3. Prevention Asymptomatic Population – Colorectal Cancer
3.1 Lifestyle Habits
To reduce the risk of colorectal cancer regular physical activity is recommended.
Evidence from update literature search[1].
[1]: Systematic research for a limited time interval (starting 2003, the end point for the de novo literature search for the last guideline update)
- Recommendation grade
- B: Empfehlung für oder gegen eine Maßnahme - verwendete Ausdrucksweise = sollte/sollte nicht
- Level of evidence
- 2a
- Consensus
- Strong consensus
- References
- [1] [2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13]
Evidence tables (1)
klkjlkjlölöklkBackground
Cross-studies and prospective cohort studies have shown that people with a high level of physical activity have fewer colon polyps (adenomas). In addition, they have an up to 30 % lower risk of cancer. Already 30 to 60 minutes of moderate physical activity per day is associated with a lower cancer risk [2][3][4][5][11][12][13][6][7][8][9][10].
There is a positive association between occurrence of colon polyps (adenomas) and colorectal cancer and a higher BMI as well as an increase in waist circumference. This effect is seen with a BMI >25 kg/m2 , increases linearly with the BMI, and is more pronounced in men than women. The risk of colon cancer was up to twice as high in overweight persons especially with truncal obesity [19] It is not clear whether the risk increase is due to obesity, altered hormone levels, increased calorie uptake, or absence of physical activity [2][10][14][15][16][17][18][19].
Smoking is associated with a risk for colon adenomas that is twice as high and an increased risk of cancer [2][11][20][21][22][23][24][25][26].
3.2 Diet Recommendations
The general diet recommendations of the DGEM should be followed.
- Consensus
- Consent
Background
In a detailed literature review from 2010, a connection between a "healthy" or an "unhealthy" diet and colorectal cancer was viewed as probable. A "healthy" diet was designated by the authors as including a high consumption of fruit and vegetables as well as reduced intake of red and processed meat. In contrast, an "unhealthy" was characterized by a large uptake of red and processed meat, potatoes, and refined starch © German Guideline Program in Oncology | Evidenced-based Guideline for Colorectal Cancer | Version 2.1 | Januar 2019 Error! Style not defined. Error! Style not defined. 31 [27]. Original publications in the last years have repeatedly observed an association between diet factors and the manifestation of CRC. They were rated with an evidence level between 2b and 4 [28][29][30][31]. However, there have also been studies that found no correlation between diet factors and CRC [32][33]. These are associations and not intervention studies. Whether these observations warrant specific diet recommendations for the prevention of CRC has not been studied so far. Therefore, despite the outlined relationships, currently no specific diet recommendations can be made. Instead, to reduce the risk of cancer, it is recommended to follow the current diet recommendations of the DGE. The associations between the uptake of specific foods and the risk of CRC will be demonstrated in more detail below. It should also be stressed here that a diet that does not cause weight gain is recommended (see Chapter 3.1).
Background
Despite controversial data, the evidence is sufficient to recommend a fiber rich diet of 30 g/day [34][35][36][37][38]. A current British study that summarizes data from seven cohort studies showed an inverse correlation between fiber uptake and cancer risk. The comparison of the daily fiber consumption of 10 and 24 g in this study demonstrated that a higher consumption was associated with a colon cancer risk reduction of 30 % [34]. In another study which summarized 13 prospective cohort studies showed similar results. Although the pooling project of prospective studies of diet and cancer demonstrated an even greater range between the lowest and highest quintile of fiber uptake, a significant inverse correlation was observed between fiber consumption and cancer risk after age-adjusted analysis, but not after adjustment according to other diet related risk factors [37]. These limited positive data may be due to the fact that the recording of the fiber consumption was merely done at the start of the study, which may reflect an incorrect long-term uptake. Despite the limited results, the remaining statements are very robust, because they are based on a large collective. Therefore, the Grade of Recommendation B was determined.
To reduce the risk of CRC alcohol consumption should be restricted.
- Recommendation grade
- B: Empfehlung für oder gegen eine Maßnahme - verwendete Ausdrucksweise = sollte/sollte nicht
- Level of evidence
- 2a
- Consensus
- Consent
Background
There is a positive correlation between high alcohol consumption and the development of CRC [39][40][41][42] especially in persons with low folic acid and/or methionine uptake [40]. Abstinent persons and persons who drink little alcohol have a significantly lower cancer risk [39][40][41][41][42]. A meta-analysis of 14 prospective cohort studies showed that already an alcohol intake of 100 g per week is associated with a 15 % increase in colon as well as rectal cancer risk [42]. The risk correlates with the amount of alcohol consumed not with the type of alcoholic beverage [40].
Background
A high consumption of red meat (beef, veal, pork, and lamb) and processed meat is associated with a higher CRC risk [38][43][44][45][46][47]. There is no positive correlation between poultry and/or poultry products [46]. The positive association is most likely due to the processing and preparation as demonstrated by data of the Prostate, lung, colorectal, and ovarian cancer trials. Especially the regular consumption of well-done red meat, bacon, and sausages correlates with a significantly increased CRC risk [47].
