The majority of cancers are sporadic and epidemiological estimates suggest
that up to 80% of colorectal cancer is attributable to diet. Epidemiologica
lly, cross-sectional comparisons, case-control studies and trends in food i
ntake show high rates of colorectal cancer in populations consuming diets h
igh in meat: and fat, and low in starch, NSP (non-starch polysaccharides, f
ibre) and vegetables. In general, prospective studies tend to support these
findings although estimates of relative risk are not high. Existing prospe
ctive studies have however used crude indices of diet subject to substantia
l measurement error, and interactions with genetic polymorphisms in, for ex
ample, phase-I and -II enzymes have been studied only rarely. The associati
on between meat consumption and colorectal cancer is usually attributed to
the formation of heterocyclic amines in meat when it is cooked. In addition
, in humans high-meat diets increase the level of nitrosatable material ent
ering the colon so that faecal N-nitroso compounds (NOCs) increase in a dos
e-responsive manner following endogenous synthesis in the colon. Some of th
e mutations and guanine adducts accumulated during colorectal cancer progre
ssion are characteristic of alkylative damage, which would be compatible wi
th NOC exposure. To date, NSP, resistant starch and vegetables have not red
uced faecal NOC levels.