New Concepts In Colorectal Cancer


Emma Maitland-Carew, BSc, Nutritional Therapist

Year of publication: 

Incidences of colorectal cancer

In the UK, more than 36,500 cases of colorectal cancer are diagnosed every year (13% of all cancers). Incidences begin to rise at 40 years old with 83% of cases in people over 60. It is more common in men than women (1). Incidences of colorectal cancer are three to four times greater in developed countries compared with less developed countries (2). People moving from their native cultures to a developed country have the same risk of colorectal cancer within one generation. This is strong evidence that environmental factors, as well as genetic factors, are involved in the aetiology. It has been suggested that between 60% and 80% of colorectal cancer is attributable to diet (3), although national statistics (2005) suggest only between 15% and 25% (4).

Aetiology of colorectal cancer

Colorectal cancer begins as small, round swellings on the surface of the intestinal or rectal epithelial tissue lining, or on a polyp and takes several decades to develop into an adenocarcinoma. When the cancer begins to invade nearby lymph nodes it can quickly spread to the liver via the portal vein.

A recent meta-analysis suggested that colorectal cancer is part of a ‘complex metabolic syndrome’ due to its association with obesity, insulin resistance, hyperglycaemia and diabetes (5). High circulating c-peptide (an insulin marker), circulating c-reactive protein (an inflammatory marker), physical inactivity and excessive energy intake, all associated with metabolic syndrome, are also markers associated with colorectal cancer. Inherited genes are responsible for 20% of all colorectal cancer cases (6).

 Early case-control and cohort studies showed that colorectal cancer was statistically significantly associated with dietary glycaemic load (GL) and carbohydrate intake. However, due to many confounding factors missed in these studies, and the poor data collection, these results were considered unreliable. Two cohort studies found there was an association in men but not in women but these results were weakened by missing Hormone Replacement Therapy (HRT) treatment as a variable. The latest cohort study showed no association, and one study found an inverse in women.

Studies in vitro and in vivo show that insulin, IGF-1 and IGFBP-3 drives colorectal cancer (7, 8). Dietary glycaemic index (GI) is considered a good predictor of insulin release from a given carbohydrate but many factors including type of foods, extent of processing, length of cooking time, amount of fibre and the presence of fat and protein in a meal, all affect the GI value, are not included in the calculations.

Therefore dietary GI or GL are not good surrogate measures of the insulin response which may explain the negative association found particularly in later studies. This is further supported when colorectal cancer is considered part of a ‘complex metabolic syndrome’.

Several confounding factors were not considered in any of the studies which would only strengthen any negative results. These included psychological stress, genetics, diet in childhood, gut integrity and the side-effect of drugs. To conclude, findings suggest that dietary GL and carbohydrate intake are not associated with colorectal cancer, possibly because they are not a good surrogate measure of serum insulin levels and it is serum insulin levels that are associated with colorectal cancer.

 Reducing Risk

 Eating a highly nutritious diet, rich in fish, saturated fat, polyunsaturates, calcium-rich dairy produce, fruit and vegetables, vitamin C, folate and vitamins B12 and B6 all help to reduce risk of colon cancer. The good news is that these are very easy to include in our diets. 

HEALTH CONDITIONS, adenocarcinoma, metablic syndrome
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