Background
A meta-analysis by Geelen et al. which summarized 19 cohort studies investigated the influence of fish consumption on the CRC risk. A comparison of the lowest and highest weekly fish uptake showed that higher consumption is associated with a 12 % lower cancer risk. The greater the difference between the lowest and highest fish uptake was, the more pronounced the correlation became [48]. However, the data are contradictory. This is probably due to the different amounts of fish that were consumed in the different studies [43][45][46][48][49][50]. Even though it can be assumed that eating more fish can slightly lower the CRC risk, no recommendation is currently given, because the data are not conclusive.
A connection between consumption of coffee/tea and a reduced risk of CRC has not been confirmed. Therefore, no recommendation can be given for coffee and tea consumption.
- Consensus
- Strong consensus
Even though the data on the prevention of CRC are not conclusive, increased amounts of fruits and vegetables should be eaten (5 portions per day).
- Consensus
- Consent
Background
In a case control study and a cohort study an inverse correlation was seen between increased ingestion of fruits and vegetables and a reduced CRC risk [54][55]. However, a meta-analysis showed that increased fruit and vegetable consumption is merely associated with a 6-9% reduced CRC risk. A stronger inverse correlation was observed for distal colon cancer [56]. However, it is unknown which components (fiber, secondary plant products) have this protective effect. Even though the data on the reduction of CRC risk are not consistent, it is viewed as beneficial to eat more fruits and vegetables, because regular consumption probably decreases disease risk in general.
There is no connection between food preparation or food fat components and CRC risk.
- Consensus
- Consent
Background
It has been repeatedly discussed whether food preparation or the proportion of potentially toxic fatty acids e.g. trans fatty acids resulting from cooking increase the risk of CRC. The data from the literature on this issue are scarce and inconsistent. Thus, it must be concluded that there is no clear connection. This was studied in the US in a recent prospective population-based cohort study. This trial in 35,000 women confirmed that trans fatty acids do not increase the risk of CRC [57]. Furthermore, there are no specific recommendations on the consumption of fat with respect to CRC risk reduction. Several studies exist that did not find a connection between fat consumption and manifestation of CRC. An effect resulting from cofactors such as intake of red meat or type of preparation cannot be sufficiently differentiated [31][32][38][48][58][59][60].
Background
A Swedish prospective population-based cohort study in more than 45,000 men found no connection between acrylamide in food and CRC risk using a Food Frequency Questionnaire (FFQ) [61]. This study confirmed previous trials that showed no connection between acrylamide and CRC manifestation in men and women [62][63][64].
3.3 Micronutrients
At this time there are no verified data on the effective prevention of colorectal cancer by micronutrients. Therefore, supplementation with these substances is not recommended for primary CRC prevention.
- Recommendation grade
- B: Empfehlung für oder gegen eine Maßnahme - verwendete Ausdrucksweise = sollte/sollte nicht
- Level of evidence
- 2b
...vitamins...
3b... including -carotene
3b... vitamin A
4... vitamin C, vitamin D, vitamin E
1a... and folic acid
1bThese recommendations are also valid for calcium
2b... magnesium
2b... and selenium.
- Consensus
- Strong consensus
- References
- [65] [66] [67] [68] [69] [70] [71] [72] [73] [74] [75] [76] [77] [78]
Background
The following list pertains to micronutrient supplements, some in pharmacological doses which can usually not be reached by eating foods such as fruits, vegetables, and milk products.
A moderate clinically non-relevant inhibitory effect on the recurrence of colon adenomas was observed for calcium [73][74][75] . However, data on a CRC risk reducing effect of calcium or vitamin D, alone or in combination, were not convincing [66][67].
There is no evidence that the intake of beta-carotene, vitamin A, or vitamin E can reduce the CRC risk. A meta-analysis [65] demonstrated, on the contrary, that supplementation of the aforementioned vitamins, alone or in combination was associated with an increased general mortality.
There is no clear evidence that taking high doses of vitamin C will reduce CRC risk.
A CRC risk reducing effect of folic acid has so far not been conclusively proven [68]. Studies on the recurrence of colon adenomas led to divergent results [69][70][71][72].
An intervention study with a selenium supplement and the primary endpoint "CRC- incidence" has not been done to date. The correlation of low selenium levels in serum and an increased adenoma risk is not sufficient to make a recommendation on selenium supplementation [77][78].
3.4 Drugs
Statines should not be taken as a primary prophylaxis against CRC.
- Recommendation grade
- B: Empfehlung für oder gegen eine Maßnahme - verwendete Ausdrucksweise = sollte/sollte nicht
- Level of evidence
- 2b
- Consensus
- Strong consensus
- References
- [83]
Hormone therapy[1] should not be given for CRC risk reduction in women.
[1]: The expression “hormone replacement therapy” is misleading. Therefore the expression “hormone therapy” is used in the guideline instead.
Background
One positive case control study, but no randomized studies exist for the use of cyclooxygenase-2 (COX-2) inhibitors for primary CRC prevention [79]. Three randomized studies on the secondary prevention with Celecoxib or Rofecoxib following polypectomy show consistently that COX-2-inhibitors significantly decrease the relapse risk for colorectal adenomas [80][81][82]. However, all three studies showed a pronounced increase in cardiovascular morbidity.
A current meta-analysis of case control, cohort, and randomized studies confirms a significant, but small effect of statines on primary prevention of CRC [83]. A phase III study on secondary prevention of colon adenomas demonstrated that ursodesoxycholic acid only reduced the risk of adenomas with high-grade dysplasia, but not for adenomas in general [90]. Prospective studies on the primary prevention of adenomas using ursodesoxycholic acid do not exist.
