Colorectal cancer

Dietary and lifestyle strategies

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  Cite this page

Macrae, F, Trevor Lockett, Julie Clarke, Chetcuti, A, Emery, J, Professor Mark Jenkins PhD BSc, McNeil, J, Prof Allan Spigelman, Dr Aung Ko Win, A/Prof Robyn Woods, Young, G, "[Pachter],[NP]", Professor John Zalcberg MB BS, PhD, FRACP, FRACMA FAICD, Cancer Council Australia Colorectal Cancer Guidelines Working Party. Guidelines:Colorectal cancer/Primary prevention dietary and lifestyle . In: Clinical practice guidelines for the prevention, early detection and management of colorectal cancer. Sydney: Cancer Council Australia. [Version URL: https://wiki.cancer.org.au/australiawiki/index.php?oldid=173036, cited 2023 Nov 29]. Available from: https://wiki.cancer.org.au/australia/Guidelines:Colorectal_cancer.


Last modified:
7 November 2017 23:29:40




Overview of evidence (non-systematic literature review)[edit source]

No systematic reviews on this topic were undertaken in the development of this clinical practice guideline section.

Evidence sources[edit source]

Two comprehensive literature reviews undertaken jointly by the World Cancer Research Fund and the American Institute for Cancer Research have reported the evidence for lifestyle factors in the prevention of cancers:

  • the Second Expert Report (SER) on food, nutrition and physical activity in the prevention of cancer (2007)[1]
  • the Continuous Update Project (CUP) review of food, nutrition and physical activity in the prevention of colorectal cancer (2011).[2]

The lifestyle and dietary guidance in this chapter is primarily summarised from these reviews. Updated information was included, where available. New systematic reviews were not undertaken for this guideline.

Updated systematic reviews are currently in progress by World Cancer Research Fund/American Institute for Cancer Research.i


iThese guidelines may be updated after 2017 as a result of updated guidance from the World Cancer Research Fund/American Institute for Cancer Research. The provisional publication dates for The Colorectal Cancer Report and the Expert Report are April 2017 and November 2017, respectively.

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Summary of associations between lifestyle factors and colorectal cancer risk[edit source]

Table 2.2 summarises the World Cancer Research Fund/American Institute for Cancer Research conclusions on the evidence for dietary and lifestyle factors as risk factors for, or protective against, colorectal cancer.[2]

Table 2.2. Food, nutrition, physical activity and risk of cancers of the colon and the rectum[edit source]

Strength of association Decreases risk Increases risk
Convincing Physical activity1, 2

Foods containing dietary fibre3

Red meat4,5

Processed meat4,6
Alcoholic drinks (men)7
Body fatness
Abdominal fatness
Adult attained height8

Probable Garlic

Milk9
Calcium10

 Alcoholic drinks (women)7
Limited – suggestive Non-starchy vegetables

Fruits
Foods containing vitamin D312

 Foods containing iron3,4

Cheese11
Foods containing animal fats3
Foods containing sugars13

Limited – no conclusion Fish, glycaemic index, folate, vitamin C, vitamin E, selenium, low fat, dietary pattern
Substantial effect on risk unlikely None identified
1. Physical activity of all types: occupational, household, transport, and recreational.

2. The Panel judges that the evidence is stronger for colon cancer is convincing. No conclusion was drawn for rectal cancer.
3. Includes both foods naturally containing the constituent and foods which have the constituent added. Dietary fibre is contained in plant foods.
4. Although red and processed meats contain iron, the general category of ‘foods containing iron’ comprises many other foods, including those of plant origin.
5. The term ‘red meat’ refers to beef, pork, lamb, and goat from domesticated animals.
6. The term ‘processed meat’ refers to meats preserved by smoking, curing, or salting, or addition of chemical preservatives.
7. The judgements for men and women are different because there are fewer data for women. For colorectal cancers, the effect appears stronger in men than women.
8. Adult attained height is unlikely directly to modify the risk of cancer. It is a marker for genetic, environmental, hormonal, and also nutritional factors affecting growth during the period from preconception to completion of linear growth.
9. Milk from cows. Most data are from high-income populations, where calcium can be taken to be a marker for milk/dairy consumption. The Panel judges that a higher intake of dietary calcium is one way in which milk could have a protective effect.
10. The evidence is derived from studies using supplements at a dose of 1200 mg/day.
11. Although both milk and cheese are included in the general category of dairy products, their different nutritional composition and consumption patterns may result in different findings.
12. Found mostly in fortified foods and animal foods.
13. ‘Sugars’ here means all ‘non-milk extrinsic’ sugars, including refined and other added sugars, honey, and as contained in fruit juices and syrups. It does not include sugars naturally present in whole foods such as fruits. It also does not include lactose as contained in animal or human milks.

Source: World Cancer Research Fund/American Institute for Cancer Research. Continuous Update Project Report. Food, Nutrition, Physical Activity, and the Prevention of Colorectal Cancer. 2011.[2] Seeking permission from publisher, note title amendment.

