The association between meat and colorectal cancer is controversial. This controversy stems in large part from studies that show that different types of meat may have very different effects on the risk of carcinogenesis. In particular, the association between meat and colorectal cancer is strongest for cured meat, possibly because chemicals used during curing are the actual cause of the effect. The use of nitrites and nitrates in cured meat has been highlighted as a possible cause of the carcinogenic effects of such foods, and this results from their ability to be converted into nitroso compounds (NOC) in the mammalian gut. Nitroso compounds may be able to initiate cancer in the cells of the gastrointestinal tract, thus explaining the association between cured meat and cancer. Another possibility is that cooking the meats at high temperatures causes the production of heterocyclic amines (HCA) which are known carcinogens. Haem in red meat can stimulate the formation of NOCs and thus may be a contributory factor.
Animal studies show a carcinogenic effects for NOCs and so researchers are interested in investigating dietary components that may inhibit their detrimental effects in the mammalian gut. For example, in one study1, a group of rats received a number of dietary components including calcium carbonate, inulin, rutin, carnosol, α-tocopherol and trisodium pyrophosphate in addition to cured meat for 14 days. Cured meat in the diet of the rats increased the production of NOCs and lipid peroxides in the faeces of the rats but calcium was able to normalise this affects. In addition α-tocopherol normalised the NOCs in the faeces of the rats. When the experiment was repeated on human volunteers cured meat also raised levels of NOCs and lipid peroxides in faeces, but calcium was able to normalise both parameters, while α-tocopherol normalised just lipid peroxidation. Calcium and α-tocopherol therefore appear to have beneficial effects at reducing some of the biomarkers associated with colorectal cancer development.
In addition, when the researchers assessed the effects of calcium and α-tocopherol on the gut wall structure, they found that both compounds decreased the number of mucin depleted foci (precancerous lesions that harbour mutations in genes) in the rats. This result suggested that that the risk of carcinogenesis had been suppressed through a reduction in the amount of potentially precancerous tissue. The haem from red meat is likely able to increase the risk of gut cancer because it is able to oxidise the nitrites and nitrates in meat to form carcinogenic NOCs. This suggests that it is not the iron per se that is the cause of the cancer but the presence of the preservatives in cured meat. This may explain the weaker association between red meat and gut cancer when compared to cured meat and gut cancer Antioxidants such as vitamin C can prevent the formation of NOCs because they inhibit the oxidation of nitrites and nitrates in the gut.
Dr Robert Barrington’s Comments: Nitrite and nitrate compounds in combination with haem appears to be necessary for the initiation of cancer of the gut. Reducing intakes of one or both compounds therefore makes sense. High intakes of cured meat are associated with the typical Western diet, and this explains the reason that colorectal cancer is now the third most common type of cancer in Western nations. Avoiding cured meat and ensuring a high intake of antioxidants from plant foods in order to maintain nitrites and nitrates in their reduced form is likely an effective strategy in beating colorectal cancer. Whether red meat of high quality is carcinogenic in isolation is unknown, but evidence certainly suggests it can be incorporated as part of a high quality diet if consumed with antioxidant plant foods. Haem can oxidise secondary amines in proteins to form NOCs but the significance of this with respect to colorectal cancer is not as clear as with cured meat.Calcium can likely reduce the carcinogenic effects of cured meat because it can bind to haem iron and thus modulate its ability to initiate the formation of NOCs.
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