A meta-analysis of 2 large randomized studies with a total of 7500 participants showed that the use of 300 mg or more of acetylsalicylic acid per day for 5 years reduces the risk of CRC with a latency of 10 and more years [85]. Another meta-analysis of 8 randomized studies with a total of 25,570 participants indicates that the daily use of at least 75 mg ASS reduces the mortality of CRC with a latency of 10 years [86]. Cohort and case control studies on the use of non-steroidal antirheumatics (NSAR) describe a reduced incidence of CRC. However, this has not been confirmed in randomized studies [85]. Due to the frequent incidence of gastrointestinal bleeding under ASS [87] and the missing evaluation of the benefit/risk ratio, the guideline group follows the guideline of the US Preventive Services Task Force on the use of ASS or NSAR for the primary prevention of CRC from the year 2007. It does not recommend the use ASS and NSAR for the primary prevention of CRC [84].
Hormone therapy can reduce the risk of CRC [89]. Due to the increased incidence of adverse events especially venous thromboembolisms, hormone therapy can be recommended for postmenopausal women, but not for primary prevention of CRC. The guideline group is following the recommendations of the U.S. Preventive Services Task Force Guideline on the use of hormone therapy in postmenopausal women [88] and the guideline Hormone Therapy in Peri- and Postmenopause of the German Society for Gynecology and Obstetrics [91].
Evidence tables
klkjlkjlölöklk
| asda | asd |
| sda | asd |
References
[1] Arbeitsgemeinschaft der Wissenschaftlichen Medizinischen Fachgesellschaften - Ständige Kommission, Leitlinien, AWMF-Regelwerk "Leitlinien", 1. Auflage 2012. 09.12.2013:, http://www.awmf.org/leitlinien/awmf-regelwerk/awmf-regelwerk.html
[2] Kirkegaard, H., Johnsen, N. F., Christensen, J., Frederiksen, K., Overvad, K., Tjonneland, A., Association of adherence to lifestyle recommendations and risk of colorectal cancer: a prospective Danish cohort study, BMJ, 2010. 341: p. c5504., http://www.ncbi.nlm.nih.gov/pubmed/20978063
[3] Halle, M., Schoenberg, M. H., Physical activity in the prevention and treatment of colorectal carcinoma, Dtsch Arztebl Int, 2009. 106(44): p. 722-7., http://www.ncbi.nlm.nih.gov/pubmed/19997551
[4] Wolin, K. Y., Yan, Y., Colditz, G. A., Lee, I. M., Physical activity and colon cancer prevention: a meta-analysis, Br J Cancer, 2009. 100(4): p. 611-6., http://www.ncbi.nlm.nih.gov/pubmed/19209175
[5] Friedenreich, C. M., Orenstein, M. R., Physical activity and cancer prevention: etiologic evidence and biological mechanisms, J Nutr, 2002. 132(11 Suppl): p. 3456S-3464S., http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12421870, http://jn.nutrition.org/content/132/11/3456S.full.pdf
[6] Wolin, K. Y., Yan, Y., Colditz, G. A., Physical activity and risk of colon adenoma: a meta-analysis, Br J Cancer, 2011. 104(5): p. 882-5., http://www.ncbi.nlm.nih.gov/pubmed/21304525
[7] Wolin, K. Y., Lee, I. M., Colditz, G. A., Glynn, R. J., Fuchs, C., Giovannucci, E., Leisure-time physical activity patterns and risk of colon cancer in women, Int J Cancer, 2007. 121(12): p. 2776-81., http://www.ncbi.nlm.nih.gov/pubmed/17722094
[8] Friedenreich, C., Norat, T., Steindorf, K., Boutron-Ruault, M. C., Pischon, T., Mazuir, M., et.al. Physical activity and risk of colon and rectal cancers: the European prospective investigation into cancer and nutrition, Cancer Epidemiol Biomarkers Prev, 2006. 15(12): p. 2398-407., http://www.ncbi.nlm.nih.gov/pubmed/17164362
[9] Lubin, F., Rozen, P., Arieli, B., Farbstein, M., Knaani, Y., Bat, L., et.al. Nutritional and lifestyle habits and water-fiber interaction in colorectal adenoma etiology, Cancer Epidemiol Biomarkers Prev, 1997. 6(2): p. 79-85., http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9037557, http://cebp.aacrjournals.org/content/6/2/79.full.pdf
[10] Giacosa, A., Franceschi, S., La Vecchia, C., Favero, A., Andreatta, R., Energy intake, overweight, physical exercise and colorectal cancer risk, Eur J Cancer Prev, 1999. 8 Suppl 1: p. S53-60., http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10772419
