Colorectal cancers supporting evidence

Colorectal cancer is a well-established complication of ulcerative colitis (Lennard-Jones era/., 1990 Ekbom et al., 1990). It has been shown that inflammation enhances the formation of colonic tumours in experimental animals given known carcint ens (Chester etal., 1986) and it is tempting to speculate that the longterm inflammatory response is respronsible for the increased risk of malignancy in ulcerative colitis. However, there is very little direct evidence to support this. It has also been postulated that free radicals may play a part in the development of sporadic cancers (Babbs,... 

An association between black tea consumption and the subsequent risk of colorectal cancer was sought in The Netherlands Cohort Study on Diet and Cancer (Goldbohm et al., 1996). No association was observed between tea consumption and risk of colorectal cancer The risk among tea drinkers in each consumption category was similar to that among nondrinkers. The authors concluded that this study did not support the hypothesis that consumption of black tea protects against fom of the major cancers in humans, and there was no evidence that black tea has a cancer-enhancing effect. 

The majority of evidence supports that, although anthraquinone-containing glycosides cause dark patches in the colon that can last for months (known as pseudomelanosis coli), this is not a precursor to nor does it increase the risk of colorectal cancer (Sonnenberg and Muller 1993). 

Case-control studies have shown that colorectal cancer risk increases with high intakes of sugar-rich foods, while other studies have failed to prove such a relationship. Thus, there is insufficient evidence to support the role of sugar in the risk for colorectal cancer. On the contrary, carbohydrate consumption in the form of fruit, vegetables, and cereals has been shown to be protective against colorectal cancer. 

Previous reports indicating an increase of A -acetylspermidine in colorectal cancer and breast cancer tissues may be consistent with the first alternative (Takenoshita et al. 1984 Kingsnorth and Wallace 1985), although the presence of DiAcSpm in cancer tissues was only demonstrated recently. However, evidence suggesting the involvement of peritoneal macrophages in DiAcSpm production supports the second alternative (Hamaoki and Nagata 2006). 

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