Objective. A shift in the total incidence from left- to right-sided colon cancer has been reported and raises the question as to whether lifestyle risk factors are responsible for the changing subsite distribution of colon cancer. The present study provides a review of the subsite-specific risk estimates for the dietary components presently regarded as convincing or probable risk factors for colorectal cancer: red meat, processed meat, fiber, garlic, milk, calcium, and alcohol. Methods. Studies were identified by searching PubMed through October 8, 2012 and by reviewing reference lists. Thirty-two prospective cohort studies are included, and the estimates are compared by sex for each risk factor. Results. For alcohol, there seems to be a stronger association with rectal cancer than with colon cancer, and for meat a somewhat stronger association with distal colon and rectal cancer, relative to proximal colon cancer. For fiber, milk, and calcium, there were only minor differences in relative risk across subsites. No statement could be given regarding garlic. Overall, many of the subsite-specific risk estimates were nonsignificant, irrespective of exposure. Conclusion. For some dietary components the associations with risk of cancer of the rectum and distal colon appear stronger than for proximal colon, but not for all. 1. Introduction Global estimates for 2008 indicate that colorectal cancer is the third most common cancer in the world [1]. Reports in several countries have described diverging incidence rates in colorectal cancer by subsite, including, in relative terms, an increasing proportion of proximal tumors [2–15], and thus a shift in absolute incidence from left- to right-sided colon cancers. The reasons for this trend are not well understood; the subsites differ in physical function, artery supply, histology, and innervation, and they also derive from different segments in the primitive intestinal tract in the embryo [16]. The proximal colon originates from the midgut, whereas the distal colon and the rectum derivate originate from the hindgut. Comparisons have also shown that proximal colon tumors tend to have different molecular characteristics, with a higher proportion of microsatellite instability, and are more likely to have CpG island methylator phenotype and Ki-ras mutations than distal colon and rectal tumors [17]. It has been estimated that 45 percent of all colorectal cancer cases can be prevented in high-risk populations through modifications of diet, physical activity habits, and weight control [18]. According to the recent report
References
[1]
J. Ferlay, H. R. Shin, F. Bray, D. Forman, C. Mathers, and D. M. Parkin, GLOBOCAN 2008: Cancer Incidence and Mortality Worldwide, IARC Cancer Base, no. 10, International Agency for Research on Cancer, Lyon, France, 2012.
[2]
F. Kee, R. H. Wilson, R. Gilliland, J. M. Sloan, B. J. Rowlands, and R. J. Moorehead, “Changing site distribution of colorectal cancer,” British Medical Journal, vol. 305, no. 6846, p. 158, 1992.
[3]
G. I. Slater, R. H. Haber, and A. H. Aufses Jr., “Changing distribution of carcinoma of the colon and rectum,” Surgery, Gynecology & Obstetrics, vol. 158, pp. 216–218, 1984.
[4]
Y. Toyoda, T. Nakayama, Y. Ito, A. Ioka, and H. Tsukuma, “Trends in colorectal cancer incidence by subsite in Osaka, Japan,” Japanese Journal of Clinical Oncology, vol. 39, no. 3, pp. 189–191, 2009.
[5]
C. Cucino, A. M. Buchner, and A. Sonnenberg, “Continued rightward shift of colorectal cancer,” Diseases of the Colon and Rectum, vol. 45, no. 8, pp. 1035–1040, 2002.
[6]
S. L. Saltzstein and C. A. Behling, “Age and time as factors in the left-to-right shift of the subsite of colorectal adenocarcinoma: a study of 213,383 cases from the California Cancer Registry,” Journal of Clinical Gastroenterology, vol. 41, no. 2, pp. 173–177, 2007.
[7]
R. W. Beart, L. J. Melton, M. Maruta, M. B. Dockerty, H. B. Frydenberg, and W. M. O'Fallon, “Trends in right and left-sided colon cancer,” Diseases of the Colon & Rectum, vol. 26, pp. 393–398, 1983.
[8]
F. Levi, L. Randimbison, and C. La Vecchia, “Trends in subsite distribution of colorectal cancers and polyps from the Vaud Cancer Registry,” Cancer, vol. 72, no. 1, pp. 46–50, 1993.
