The question of whether supplementation with ALA affects platelet aggregation remains unclear. A major determinant appears to be the degree of conversion to EPA (Garg et al 1989). When there is an increase in total EPA and reduced AA, due to ALA inhibition of LA conversion, the result is EPA replacing AA in the cell membrane and a decrease in thromboxane synthesis. In addition, SDG, another component of FSO, is metabolised to enterolactone and enterodiol and these substances may have antiplatelet-activating factor activity. Due to the variable lignan content of FSO it is difficult to determine the clinical significance of this (Prasad 1999). Studies assessing the actual antiaggregatory effect of FSO in humans have produced mixed results.
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