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Colorectal Cancer Prevention (PDQ®)—Health Professional Version - National Cancer Institute

Colorectal Cancer Prevention (PDQ®)—Health Professional Version - National Cancer Institute



National Cancer Institute

Colorectal Cancer Prevention (PDQ®)–Health Professional Version

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Who Is at Risk?

For the great majority of people, the major factor that increases a person’s risk for colorectal cancer (CRC) is increasing age. Risk increases dramatically after age 50 years; 90% of all CRCs are diagnosed after this age. Incidence and mortality rates are higher in African Americans compared with other races.[1] The history of CRC in a first-degree relative, especially if before the age of 55 years, roughly doubles the risk. A personal history of CRC, high-risk adenomas, or ovarian cancer also increases the risk.[2] Other risk factors are weaker than age and family history. People with an inflammatory bowel disease, such as ulcerative colitis or Crohn disease, have a much higher risk of CRC starting about 8 years after disease onset and are recommended to have frequent colonoscopic surveillance.[3] A small percentage (<5%) of CRCs occur in people with a genetic predisposition, including familial adenomatous polyposis and hereditary nonpolyposis coli.
References
  1. Lansdorp-Vogelaar I, Kuntz KM, Knudsen AB, et al.: Contribution of screening and survival differences to racial disparities in colorectal cancer rates. Cancer Epidemiol Biomarkers Prev 21 (5): 728-36, 2012. [PUBMED Abstract]
  2. Imperiale TF, Juluri R, Sherer EA, et al.: A risk index for advanced neoplasia on the second surveillance colonoscopy in patients with previous adenomatous polyps. Gastrointest Endosc 80 (3): 471-8, 2014. [PUBMED Abstract]
  3. Laukoetter MG, Mennigen R, Hannig CM, et al.: Intestinal cancer risk in Crohn's disease: a meta-analysis. J Gastrointest Surg 15 (4): 576-83, 2011. [PUBMED Abstract]

Overview

Note: Separate PDQ summaries on Colorectal Cancer Screening; Colon Cancer Treatment; and Rectal Cancer Treatment are also available.

Factors With Adequate Evidence of Increased Risk of Colorectal Cancer

Excessive alcohol use

Based on solid evidence from observational studies, excessive alcohol use is associated with an increased risk of colorectal cancer (CRC).[1,2]
Magnitude of Effect: A pooled analysis of eight cohort studies estimated an adjusted relative risk (RR) of 1.41 (95% confidence interval [CI], 1.16–1.72) for consumption exceeding 45 g/day.[1]
  • Study Design: Cohort studies.
  • Internal Validity: Fair.
  • Consistency: Fair.
  • External Validity: Fair.

Cigarette smoking

Based on solid evidence, cigarette smoking is associated with increased incidence and mortality from CRC.
Magnitude of Effect: A pooled analysis of 106 observational studies estimated an adjusted RR (current smokers vs. never smokers) for developing CRC of 1.18 (95% CI, 1.11–1.25).[3,4]
  • Study Design: 106 observational studies.
  • Internal Validity: Fair.
  • Consistency: Good.
  • External Validity: Good.

Obesity

Based on solid evidence, obesity is associated with increased incidence and mortality from CRC.
Magnitude of Effect: In one large cohort study, the adjusted RR for developing colon cancer for women with a body mass index of more than 29 was 1.45 (95% CI, 1.02–2.07).[5,6] A similar increase in CRC mortality was found in another large cohort study.[7,8]
  • Study Design: Large cohort studies.
  • Internal Validity: Fair.
  • Consistency: Good.
  • External Validity: Good.

Family/personal history of colorectal cancer and other hereditary conditions

Based on solid evidence, a family history of CRC in a first-degree relative or a personal history of CRC increases the risk of CRC.[9-12] Having a genetic predisposition, including familial adenomatous polyposis and hereditary nonpolyposis coli, also increases risk for CRC.[13]
Magnitude of Effect: In persons with adenomatous polyposis coli, the risk of CRC by age 40 can be as high as 100%. Persons with hereditary nonpolyposis coli can have a lifetime risk of CRC of about 80%.
  • Study Design: Case-control and cohort studies.
  • Internal Validity: Good.
  • Consistency: Good.
  • External Validity: Good.
Refer to the PDQ summary on Genetics of Colorectal Cancer for more information about family history and hereditary conditions.

Factors With Adequate Evidence for a Decreased Risk of Colorectal Cancer

Physical activity

Based on solid evidence, regular physical activity is associated with a decreased incidence of CRC.
Magnitude of Effect: A meta-analysis of 52 observational studies found a statistically significant 24% reduction in CRC incidence (RR, 0.76; 95% CI, 0.72–0.81).[14]
  • Study Design: Cohort studies and meta-analysis.
  • Internal Validity: Fair.
  • Consistency: Good.
  • External Validity: Good.