[9]
E. Mitry, A. M. Benhamiche, C. Couillault et al., “Effect of age, period of diagnosis and birth cohort on large bowel cancer incidence in a well-defined French population, 1976–1995,” European Journal of Cancer Prevention, vol. 11, no. 6, pp. 529–534, 2002.
[10]
H. Singh, A. A. Demers, L. Xue, D. Turner, and C. N. Bernstein, “Time trends in colon cancer incidence and distribution and lower gastrointestinal endoscopy utilization in Manitoba,” American Journal of Gastroenterology, vol. 103, no. 5, pp. 1249–1256, 2008.
[11]
H. Takada, T. Ohsawa, S. Iwamoto, et al., “Changing site distribution of colorectal cancer in Japan,” Diseases of the Colon & Rectum, vol. 45, pp. 1249–1254, 2002.
[12]
M. Th？rn, R. Bergstr？m, U. Kressner, P. Sparén, M. Zack, and A. Ekbom, “Trends in colorectal cancer incidence in Sweden 1959–93 by gender, localization, time period, and birth cohort,” Cancer Causes and Control, vol. 9, no. 2, pp. 145–152, 1998.
[13]
J. R. Jass, “Subsite distribution and incidence of colorectal cancer in New Zealand, 1974–1983,” Diseases of the Colon & Rectum, vol. 34, pp. 56–59, 1991.
[14]
R. Scheiden, P. Pescatore, Y. Wagener, N. Kieffer, and C. Capesius, “Colon cancer in Luxembourg: a national population-based data report, 1988–1998,” BMC Cancer, vol. 5, article 52, 2005.
[15]
I. K. Larsen and F. Bray, “Trends in colorectal cancer incidence in Norway 1962–2006: an interpretation of the temporal patterns by anatomic subsite,” International Journal of Cancer, vol. 126, no. 3, pp. 721–732, 2010.
[16]
F. Y. Li and M. D. Lai, “Colorectal cancer, one entity or three,” Journals of Zhejiang University-Science B, vol. 10, pp. 219–229, 2009.
[17]
M. L. Slattery, K. Curtin, R. K. Wolff et al., “A comparison of colon and rectal somatic DNA alterations,” Diseases of the Colon & Rectum, vol. 52, no. 7, pp. 1304–1311, 2009.
[18]
World Cancer Research Found and American Institute for Cancer Research, Food, Nutrition, Physical Activity, and the Prevention of Cancer: A Global Perspective, Washington, DC, USA, 2007.
[19]
World Cancer Research Found and American Institute for Cancer Research, Food, Nutrition, Physical Activity, and the Prevention of Colorectal Cancer. Continuous Update Project, Colorectal Cancer Report 2010, Summary, Washington, DC, USA, 2011.
[20]
M. Huncharek, J. Muscat, and B. Kupelnick, “Colorectal cancer risk and dietary intake of calcium, vitamin D, and dairy products: a meta-analysis of 26,335 cases from 60 observational studies,” Nutrition and Cancer, vol. 61, no. 1, pp. 47–69, 2009.
[21]
J. A. Bergsma-Kadijk, P. van't Veer, E. Kampman, and J. Burema, “Calcium does not protect against colorectal neoplasia,” Epidemiology, vol. 7, no. 6, pp. 590–597, 1996.
[22]
S. C. Larsson and A. Wolk, “Meat consumption and risk of colorectal cancer: a meta-analysis of prospective studies,” International Journal of Cancer, vol. 119, no. 11, pp. 2657–2664, 2006.
[23]
D. S. Chan, R. Lau, D. Aune et al., “Red and processed meat and colorectal cancer incidence: meta-analysis of prospective studies,” PLoS ONE, vol. 6, no. 6, article e20456, 2011.
[24]
E. Cho, S. A. Smith-Warner, D. Spiegelman, et al., “Dairy foods, calcium, and colorectal cancer: a pooled analysis of 10 cohort studies,” Journal of the National Cancer Institute, vol. 96, pp. 1015–1022, 2004.