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Tobacco smoking[edit source]

The CUP review[2] reported significant associations between daily cigarette consumption, duration, pack years and age of initiation with colorectal cancer incidence, with an increase in risk of 38% for every 40 cigarettes smoked per day.[3] The large European Prospective Investigation into Cancer and Nutrition (EPIC) study found that smokers have an increased risk of colon cancer with most occurring in the proximal rather than distal colon.[4] The incidence of smoking-related colon cancer in the US is now the same for women and men, likely reflecting converging smoking patterns.[5]

Tobacco smoking is considered to be an established cause of colorectal cancer,[6] with 8.1% of colorectal cancer in the UK attributed to tobacco use.[7]


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Obesity and abdominal fatness[edit source]

The CUP review[2] concluded that cohort studies investigating body mass index published between 2007 and 2011 showed increased risk of colorectal cancer with increased body fatness. The meta-analyses showed increased risks of 2%, 3% and 1% per kg/m2 for colorectal, colon and rectal cancers, respectively. There tended to be a larger effect for men than women and the effect was stronger for the USA and Asia than Europe.

The CUP review[2] agreed with the SER[1] finding that there was convincing evidence that greater body fatness is associated with colorectal cancer risk. Similarly, the CUP review[2] found that all new cohort studies demonstrated that increasing waist circumference and/or waist-to-hip ratio measurements increased risk for colorectal cancer. The meta-analyses showed increased risks of 3%, 5% and 3% (per inch in waist circumference for studies that did not adjust for body mass index) for colorectal, colon and rectal cancers respectively. In the UK, 13% of colorectal cancer has been attributed to overweight and obesity.[7] In the large EPIC cohort study, individuals who gained > 20 kg of weight since age 20 had a 38% higher risk of colon, but not rectal cancer, compared with those whose weight remained stable. In a recent meta-analysis of observational studies, each 5 kg of adult body weight gain was associated with a 4% higher risk of colorectal cancer.[8] This association only applied to those with high attained waist circumference, suggesting fat accumulation in the abdominal area is important in relation to colorectal cancer risk.[9][10][11][12][13] In the Women’s Health Initiative Study, the risk of colorectal cancer in postmenopausal women increased when BMI exceeded 27 kg/m2.[14] A recent review, which included seven studies, found obese patients were more likely to have distal tumours, show intact DNA mismatch repair, and have increased lymph node metastases, compared with normal-weight patients.[15] The incidence of colorectal cancer in individuals under 50 years for whom screening is limited is increasing[16] and the rising prevalence of excess weight may play a role in this trend.[17]

Other recent reviews made similar conclusions, with the risk of colorectal cancer from excess body fatness being stronger in men than women, rectal cancer being less affected by body fatness than colon cancer, and with general and regional fatness both playing a role.[9][10][11][12][13][18] Body and abdominal adiposity may increase risk through systemic effects, in which insulin and oestrogen levels encourage carcinogenesis and discourage apoptosis.[19] Patients with type-2 diabetes are at greater risk of cancers[20], including of the colorectum,[21] but particularly the proximal colon.[22][23]

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Nutrition[edit source]

Dietary fibre[edit source]

Dietary fibre is a heterogeneous group comprising primarily plant-derived structural components not digested by human digestive enzymes, consisting largely of non-starch polysaccharides and resistant starch. The suggested mechanisms for protection from colorectal cancer by high dietary fibre include fibre diluting or adsorbing digesta carcinogens, reducing intestinal transit time, reducing secondary bile acid production, reducing colonic pH and increasing the production of short chain fatty acids.[18] The short-chain fatty acid butyrate may play an important role,[24] as it enhances the deletion of genetically damaged cells by inducing cell cycle arrest, differentiation and apoptosis.[25]

The CUP review[2] concluded that 13 of 18 studies published since the SER (2007)[1] showed decreased risk of colorectal cancer with increased intake of total dietary fibre. The updated meta-analyses showed a 12% decreased risk for men and an 8% decreased risk for women (per 10 g dietary fibre/day), with a 21% decreased risk per three daily servings of wholegrains for colorectal cancer and a 16% decreased risk for colon cancer. The CUP review[2] also reported a further 12 new studies examining colon cancer alone and 10 studies looking at rectal cancer only since SER.[1] Meta-analyses undertaken for the CUP review[2] showed an 11% decrease in colon cancer risk per 10 g of dietary fibre consumed per day. For rectal cancer meta-analyses revealed a trend towards decreased risk that did not reach statistical significance as was reported previously in the SER (2007).[1]

Based on consistent evidence, with clear dose-response relationships for both women and men, the CUP review[2] concluded that the protective effect of dietary fibre had strengthened from ‘probable’ to ‘convincing’. The CUP review[2] agreed with the SER[1] conclusion that evidence of protection from non-starchy fruits and vegetables was limited. The CUP review[2] included a pooled analysis of 756,217 participants from 14 cohort studies, followed up for between 6 and 20 years[26].

Since the CUP review[2] published its conclusions, another large systematic review and meta-analysis confirmed that ingestion of dietary fibre, in particular cereal fibre and whole grains, was inversely associated with risk of colon cancer.[27] The investigators found no association between intake of fruit or vegetable fibre and risk of colorectal cancer, but suggested that level of fibre intake from these sources may have been too low to detect effects. Intake of whole grains did not protect against colorectal cancer in the Norwegian Women Study, although consumption tended to be weakly associated with a lower risk of proximal colon cancer.[28] Intake of whole grain products, in particular whole grain wheat, was found to be associated with a lower incidence of colorectal cancer in the prospective HELGA study.[29]

The large NIH-AARP American cohort study was not included in the CUP review[2] and reported a reduction in risk of colon cancer in adults from high intake of vegetables consumed during ages 12–13 years and during the previous 10 years. High intakes of fruit consumed in the previous 10 years were also protective.[30] A healthy diet can also improve overall survival after diagnosis of colorectal cancer.[31]

