Colorectal cancer

Graphic of colorectal cancer statisticsHow diet, nutrition and physical activity affect colorectal (bowel) cancer risk. In total, we analysed 99 studies from around the world, comprising more than 29 million adults and over 247,000 cases of colorectal cancer.

The colon is the lower part of the intestinal tract. It extends from the caecum to the rectum. In the colon, water and salts are absorbed from undigested foods, and muscles move the waste products towards the rectum.

The colon contains a vast population of many types of bacteria, which have potentially important functions. These include the fermentation of unabsorbed carbohydrate (non-starch polysaccharides and resistant starch) to release energy and short-chain fatty acids that influence the health of the colonic mucosa. The colon is lined with mucous membranes and contains lymphoid cells that form part of the body’s immune defences.

> Find the latest colorectal cancer statistics

What causes colorectal cancer?

Our Expert Panel has reviewed the evidence on diet, weight, physical activity and the risk of colorectal cancer.

There is strong evidence that:

There is some evidence that:

  • consuming foods containing vitamin C might decrease the risk of colon cancer
  • consuming fish might decrease the risk of colorectal cancer
  • vitamin D might decrease the risk of colorectal cancer
  • consuming multivitamin supplements might decrease the risk of colorectal cancer
  • low consumption of non-starchy vegetables might increase the risk of colorectal cancer
  • low consumption of fruit might increase the risk of colorectal cancer
  • consumption of foods containing haem iron might increase the risk of colorectal cancer

> Download our 2018 colorectal cancer report

> See more graphics in our toolkit

Other causes of colorectal cancer

In addition to the findings on diet, nutrition and physical activity outlined above, other established causes of colorectal cancer include:

Smoking

Smoking 40 cigarettes (two packs) per day increases risk of colorectal cancer by about 40% and nearly doubles the risk of colorectal cancer death.

Other diseases

Inflammatory bowel disease (Crohn’s disease and ulcerative colitis) increases the risk of colon cancer.

Medication

Long-term use (five years or more) of at least 75 mg per day of the non-steroidal antiinflammatory drug aspirin can reduce the risk of colorectal cancer. Hormone therapy in postmenopausal women decreases colorectal cancer risk.

Emerging research on colorectal cancer

We fund research on colorectal cancer through our grant programme. Read about the latest findings and ongoing projects in our database of projects.

Pathogenesis: how does colorectal cancer develop?

Approximately 95 per cent of colorectal cancers are adenocarcinomas. Other types of cancer that can occur include mucinous carcinomas and adenosquamous carcinomas.

Carcinogens can interact directly with the cells that line the colon and rectum. Between five and 10 per cent of colorectal cancers are a consequence of recognised hereditary conditions. The two major ones are familial adenomatous polyposis (FAP) and hereditary non-polyposis colorectal cancer (HNPCC). A further 20% of cases occur in people who have a family history of colorectal cancer.

People with FAP have a mutation in the tumour-suppressor gene APC which regulates cell growth and develop a large number of adenomas at a relatively young age; if left untreated, nearly all will develop colorectal cancer by the time they reach age 40. On average, people develop HNPCC in their mid-40s; having this form of the disease also increases the risk of a number of other gastrointestinal cancers. HNPCC involves mutations in DNA repair genes.

These two conditions also lead to sporadic colorectal cancer. The so-called ‘gatekeeper’ pathway involves the disruption of genes that regulate growth – principally APC, as in FAP – and is involved in 85% of sporadic colorectal cancers. The ‘caretaker’ pathway, which is characterised by disruption to genes that maintain genetic stability as in HNPCC, leads to 15% of sporadic cancers.

Full references and a summary of the mechanisms underpinning all the findings can be found in the colorectal cancer report.

Diet and Cancer Report 2018

In 2018, World Cancer Research Fund International published Diet, Nutrition, Physical Activity and Cancer: a Global Perspective on behalf of AICR, WCRF and WKOF. This was the third in our series of major reports looking at the many ways in which our diets, and how active we are, affect our cancer risk. You can find out much more about colorectal cancer by downloading a pdf of the relevant chapter in the 2018 report. Please note, however, that this webpage may have been updated since the report was published.

