THESIS

Cassidy et al. (1994), in an international correlative study, found a
strong inverse relationship between starch intake and colon ad rectal cancer, even
after adjusting for fat and protein intake. Non starch polysaccharides were only
significantly correlated when combined with starch. In this study, the authors assumed
that 5% of all starch consumed was resistant and that this RS contributed to the
protective effect of starch. However, this estimate represents a substantial amount of
RS reaching the colon as dietary intakes of starch are approximately 8-10 times higher
than intakes of non starch polysaccharides.
1.2.2 Resistant starch and short chain fatty acid production
The fermentation of resistant starch in the colon by colonic bacteria
to produce short-chain fatty acids has been associated with various health benefits
(Escarpa et al. 1996; Topping and Clifton, 2001). The formation of butyrate seems to
be especially beneficial, as its function has been linked to lowering cancer risk by
various mechanisms. Butyrate inhibits division of cancer cells, induces apoptosis in
colon tumor cell lines and inhibits proliferation of colonic mucosal cells (Van et al.
1994). Butyrate induces the chemo preventive enzyme, glutathione transferase in rat
colon (Escarpa et al. 1996).
Furthermore, the toxicity of potential mutagens such as nitrosamide
and hydrogen peroxide in human colon cells is inhibited by butyrate. In addition to
the production of short-chain fatty acids, the presence of resistant starch in the colon
results in lowers concentrations of bile acids such as cholic acid and enhances their
excretion, probably protecting against colorectal cancer. In particular, RS II (from
raw potatoes starch) is reported to increase the concentration of butyrate in humans
and rats (Cummings et al. 1996; Martin et al. 2000; Henningsson et al. 2003). While
RS3 (retrograded starch) reported to increase the concentration of acetate in pigs
(Martin et al. 2000), but not in humans (Cummings et al. 1996).
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