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Red and processed meat[edit source]

Based on the findings of nine of 12 studies published between 2007–2011, the CUP review[2] confirmed the SER[1] finding that there was convincing evidence that higher intakes of red meat increase the risk of colorectal cancer. Meta-analysis showed a 17% increase in risk of colorectal cancer per 100 g red meat consumed per day.[32]

The risk of colorectal cancer and rectal cancer differ according to the subtype of red meat consumed.[33] The mechanism underlying the increase in risk may be associated with the presence of haem in red meat, which undergoes endogenous nitrosylation with the formation of potentially carcinogenic N-nitroso compounds,[31] or due to the production of potentially carcinogenic heterocyclic amines and polycyclic aromatic hydrocarbons during the cooking of meat, or the presence of nitrites and nitrates.[34]

In 10 of 13 studies included in the CUP review, increased risk of colorectal cancer with higher intake of processed meat was observed.[2] The meta-analysis showed an 18% increased risk for colorectal cancer and a 24% increased risk of colon cancer per 50 g processed meat/day intake.[2] There was a nonsignificant trend towards increased risk of rectal cancer.

The CUP review[2] concluded there was a dose-response relationship apparent from cohort studies and agreed with the SER that processed meat was a convincing cause of colorectal cancer. These conclusions are further supported by more recent studies confirming red meat consumption is a risk factor for cancer of several sites, including colon and rectum, with no effect of cooking method.[15] Further, the American Institute for Cancer Research working group on red and processed meats classified red meat as ‘probably carcinogenic to humans’ based on limited evidence for positive associations between red meat consumption and colorectal cancer development, but strong mechanistic evidence. The working group also upgraded their classification for processed meats to ‘carcinogenic in humans’ based on there being sufficient epidemiological evidence that these meats causes colorectal cancer.[35][36] Others have found an association between cooking method and colorectal cancer and rectal adenoma risk.[34][37] Recent studies have also confirmed a positive association between red processed meat and proximal colon cancer,[34] and that in Europe the negative effect of processed meat was mainly driven by the consumption of sausages.[38]

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Other nutrients[edit source]

The CUP review and SER concluded milk probably protected from colorectal cancer, with a 9% decreased risk for colorectal cancer per 200 g milk consumed/day.[2][1] This conclusion is supported by the EPIC study, which found dairy products protective irrespective of fat content of the products,[39] and a meta-analysis of cohort studies that showed that milk and total dairy products are associated with a reduction in colorectal cancer risk.[40]

However, the CUP review[2] and SER review[1] found that, in six of seven cohort studies, calcium supplements reduced the risk of colorectal cancer, and the CUP panel concluded that calcium probably protected against colorectal cancer. The NIH-AARP Diet and Health study was not included in CUP review,[2] and this large study found that high intake of milk and calcium over the previous 10 years reduced the risk of colon cancer, and that intake of milk was inversely associated with risk of rectal cancer.[30] However a 2013 meta-analysis showed that calcium supplementation (≥ 500 mg/d) did not alter the risk of colorectal cancer (risk ratio [RR] 1•38, 95% confidence interval [CI] 0•89 to 2•15, P = 0•15).[41]

In contrast to the benefits seen for colorectal cancer risk, a recent randomised controlled trial investigating the impact of calcium and vitamin D alone and in combination on metachronous adenoma revealed no significant reduction of risk associated with any of the treatments:[42]

  • vitamin D versus no vitamin D (adjusted RR 0.99; 95% CI 0.89 to 1.09)
  • calcium versus no calcium (RR 0.95; 95% CI 0.85 to 1.06)
  • both vitamin D and calcium versus neither (RR 0.93; 95% CI, 0.80 to 1.08).

The findings for advanced adenomas were similar.[42] There were few serious adverse events.

In combination, the evidence suggests that calcium and vitamin D may elicit their protective effects at points in colorectal carcinogenesis beyond the advanced adenoma stage.

The SER reviewed 15 case-controlled studies on dietary selenium that showed a decreased risk for colorectal cancer with increased serum selenium levels, but no cohort studies were identified.[1] The Panel concluded there was limited evidence that foods containing selenium protect against colorectal cancer. The updated CUP review report included two new cohort studies published since the SER but the results were inconsistent and the report concluded there was inadequate evidence to draw conclusions about the relationship between dietary selenium and colorectal cancer.[2] There were few, relatively small studies investigating selenium supplements and the World Cancer Research Fund concluded the results were inconsistent and the outcomes too limited to draw a conclusion.[1][2]

Folic acid[edit source]

A joint position statement between Cancer Council Australia and the Cancer Society of New Zealand[43] on folate and cancer risk, including folic acid supplementation, was published in August 2010 and updated in March 2014. The statement included evidence from a review of recommendations for folic acid supplementation by the Scientific Advisory Committee on Nutrition of the British Food Standards Agency.[44] The British review included publications from the Aspirin/Folate Polyp Prevention Study[45][46] and an ecological study highlighting a temporal association between folic acid fortification and an increase in bowel cancer incidence in the USA and Canada.[47]

The position statement included the following recommendation in relation to folic acid fortification:

Based on current evidence, the benefits of folic acid fortification for reducing the incidence of neural tube defects outweigh any potential increased risk of cancer. Therefore the Cancer Society of New Zealand and Cancer Council Australia are not opposed to mandatory fortification of foods with folic acid. However careful monitoring of emerging evidence on any adverse effects of folic acid fortification, particularly cancer incidence, is required.