[25]
Y. Park, D. J. Hunter, D. Spiegelman, et al., “Dietary fiber intake and risk of colorectal cancer: a pooled analysis of prospective cohort studies,” The Journal of the American Medical Association, vol. 294, pp. 2849–2857, 2005.
[26]
E. Cho, S. A. Smith-Warner, J. Ritz, et al., “Alcohol intake and colorectal cancer: a pooled analysis of 8 cohort studies,” Annals of Internal Medicine, vol. 140, pp. 603–613, 2004.
[27]
A. L. Klatsky, M. A. Armstrong, G. D. Friedman, and R. A. Hiatt, “The relations of alcoholic beverage use to colon and rectal cancer,” American Journal of Epidemiology, vol. 128, no. 5, pp. 1007–1015, 1988.
[28]
G. N. Stemmermann, A. Nomura, and P. H. Chyou, “The influence of dairy and nondairy calcium on subsite large-bowel cancer risk,” Diseases of the Colon and Rectum, vol. 33, no. 3, pp. 190–194, 1990.
[29]
A. A. Razzak, A. S. Oxentenko, R. A. Vierkant, et al., “Alcohol intake and colorectal cancer risk by molecularly defined subtypes in a prospective study of older women,” Cancer Prevention Research, vol. 4, pp. 2035–2043, 2011.
[30]
E. Giovannucci, E. B. Rimm, M. J. Stampfer, G. A. Colditz, A. Ascherio, and W. C. Willett, “Intake of fat, meat, and fiber in relation to risk of colon cancer in men,” Cancer Research, vol. 54, no. 9, pp. 2390–2397, 1994.
[31]
A. Chao, M. J. Thun, C. J. Connell, et al., “Meat consumption and risk of colorectal cancer,” The Journal of the American Medical Association, vol. 293, pp. 172–182, 2005.
[32]
S. C. Larsson, J. Rafter, L. Holmberg, L. Bergkvist, and A. Wolk, “Red meat consumption and risk of cancers of the proximal colon, distal colon and rectum: the Swedish Mammography Cohort,” International Journal of Cancer, vol. 113, no. 5, pp. 829–834, 2005.
[33]
T. Norat, S. Bingham, P. Ferrari, et al., “Meat, fish, and colorectal cancer risk: the European Prospective Investigation into cancer and nutrition,” Journal of the National Cancer Institute, vol. 97, no. 12, pp. 906–916, 2005.
[34]
Y. Sato, N. Nakaya, S. Kuriyama, Y. Nishino, Y. Tsubono, and I. Tsuji, “Meat consumption and risk of colorectal cancer in Japan: the Miyagi cohort study,” European Journal of Cancer Prevention, vol. 15, no. 3, pp. 211–218, 2006.
[35]
A. J. Cross, L. M. Ferrucci, A. Risch et al., “A large prospective study of meat consumption and colorectal cancer risk: an investigation of potential mechanisms underlying this association,” Cancer Research, vol. 70, no. 6, pp. 2406–2414, 2010.
[36]
A. Shin, J. Joo, J. Bak, et al., “Site-specific risk factors for colorectal cancer in a Korean population,” PLoS One, vol. 6, article e23196, 2011.
[37]
K. A. Steinmetz, L. H. Kushi, R. M. Bostick, A. R. Folsom, and J. D. Potter, “Vegetables, fruit, and colon cancer in the Iowa women's health study,” American Journal of Epidemiology, vol. 139, no. 1, pp. 1–15, 1994.
[38]
C. S. Fuchs, E. L. Giovannucci, G. A. Colditz et al., “Dietary fiber and the risk of colorectal cancer and adenoma in women,” New England Journal of Medicine, vol. 340, no. 3, pp. 169–176, 1999.
[39]
S. C. Larsson, E. Giovannucci, L. Bergkvist, and A. Wolk, “Whole grain consumption and risk of colorectal cancer: a population-based cohort of 60 000 women,” British Journal of Cancer, vol. 92, no. 9, pp. 1803–1807, 2005.
