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      Consumption of Buglossoides arvensis seed oil is safe and increases tissue long-chain n-3 fatty acid content more than flax seed oil – results of a phase I randomised clinical trial

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          Abstract

          Enrichment of tissues with ≥20-carbon n-3 PUFA like EPA is associated with positive cardiovascular outcomes. Stearidonic acid (SDA; 18 : 4 n-3) and α-linolenic acid (ALA; 18 : 3 n-3) are plant-derived dietary n-3 PUFA; however, direct comparisons of their impact on tissue n-3 PUFA content are lacking. Ahiflower ® oil extracted from Buglossoides arvensis seeds is the richest known non-genetically modified source of dietary SDA. To investigate the safety and efficacy of dietary Ahiflower oil, a parallel-group, randomised, double-blind, comparator-controlled phase I clinical trial was performed. Diets of healthy subjects ( n 40) were supplemented for 28 d with 9·1 g/d of Ahiflower (46 % ALA, 20 % SDA) or flax seed oil (59 % ALA). Blood and urine chemistries, blood lipid profiles, hepatic and renal function tests and haematology were measured as safety parameters. The fatty acid composition of fasting plasma, erythrocytes, polymorphonuclear cells and mononuclear cells were measured at baseline and after 14 and 28 d of supplementation. No clinically significant changes in safety parameters were measured in either group. Tissue ALA and EPA content increased in both groups compared with baseline, but EPA accrual in plasma and in all cell types was greater in the Ahiflower group (time × treatment interactions, P ≤ 0·01). Plasma and mononuclear cell eicosatetraenoic acid (20 : 4 n-3) and docosapentaenoic acid (22 : 5 n-3) content also increased significantly in the Ahiflower group compared with the flax group. In conclusion, the consumption of Ahiflower oil is safe and is more effective for the enrichment of tissues with 20- and 22-carbon n-3 PUFA than flax seed oil.

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          Most cited references51

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          A rapid method of total lipid extraction and purification.

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            Proresolving lipid mediators and mechanisms in the resolution of acute inflammation.

            Inflammatory responses, like all biological cascades, are shaped by a delicate balance between positive and negative feedback loops. It is now clear that in addition to positive and negative checkpoints, the inflammatory cascade rather unexpectedly boasts an additional checkpoint, a family of chemicals that actively promote resolution and tissue repair without compromising host defense. Indeed, the resolution phase of inflammation is just as actively orchestrated and carefully choreographed as its induction and inhibition. In this review, we explore the immunological consequences of omega-3-derived specialized proresolving mediators (SPMs) and discuss their place within what is currently understood of the role of the arachidonic acid-derived prostaglandins, lipoxins, and their natural C15-epimers. We propose that treatment of inflammation should not be restricted to the use of inhibitors of the acute cascade (antagonism) but broadened to take account of the enormous therapeutic potential of inducers (agonists) of the resolution phase of inflammation.
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              Resolvins and protectins in inflammation resolution.

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                Author and article information

                Journal
                J Nutr Sci
                J Nutr Sci
                JNS
                Journal of Nutritional Science
                Cambridge University Press (Cambridge, UK )
                2048-6790
                2016
                08 January 2016
                : 5
                : e2
                Affiliations
                [1 ]Department of Chemistry and Biochemistry, Université de Moncton , Moncton, NB, Canada
                [2 ]Réseau de Santé Vitalité Health Network, Centre hospitalier universitaire Dr-Georges-L.-Dumont , Moncton, NB, Canada
                [3 ]Department of Biology, Université de Moncton , Moncton, NB, Canada
                [4 ]Department of Biology, Université du Québec à Rimouski , Rimouski, QC, Canada
                Author notes
                [* ]Corresponding author:, Dr M. E. Surette, fax +1 506 858 4541, email marc.surette@ 123456umoncton.ca
                Article
                S2048679015000348 00034
                10.1017/jns.2015.34
                4709838
                26793308
                ac5e195f-19c3-49fe-8458-2b115a8cf61b
                © The Author(s) 2016

                This is an Open Access article, distributed under the terms of the Creative Commons Attribution licence ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted re-use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 22 September 2015
                : 19 October 2015
                Page count
                Figures: 3, Tables: 7, References: 64, Pages: 12
                Categories
                Research Article

                stearidonic acid,leucocytes,epa,ae, adverse event,ala, α-linolenic acid,ar, adverse reaction,dpa, docosapentaenoic acid,dgla, dihomo-γ-linolenic acid,eta, eicosatetraenoic acid,fame, fatty acid methyl esters,gla, γ-linolenic acid,hbss, hanks' balanced salt solution,pmn, polymorphonuclear cells,sda, stearidonic acid

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