Poor diet is now considered to play a significant role in the development of cancer. In particular, the low quality foods that characterise the typical Western diet are thought to be particularly problematic. Plant foods are thought to confer protection from cancer for two main reasons. Firstly, they are rich in phytochemicals such as the polyphenol, carotenoid and glucosinolate groups of chemicals, that act pharmacologically to inhibit the initiation, progression and propagation of cancer. Secondly, plant foods are rich in fibre which may protect from cancers of the gut through multiple mechanisms such as binding to carcinogens, decreasing transit times through the gut and through establishing healthy colonies of gram negative strains of bacteria. The absence of fibre in the typical Western diet is therefore problematic because not only does the low fibre intake increase the risk of cancer directly, it also acts as a marker for low intakes of plant food generally, indicating that potential anti-cancer phytochemicals are also absent from the diet.
For example, in one study researchers used a large prospective style study to assess the possible associations between dietary fibre intake and colorectal cancer risk1. Subjects completed a health questionnaire and over a 9 year follow up, cases of colorectal cancer were identified within the cohort. The results showed that a high intake of total dietary fibre was associated with a 15 to 20 % reduction in the risk of colorectal cancer compared to a low intake of fibre. Analysis of this data revealed that the protective effects were conferred from legume fibre intake only. Legumes, whole grains and cruciferous vegetables were associated with a reduction in the risk of colorectal cancer, whereas refined grains were associated with an increased risk of colorectal cancer. These results are interesting because they may indicate that fibre has protective effects on colorectal cancer. However, the possibility that the fibre is simply a marker for a diet rich in anti-cancer phytochemicals and plant antioxidants cannot be excluded.
The possible protective effects of plant phytochemicals on gut cancer is well researched. It is thought that the antioxidant phytochemicals in certain plants are able to inhibit the formation of carcinogenic substances within the gut. Antioxidants may prevent the conversion of nitrites and nitrates in processed meat to carcinogenic nitrosamines and thus limit the interaction between potential carcinogens and the tissues of the gut. For example, the associations between oxidative stress, gastric cancer and antioxidant intake has been measured in Zambian subjects2. The results of this study showed that urinary excretion of the oxidative stress marker 8-iso prostaglandin F2α was higher in those subjects with gastric cancer, compared to pair matched healthy control subjects. In addition, dietary analysis revealed that fruit intake was significantly lower in the subjects with gastric cancer, when compared to healthy controls. Associations between low fruit intake and high levels of oxidative stress were also significant.
Therefore it is unclear if the fibre content of plants is protective of cancer directly, or whether the fibre may be a marker for phytochemical antioxidant intake. For example, oats contain high concentrations of soluble fibre and traditionally this has been suggested to be responsible for their health effects. However recent studies have highlighted a group of phytochemicals in oats, the alkylresorcinols, that have potent antioxidant effects in humans. It is therefore very difficult to identify which component is having protective effects against diseases such as cancer. Mechanisms exist to explain anti-cancer effects for both fibre and phytochemical antioxidants, and so it likely that both fibre and phytochemicals such as polyphenols are protective of gut cancer. In fact, the different mechanisms of action hint at synergistic effects. For example, while antioxidant phytochemicals may inhibit carcinogen formation in the upper gut, fibre may be converted to short chain fatty acids (SCFA) in the lower gut through the action of beneficial bacteria.
The association between high levels of SCFA such as propionate, butyrate and acetate in the colon, and a lower risk of colorectal cancer has been reported in the nutritional literature. For example, in one study3. researchers assessed the effects of dietary fibre on the bacterial colonies within the colon in patients with advanced colorectal cancer. The results showed that lower dietary intakes of fibre were associated with lower SCFA synthesis in the colon of patients with cancer compared to controls. Analysis of the bacterial populations showed that those subject with colorectal cancer had altered bacterial populations in their colon, such that Clostridium, Roseburia and Eubacterium spp were less prevalent in the colon of the cancer patients compared to the healthy controls. In contrast, Enterococcus and Streptococcus spp were more prevalent in those subject with colorectal cancer. Higher fibre diets may therefore cause changes the bacterial populations in the gut and this may protect from cancer through conversion of fibre to SCFA.
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