[11] Terry, M. B., Neugut, A. I., Bostick, R. M., Sandler, R. S., Haile, R. W., Jacobson, J. S., et.al. Risk factors for advanced colorectal adenomas: a pooled analysis, Cancer Epidemiol Biomarkers Prev, 2002. 11(7): p. 622-9., http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12101109, http://cebp.aacrjournals.org/content/11/7/622.full.pdf
[12] Lee, I. M., Physical activity and cancer prevention--data from epidemiologic studies, Med Sci Sports Exerc, 2003. 35(11): p. 1823-7., http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14600545
[13] Wei, E. K., Giovannucci, E., Wu, K., Rosner, B., Fuchs, C. S., Willett, W. C., et.al. Comparison of risk factors for colon and rectal cancer, Int J Cancer, 2004. 108(3): p. 433-42., http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14648711, http://onlinelibrary.wiley.com/store/10.1002/ijc.11540/asset/11540_ftp.pdf?v=1&t=ik57p9sa&s=d9839afe4670a7de533f74cc0bbbd4e22fed258e
[14] Martinez, M. E., Heddens, D., Earnest, D. L., Bogert, C. L., Roe, D., Einspahr, J., et.al. Physical activity, body mass index, and prostaglandin E2 levels in rectal mucosa, J Natl Cancer Inst, 1999. 91(11): p. 950-3., http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10359547, http://jnci.oxfordjournals.org/content/91/11/950.full.pdf
[15] Giovannucci, E., Modifiable risk factors for colon cancer, Gastroenterol Clin North Am, 2002. 31(4): p. 925-43., http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12489270
[16] Giovannucci, E., Diet, body weight, and colorectal cancer: a summary of the epidemiologic evidence, J Womens Health (Larchmt), 2003. 12(2): p. 173-82., http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12737716, http://online.liebertpub.com/doi/abs/10.1089/154099903321576574
[17] Renehan, A. G., Tyson, M., Egger, M., Heller, R. F., Zwahlen, M., Body-mass index and incidence of cancer: a systematic review and meta-analysis of prospective observational studies, Lancet, 2008. 371(9612): p. 569-78., http://www.ncbi.nlm.nih.gov/pubmed/18280327
[18] Pischon, T., Lahmann, P. H., Boeing, H., Friedenreich, C., Norat, T., Tjonneland, A., et.al. Body size and risk of colon and rectal cancer in the European Prospective Investigation Into Cancer and Nutrition (EPIC), J Natl Cancer Inst, 2006. 98(13): p. 920-31., http://www.ncbi.nlm.nih.gov/pubmed/16818856
[19] Ning, Y., Wang, L., Giovannucci, E. L., A quantitative analysis of body mass index and colorectal cancer: findings from 56 observational studies, Obes Rev, 2010. 11(1): p. 19-30., http://www.ncbi.nlm.nih.gov/pubmed/19538439
[20] Terry, M. B., Neugut, A. I., Cigarette smoking and the colorectal adenoma-carcinoma sequence: a hypothesis to explain the paradox, Am J Epidemiol, 1998. 147(10): p. 903-10., http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9596467, http://aje.oxfordjournals.org/content/147/10/903.full.pdf
[21] Almendingen, K., Hofstad, B., Trygg, K., Hoff, G., Hussain, A., Vatn, M. H., Smoking and colorectal adenomas: a case-control study, Eur J Cancer Prev, 2000. 9(3): p. 193-203., http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10954259
[22] Chao, A., Thun, M. J., Jacobs, E. J., Henley, S. J., Rodriguez, C., Calle, E. E., Cigarette smoking and colorectal cancer mortality in the cancer prevention study II, J Natl Cancer Inst, 2000. 92(23): p. 1888-96., http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11106680, http://jnci.oxfordjournals.org/content/92/23/1888.full.pdf
[23] Giovannucci, E., An updated review of the epidemiological evidence that cigarette smoking increases risk of colorectal cancer, Cancer Epidemiol Biomarkers Prev, 2001. 10(7): p. 725-31., http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11440957, http://cebp.aacrjournals.org/content/10/7/725.full.pdf
[24] Reid, M. E., Marshall, J. R., Roe, D., Lebowitz, M., Alberts, D., Battacharyya, A. K., et.al. Smoking exposure as a risk factor for prevalent and recurrent colorectal adenomas, Cancer Epidemiol Biomarkers Prev, 2003. 12(10): p. 1006-11., http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14578135, http://cebp.aacrjournals.org/content/12/10/1006.full.pdf
[25] Botteri, E., Iodice, S., Raimondi, S., Maisonneuve, P., Lowenfels, A. B., Cigarette smoking and adenomatous polyps: a meta-analysis, Gastroenterology, 2008. 134(2): p. 388-95., http://www.ncbi.nlm.nih.gov/pubmed/18242207
