Key Findings:
This review focuses on estimating the percentage conversion through the desaturation – chain elongation pathway of LA and ALA to their respective long-chain PUFA, ie metabolism of LA to AA or ALA to DHA, and the implications of inefficient conversion of parent to long-chain PUFA in humans for the nutritional or potentially health protective roles of individual PUFA. The context is that the limited conversion in humans presents an opportunity to investigate the clinical effects of individual PUFA, especially ALA, eicosapentaenoic acid (EPA), and DHA, with minimal confounding due to conversion of ALA or EPA to DHA.
ABSTRACT:
There is considerable interest in the potential impact of several polyunsaturated fatty acids (PUFAs) in mitigating the significant morbidity and mortality caused by degenerative diseases of the cardiovascular system and brain. Despite this interest, confusion surrounds the extent of conversion in humans of the parent PUFA, linolenic or a-linolenic acid (ALA), to their respective long-chain PUFA products. As a result, there is uncertainty about the potential benefits of ALA versus eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA). Some of the confusion arises because although mammals have the necessary enzymes to make the long-chain PUFA from the parent PUFA, in vivo studies in humans show that ≈5% of ALA is converted to EPA and <0.5% of ALA is converted to DHA. Because the capacity of this pathway is very low in healthy, nonvegetarian humans, even large amounts of dietary ALA have a negligible effect on plasma DHA, an effect paralleled in the n6 PUFA by a negligible effect of dietary linoleic acid on plasma arachidonic acid. Despite this inefficient conversion, there are potential roles in human health for ALA and EPA that could be independent of their metabolism to DHA through the desaturation – chain elongation pathway. (Authors abstract)
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