The Cancer Society of New Zealand and Cancer Council Australia support the respective government guidelines for food and nutrition (New Zealand Food and Nutrition Guidelines and Australian Dietary Guidelines[48]) and recommend people obtain their nutritional requirements from whole foods, such as fruits, vegetables, breads and cereals rather than individual nutrients in a supplement form.

People with existing bowel adenomas and those with an increased risk of developing bowel adenomas should avoid taking high-dose (above the upper limit of 1mg per day[49]) supplements that contain folic acid”.[43]


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Folic acid intake outside pregnancy should not exceed 1mg per day and those with a history of colorectal adenomas should not take more than 200mcg as a supplement.

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Alcohol[edit source]

The 15 new papers reviewed by the CUP review showed an increased risk with increased intake of ethanol for colorectal cancer and colon cancers.[2] The meta-analyses showed a 10% increased risk for colorectal cancer and rectal cancers, and an 8% increased risk for colon cancer per 10 g ethanol consumed per day. The effect was stronger in men than women, with 11% increased risk in men, compared with 7% in women.

The CUP review[2] agreed with the SER[1] conclusion that the evidence for ethanol from alcoholic drinks as a cause of colorectal cancer in men was convincing, and was probably a cause of colorectal cancer in women. In the UK, 15.5% of colorectal cancers in men and 6.9% in women have been attributed to consumption of alcohol.[7] In a recent meta-analysis, alcohol consumption was associated with an increase of risk of colorectal adenomas which was the same for both sexes and stronger in European than US and Asian studies.[50] In 2010, there were 10,865 colon cancers diagnosed in Australia, of which 868 were attributed to alcohol consumption, with 80% of those diagnosed in men.[51] The European Code against Cancer (4th edition) concluded that even low and moderate alcohol intakes increase the risk of colorectal cancer in a dose-dependent manner.[52]

Alcohol also interacts with tobacco by interfering with the repair of specific DNA mutations caused by smoking, and may also enhance the penetration of other carcinogenic molecules into mucosal surfaces.

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Physical activity[edit source]

The SER recommended that, to prevent colorectal cancer, people should be moderately physically active (equivalent to brisk walking for at least 30 minutes a day, with the objective of ≥ 60 minutes of moderate or ≥ 30 minutes of vigorous physical activity every day).[1]

The CUP review reviewed the outcomes of cohort studies published since 2007, and concluded that a lower risk of colon cancer was associated with higher overall levels of physical activity, with evidence of a dose-response effect within the range studied.[2][53][54] The effect was strong for colon cancer, but there was no evidence of an effect for rectal cancer. The effect was strong and consistent for men, but less strong in women. The meta-analyses showed that recreational physical activity resulted in an 11% decrease in risk for colorectal and 12% decrease for colon cancer per 30 minutes of exercise per day, with maximum effect observed with approximately 10 hours per week of average-paced walking.[55] Another meta-analysis found a similar inverse relationship between colonic adenoma risk and physical activity.[53][54]

While these effects were independent of any effect of exercise on obesity, additional benefits of longer-term, sustained, moderate physical activity may also be realised through reduced body fatness and may protect against colon cancer by decreasing inflammation, reducing insulin levels and reducing insulin resistance. Physical activity and fewer sitting hours were found to significantly reduce colon cancer risk in both the distal and proximal colon, although results for rectal cancer were mixed.[53][19][56]

Increasing exercise after non-metastatic colorectal cancer treatment was associated with reduced risk of colorectal cancer-specific and overall mortality for women and men[57][58] and lower rectum cancer mortality[19]. In a meta-analysis of prospective studies both prediagnosis and postdiagnosis physical activity was found to reduce the risk of colorectal cancer-specific mortality and all-cause mortality.[59]

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Summary of key messages based on the World Cancer Research Fund/American Institute for Cancer Research and updated evidence[edit source]

Table 2.3. Key messages regarding primary prevention of colorectal cancer[edit source]

Factor Key message
Smoking Avoid tobacco smoking.
Alcohol (Men) Avoid alcohol or limit intake to less than 2 standard drinks per day.
(Women) Avoid alcohol or limit intake to less than 1 standard drink per day.
Diet
Increase intake of cereal fibre, particularly poorly soluble cereal.
Moderate amounts of lean red meat (up to 100 g/day) can be eaten as part of a mixed diet. Charring of red meat is best avoided and consumption of processed meats should be limited.
Garlic is probably protective against cancer.
Milk is probably protective against cancer.
There is limited evidence that foods containing iron increase risk of cancer.
There is limited evidence that cheese intake increases risk of cancer.
There is limited evidence that foods containing animal fats increase risk of cancer.
There is limited evidence that foods containing sugars increase risk of cancer.
There is limited evidence that non-starchy vegetables and fruits reduce risk of cancer.
There is limited evidence that foods containing vitamin D reduce risk of cancer.
There is no evidence that foods containing folate reduce risk of cancer.
There is no evidence that fish intake reduces risk of cancer.
There is no evidence that foods containing selenium reduce risk of cancer.
Body fatness
Maintain weight in healthy BMI range.
Avoid abdominal fatness.
Physical activity
Aim for 30–60 minutes/day of moderate physical activity.
Avoid sedentary behaviour.

