Omega-3, Omega-6 and Omega-9 Fatty Acids: Implications for Cardiovascular and Other Diseases

Strategic in pathophysiological homeostasis (following injury), as well as cellular, tissue and organismic protection are acute and chronic inflammatory responses [1,2]. Consequently, the pathogenesis and progression of cardiovascular and other diseases is initiated and perpetuated by this phenomenon. Efforts to normalize or control inflammatory processes include pharmacological, dietary and behavioral therapies, aimed at regulating biologically stimulatory molecules that may stimulate or suppress the synthesis of inflammatory triggers and subsequent byproducts [3-9]. The most recognizable potent bioactive lipid mediators are Arachidonic Acid (AA, C20:4n6), Eicosapentaenoic Acid (EPA, C22:5n3) and Docosahexaenoic Acid (DHA, C20:6n3), synthesized from their dietarly essential precursors linoleic (LA, C18:3n6) and αlinolenic (ALA, C18:3n3) acids (Figure 1). The omega-9 fatty acid, oleic acid, has been suggested to occupy a role in the metabolism of the essential fatty acids [10,11]. These bioactive lipid mediators regulate pro-and anti-inflammatory processes via their ability to stimulate enzymes and produce cytokines and other acute phase molecules [12]. Further, these mediators occupy a central role in the synthesis of lipoxins and resolvins that hinder inflammatory pathways, increase the production of anti-inflammatory cytokines and facilitate the resolution of acute inflammation [13-17]. Decreasing dietary omega-6 fatty acid (i.e. linoleic acid) intake increases the bioavailability of omega-3 fatty acids [18], which may in turn lower tissue concentrations of the omega-6/omega-3 fatty acid ratio, mitigate the intensity and duration of inflammatory responses and subsequently reduce disease risk [19-21].