Antiproliferative

ALA has demonstrated the capacity to inhibit tumour progression in animal models of mammary tumour (Chen et al 2002, Cognault et al 2000); however, the clinical significance of these findings needs to be examined further. An immunostimulant action, which is both eicosanoid and non-eicosanoid mediated, has been suggested as one possible mechanism of action. Another theory suggests that through ALA's competitive inhibition of LA, tumour cells may not receive sufficient LA, which would inhibit further cell growth (Johnston 1995). It is interesting to observe that higher dietary ALA intake is associated with a reduction in cancer deaths; however, this is not seen with higher EPA/DHA intakes, suggesting that the protective effect is not reliant on the conversion of ALA to EP/VDHA (Cunnane 1995). In addition, results from © 2007 Elsevier Australia

epidemiological studies show an association between low ALA consumption in humans and increased cancer deaths in general (Dolecek 1992).

Animal studies testing SDG and its metabolites from the seeds have produced promising results and suggest that they may act as selective oestrogen receptor modulating agents and therefore play a protective role against oestrogen-dependent cancers (Kitts et al 1999, Wang et al 2005).

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