Source: World Cancer Research Fund and American Institute for Cancer Research SER[1] and CUP[2] reports.


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It is recommended to follow the primary prevention messages from the World Cancer Research Fund/American Institute for Cancer Research on tobacco smoking, alcohol, diet, body fatness, physical activity (see Table 2.3).

Next section: Aspirin for prevention of colorectal cancer


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References[edit source]

  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 World Cancer Research Fund/American Institute for Cancer Research. Food, nutrition, physical activity and the prevention of cancer: a global perspective. 2007 Available from: http://www.dietandcancerreport.org/.
  2. ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 2.16 2.17 2.18 2.19 2.20 2.21 2.22 2.23 2.24 2.25 2.26 2.27 World Cancer Research Fund/American Institute for Cancer Research. Continuous Update Project Report: Food, Nutrition, Physical Activity, and the Prevention of Colorectal Cancer. WCRF; 2011.
  3. ↑ Liang PS, Chen TY, Giovannucci E. Cigarette smoking and colorectal cancer incidence and mortality: systematic review and meta-analysis. Int J Cancer 2009 May 15;124(10):2406-15 Available from: http://www.ncbi.nlm.nih.gov/pubmed/19142968.
  4. ↑ Leufkens AM, Van Duijnhoven FJ, Siersema PD, Boshuizen HC, Vrieling A, Agudo A, et al. Cigarette smoking and colorectal cancer risk in the European Prospective Investigation into Cancer and Nutrition study. Clin Gastroenterol Hepatol 2011 Feb;9(2):137-44 Available from: http://www.ncbi.nlm.nih.gov/pubmed/21029790.
  5. ↑ Freedman ND, Abnet CC, Caporaso NE, Fraumeni JF Jr, Murphy G, Hartge P, et al. Impact of changing US cigarette smoking patterns on incident cancer: risks of 20 smoking-related cancers among the women and men of the NIH-AARP cohort. Int J Epidemiol 2016 Jun;45(3):846-56 Available from: http://www.ncbi.nlm.nih.gov/pubmed/26411408.
  6. ↑ Secretan B, Straif K, Baan R, Grosse Y, El Ghissassi F, Bouvard V, et al. A review of human carcinogens--Part E: tobacco, areca nut, alcohol, coal smoke, and salted fish. Lancet Oncol 2009 Nov;10(11):1033-4 Available from: http://www.ncbi.nlm.nih.gov/pubmed/19891056.
  7. ↑ 7.0 7.1 7.2 Parkin DM, Boyd L, Walker LC. 16. The fraction of cancer attributable to lifestyle and environmental factors in the UK in 2010. Br J Cancer 2011 Dec 6;105 Suppl 2:S77-81 Available from: http://www.ncbi.nlm.nih.gov/pubmed/22158327.
  8. ↑ Schlesinger S, Lieb W, Koch M, Fedirko V, Dahm CC, Pischon T, et al. Body weight gain and risk of colorectal cancer: a systematic review and meta-analysis of observational studies. Obes Rev 2015 Jul;16(7):607-19 Available from: http://www.ncbi.nlm.nih.gov/pubmed/25925734.
  9. ↑ 9.0 9.1 Aleksandrova K, Nimptsch K, Pischon T. Obesity and colorectal cancer. Front Biosci (Elite Ed) 2013 Jan 1;5:61-77 Available from: http://www.ncbi.nlm.nih.gov/pubmed/23276970.
  10. ↑ 10.0 10.1 Gribovskaja-Rupp I, Kosinski L, Ludwig KA. Obesity and colorectal cancer. Clin Colon Rectal Surg 2011 Dec;24(4):229-43 Available from: http://www.ncbi.nlm.nih.gov/pubmed/23204938.
  11. ↑ 11.0 11.1 Whitlock K, Gill RS, Birch DW, Karmali S. The Association between Obesity and Colorectal Cancer. Gastroenterol Res Pract 2012;2012:768247 Available from: http://www.ncbi.nlm.nih.gov/pubmed/23304128.
  12. ↑ 12.0 12.1 Ma Y, Yang Y, Wang F, Zhang P, Shi C, Zou Y, et al. Obesity and risk of colorectal cancer: a systematic review of prospective studies. PLoS One 2013;8(1):e53916 Available from: http://www.ncbi.nlm.nih.gov/pubmed/23349764.
  13. ↑ 13.0 13.1 Boeing H. Obesity and cancer--the update 2013. Best Pract Res Clin Endocrinol Metab 2013 Apr;27(2):219-27 Available from: http://www.ncbi.nlm.nih.gov/pubmed/23731883.
  14. ↑ Heo M, Kabat GC, Strickler HD, Lin J, Hou L, Stefanick ML, et al. Optimal cutoffs of obesity measures in relation to cancer risk in postmenopausal women in the Women's Health Initiative Study. J Womens Health (Larchmt) 2015 Mar;24(3):218-27 Available from: http://www.ncbi.nlm.nih.gov/pubmed/25587642.
  15. ↑ 15.0 15.1 Sinicrope FA, Foster NR, Sargent DJ, O'Connell MJ, Rankin C. Obesity is an independent prognostic variable in colon cancer survivors. Clin Cancer Res 2010 Mar 15;16(6):1884-93 Available from: http://www.ncbi.nlm.nih.gov/pubmed/20215553.
