Dietary and lifestyle strategies
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)
- the Continuous Update Project (CUP) review of food, nutrition and physical activity in the prevention of colorectal cancer (2011).
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.
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.
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
|Alcoholic drinks (women)7|
|Limited – suggestive||Non-starchy vegetables
|Foods containing iron3,4|
|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.
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. Seeking permission from publisher, note title amendment.
Tobacco smoking[edit source]
The CUP review 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. 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. The incidence of smoking-related colon cancer in the US is now the same for women and men, likely reflecting converging smoking patterns.
Obesity and abdominal fatness[edit source]
The CUP review 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 agreed with the SER finding that there was convincing evidence that greater body fatness is associated with colorectal cancer risk. Similarly, the CUP review 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. 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. 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. In the Women’s Health Initiative Study, the risk of colorectal cancer in postmenopausal women increased when BMI exceeded 27 kg/m2. 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. The incidence of colorectal cancer in individuals under 50 years for whom screening is limited is increasing and the rising prevalence of excess weight may play a role in this trend.
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. Body and abdominal adiposity may increase risk through systemic effects, in which insulin and oestrogen levels encourage carcinogenesis and discourage apoptosis. Patients with type-2 diabetes are at greater risk of cancers, including of the colorectum, but particularly the proximal colon.
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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. The short-chain fatty acid butyrate may play an important role, as it enhances the deletion of genetically damaged cells by inducing cell cycle arrest, differentiation and apoptosis.
The CUP review concluded that 13 of 18 studies published since the SER (2007) 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 also reported a further 12 new studies examining colon cancer alone and 10 studies looking at rectal cancer only since SER. Meta-analyses undertaken for the CUP review 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).
Based on consistent evidence, with clear dose-response relationships for both women and men, the CUP review concluded that the protective effect of dietary fibre had strengthened from ‘probable’ to ‘convincing’. The CUP review agreed with the SER conclusion that evidence of protection from non-starchy fruits and vegetables was limited. The CUP review included a pooled analysis of 756,217 participants from 14 cohort studies, followed up for between 6 and 20 years.
Since the CUP review 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. 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. 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.
The large NIH-AARP American cohort study was not included in the CUP review 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. A healthy diet can also improve overall survival after diagnosis of colorectal cancer.
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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 confirmed the SER 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.
The risk of colorectal cancer and rectal cancer differ according to the subtype of red meat consumed. 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, 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.
In 10 of 13 studies included in the CUP review, increased risk of colorectal cancer with higher intake of processed meat was observed. 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. There was a nonsignificant trend towards increased risk of rectal cancer.
The CUP review 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. 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. Others have found an association between cooking method and colorectal cancer and rectal adenoma risk. Recent studies have also confirmed a positive association between red processed meat and proximal colon cancer, and that in Europe the negative effect of processed meat was mainly driven by the consumption of sausages.
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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. This conclusion is supported by the EPIC study, which found dairy products protective irrespective of fat content of the products, and a meta-analysis of cohort studies that showed that milk and total dairy products are associated with a reduction in colorectal cancer risk.
However, the CUP review and SER review 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, 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. 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).
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:
- 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. 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. 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. 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.
Folic acid[edit source]
A joint position statement between Cancer Council Australia and the Cancer Society of New Zealand 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. The British review included publications from the Aspirin/Folate Polyp Prevention Study and an ecological study highlighting a temporal association between folic acid fortification and an increase in bowel cancer incidence in the USA and Canada.
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) 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) supplements that contain folic acid”.
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.
The 15 new papers reviewed by the CUP review showed an increased risk with increased intake of ethanol for colorectal cancer and colon cancers. 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 agreed with the SER 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. 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. 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. 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.
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.
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).
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. 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. Another meta-analysis found a similar inverse relationship between colonic adenoma risk and physical activity.
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.
Increasing exercise after non-metastatic colorectal cancer treatment was associated with reduced risk of colorectal cancer-specific and overall mortality for women and men and lower rectum cancer mortality. 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.
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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]
|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.|
|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.|
|Maintain weight in healthy BMI range.|
|Avoid abdominal fatness.|
|Aim for 30–60 minutes/day of moderate physical activity.|
|Avoid sedentary behaviour.|
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).
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