[26] Botteri, E., Iodice, S., Bagnardi, V., Raimondi, S., Lowenfels, A. B., Maisonneuve, P., Smoking and colorectal cancer: a meta-analysis, JAMA, 2008. 300(23): p. 2765-78., http://www.ncbi.nlm.nih.gov/pubmed/19088354
[27] Miller, P. E., Lesko, S. M., Muscat, J. E., Lazarus, P., Hartman, T. J., Dietary patterns and colorectal adenoma and cancer risk: a review of the epidemiological evidence, Nutr Cancer, 2010. 62(4): p. 413-24., http://www.ncbi.nlm.nih.gov/pubmed/20432162
[28] Cottet, V., Bonithon-Kopp, C., Kronborg, O., Santos, L., Andreatta, R., Boutron-Ruault, M. C., et.al. Dietary patterns and the risk of colorectal adenoma recurrence in a European intervention trial, Eur J Cancer Prev, 2005. 14(1): p. 21-9., http://www.ncbi.nlm.nih.gov/pubmed/15677892
[29] Mai, V., Kant, A. K., Flood, A., Lacey, J. V., Jr., Schairer, C., Schatzkin, A., Diet quality and subsequent cancer incidence and mortality in a prospective cohort of women, Int J Epidemiol, 2005. 34(1): p. 54-60., http://www.ncbi.nlm.nih.gov/pubmed/15649959
[30] Sansbury, L. B., Wanke, K., Albert, P. S., Kahle, L., Schatzkin, A., Lanza, E., The effect of strict adherence to a high-fiber, high-fruit and -vegetable, and low-fat eating pattern on adenoma recurrence, Am J Epidemiol, 2009. 170(5): p. 576-84., http://www.ncbi.nlm.nih.gov/pubmed/19643809
[31] Wakai, K., Hirose, K., Matsuo, K., Ito, H., Kuriki, K., Suzuki, T., et.al. Dietary risk factors for colon and rectal cancers: a comparative case-control study, J Epidemiol, 2006. 16(3): p. 125-35., http://www.ncbi.nlm.nih.gov/pubmed/16710081
[32] Beresford, S. A., Johnson, K. C., Ritenbaugh, C., Lasser, N. L., Snetselaar, L. G., Black, H. R., et.al. Low-fat dietary pattern and risk of colorectal cancer: the Women's Health Initiative Randomized Controlled Dietary Modification Trial, JAMA, 2006. 295(6): p. 643-54., http://www.ncbi.nlm.nih.gov/pubmed/16467233
[33] Lanza, E., Yu, B., Murphy, G., Albert, P. S., Caan, B., Marshall, J. R., et.al. The polyp prevention trial continued follow-up study: no effect of a low-fat, high-fiber, high-fruit, and -vegetable diet on adenoma recurrence eight years after randomization, Cancer Epidemiol Biomarkers Prev, 2007. 16(9): p. 1745-52., http://www.ncbi.nlm.nih.gov/pubmed/17855692
[34] Dahm, C. C., Keogh, R. H., Spencer, E. A., Greenwood, D. C., Key, T. J., Fentiman, I. S., et.al. Dietary fiber and colorectal cancer risk: a nested case-control study using food diaries, J Natl Cancer Inst, 2010. 102(9): p. 614-26., http://www.ncbi.nlm.nih.gov/pubmed/20407088
[35] Ishikawa, H., Akedo, I., Otani, T., Suzuki, T., Nakamura, T., Takeyama, I., et.al. Randomized trial of dietary fiber and Lactobacillus casei administration for prevention of colorectal tumors, Int J Cancer, 2005. 116(5): p. 762-7., http://www.ncbi.nlm.nih.gov/pubmed/15828052
[36] Jacobs, E. T., Lanza, E., Alberts, D. S., Hsu, C. H., Jiang, R., Schatzkin, A., et.al. Fiber, sex, and colorectal adenoma: results of a pooled analysis, Am J Clin Nutr, 2006. 83(2): p. 343-9., http://www.ncbi.nlm.nih.gov/pubmed/16469993
[37] Park, Y., Hunter, D. J., Spiegelman, D., Bergkvist, L., Berrino, F., van den Brandt, P. A., et.al. Dietary fiber intake and risk of colorectal cancer: a pooled analysis of prospective cohort studies, JAMA, 2005. 294(22): p. 2849-57., http://www.ncbi.nlm.nih.gov/pubmed/16352792
[38] Robertson, D. J., Sandler, R. S., Haile, R., Tosteson, T. D., Greenberg, E. R., Grau, M., et.al. Fat, fiber, meat and the risk of colorectal adenomas, Am J Gastroenterol, 2005. 100(12): p. 2789-95., http://www.ncbi.nlm.nih.gov/pubmed/16393237
[39] Austin, G. L., Galanko, J. A., Martin, C. F., Sandler, R. S., Moderate alcohol consumption protects against colorectal adenomas in smokers, Dig Dis Sci, 2008. 53(1): p. 116-22., http://www.ncbi.nlm.nih.gov/pubmed/17510802
[40] Cho, E., Smith-Warner, S. A., Ritz, J., van den Brandt, P. A., Colditz, G. A., Folsom, A. R., et.al. Alcohol intake and colorectal cancer: a pooled analysis of 8 cohort studies, Ann Intern Med, 2004. 140(8): p. 603-13., http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15096331, http://annals.org/article.aspx?articleid=717373