  16. ↑ Ahnen DJ, Wade SW, Jones WF, Sifri R, Mendoza Silveiras J, Greenamyer J, et al. The increasing incidence of young-onset colorectal cancer: a call to action. Mayo Clin Proc 2014 Feb;89(2):216-24 Available from: http://www.ncbi.nlm.nih.gov/pubmed/24393412.
  17. ↑ Patel P, De P. Trends in colorectal cancer incidence and related lifestyle risk factors in 15-49-year-olds in Canada, 1969-2010. Cancer Epidemiol 2016 Jun;42:90-100 Available from: http://www.ncbi.nlm.nih.gov/pubmed/27060626.
  18. ↑ 18.0 18.1 Topping DL, Clifton PM. Short-chain fatty acids and human colonic function: roles of resistant starch and nonstarch polysaccharides. Physiol Rev 2001 Jul;81(3):1031-64 Available from: http://www.ncbi.nlm.nih.gov/pubmed/11427691.
  19. ↑ 19.0 19.1 19.2 Morrison DS, Parr CL, Lam TH, Ueshima H, Kim HC, Jee SH, et al. Behavioural and metabolic risk factors for mortality from colon and rectum cancer: analysis of data from the Asia-Pacific Cohort Studies Collaboration. Asian Pac J Cancer Prev 2013;14(2):1083-7 Available from: http://www.ncbi.nlm.nih.gov/pubmed/23621191.
  20. ↑ Anderson AS, Key TJ, Norat T, Scoccianti C, Cecchini M, Berrino F, et al. European Code against Cancer 4th Edition: Obesity, body fatness and cancer. Cancer Epidemiol 2015 Dec;39 Suppl 1:S34-45 Available from: http://www.ncbi.nlm.nih.gov/pubmed/26205840.
  21. ↑ De Bruijn KM, Arends LR, Hansen BE, Leeflang S, Ruiter R, van Eijck CH. Systematic review and meta-analysis of the association between diabetes mellitus and incidence and mortality in breast and colorectal cancer. Br J Surg 2013 Oct;100(11):1421-9 Available from: http://www.ncbi.nlm.nih.gov/pubmed/24037561.
  22. ↑ Limburg PJ, Anderson KE, Johnson TW, Jacobs DR Jr, Lazovich D, Hong CP, et al. Diabetes mellitus and subsite-specific colorectal cancer risks in the Iowa Women's Health Study. Cancer Epidemiol Biomarkers Prev 2005 Jan;14(1):133-7 Available from: http://www.ncbi.nlm.nih.gov/pubmed/15668486.
  23. ↑ Lim E, Jones IT, Gibbs P, McLaughlan S, Faragher I, Skinner I, et al. Subsite-specific colorectal cancer in diabetic and nondiabetic patients. Cancer Epidemiol Biomarkers Prev 2005 Jun;14(6):1579-82 Available from: http://www.ncbi.nlm.nih.gov/pubmed/15941979.
  24. ↑ Cassidy A, Bingham SA, Cummings JH. Starch intake and colorectal cancer risk: an international comparison. Br J Cancer 1994 May;69(5):937-42 Available from: http://www.ncbi.nlm.nih.gov/pubmed/8180027.
  25. ↑ Hague A, Manning AM, Hanlon KA, Huschtscha LI, Hart D, Paraskeva C. Sodium butyrate induces apoptosis in human colonic tumour cell lines in a p53-independent pathway: implications for the possible role of dietary fibre in the prevention of large-bowel cancer. Int J Cancer 1993 Sep 30;55(3):498-505 Available from: http://www.ncbi.nlm.nih.gov/pubmed/8397167.
  26. ↑ Koushik A, Hunter DJ, Spiegelman D, Beeson WL, van den Brandt PA, Buring JE, et al. Fruits, vegetables, and colon cancer risk in a pooled analysis of 14 cohort studies. J Natl Cancer Inst 2007 Oct 3;99(19):1471-83 Available from: http://www.ncbi.nlm.nih.gov/pubmed/17895473.
  27. ↑ Aune D, Chan DS, Lau R, Vieira R, Greenwood DC, Kampman E, et al. Dietary fibre, whole grains, and risk of colorectal cancer: systematic review and dose-response meta-analysis of prospective studies. BMJ 2011 Nov 10;343:d6617 Available from: http://www.ncbi.nlm.nih.gov/pubmed/22074852.
  28. ↑ Bakken T, Braaten T, Olsen A, Kyrø C, Lund E, Skeie G. Consumption of Whole-Grain Bread and Risk of Colorectal Cancer among Norwegian Women (the NOWAC Study). Nutrients 2016 Jan 13;8(1) Available from: http://www.ncbi.nlm.nih.gov/pubmed/26771634.
  29. ↑ Kyrø C, Skeie G, Loft S, Landberg R, Christensen J, Lund E, et al. Intake of whole grains from different cereal and food sources and incidence of colorectal cancer in the Scandinavian HELGA cohort. Cancer Causes Control 2013 Jul;24(7):1363-74 Available from: http://www.ncbi.nlm.nih.gov/pubmed/23624874.
  30. ↑ 30.0 30.1 Ruder EH, Thiébaut AC, Thompson FE, Potischman N, Subar AF, Park Y, et al. Adolescent and mid-life diet: risk of colorectal cancer in the NIH-AARP Diet and Health Study. Am J Clin Nutr 2011 Dec;94(6):1607-19 Available from: http://www.ncbi.nlm.nih.gov/pubmed/22071715.
