Diet is an important factor in the development of colonic cancer. Fibre has been shown to decrease this risk. Part of this protective effect is probably mediated by colonic fermentation. About 10% of starch in the normal diet escapes digestion and absorption in the small bowel, and is therefore called resistant starch. This is a considerably larger source of fermentable substrate than fibre in the diet and could thus contribute significantly to the prevention of this malignancy. Short chain fatty acids, produced during fermentation, reduce colonic pH, affecting the intraluminal concentration of the putative co-carcinogenic secondary bile acids by precipitation, and by inhibition of their enzymatic formation from primary bile acids. The role of secondary bile acids in promoting colonic carcinogenesis is probably mediated by their cytotoxic effect on colonic mucosa, leading to a compensatory increase in proliferation. A hyper-proliferative mucosa, having an enhanced sensitivity to mutagenic substances, is associated with an increased risk of colorectal cancer. Butyrate, one of the short chain fatty acids, could be significant, as it has anti-neoplastic properties in vitro and in vivo. We conclude that fermentation is probably the key factor in the protective effect of fibre on colon carcinogenesis. Furthermore, consumption of resistant starch seems to be another way of stimulating fermentation.