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Dietary fibre has been purported to have beneficial effects on colorectal cancer presumably by reducing colon transit time and thus reducing exposure of the intestine lining to potentially harmful carcinogenous chemicals present in our diet. The lack of fibre in our diet coupled with increased red meat and saturated fat intake has long been associated with increased colorectal cancer rates.

Evidence in this regard has been noted in population based studies which show that immigrant populations develop the same rates of colorectal cancer as the resident population after prolonged exposure (Japanese Hawaiians) to the environment.Some population based studies at variance with this theory. What is thought to be a confounding problem is that there are now known to be 2 mechanisms that cause colorectal cancer. Cancers have been shown to grow from abnormal tissue growths (polyps) in the lining of the intestine (mucosa). This is a size, shape and tissue type dependent phenomenon.

The first mechanism for cancer development from polyps is the "carcinoma-adenoma sequence" (CA). This affects more left sided (distal) tumours. 

The second mechanism of "micro satellite-instability" (MSI) is due to mutations of genes that prevent cell repair.  These increase the chances of cancer developing. This form of cancer affects more the right-sided (proximal) tumours. 

The third pathway is the serrated polyp pathway. Mutation of  BRAF is usually associated.

 “Serrated polyps” is the term used for epithelial lesions of the colon and rectum that have a “sawtooth” pattern on the polyp's surface and crypt epithelium. The so-called serrated pathway describes the progression of sessile serrated adenomas and traditional serrated adenomas to colorectal cancer.

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