Dr John P Wright
Updated: 5 September 2005
As the cause of colon cancer is unknown it is not yet possible to determine the antidote by the traditional scientific approach. Epidemiological evidence however has shown that certain factors are involved in the development of colon cancer. Modification of these factors may reverse, suppress or prevent the carcinogenic process from progressing to invasive cancer.
The ideal approach would probably be dietary. High protein diets, high fat diets and deep frying have been suspected of promoting the development of colon cancer. Equally popular is the idea that our diets lack fruit, vegetables and fiber. Large epidemiological studies have both supported and refuted these suggestions. A number of meta-analyses have been published recently without any clear supporting evidence being found.
Lifestyle aberrations such as obesity, sedentary lifestyle and a low level of fitness appear to be associated with a higher incidence of colon cancer but the relative importance of each aspect is unknown. It is clear that cigarette smoking for more than 10 years has been shown to increase the incidence of cancer of the colon by well over 50%. The effect of alcohol ingestion is very much less clear.
A more physiological suggestion has been the carcinogenic effects of bile acids and their metabolites. The latter are produced by bacterial action and are thought to have an important role in cancer formation. The decrease in colonic transit time as a result of a high fibre diet was thought to be the underlying mechanism for the apparently low incidence of colon cancer in black Africans on a high fibre cereal diet. This scenario is still to be confirmed.
Hormone replacement therapy has had a chequered career recently but it is clear that HRT reduces the rate of invasive colonic cancer but not rectal cancer. The mechanism of this observation is unknown.
Vitamins, anti-oxidants and trace elements are being taken for all manner of ills. It is therefore not surprising that preventing colon cancer has become another objective of this type of therapy. At present it is suggested that calcium binds toxic fatty acids thereby protecting colonic epithelial cells. The specific calcium molecule and dose is still to be determined but controlled clinical studies are currently underway.
Isolated studies have shown a reduction in the incidence of cancer colon associated with the ingestion of vitamin E, D and folic acid but a meta-analysis of 14 randomised trials published last year showed no protective benefit.
The most exciting proven way to reduce the incidence of colon cancer is with non-steroidal anti-inflammatory drugs. The regular ingestion of aspirin has been shown to reduce the mortality. In a study of 600 000 subjects the mortality due to cancer of the colon was reduced by 40%. In familial adenomatous polyposis, celecoxib reduced the number of adenomas by 28%. The documented reduction in incidence and the prevention of progress of adenoma to carcinoma by non-steroidal anti-inflammatory is currently the most important area of hope in the prevention of colon cancer. The problems associated with this type of therapy include gastric ulceration and intracerebral haemorrhage. It can not therefore be recommended yet to the population at large until the relative risks and benefits are established.
At present full examination by colonoscopy of the colon in all 50 year olds will detect the majority of colon cancers at a treatable stage. The future may still bring a safe preventative strategy along with a better understanding of the pathogenesis of colon cancer but meanwhile a screening colonoscopy at 50 years of age is probably the safest approach.