  31. ↑ 31.0 31.1 Norat T, Bingham S, Ferrari P, Slimani N, Jenab M, Mazuir M, et al. Meat, fish, and colorectal cancer risk: the European Prospective Investigation into cancer and nutrition. J Natl Cancer Inst 2005 Jun 15;97(12):906-16 Available from: http://www.ncbi.nlm.nih.gov/pubmed/15956652.
  32. ↑ Chan DS, Lau R, Aune D, Vieira R, Greenwood DC, Kampman E, et al. Red and processed meat and colorectal cancer incidence: meta-analysis of prospective studies. PLoS One 2011;6(6):e20456 Available from: http://www.ncbi.nlm.nih.gov/pubmed/21674008.
  33. ↑ Egeberg R, Olsen A, Christensen J, Halkjær J, Jakobsen MU, Overvad K, et al. Associations between red meat and risks for colon and rectal cancer depend on the type of red meat consumed. J Nutr 2013 Apr;143(4):464-72 Available from: http://www.ncbi.nlm.nih.gov/pubmed/23427329.
  34. ↑ 34.0 34.1 34.2 Miller PE, Lazarus P, Lesko SM, Cross AJ, Sinha R, Laio J, et al. Meat-related compounds and colorectal cancer risk by anatomical subsite. Nutr Cancer 2013;65(2):202-26 Available from: http://www.ncbi.nlm.nih.gov/pubmed/23441608.
  35. ↑ International Agency for Research on Cancer IARC Working Group. Volume 114: Consumption of red meat and processed meat.; 2015.
  36. ↑ Bouvard V, Loomis D, Guyton KZ, Grosse Y, Ghissassi FE, Benbrahim-Tallaa L, et al. Carcinogenicity of consumption of red and processed meat. Lancet Oncol 2015 Dec;16(16):1599-600 Available from: http://www.ncbi.nlm.nih.gov/pubmed/26514947.
  37. ↑ Ferrucci LM, Sinha R, Huang WY, Berndt SI, Katki HA, Schoen RE, et al. Meat consumption and the risk of incident distal colon and rectal adenoma. Br J Cancer 2012 Jan 31;106(3):608-16 Available from: http://www.ncbi.nlm.nih.gov/pubmed/22166801.
  38. ↑ Parr CL, Hjartåker A, Lund E, Veierød MB. Meat intake, cooking methods and risk of proximal colon, distal colon and rectal cancer: the Norwegian Women and Cancer (NOWAC) cohort study. Int J Cancer 2013 Sep 1;133(5):1153-63 Available from: http://www.ncbi.nlm.nih.gov/pubmed/23401013.
  39. ↑ Murphy N, Norat T, Ferrari P, Jenab M, Bueno-de-Mesquita B, Skeie G, et al. Consumption of dairy products and colorectal cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC). PLoS One 2013;8(9):e72715 Available from: http://www.ncbi.nlm.nih.gov/pubmed/24023767.
  40. ↑ Aune D, Lau R, Chan DS, Vieira R, Greenwood DC, Kampman E, et al. Dairy products and colorectal cancer risk: a systematic review and meta-analysis of cohort studies. Ann Oncol 2012 Jan;23(1):37-45 Available from: http://www.ncbi.nlm.nih.gov/pubmed/21617020.
  41. ↑ Bristow SM, Bolland MJ, MacLennan GS, Avenell A, Grey A, Gamble GD, et al. Calcium supplements and cancer risk: a meta-analysis of randomised controlled trials. Br J Nutr 2013 Oct;110(8):1384-93 Available from: http://www.ncbi.nlm.nih.gov/pubmed/23601861.
  42. ↑ 42.0 42.1 Baron JA, Barry EL, Mott LA, Rees JR, Sandler RS, Snover DC, et al. A Trial of Calcium and Vitamin D for the Prevention of Colorectal Adenomas. N Engl J Med 2015 Oct 15;373(16):1519-30 Available from: http://www.ncbi.nlm.nih.gov/pubmed/26465985.
  43. ↑ 43.0 43.1 Cancer Council Australia and the Cancer Society of New Zealand. Position statement - Folate and reducing cancer risk. http://wiki.cancer.org.au/policy/Position_statement_-_Folate_and_reducing_cancer_risk#Folic_acid_fortification; 2014 Mar.
  44. ↑ Scientific Advisory Committee on Nutrition. Folic acid and colorectal cancer risk: review of recommendation for mandatory folic acid fortification. http://www.sacn.gov.uk/pdfs/summary_of_sacn_report_to_cmo_19_october_2009.pdf: Scientific Advisory Committee on Nutrition; 2009 Oct.
  45. ↑ Cole BF, Baron JA, Sandler RS, Haile RW, Ahnen DJ, Bresalier RS, et al. Folic acid for the prevention of colorectal adenomas: a randomized clinical trial. JAMA 2007 Jun 6;297(21):2351-9 Available from: http://www.ncbi.nlm.nih.gov/pubmed/17551129.
  46. ↑ Figueiredo JC, Levine AJ, Grau MV, Barry EL, Ueland PM, Ahnen DJ, et al. Colorectal adenomas in a randomized folate trial: the role of baseline dietary and circulating folate levels. Cancer Epidemiol Biomarkers Prev 2008 Oct;17(10):2625-31 Available from: http://www.ncbi.nlm.nih.gov/pubmed/18843003.
  47. ↑ Mason JB, Dickstein A, Jacques PF, Haggarty P, Selhub J, Dallal G, et al. A temporal association between folic acid fortification and an increase in colorectal cancer rates may be illuminating important biological principles: a hypothesis. Cancer Epidemiol Biomarkers Prev 2007 Jul;16(7):1325-9 Available from: http://www.ncbi.nlm.nih.gov/pubmed/17626997.