Interventions With Adequate Evidence for a Decreased Risk of Colorectal Cancer

Aspirin

Benefits
Based on solid evidence, daily aspirin (acetylsalicylic acid [ASA]) reduces CRC incidence and mortality after 10 to 20 years. This is based on three individual participant level data meta-analyses of trials of aspirin used for the primary and secondary prevention of cardiovascular disease.[15-17]
Magnitude of Effect: ASA use reduces the long-term risk for developing CRC by 40% about 10 to 19 years after initiation (hazard ratio [HR], 0.60; 95% CI, 0.47–0.76).[18] Daily doses of 75 to 1,200 mg of ASA reduce the 20-year risk of CRC death by about 33% (HR, 0.67; 95% CI, 0.52–0.86).[16,17]
  • Study Design: Individual patient level data meta-analyses of randomized controlled trials (RCTs) of ASA for primary and secondary cardiovascular prevention.
  • Internal Validity: Fair, some data from registries and death certificates, some loss to follow-up; variations in ASA dose and timing; adherence to ASA unknown after end of trials (5–9 years); trials designed to answer a different primary hypothesis (cardiovascular disease prevention).
  • Consistency: Generally consistent.
  • External Validity: Fair, most data (>75%) from men.
Harms
Based on solid evidence, harms of ASA use include excessive bleeding, including gastrointestinal bleeds and hemorrhagic stroke.
Magnitude of Effect: Very low-dose ASA use (i.e., ≤100 mg every day or every other day) results in an estimated 14 (95% CI, 7–23) additional major gastrointestinal bleeding events and 3.2 (95% CI, -0.5 to 0.82) extra hemorrhagic strokes per 1,000 persons over 10 years. These risks increase with advancing age.[19]
  • Study Design: Evidence obtained from RCTs, cohort studies, and meta-analyses comparing ASA with placebo or no treatment for the primary prevention of cardiovascular disease.[19]
  • Internal Validity: Fair, data is from clinically and methodologically heterogeneous trials.
  • Consistency: Good.
  • External Validity: Fair, data on specific subgroups is limited.

Hormone therapy (estrogen plus progestin)

Based on solid evidence, combined hormone therapy (conjugated equine estrogen and progestin) decreases the incidence of invasive CRC.[20]
Based on fair evidence, combination conjugated equine estrogen and progestin has little or no benefit in reducing mortality from CRC. Data from the Women’s Health Initiative (WHI), a randomized, placebo-controlled trial evaluating estrogen plus progestin, with a mean intervention of 5.6 years and a follow-up of 11.6 years showed that women taking combined hormone therapy had a statistically significant higher stage of cancer (regional and distant) at diagnosis but not a statistically significant number of deaths from CRC compared with women taking the placebo.[20]
Magnitude of Effect: There were fewer CRCs in the combined hormone therapy group than in the placebo group (0.12% vs. 0.16%; HR, 0.72; 95% CI, 0.56–0.94). A meta-analysis of cohort studies observed a RR of 0.86 (95% CI, 0.76–0.97) for incidence of CRC associated with combined hormone therapy.
There were 37 CRC deaths in the combined hormone therapy arm compared with 27 deaths in the placebo arm (0.04% vs. 0.03%; HR, 1.29; 95% CI, 0.78–2.11).
  • Study Design: RCT and cohort studies.
  • Internal Validity: Good.
  • Consistency: Good for effect on incidence; not applicable (N/A) for effect on mortality; results were based on one trial.
  • External Validity: Good.
Harms
Based on solid evidence, harms of postmenopausal combined estrogen-plus-progestin hormone use include increased risk of breast cancer, coronary heart disease, and thromboembolic events.
Magnitude of Effect: The WHI showed a 26% increase in invasive breast cancer in the combined hormone group, a 29% increase in coronary heart disease events, a 41% increase in stroke rates, and a twofold higher rate of thromboembolic events.[21]
  • Study Design: Evidence from RCTs.
  • Internal Validity: Good.
  • Consistency: Good.
  • External Validity: Fair.

