The main actions of FSO have been attributed to its high ALA content. ALA is subject to three different metabolic fates: (a) incorporation into structural, transport or storage pools, (b) beta-oxidation as an energy source and (c) elongation and further desaturation to form EPA, DPA and DHA. It appears that all three contribute to the biological effects of this oil.
ALA's direct role in cell membrane structure is likely to be minor, with ALA representing less than 0.5% of the total FA in cell membranes and blood lipids in healthy adults. However, its limited propensity to generate the n-3 metabolites, EPA and DHA, the major FAs in cell membranes, could represent an indirect effect via this mechanism (Burdge 2004).
Studies exploring the metabolism of ALA have revealed that 22% of ALA undergoes beta-oxidation in women and 33% in men. Once broken down the carbon chain can be used as fuel or in the synthesis of cholesterol and other fatty acids such as palmitic, palmitoleic, stearic and oleic acids de novo (Burdge 2004). FSO also influences the eicosanoid production cascade via conversion of the n-3 and n-6 parent FAs in FSO to their respective metabolites.
It Is also thought that some of the actions of FSO may be Independent of Its FA content and can be attributed to the lignan SDG. This has been partly supported by research conducted by Prasad et al In 1998 and again in 1999. ANTI-INFLAMMATORY
Metabolites of ALA and LA act as substrates for the formation of the antiinflammatory eicosanoids, comprising prostaglandins, thromboxanes, and leukotrienes (Gerster 1998). ALA suppresses AA production by interfering with the conversion of LA to AA, and reduces the biosynthesis of inflammatory eicosanoids, although not to the same extent as EPA and DHA (Morris 2001). Cytokines, another important group of inflammatory mediators, are generated in response to these eicosanoids and are influenced by changes in the n-3:n-6 ratios in cell membranes (James et al 2000). In one study, ingestion of FSO (equivalent to 13.7 g/day ALA) for 4 weeks by healthy male subjects resulted in a 30% reduction in TNF-alpha, 31 % reduction in IL-1 -beta, 29% reduction in eicosanoids thromboxane B(2) and 30% reduction in PGE2 (Caughey et al 1996).
In animal models ALA has consistently demonstrated eicosanoid-mediated antiinflammatory effects; however, the extent of these has been dependent on the levels of both ALA and LA in the diet, duration of use and type of tissue studied (Cunnane & Thompson 1995).
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