Published findings in peer-reviewed journals

Selected findings from this report have been published in peer-reviewed journals. Details of the papers and links to the abstract in PubMed are below:

Height and body fatness and colorectal cancer risk: an update of the WCRF-AICR systematic review of published prospective studies. Abar, Vieira AR, Aune, Sobiecki JG, Vingeliene S, Polemiti E, Stevens C, Greenwood DC, Chan DSM, Schlesinger S, Norat T. Eur J Nutr. 2017 Oct 28. doi: 10.1007/s00394-017-1557-1. Abstract

Adult weight gain and colorectal adenomas-a systematic review and meta-analysis. Schlesinger S, Aleksandrova K, Abar L, Vieira AR, Vingeliene S, Polemiti E, Stevens CAT, Greenwood DC, Chan DSM, Aune D & Norat T. Ann Oncol 2017 Jun 1;28(6):1217-1229. doi: 10.1093/annonc/mdx080. Abstract

Foods and beverages and colorectal cancer risk: a systematic review and meta-analysis of cohort studies, an update of the evidence of the WCRF-AICR Continuous Update Project. Vieira AR, Abar L, Chan DSM, Vingeliene S, Polemiti E, Stevens C, Greenwood D, Norat T. Ann Oncol. 2017 Aug 1;28(8):1788-1802. Abstract

Red and processed meat intake and risk of colorectal adenomas: a systematic review and meta-analysis of epidemiological studies. Aune D, Chan DS, Vieira AR, Navarro Rosenblatt DA, R Vieira, Greenwood DC, Kampman E & Norat T. Cancer Causes Control. 2013; 24 (4): 611-27. Abstract

Carbohydrates, glycemic index, glycemic load, and colorectal cancer risk: a systematic review and meta-analysis of cohort studies. Aune D, Chan DS, Lau R, Vieira R, Greenwood DC, Kampman E & Norat T. Cancer Causes Control. 2012; 23 (4): 521-535. Abstract

Recent Evidence for Colorectal Cancer Prevention Through Healthy Food, Nutrition, and Physical Activity: Implications for Recommendations. Perera PS, Thompson RL & Wiseman MJ. Curr Nutr Rep. 2012 DOI 10.1007/s13668-011-0006-7 Abstract

Dairy products and colorectal cancer risk: a systematic review and meta-analysis of cohort studies. Aune D, Lau R, Chan DS, Vieira R, Greenwood DC, Kampman E & Norat T. Ann Oncol. 2012 (1); 23: 37-45. Abstract

Nonlinear reduction in risk for colorectal cancer by fruit and vegetable intake based on meta-analysis of prospective studies. Hurst R, Hooper L, Norat T, Lau R, Aune D, Greenwood DC, Vieira R, Collings R, Harvey LJ, Sterne JA, Beynon R, Savovic J & Fairweather-Tait SJ.  Am J Clin Nutr. 2012; 96(1): 111-22. Abstract

Red and processed meat and colorectal cancer incidence: meta-analysis of prospective studies. Chan DS, Lau R, Aune D, Vieira R, Greenwood DC, Kampman E & Norat T. PLoS ONE. 2011; 6: e20456. Abstract

Dietary fibre, whole grains, and risk of colorectal cancer: systematic review and dose-response meta-analysis of prospective cohort studies. Aune D, Chan DSM, Lau R, Vieira R, Greenwood DC, Kampman E & Norat T. BMJ 2011; 343:d6617 Nov 10. Abstract

Meta-analyses of vitamin D intake, 25-hydroxyvitamin D status, vitamin D receptor polymorphisms and colorectal cancer risk. Touvier M, Chan DS, Lau R, Aune D, Vieira R, Greenwood DC, Kampman E, Riboli E, Hercberg S & Norat T. Cancer Epidemiol Biomarkers Prev. 2011; 20: 1003-16. Abstract