Abstract

We have previously shown racial differences in Omega‐6 (ω‐6) long chain polyunsaturated fatty acid (LC‐PUFA) levels and the frequency of genetic variants in genes that enhance ω‐6 LC‐PUFA synthesis. In this study we examine if racial differences also exist in Omega‐3 (ω3) and ω6 LC‐PUFA metabolism in patients with coronary artery disease (CAD). We used Gas Chromatography to measure the LC‐PUFA precursors α‐linolenic (18:3 ALA) and linoleic (18:2 LA) and the major ω3/ω6 LC‐PUFA products, eicosapentanoic (22:5, EPA), docosapentaenoic (24:5 DPA) docosahexanoic (24:6 DHA), gamma‐linoleic (18:3 GLA), dihomo‐gamma linoleic (20:3 DGLA) and arachidonic (20:4 AA) in fasting serum from 74 African Americans (AfAm) and 334 European Americans (Eam) with CAD. Compared to EAm, AfAm had lower ALA (0.71 ± 0.22 vs 0.79 ± 0.26 p=0.01), whereas DHA levels were higher (2.12 ± 0.69 vs 1.71 ± 0.68 p<0.001). AfAm also had higher AA levels (10.00 ± 2.07 vs 7.95 ± 2.11 p<0.0001). Compared to EAm, PUFA product:precursor ratios were higher in AfAm for DHA:ALA (3.33 ± 1.6 vs 2.38 ± 1.20 p<0.001), DHA:EPA (3.28 ± 1.56 vs 2.47 ± 1.04 p<0.001), DHA:DPA (3.77 ± 1.13 vs 2.85 ± 0.96 P<0.001), AA/LA (0.33 ± 0.08 vs 0.27 ± 0.08 p<0.001) and AA/DGLA (6.93 ± 2.17 vs 5.35 ± 1.99 p<0.001). Product:precursor ratios of PUFAs provide a surrogate measure of activity in LC‐PUFA synthesis and suggests enhanced precursor conversion in AfAm which may be genetically determined.

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