Polyp removal

Benefits
Based on fair evidence, removal of adenomatous polyps reduces the risk of CRC. Much of this reduction likely comes from removal of large (i.e., >1.0 cm) polyps, while the benefit of removing smaller polyps—which are much more common—is unknown. Some but not all observational evidence indicates that this reduction may be greater for left-sided CRC than for right-sided CRC.[22-24]
Magnitude of Effect: Unknown, probably greater for larger polyps (i.e., >1.0 cm) than smaller ones.[25]
  • Study Design: Evidence obtained from cohort studies and one RCT of sigmoidoscopy.[23]
  • Internal Validity: Good.
  • Consistency: Consistent.
  • External Validity: Good.
Harms
Based on solid evidence, the major harms of polyp removal include perforation of the colon and bleeding.
Magnitude of Effect: Seven to nine events per 1,000 procedures.[26-28]
  • Study Design: Evidence from retrospective cohort studies.[27,28]
  • Internal Validity: Good.
  • Consistency: Good.
  • External Validity: Good.

Factors With Inadequate Evidence of an Association With Colorectal Cancer

Nonsteroidal anti-inflammatory drugs (NSAIDs)

Benefits
There is inadequate evidence that the use of NSAIDs reduces the risk of CRC. In people without genetic predisposition but with a prior history of a colonic adenoma that had been removed, three RCT found that celecoxib [29,30] and rofecoxib [31] decreased the incidence of recurrent adenoma, although follow-up was too short to determine whether CRC incidence or mortality would have been affected.
Based on solid evidence, NSAIDs reduce the risk of adenomas, but the extent to which this translates into a reduction of CRC is uncertain.
  • Study Design: No adequate studies with CRC outcome.
  • Internal Validity: N/A.
  • Consistency: N/A.
  • External Validity: N/A.
Harms
Based on solid evidence, harms of NSAID use are relatively common and potentially serious, and include upper gastrointestinal bleeding, chronic kidney disease, and serious cardiovascular events such as myocardial infarction, heart failure, and hemorrhagic stroke.[32] A recent report compared the COX-2 inhibitor celecoxib (200 mg/d) with the nonselective nonsteroidals naproxen (850 mg/d) and ibuprofen (2,000 mg/d) in individuals with severe arthritis (i.e., not using lower doses as for primary prevention). The results showed that serious cardiovascular events were not less common for those taking the nonselective nonsteroidals. However, this study did not assess the comparative safety of lower doses or the safety of the COX-2 inhibitor rofecoxib.[33]
Magnitude of Effect: The estimated average excess risk of upper gastrointestinal complications in average-risk people attributable to NSAIDs is 4 to 5 per 1,000 people per year.[34,35] The excess risk varies with the underlying gastrointestinal risk, however, it likely exceeds ten extra cases per 1,000 people per year in more than 10% of users.[36] Serious cardiovascular events are increased by 50% to 60%.[35]
  • Study Design: Evidence obtained from RCTs and high-quality systematic reviews and meta-analyses.[34,35]
  • Internal Validity: Good.
  • Consistency: Good.
  • External Validity: Good.

Calcium supplementation

The evidence is inadequate to determine whether calcium supplementation reduces the risk of CRC.

Dietary factors

There is no reliable evidence that a diet started in adulthood that is low in fat and meat and high in fiber, fruits, and vegetables reduces the risk of CRC by a clinically important degree.

Factors and Interventions With Adequate Evidence of no Association With Colorectal Cancer

Estrogen-only therapy

Benefits
Based on fair evidence, conjugated equine estrogens do not affect the incidence of, or survival from, invasive CRC.[37]
Magnitude of Effect: N/A.
  • Study Design: Evidence from RCTs.
  • Internal Validity: Good.
  • Consistency: Good.
  • External Validity: Fair.

