a-Linolenic acid supplementation and conversion to n-3 long-chain polyunsaturated fatty acids in humans

January 1, 2009 Human Health and Nutrition Data 0 Comments

a-Linolenic acid supplementation and conversion to n-3 long-chain polyunsaturated fatty acids in humans

Year: 2009
Authors: Brenna, J.T. Salem Jr., N. Sinclair, A.J. Cunnane, S.C
Publication Name: Prostaglandins, Leukotrienes and Essential Fatty Acids
Publication Details: Volume 80; Pages 85 to 91.


Blood levels of polyunsaturated fatty acids (PUFA) are considered biomarkers of status. Alpha-linolenic acid, ALA, the plant omega-3, is the dietary precursor for the long-chain omega-3 PUFA eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and docosahexaenoic acid (DHA). Studies in normal healthy adults consuming western diets, which are rich in linoleic acid (LA), show that supplemental ALA raises EPA and DPA status in the blood and in breast milk. However, ALA or EPA dietary supplements have little effect on blood or breast milk DHA levels, whereas consumption of preformed DHA is effective in raising blood DHA levels. Addition of ALA to the diets of formula-fed infants does raise DHA, but no level of ALA tested raises DHA to levels achievable with preformed DHA at intakes similar to typical human milk DHA supply. The DHA status of infants and adults consuming preformed DHA in their diets is, on average, greater than that of people who do not consume DHA. With no other changes in diet, improvement of blood DHA status can be achieved with dietary supplements of preformed DHA, but not with supplementation of ALA, EPA, or other precursors. (Author's abstract)
This article provides a review of the conversion of ALA and EPA into DHA. The author provides several conclusions in this regard. ALA conversion to EPA, DPAn-3 and DHA in tracer studies has been observed in nearly all humans studied from birth through late middle age and in both males and females. The majority of evidence from isotopic tracer studies show that the conversion of ALA to DHA is of the order of 1% in infants, and considerably lower in adults. This is consistent with measurements of whole body ALA oxidation which is the predominant fate of ALA in both rodents and humans. These conversion rates must be viewed as markers of flux through this metabolic pathway but must not be assumed to represent a net change in mass. Very few studies in adults show that blood stream or breast milk DHA concentrations increase following several weeks of increased dietary ALA supply, whereas most studies do not. ALA appears to contribute little to circulating DHA when added to a diet that already contains some ALA and high LA levels.  Supplementation of the diet with high levels of ALA leads to small but significant increases in EPA and DPAn-3 although supplementation with preformed EPA is approximately 15-fold more efficacious in this regard. Dietary DHA increases blood and tissue DHA beyond that achievable with consumption of usual intakes of any precursor omega-3 PUFA, against a background of western diets providing ample n-6 fatty acids. For a given dietary concentration of ALA, the conversion of ALA to LCPUFA is decreased by high dietary ratios of LA/ALA. Moreover, n-6 fatty acid intake influences tissue concentrations of the n-3 LCPUFA. Present evidence indicates that n-3 LCPUFA status can be improved by increasing their intake or by decreasing LA intake, and a combination of the two is likely to be most effective.  (Editor's comments)

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