Colorectal Cancer

Colorectal cancer develops through a process involving genetic change in the epithelial cells of the colon lining. The main factors that initiate colorectal cancer are consumption of cooked red meat (due to heterocyclic amines) (Gerhardsson de V et al 1991; Reddy S et al 1987), high intake of refined carbohydrates (Franceschi S et al 2001), poor vitamin and mineral intake, alcohol consumption, smoking, bile acids, fecal mutagens (DNA-damaging agents), fecal pH, and compromised detoxification enzymes (Winawer SJ et al 1992). An example of one important detoxification enzyme is N-acetyltransferase, which catalyzes the formation of DNA-damaging products from heterocyclic amines that form in cooked meats. Differences in the activity of this enzyme classify individuals as slow or fast acetylators. The level of red meat consumption in fast but not slow acetylators is associated with risk for colorectal cancer development (Welfare MR et al 1997).

In industrialized Western societies, both polyps and colon cancer occur more frequently due in part to diets low in fruits, vegetables, vegetable protein, and fiber (Satia-Aboutaj J et al 2003). Fecal mutagens are produced by certain diets such as those containing overcooked or burnt meat or fish. Increased intake of fiber, on the other hand, shortens the intestinal transit time, which in turn reduces the exposure of the colorectal lining to mutagens within the stool (Johansson G et al 1997).

Low folate intake, especially when combined with alcohol consumption and a low-protein diet, increases colorectal cancer risk (Kato I et al 1999). Dietary folate influences DNA methylation, synthesis, and repair. Abnormalities in these DNA processes enhance cancer development, particularly in rapidly growing tissues such as the colorectal mucosa (Lengauer C et al 1997; Feinberg AP et al 1983). Higher folate intake from either dietary sources or supplements may protect against the initiation of colorectal cancer (Giovannucci E 2002, 1998).