[40]
A. M. Nomura, J. H. Hankin, B. E. Henderson et al., “Dietary fiber and colorectal cancer risk: the multiethnic cohort study,” Cancer Causes and Control, vol. 18, no. 7, pp. 753–764, 2007.
[41]
A. Schatzkin, T. Mouw, Y. Park et al., “Dietary fiber and whole-grain consumption in relation to colorectal cancer in the NIH-AARP Diet and Health Study,” American Journal of Clinical Nutrition, vol. 85, no. 5, pp. 1353–1360, 2007.
[42]
G. C. Kabat, J. M. Shikany, S. A. Beresford et al., “Dietary carbohydrate, glycemic index, and glycemic load in relation to colorectal cancer risk in the Women's Health Initiative,” Cancer Causes and Control, vol. 19, no. 10, pp. 1291–1298, 2008.
[43]
R. Egeberg, A. Olsen, S. Loft et al., “Intake of wholegrain products and risk of colorectal cancers in the Diet, Cancer and Health cohort study,” British Journal of Cancer, vol. 103, no. 5, pp. 730–734, 2010.
[44]
N. Murphy, T. Norat, P. Ferrari, et al., “Dietary fibre intake and risks of cancers of the colon and rectum in the European Prospective Investigation into Cancer and Nutrition (EPIC),” PLoS One, vol. 7, article e39361, 2012.
[45]
M. L. McCullough, A. S. Robertson, C. Rodriguez et al., “Calcium, vitamin D, dairy products, and risk of colorectal cancer in the Cancer Prevention Study II Nutrition Cohort (United States),” Cancer Causes and Control, vol. 14, no. 1, pp. 1–12, 2003.
[46]
S. C. Larsson, L. Bergkvist, and A. Wolk, “High-fat dairy food and conjugated linoleic acid intakes in relation to colorectal cancer incidence in the Swedish Mammography Cohort,” American Journal of Clinical Nutrition, vol. 82, no. 4, pp. 894–900, 2005.
[47]
S. C. Larsson, L. Bergkvist, J. Ruteg？rd, E. Giovannucci, and A. Wolk, “Calcium and dairy food intakes are inversely associated with colorectal cancer risk in the Cohort of Swedish Men,” American Journal of Clinical Nutrition, vol. 83, no. 3, pp. 667–673, 2006.
[48]
P. Terry, J. A. Baron, L. Bergkvist, L. Holmberg, and A. Wolk, “Dietary calcium and vitamin D intake and risk of colorectal cancer: a prospective cohort study in women,” Nutrition and Cancer, vol. 43, no. 1, pp. 39–46, 2002.
[49]
K. Wu, W. C. Willett, C. S. Fuchs, G. A. Colditz, and E. L. Giovannucci, “Calcium intake and risk of colon cancer in women and men,” Journal of the National Cancer Institute, vol. 94, no. 6, pp. 437–446, 2002.
[50]
A. Flood, U. Peters, N. Chatterjee, J. V. Lacey Jr., C. Schairer, and A. Schatzkin, “Calcium from diet and supplements is associated with reduced risk of colorectal cancer in a prospective cohort of women,” Cancer Epidemiology Biomarkers and Prevention, vol. 14, no. 1, pp. 126–132, 2005.
[51]
J. Ishihara, M. Inoue, M. Iwasaki, S. Sasazuki, and S. Tsugane, “Dietary calcium, vitamin D, and the risk of colorectal cancer,” American Journal of Clinical Nutrition, vol. 88, no. 6, pp. 1576–1583, 2008.
[52]
A. H. Wu, A. Paganini-Hill, R. K. Ross, and B. E. Henderson, “Alcohol, physical activity and other risk factors for colorectal cancer: a prospective study,” British Journal of Cancer, vol. 55, no. 6, pp. 687–694, 1987.
[53]
E. Giovannucci, E. B. Rimm, A. Ascherio, M. J. Stampfer, G. A. Colditz, and W. C. Willett, “Alcohol, low-methionine—low-folate diets, and risk of colon cancer in men,” Journal of the National Cancer Institute, vol. 87, no. 4, pp. 265–273, 1995.