Statins

Benefits
Based on solid evidence, statins do not reduce the incidence or mortality from CRC.
  • Study Design: Meta-analyses of RCTs.[38-40]
  • Internal Validity: Good.
  • Consistency: Good.
  • External Validity: N/A.
Harms
Based on solid evidence, the harms of statins are small.
  • Study Design: Observational studies,[41] multiple RCTs, and a review.[42]
  • Internal Validity: Good.
  • Consistency: Good.
  • External Validity: Good.
References
  1. Cho E, Smith-Warner SA, Ritz J, et al.: Alcohol intake and colorectal cancer: a pooled analysis of 8 cohort studies. Ann Intern Med 140 (8): 603-13, 2004. [PUBMED Abstract]
  2. Fedirko V, Tramacere I, Bagnardi V, et al.: Alcohol drinking and colorectal cancer risk: an overall and dose-response meta-analysis of published studies. Ann Oncol 22 (9): 1958-72, 2011. [PUBMED Abstract]
  3. Botteri E, Iodice S, Bagnardi V, et al.: Smoking and colorectal cancer: a meta-analysis. JAMA 300 (23): 2765-78, 2008. [PUBMED Abstract]
  4. Liang PS, Chen TY, Giovannucci E: Cigarette smoking and colorectal cancer incidence and mortality: systematic review and meta-analysis. Int J Cancer 124 (10): 2406-15, 2009. [PUBMED Abstract]
  5. Martínez ME, Giovannucci E, Spiegelman D, et al.: Leisure-time physical activity, body size, and colon cancer in women. Nurses' Health Study Research Group. J Natl Cancer Inst 89 (13): 948-55, 1997. [PUBMED Abstract]
  6. Giovannucci E, Ascherio A, Rimm EB, et al.: Physical activity, obesity, and risk for colon cancer and adenoma in men. Ann Intern Med 122 (5): 327-34, 1995. [PUBMED Abstract]
  7. Calle EE, Rodriguez C, Walker-Thurmond K, et al.: Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. N Engl J Med 348 (17): 1625-38, 2003. [PUBMED Abstract]
  8. Ma Y, Yang Y, Wang F, et al.: Obesity and risk of colorectal cancer: a systematic review of prospective studies. PLoS One 8 (1): e53916, 2013. [PUBMED Abstract]
  9. Johns LE, Houlston RS: A systematic review and meta-analysis of familial colorectal cancer risk. Am J Gastroenterol 96 (10): 2992-3003, 2001. [PUBMED Abstract]
  10. Schoen RE, Razzak A, Yu KJ, et al.: Incidence and mortality of colorectal cancer in individuals with a family history of colorectal cancer. Gastroenterology 149 (6): 1438-1445.e1, 2015. [PUBMED Abstract]
  11. Butterworth AS, Higgins JP, Pharoah P: Relative and absolute risk of colorectal cancer for individuals with a family history: a meta-analysis. Eur J Cancer 42 (2): 216-27, 2006. [PUBMED Abstract]
  12. Samadder NJ, Curtin K, Tuohy TM, et al.: Increased risk of colorectal neoplasia among family members of patients with colorectal cancer: a population-based study in Utah. Gastroenterology 147 (4): 814-821.e5; quiz e15-6, 2014. [PUBMED Abstract]
  13. Mork ME, You YN, Ying J, et al.: High Prevalence of Hereditary Cancer Syndromes in Adolescents and Young Adults With Colorectal Cancer. J Clin Oncol 33 (31): 3544-9, 2015. [PUBMED Abstract]
  14. Wolin KY, Yan Y, Colditz GA, et al.: Physical activity and colon cancer prevention: a meta-analysis. Br J Cancer 100 (4): 611-6, 2009. [PUBMED Abstract]
  15. Flossmann E, Rothwell PM; British Doctors Aspirin Trial and the UK-TIA Aspirin Trial: Effect of aspirin on long-term risk of colorectal cancer: consistent evidence from randomised and observational studies. Lancet 369 (9573): 1603-13, 2007. [PUBMED Abstract]
  16. Rothwell PM, Wilson M, Elwin CE, et al.: Long-term effect of aspirin on colorectal cancer incidence and mortality: 20-year follow-up of five randomised trials. Lancet 376 (9754): 1741-50, 2010. [PUBMED Abstract]
  17. Rothwell PM, Fowkes FG, Belch JF, et al.: Effect of daily aspirin on long-term risk of death due to cancer: analysis of individual patient data from randomised trials. Lancet 377 (9759): 31-41, 2011. [PUBMED Abstract]
  18. Chubak J, Whitlock EP, Williams SB, et al.: Aspirin for the Prevention of Cancer Incidence and Mortality: Systematic Evidence Reviews for the U.S. Preventive Services Task Force. Ann Intern Med 164 (12): 814-25, 2016. [PUBMED Abstract]
  19. Whitlock EP, Burda BU, Williams SB, et al.: Bleeding Risks With Aspirin Use for Primary Prevention in Adults: A Systematic Review for the U.S. Preventive Services Task Force. Ann Intern Med 164 (12): 826-35, 2016. [PUBMED Abstract]
  20. Simon MS, Chlebowski RT, Wactawski-Wende J, et al.: Estrogen plus progestin and colorectal cancer incidence and mortality. J Clin Oncol 30 (32): 3983-90, 2012. [PUBMED Abstract]
