Colorectal, commonly known as bowel cancer, refers to any cancer of the colon or rectum. It is the third most common cancer worldwide, representing over 9% of all cancers, with Australia and New Zealand having some of the highest rates globally.[1,2]
Colon and rectal cancers are often preceded by adenomatous polyps, which have both genetic and environmental triggers. 3] While polyps are seldom symptomatic, they are the precursor lesion for a large majority of colorectal cancers. Larger adenomas, or when multiple are present, increases the risk of future cancer diagnosis. A number of studies suggest that Western dietary and lifestyle factors are responsible for the high incidence of colorectal cancer seen in industrialised countries, with significantly increased incidence observed in developing countries as Western lifestyles are increasingly adopted.[1,5]
Lifestyle factors, especially the standard Western diet, appear to play a major role in the development of colorectal cancer. There is convincing evidence that obesity and physical inactivity are also associated with an increased risk.[6,7] Chronic inflammation, such as that seen in inflammatory bowel diseases, upregulates metabolic activity which promotes tumorigenesis.[8–10] These inflammatory processes are regulated by the composition of the microbiota. See our topic summary on the gut microbiota for further information.
Well-researched dietary factors are:
- Dietary fat, which has been shown to upregulate colonic inflammation and increase permeability of the mucosal layer, mediated by the production of secondary bile acids [12,13]
- Red and processed meats. These have been classified as carcinogenic, with mechanisms proposed to be related to the formation of toxic heterocyclic amines, polycyclic aromatic hydrocarbons, heme, N-Nitroso compounds and N-glycolylneuraminic acid 
Figure 1. (from Yang et al., 2018 ) shows the mechanisms by which diet either disrupts or protects the colonic environment from DNA damage. As this illustrates, a diet high in fibre, antioxidants and phenolic compounds reduces production of toxic secondary bile acids, ammonia and hydrogen sulfide and promotes the production of an abundance of short chain fatty acids, protecting colonocytes and the mucosal barrier. Therefore, the consumption of whole grains, fruit and vegetables is associated with reduced risk of colorectal cancer.[6,7,15]
The nutrition prescription
A whole food plant-based diet is naturally high in overall dietary fibre, nutrients and antioxidants, all of which support a healthy gut microbiome and reduce the risk of inflammation occurring in the colonic environment.
Of the short chain fatty acids, butyrate has been shown to be particularly beneficial. Butyrate production increases on high fibre diets and is linked with reduced inflammation and prevention of colon cancer.  A landmark study showed a two-week dietary switch to a predominantly plant-based diet produced remarkable reductions in inflammatory and proliferative markers in colonic biopsies, while more than doubling butyrate production. Dietary fibre provides prebiotic activity and thus stimulates the growth of beneficial bacteria and drives short chain fatty acid production. It also supports epidemiological and clinical evidence showing whole grains, fruits and vegetables reduce colorectal cancer risk.
Other components consumed in abundant quantities on a plant-based diet are phenolic compounds and antioxidants, which reach the colonic microbiome largely intact.  Although research surrounding their impact on colorectal cancer is in its infancy, they have significant anti-inflammatory and anti-proliferative effects.
A whole food plant-based diet low in fat also reduces the production of bile acids, and the subsequent formation of secondary bile acids in the colon, which have already been shown to promote tumours within the colonic environment.
Medical supervision of diet change is essential
People with signs and symptoms of poor gut health should always consult their general practitioner or specialist for diagnosis, treatment and supervision of diet change.
Video overview from Physicians Committee for Responsible Medicine
The Nutrient Reference Values for Australia and New Zealand recommend a daily intake of 25g of dietary fibre for women and 30g for men.  However, it appears that this may not be sufficient to protect against colorectal cancer, given that consumption approaches these levels, but the prevalence of colorectal cancer is amongst the highest in the developed world. [5,21] A whole food plant-based diet comprising a variety of whole grains, fruits, vegetables, legumes and nuts naturally provides well in excess of these requirements. It is important that a wide variety of plant foods are chosen to ensure that a diversity of microbiome-stimulating fibres are provided to the colon.
Resistant starch, a form of fibre naturally found in starch-rich foods, such as legumes, whole grains, tuberous vegetables and slightly under-ripe bananas has been shown to be particularly effective at increasing butyrate production in the colon and confer protection against colorectal cancer development. [9,10] A whole food plant-based dietary pattern that comprises a wide variety of whole grains, tuberous vegetables, legumes and fruit will provide significantly greater resistant starch intake than a standard Australian diet.
While the microbiome adapts rapidly to dietary change,  sudden increases of dietary fibre consumption via additional fruit, vegetables and legumes can cause discomfort in the initial stages. We recommend taking a stepwise approach to increasing intake to allow a smooth transition to increased whole foods which is sustainable.
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Le Leu RK, Hu Y, Brown IL, Woodman RJ, Young GP. Synbiotic intervention of Bifidobacterium lactis and resistant starch protects against colorectal cancer development in rats. Carcinogenesis. 2010;31(2):246-251. https://doi.org/10.1093/carcin/bgp197
Hu Y, Le Leu RK, Christophersen CT, et al. Manipulation of the gut microbiota using resistant starch is associated with protection against colitis-associated colorectal cancer in rats. Carcinogenesis. 2016;37(4):366-375. https://doi.org/10.1093/carcin/bgw019
Yang J, Yu J. The association of diet, gut microbiota and colorectal cancer: what we eat may imply what we get. Protein Cell. 2018;9(5):474-487. https://doi.org/10.1007/s13238-018-0543-6
Ocvirk S, O’Keefe SJ. Influence of Bile Acids on Colorectal Cancer Risk: Potential Mechanisms Mediated by Diet – Gut Microbiota Interactions. Curr Nutr Rep. 2017;6(4):315-322. https://doi.org/10.1007/s13668-017-0219-5
Stenman LK, Holma R, Eggert A, Korpela R. A novel mechanism for gut barrier dysfunction by dietary fat: epithelial disruption by hydrophobic bile acids. Am J Physiol-Gastrointest Liver Physiol. 2013;304(3):G227-G234. https://doi.org/10.1152/ajpgi.00267.2012
Cascella M, Bimonte S, Barbieri A, et al. Dissecting the mechanisms and molecules underlying the potential carcinogenicity of red and processed meat in colorectal cancer (CRC): an overview on the current state of knowledge. Infect Agent Cancer. 2018;13(1):3.
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O’Keefe SJD, Li JV, Lahti L, et al. Fat, fibre and cancer risk in African Americans and rural Africans. Nat Commun. 2015;6(1):6342. https://doi.org/10.1038/ncomms7342
Bishehsari F, Engen PA, Preite NZ, et al. Dietary Fiber Treatment Corrects the Composition of Gut Microbiota, Promotes SCFA Production, and Suppresses Colon Carcinogenesis. Genes. 2018;9(2):102. https://doi.org/10.3390/genes9020102
Orlich MJ, Singh PN, Sabaté J, et al. Vegetarian Dietary Patterns and the Risk of Colorectal Cancers. JAMA Intern Med. 2015;175(5):767-776. https://doi.org/10.1001/jamainternmed.2015.59
Cueva C, Silva M, Pinillos I, Bartolomé B, Moreno-Arribas MV. Interplay between Dietary Polyphenols and Oral and Gut Microbiota in the Development of Colorectal Cancer. Nutrients. 2020;12(3):625. https://doi.org/10.3390/nu12030625
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