  48. ↑ National Health and Medical Research Council. Australian dietary guidelines. Canberra: NHMRC; 2013 Available from: http://www.nhmrc.gov.au/_files_nhmrc/publications/attachments/n55_australian_dietary_guidelines_130530.pdf.
  49. ↑ National Health and Medical Research Council. Nutrient reference values for Australia and New Zealand including recommended dietary intakes. Canberra: NHMRC; 2006 Available from: http://www.nhmrc.gov.au/_files_nhmrc/publications/attachments/n35.pdf.
  50. ↑ Zhu JZ, Wang YM, Zhou QY, Zhu KF, Yu CH, Li YM. Systematic review with meta-analysis: alcohol consumption and the risk of colorectal adenoma. Aliment Pharmacol Ther 2014 Aug;40(4):325-37 Available from: http://www.ncbi.nlm.nih.gov/pubmed/24943329.
  51. ↑ Pandeya N, Wilson LF, Webb PM, Neale RE, Bain CJ, Whiteman DC. Cancers in Australia in 2010 attributable to the consumption of alcohol. Aust N Z J Public Health 2015 Oct;39(5):408-13 Available from: http://www.ncbi.nlm.nih.gov/pubmed/26437723.
  52. ↑ Scoccianti C, Cecchini M, Anderson AS, Berrino F, Boutron-Ruault MC, Espina C, et al. European Code against Cancer 4th Edition: Alcohol drinking and cancer. Cancer Epidemiol 2015 Dec;39 Suppl 1:S67-74 Available from: http://www.ncbi.nlm.nih.gov/pubmed/26115567.
  53. ↑ 53.0 53.1 53.2 Boyle T, Keegel T, Bull F, Heyworth J, Fritschi L. Physical activity and risks of proximal and distal colon cancers: a systematic review and meta-analysis. J Natl Cancer Inst 2012 Oct 17;104(20):1548-61 Available from: http://www.ncbi.nlm.nih.gov/pubmed/22914790.
  54. ↑ 54.0 54.1 Robsahm TE, Aagnes B, Hjartåker A, Langseth H, Bray FI, Larsen IK. Body mass index, physical activity, and colorectal cancer by anatomical subsites: a systematic review and meta-analysis of cohort studies. Eur J Cancer Prev 2013 Nov;22(6):492-505 Available from: http://www.ncbi.nlm.nih.gov/pubmed/23591454.
  55. ↑ Keum N, Bao Y, Smith-Warner SA, Orav J, Wu K, Fuchs CS, et al. Association of Physical Activity by Type and Intensity With Digestive System Cancer Risk. JAMA Oncol 2016 Sep 1;2(9):1146-53 Available from: http://www.ncbi.nlm.nih.gov/pubmed/27196375.
  56. ↑ Simons CC, Hughes LA, van Engeland M, Goldbohm RA, van den Brandt PA, Weijenberg MP. Physical activity, occupational sitting time, and colorectal cancer risk in the Netherlands cohort study. Am J Epidemiol 2013 Mar 15;177(6):514-30 Available from: http://www.ncbi.nlm.nih.gov/pubmed/23420352.
  57. ↑ Meyerhardt JA, Giovannucci EL, Holmes MD, Chan AT, Chan JA, Colditz GA, et al. Physical activity and survival after colorectal cancer diagnosis. J Clin Oncol 2006 Aug 1;24(22):3527-34 Available from: http://www.ncbi.nlm.nih.gov/pubmed/16822844.
  58. ↑ Meyerhardt JA, Giovannucci EL, Ogino S, Kirkner GJ, Chan AT, Willett W, et al. Physical activity and male colorectal cancer survival. Arch Intern Med 2009 Dec 14;169(22):2102-8 Available from: http://www.ncbi.nlm.nih.gov/pubmed/20008694.
  59. ↑ Je Y, Jeon JY, Giovannucci EL, Meyerhardt JA. Association between physical activity and mortality in colorectal cancer: a meta-analysis of prospective cohort studies. Int J Cancer 2013 Oct 15;133(8):1905-13 Available from: http://www.ncbi.nlm.nih.gov/pubmed/23580314.

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Referring to the large bowel, comprising the colon and rectum.

Measures to prevent the onset of disease. This may include prevention strategies to modify cancer risk factors, such as dietary and lifestyle interventions, and medical interventions to enhance resistance to the effects of exposure to a disease agent, such as chemoprevention and vaccines.

A common medication used to treat pain, fever, and inflammation. Also known as acetylsalicylic acid (ASA).

A small growth protruding from a mucous membrane, such as the lining of the bowel.

A recommendation on a subject that is outside the scope of the search strategy for the systematic review, based on expert opinion and formulated by a consensus process.

The main part of the large bowel, which absorbs water and electrolytes from undigested food (solid waste). Its four parts are the ascending colon, transverse colon, descending colon and sigmoid colon.

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