[41] Mizoue, T., Inoue, M., Wakai, K., Nagata, C., Shimazu, T., Tsuji, I., et.al. Alcohol drinking and colorectal cancer in Japanese: a pooled analysis of results from five cohort studies, Am J Epidemiol, 2008. 167(12): p. 1397-406., http://www.ncbi.nlm.nih.gov/pubmed/18420544
[42] Moskal, A., Norat, T., Ferrari, P., Riboli, E., Alcohol intake and colorectal cancer risk: a dose-response meta-analysis of published cohort studies, Int J Cancer, 2007. 120(3): p. 664-71., http://www.ncbi.nlm.nih.gov/pubmed/17096321
[43] Chao, A., Thun, M. J., Connell, C. J., McCullough, M. L., Jacobs, E. J., Flanders, W. D., et.al. Meat consumption and risk of colorectal cancer, JAMA, 2005. 293(2): p. 172-82., http://www.ncbi.nlm.nih.gov/pubmed/15644544
[44] Larsson, S. C., Wolk, A., Meat consumption and risk of colorectal cancer: a meta-analysis of prospective studies, Int J Cancer, 2006. 119(11): p. 2657-64., http://www.ncbi.nlm.nih.gov/pubmed/16991129
[45] Mathew, A., Sinha, R., Burt, R., Caan, B., Paskett, E., Iber, F., et.al. Meat intake and the recurrence of colorectal adenomas, Eur J Cancer Prev, 2004. 13(3): p. 159-64., http://www.ncbi.nlm.nih.gov/pubmed/15167213
[46] 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. 97(12): p. 906-16., http://www.ncbi.nlm.nih.gov/pubmed/15956652
[47] Sinha, R., Peters, U., Cross, A. J., Kulldorff, M., Weissfeld, J. L., Pinsky, P. F., et.al. Meat, meat cooking methods and preservation, and risk for colorectal adenoma, Cancer Res, 2005. 65(17): p. 8034-41., http://www.ncbi.nlm.nih.gov/pubmed/16140978
[48] Geelen, A., Schouten, J. M., Kamphuis, C., Stam, B. E., Burema, J., Renkema, J. M., et.al. Fish consumption, n-3 fatty acids, and colorectal cancer: a meta-analysis of prospective cohort studies, Am J Epidemiol, 2007. 166(10): p. 1116-25., http://www.ncbi.nlm.nih.gov/pubmed/17823383
[49] Sugawara, Y., Kuriyama, S., Kakizaki, M., Nagai, M., Ohmori-Matsuda, K., Sone, T., et.al. Fish consumption and the risk of colorectal cancer: the Ohsaki Cohort Study, Br J Cancer, 2009. 101(5): p. 849-54., http://www.ncbi.nlm.nih.gov/pubmed/19638981
[50] Pot, G. K., Majsak-Newman, G., Geelen, A., Harvey, L. J., Nagengast, F. M., Witteman, B. J., et.al. Fish consumption and markers of colorectal cancer risk: a multicenter randomized controlled trial, Am J Clin Nutr, 2009. 90(2): p. 354-61., http://www.ncbi.nlm.nih.gov/pubmed/19553301
[51] Je, Y., Liu, W., Giovannucci, E., Coffee consumption and risk of colorectal cancer: a systematic review and meta-analysis of prospective cohort studies, Int J Cancer, 2009. 124(7): p. 1662-8., http://www.ncbi.nlm.nih.gov/pubmed/19115212
[52] Sun, C. L., Yuan, J. M., Koh, W. P., Yu, M. C., Green tea, black tea and colorectal cancer risk: a meta-analysis of epidemiologic studies, Carcinogenesis, 2006. 27(7): p. 1301-9., http://www.ncbi.nlm.nih.gov/pubmed/16638787
[53] Zhang, X., Albanes, D., Beeson, W. L., van den Brandt, P. A., Buring, J. E., Flood, A., et.al. Risk of colon cancer and coffee, tea, and sugar-sweetened soft drink intake: pooled analysis of prospective cohort studies, J Natl Cancer Inst, 2010. 102(11): p. 771-83., http://www.ncbi.nlm.nih.gov/pubmed/20453203
[54] Foschi, R., Pelucchi, C., Dal Maso, L., Rossi, M., Levi, F., Talamini, R., et.al. Citrus fruit and cancer risk in a network of case-control studies, Cancer Causes Control, 2010. 21(2): p. 237-42., http://www.ncbi.nlm.nih.gov/pubmed/19856118
[55] Millen, A. E., Subar, A. F., Graubard, B. I., Peters, U., Hayes, R. B., Weissfeld, J. L., et.al. Fruit and vegetable intake and prevalence of colorectal adenoma in a cancer screening trial, Am J Clin Nutr, 2007. 86(6): p. 1754-64., http://www.ncbi.nlm.nih.gov/pubmed/18065596
[56] Koushik, A., Hunter, D. J., Spiegelman, D., Beeson, W. L., van den Brandt, P. A., Buring, J. E., et.al. Fruits, vegetables, and colon cancer risk in a pooled analysis of 14 cohort studies, J Natl Cancer Inst, 2007. 99(19): p. 1471-83., http://www.ncbi.nlm.nih.gov/pubmed/17895473
[57] Limburg, P. J., Liu-Mares, W., Vierkant, R. A., Wang, A. H., Harnack, L., Flood, A. P., et.al. Prospective evaluation of trans-fatty acid intake and colorectal cancer risk in the Iowa Women's Health Study, Int J Cancer, 2008. 123(11): p. 2717-9., http://www.ncbi.nlm.nih.gov/pubmed/18767047
[58] Alexander, D. D., Cushing, C. A., Lowe, K. A., Sceurman, B., Roberts, M. A., Meta-analysis of animal fat or animal protein intake and colorectal cancer, Am J Clin Nutr, 2009. 89(5): p. 1402-9., http://www.ncbi.nlm.nih.gov/pubmed/19261724