[54]
A. Pedersen, C. Johansen, and M. Gr？nb？k, “Relations between amount and type of alcohol and colon and rectal cancer in a Danish population based cohort study,” Gut, vol. 52, no. 6, pp. 861–867, 2003.
[55]
M. Akhter, S. Kuriyama, N. Nakaya et al., “Alcohol consumption is associated with an increased risk of distal colon and rectal cancer in Japanese men: the Miyagi Cohort Study,” European Journal of Cancer, vol. 43, no. 2, pp. 383–390, 2007.
[56]
P. Ferrari, M. Jenab, T. Norat, et al., “Lifetime and baseline alcohol intake and risk of colon and rectal cancers in the European prospective investigation into cancer and nutrition (EPIC),” International Journal of Cancer, vol. 121, no. 9, pp. 2065–2072, 2007.
[57]
B. W. C. Bongaerts, P. A. van den Brandt, R. A. Goldbohm, A. F. P. M. de Goeij, and M. P. Weijenberg, “Alcohol consumption, type of alcoholic beverage and risk of colorectal cancer at specific subsites,” International Journal of Cancer, vol. 123, no. 10, pp. 2411–2417, 2008.
[58]
J. Y. Park, C. C. Dahm, R. H. Keogh et al., “Alcohol intake and risk of colorectal cancer: results from the UK Dietary Cohort Consortium,” British Journal of Cancer, vol. 103, no. 5, pp. 747–756, 2010.
[59]
M. Egger, G. D. Smith, and J. A. Sterne, “Uses and abuses of meta-analysis,” Clinical Medicine, vol. 1, pp. 478–484, 2001.
[60]
J. Lin, S. M. Zhang, N. R. Cook, J. E. Manson, I. M. Lee, and J. E. Buring, “Intakes of calcium and vitamin D and risk of colorectal cancer in women,” American Journal of Epidemiology, vol. 161, no. 8, pp. 755–764, 2005.
[61]
S. A. Bingham, R. Hughes, and A. J. Cross, “Effect of white versus red meat on endogenous N-nitrosation in the human colon and further evidence of a dose response,” Journal of Nutrition, vol. 132, no. 11, pp. 3522S–3525S, 2002.
[62]
A. C. Povey, C. N. Hall, A. F. Badawi, D. P. Cooper, and P. J. O'Connor, “Elevated levels of the pro-carcinogenic adduct, O(6)-methylguanine, in normal DNA from the cancer prone regions of the large bowel,” Gut, vol. 47, no. 3, pp. 362–365, 2000.
[63]
A. Hague, A. M. Manning, K. A. Hanlon, L. I. Huschtscha, D. Hart, and C. Paraskeva, “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,” International Journal of Cancer, vol. 55, no. 3, pp. 498–505, 1993.
[64]
W. Scheppach and F. Weiler, “The butyrate story: old wine in new bottles?” Current Opinion in Clinical Nutrition and Metabolic Care, vol. 7, no. 5, pp. 563–567, 2004.
[65]
J. M. Wong, R. de Souza, C. W. C. Kendall, A. Emam, and D. J. Jenkins, “Colonic health: fermentation and short chain fatty acids,” Journal of Clinical Gastroenterology, vol. 40, no. 3, pp. 235–243, 2006.
[66]
W. E. Roediger, “Role of anaerobic bacteria in the metabolic welfare of the colonic mucosa in man,” Gut, vol. 21, no. 9, pp. 793–798, 1980.
[67]
S. A. Lamprecht and M. Lipkin, “Chemoprevention of colon cancer by calcium, vitamin D and folate: molecular mechanisms,” Nature Reviews Cancer, vol. 3, no. 8, pp. 601–614, 2003.
[68]
G. P？schl and H. K. Seitz, “Alcohol and cancer,” Alcohol and Alcoholism, vol. 39, no. 3, pp. 155–165, 2004.
[69]
U. A. Simanowski, F. Stickel, H. Maier, U. G？rtner, and H. K. Seitz, “Effect of alcohol on gastrointestinal cell regeneration as a possible mechanism in alcohol-associated carcinogenesis,” Alcohol, vol. 12, no. 2, pp. 111–115, 1995.
