUFAs oppose the action of all n-6 PUFAs; secondly that all n-6 PUFAs are metabolically and functionally equivalent and that all n-3 PUFAs are metabolically and functionally equivalent; and thirdly that all ways of changing the ratio are equivalent. None of these is correct. This will be discussed using examples from the literature.