[59] Galeone, C., Talamini, R., Levi, F., Pelucchi, C., Negri, E., Giacosa, A., et.al. Fried foods, olive oil and colorectal cancer, Ann Oncol, 2007. 18(1): p. 36-9., http://www.ncbi.nlm.nih.gov/pubmed/17018706
[60] Nakamura, T., Ishikawa, H., Takeyama, I., Kawano, A., Ishiguro, S., Otani, T., et.al. Excessive fat restriction might promote the recurrence of colorectal tumors, Nutr Cancer, 2010. 62(2): p. 154-63., http://www.ncbi.nlm.nih.gov/pubmed/20099189
[61] Larsson, S. C., Akesson, A., Bergkvist, L., Wolk, A., Dietary acrylamide intake and risk of colorectal cancer in a prospective cohort of men, Eur J Cancer, 2009. 45(4): p. 513-6., http://www.ncbi.nlm.nih.gov/pubmed/19121931
[62] Hogervorst, J. G., Schouten, L. J., Konings, E. J., Goldbohm, R. A., van den Brandt, P. A., Dietary acrylamide intake is not associated with gastrointestinal cancer risk, J Nutr, 2008. 138(11): p. 2229-36., http://www.ncbi.nlm.nih.gov/pubmed/18936224
[63] Mucci, L. A., Wilson, K. M., Acrylamide intake through diet and human cancer risk, J Agric Food Chem, 2008. 56(15): p. 6013-9., http://www.ncbi.nlm.nih.gov/pubmed/18624443
[64] Mucci, L. A., Adami, H. O., Wolk, A., Prospective study of dietary acrylamide and risk of colorectal cancer among women, Int J Cancer, 2006. 118(1): p. 169-73., http://www.ncbi.nlm.nih.gov/pubmed/16003738
[65] Bjelakovic, G., Nikolova, D., Gluud, L. L., Simonetti, R. G., Gluud, C., Mortality in randomized trials of antioxidant supplements for primary and secondary prevention: systematic review and meta-analysis, JAMA, 2007. 297(8): p. 842-57., http://www.ncbi.nlm.nih.gov/pubmed/17327526
[66] Weingarten, M. A., Zalmanovici, A., Yaphe, J., Dietary calcium supplementation for preventing colorectal cancer and adenomatous polyps, Cochrane Database Syst Rev, 2008. p. CD003548., http://www.ncbi.nlm.nih.gov/pubmed/18254022
[67] Wactawski-Wende, J., Kotchen, J. M., Anderson, G. L., Assaf, A. R., Brunner, R. L., O'Sullivan, M. J., et.al. Calcium plus vitamin D supplementation and the risk of colorectal cancer, N Engl J Med, 2006. 354(7): p. 684-96., http://www.ncbi.nlm.nih.gov/pubmed/16481636
[68] Sanjoaquin, M. A., Allen, N., Couto, E., Roddam, A. W., Key, T. J., Folate intake and colorectal cancer risk: a meta-analytical approach, Int J Cancer, 2005. 113(5): p. 825-8., http://www.ncbi.nlm.nih.gov/pubmed/15499620
[69] Wu, K., Platz, E. A., Willett, W. C., Fuchs, C. S., Selhub, J., Rosner, B. A., et.al. A randomized trial on folic acid supplementation and risk of recurrent colorectal adenoma, Am J Clin Nutr, 2009. 90(6): p. 1623-31., http://www.ncbi.nlm.nih.gov/pubmed/19864409
[70] Jaszewski, R., Misra, S., Tobi, M., Ullah, N., Naumoff, J. A., Kucuk, O., et.al. Folic acid supplementation inhibits recurrence of colorectal adenomas: a randomized chemoprevention trial, World J Gastroenterol, 2008. 14(28): p. 4492-8., http://www.ncbi.nlm.nih.gov/pubmed/18680228
[71] Cole, B. F., Baron, J. A., Sandler, R. S., Haile, R. W., Ahnen, D. J., Bresalier, R. S., et.al. Folic acid for the prevention of colorectal adenomas: a randomized clinical trial, JAMA, 2007. 297(21): p. 2351-9., http://www.ncbi.nlm.nih.gov/pubmed/17551129
[72] Logan, R. F., Grainge, M. J., Shepherd, V. C., Armitage, N. C., Muir, K. R., Aspirin and folic acid for the prevention of recurrent colorectal adenomas, Gastroenterology, 2008. 134(1): p. 29-38., http://www.ncbi.nlm.nih.gov/pubmed/18022173
[73] Grau, M. V., Baron, J. A., Sandler, R. S., Wallace, K., Haile, R. W., Church, T. R., et.al. Prolonged effect of calcium supplementation on risk of colorectal adenomas in a randomized trial, J Natl Cancer Inst, 2007. 99(2): p. 129-36., http://www.ncbi.nlm.nih.gov/pubmed/17227996
[74] Wallace, K., Baron, J. A., Cole, B. F., Sandler, R. S., Karagas, M. R., Beach, M. A., et.al. Effect of calcium supplementation on the risk of large bowel polyps, J Natl Cancer Inst, 2004. 96(12): p. 921-5., http://www.ncbi.nlm.nih.gov/pubmed/15199111
[75] Hartman, T. J., Albert, P. S., Snyder, K., Slattery, M. L., Caan, B., Paskett, E., et.al. The association of calcium and vitamin D with risk of colorectal adenomas, J Nutr, 2005. 135(2): p. 252-9., http://www.ncbi.nlm.nih.gov/pubmed/15671222
