DIFFERENTIAL UTILIZATION OF EICOSAPENTAENOIC ACID AND DOCOSAHEXAENOICACID IN HUMAN PLASMA

It has recently been shown that the omega3 fatty acid status in humans can be predicted by the concentration of eicosapentaenoic (EPA) and d ocosahexaenoic (DHA) acids in plasma phospholipids [Bjerve, K.S., Brub akk, A.M., Fougner, K.J., Johnsen, H., Midjthell, K., and Vik, T. (199 3) Am. J. Clin. Nutr., in press]. In countries with low intake of omeg a3 fatty acids, the level of EPA in plasma phospholipids is often only about one-fifth the concentration of DHA. The purpose of this study w as to investigate whether this difference in the concentration of thes e two fatty acids was due to a selective loss of EPA relative to DHA o r to a lower dietary intake of EPA. Seven female volunteers ingested f our grams of MaxEPA daily for 2 wk and in the following 4 wk they ate a diet almost completely devoid of the long-chain omega3 fatty acids. The concentrations of the omega3 fatty acids in the plasma cholesteryl esters, triglycerides and phospholipids and the high density lipoprot ein phospholipids were examined at weekly intervals throughout the stu dy. There was a more rapid rise in the concentration of EPA than in DH A levels in the supplementation period in all lipid fractions, but the re was a disproportionate rise in DHA relative to EPA in the plasma li pids compared with the ratio in the supplement. In the depletion phase there was a rapid disappearance of EPA from all fractions, such that pre-trial levels were reached by one week post-supplementation. The di sappearance of DHA was slower, particularly for the plasma phospholipi ds: at 4 wk post-supplementation, the DHA concentration in this fracti on was still 40% above the pre-trial value. It is suggested that the l ow plasma EPA values relative to DHA are the result of increased beta- oxidation of EPA and/or low dietary intake, rather than a rapid conver sion of EPA to DHA. One practical result of this experiment is that, c ompared with DHA, the maintenance of increased EPA levels in plasma (a nd therefore tissues) would require constant inputs of EPA due to its more rapid loss from the plasma.