  21. Writing Group for the Women's Health Initiative Investigators: Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results From the Women's Health Initiative randomized controlled trial. JAMA 288 (3): 321-33, 2002. [PUBMED Abstract]
  22. Brenner H, Hoffmeister M, Arndt V, et al.: Protection from right- and left-sided colorectal neoplasms after colonoscopy: population-based study. J Natl Cancer Inst 102 (2): 89-95, 2010. [PUBMED Abstract]
  23. Atkin WS, Edwards R, Kralj-Hans I, et al.: Once-only flexible sigmoidoscopy screening in prevention of colorectal cancer: a multicentre randomised controlled trial. Lancet 375 (9726): 1624-33, 2010. [PUBMED Abstract]
  24. Brenner H, Chang-Claude J, Seiler CM, et al.: Protection from colorectal cancer after colonoscopy: a population-based, case-control study. Ann Intern Med 154 (1): 22-30, 2011. [PUBMED Abstract]
  25. Robertson DJ, Greenberg ER, Beach M, et al.: Colorectal cancer in patients under close colonoscopic surveillance. Gastroenterology 129 (1): 34-41, 2005. [PUBMED Abstract]
  26. Nelson DB, McQuaid KR, Bond JH, et al.: Procedural success and complications of large-scale screening colonoscopy. Gastrointest Endosc 55 (3): 307-14, 2002. [PUBMED Abstract]
  27. Levin TR, Zhao W, Conell C, et al.: Complications of colonoscopy in an integrated health care delivery system. Ann Intern Med 145 (12): 880-6, 2006. [PUBMED Abstract]
  28. Warren JL, Klabunde CN, Mariotto AB, et al.: Adverse events after outpatient colonoscopy in the Medicare population. Ann Intern Med 150 (12): 849-57, W152, 2009. [PUBMED Abstract]
  29. Bertagnolli MM, Eagle CJ, Zauber AG, et al.: Celecoxib for the prevention of sporadic colorectal adenomas. N Engl J Med 355 (9): 873-84, 2006. [PUBMED Abstract]
  30. Arber N, Eagle CJ, Spicak J, et al.: Celecoxib for the prevention of colorectal adenomatous polyps. N Engl J Med 355 (9): 885-95, 2006. [PUBMED Abstract]
  31. Lanas A, Baron JA, Sandler RS, et al.: Peptic ulcer and bleeding events associated with rofecoxib in a 3-year colorectal adenoma chemoprevention trial. Gastroenterology 132 (2): 490-7, 2007. [PUBMED Abstract]
  32. Bresalier RS, Sandler RS, Quan H, et al.: Cardiovascular events associated with rofecoxib in a colorectal adenoma chemoprevention trial. N Engl J Med 352 (11): 1092-102, 2005. [PUBMED Abstract]
  33. Nissen SE, Yeomans ND, Solomon DH, et al.: Cardiovascular Safety of Celecoxib, Naproxen, or Ibuprofen for Arthritis. N Engl J Med 375 (26): 2519-29, 2016. [PUBMED Abstract]
  34. Rostom A, Dubé C, Lewin G, et al.: Nonsteroidal anti-inflammatory drugs and cyclooxygenase-2 inhibitors for primary prevention of colorectal cancer: a systematic review prepared for the U.S. Preventive Services Task Force. Ann Intern Med 146 (5): 376-89, 2007. [PUBMED Abstract]
  35. Kearney PM, Baigent C, Godwin J, et al.: Do selective cyclo-oxygenase-2 inhibitors and traditional non-steroidal anti-inflammatory drugs increase the risk of atherothrombosis? Meta-analysis of randomised trials. BMJ 332 (7553): 1302-8, 2006. [PUBMED Abstract]
  36. Hernández-Díaz S, García Rodríguez LA: Cardioprotective aspirin users and their excess risk of upper gastrointestinal complications. BMC Med 4: 22, 2006. [PUBMED Abstract]
  37. Ritenbaugh C, Stanford JL, Wu L, et al.: Conjugated equine estrogens and colorectal cancer incidence and survival: the Women's Health Initiative randomized clinical trial. Cancer Epidemiol Biomarkers Prev 17 (10): 2609-18, 2008. [PUBMED Abstract]
  38. Baigent C, Keech A, Kearney PM, et al.: Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins. Lancet 366 (9493): 1267-78, 2005. [PUBMED Abstract]
  39. Dale KM, Coleman CI, Henyan NN, et al.: Statins and cancer risk: a meta-analysis. JAMA 295 (1): 74-80, 2006. [PUBMED Abstract]
  40. Browning DR, Martin RM: Statins and risk of cancer: a systematic review and metaanalysis. Int J Cancer 120 (4): 833-43, 2007. [PUBMED Abstract]
  41. Hippisley-Cox J, Coupland C: Unintended effects of statins in men and women in England and Wales: population based cohort study using the QResearch database. BMJ 340: c2197, 2010. [PUBMED Abstract]
  42. Joy TR, Hegele RA: Narrative review: statin-related myopathy. Ann Intern Med 150 (12): 858-68, 2009. [PUBMED Abstract]
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