[76] Lin, J., Cook, N. R., Lee, I. M., Manson, J. E., Buring, J. E., Zhang, S. M., Total magnesium intake and colorectal cancer incidence in women, Cancer Epidemiol Biomarkers Prev, 2006. 15(10): p. 2006-9., http://www.ncbi.nlm.nih.gov/pubmed/17035414
[77] Jacobs, E. T., Jiang, R., Alberts, D. S., Greenberg, E. R., Gunter, E. W., Karagas, M. R., et.al. Selenium and colorectal adenoma: results of a pooled analysis, J Natl Cancer Inst, 2004. 96(22): p. 1669-75., http://www.ncbi.nlm.nih.gov/pubmed/15547179
[78] Peters, U., Chatterjee, N., Church, T. R., Mayo, C., Sturup, S., Foster, C. B., et.al. High serum selenium and reduced risk of advanced colorectal adenoma in a colorectal cancer early detection program, Cancer Epidemiol Biomarkers Prev, 2006. 15(2): p. 315-20., http://www.ncbi.nlm.nih.gov/pubmed/16492922
[79] Vinogradova, Y., Hippisley-Cox, J., Coupland, C., Logan, R. F., Risk of colorectal cancer in patients prescribed statins, nonsteroidal anti-inflammatory drugs, and cyclooxygenase-2 inhibitors: nested case-control study, Gastroenterology, 2007. 133(2): p. 393-402., http://www.ncbi.nlm.nih.gov/pubmed/17681160
[80] Bertagnolli, M. M., Eagle, C. J., Zauber, A. G., Redston, M., Solomon, S. D., Kim, K., et.al. Celecoxib for the prevention of sporadic colorectal adenomas, N Engl J Med, 2006. 355(9): p. 873-84., http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16943400, http://www.nejm.org/doi/pdf/10.1056/NEJMoa061355
[81] Arber, N., Eagle, C. J., Spicak, J., Racz, I., Dite, P., Hajer, J., et.al. Celecoxib for the prevention of colorectal adenomatous polyps, N Engl J Med, 2006. 355(9): p. 885-95., http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16943401, http://www.nejm.org/doi/pdf/10.1056/NEJMoa061652
[82] Baron, J. A., Sandler, R. S., Bresalier, R. S., Quan, H., Riddell, R., Lanas, A., et.al. A randomized trial of rofecoxib for the chemoprevention of colorectal adenomas, Gastroenterology, 2006. 131(6): p. 1674-82., http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17087947, http://www.gastrojournal.org/article/S0016-5085(06)01994-9/pdf
[83] Bardou, M., Barkun, A., Martel, M., Effect of statin therapy on colorectal cancer, Gut, 2010. 59(11): p. 1572-85., http://www.ncbi.nlm.nih.gov/pubmed/20660702
[84] Routine aspirin or nonsteroidal anti-inflammatory drugs for the primary prevention of colorectal cancer: U.S. Preventive Services Task Force recommendation statement, Ann Intern Med, 2007. 146(5): p. 361-4., http://www.ncbi.nlm.nih.gov/pubmed/17339621
[85] Flossmann, E., Rothwell, P. M., Effect of aspirin on long-term risk of colorectal cancer: consistent evidence from randomised and observational studies, Lancet, 2007. 369(9573): p. 1603-13., http://www.ncbi.nlm.nih.gov/pubmed/17499602
[86] Rothwell, P. M., Fowkes, F. G., Belch, J. F., Ogawa, H., Warlow, C. P., Meade, T. W., Effect of daily aspirin on long-term risk of death due to cancer: analysis of individual patient data from randomised trials, Lancet, 2011. 377(9759): p. 31-41., http://www.ncbi.nlm.nih.gov/pubmed/21144578
[87] Chan, A. T., Giovannucci, E. L., Meyerhardt, J. A., Schernhammer, E. S., Curhan, G. C., Fuchs, C. S., Long-term use of aspirin and nonsteroidal anti-inflammatory drugs and risk of colorectal cancer, JAMA, 2005. 294(8): p. 914-23., http://www.ncbi.nlm.nih.gov/pubmed/16118381
[88] Hormone therapy for the prevention of chronic conditions in postmenopausal women: recommendations from the U.S. Preventive Services Task Force, Ann Intern Med, 2005. 142(10): p. 855-60., http://www.ncbi.nlm.nih.gov/pubmed/15897536
[89] Farquhar, C., Marjoribanks, J., Lethaby, A., Suckling, J. A., Lamberts, Q., Long term hormone therapy for perimenopausal and postmenopausal women, Cochrane Database Syst Rev, 2009. p. CD004143., http://www.ncbi.nlm.nih.gov/pubmed/19370593
[90] Alberts, D. S., Martinez, M. E., Hess, L. M., Einspahr, J. G., Green, S. B., Bhattacharyya, A. K., et.al. Phase III trial of ursodeoxycholic acid to prevent colorectal adenoma recurrence, J Natl Cancer Inst, 2005. 97(11): p. 846-53., http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15928305, http://jnci.oxfordjournals.org/content/97/11/846.full.pdf
[91] DGGG, Hormontherapie (HT) in der Peri- und Postmenopause, 2009.