QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by O'Keefe, S. J. D. Articles by van der Merwe, T. Search for Related Content PubMed PubMed Citation Articles by O'Keefe, S. J. D. Articles by van der Merwe, T. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Medline Plus Health Information Diets Hazardous Substances DB HYDROGEN

---

Supplement: International Research Conference on Food, Nutrition, and Cancer

Why Do African Americans Get More Colon Cancer than Native Africans?^1–3,

⁴ Division of Gastroenterology and Pathology, University of Pittsburgh, Pittsburgh, PA 15213 and the ⁵ University of Limpopo, Medunsa Campus, GaRankuwa, South Africa

^* To whom correspondence should be addressed. E-mail: sjokeefe{at}pitt.edu.

The incidence of colorectal cancer (CRC) is dramatically higher in African Americans (AAs) than in Native Africans (NAs) (60:100,000 vs. <1:100,000) and slightly higher than in Caucasian Americans (CAs). To explore whether the difference could be explained by interactions between diet and colonic bacterial flora, we compared randomly selected samples of healthy 50- to 65-y-old AAs (n = 17) with NAs (n = 18) and CAs (n = 17). Diet was measured by 3-d recall, and colonic metabolism by breath hydrogen and methane responses to oral lactulose. Fecal samples were cultured for 7- dehydroxylating bacteria and Lactobacillus plantarum. Colonoscopic mucosal biopsies were taken to measure proliferation rates. In comparison with NAs, AAs consumed more (P < 0.01) protein (94 ± 9.3 vs. 58 ± 4.1 g/d) and fat (114 ± 11.2 vs. 38 ± 3.0 g/d), meat, saturated fat, and cholesterol. However, they also consumed more (P < 0.05) calcium, vitamin A, and vitamin C, and fiber intake was the same. Breath hydrogen was higher (P < 0.0001) and methane lower in AAs, and fecal colony counts of 7- dehydroxylating bacteria were higher and of Lactobacilli were lower. Colonic crypt cell proliferation rates were dramatically higher in AAs (21.8 ± 1.1% vs. 3.2 ± 0.8% labeling, P < 0.0001). In conclusion, the higher CRC risk and mucosal proliferation rates in AAs than in NAs were associated with higher dietary intakes of animal products and higher colonic populations of potentially toxic hydrogen and secondary bile-salt-producing bacteria. This supports our hypothesis that CRC risk is determined by interactions between the external (dietary) and internal (bacterial) environments.

This article has been cited by other articles:

				S. J. D. O'Keefe, J. Ou, S. Aufreiter, D. O'Connor, S. Sharma, J. Sepulveda, T. Fukuwatari, K. Shibata, and T. Mawhinney Products of the Colonic Microbiota Mediate the Effects of Diet on Colon Cancer Risk J. Nutr., November 1, 2009; 139(11): 2044 - 2048. [Abstract] [Full Text] [PDF]

				S. Sharma and S. J D O'Keefe Environmental influences on the high mortality from colorectal cancer in African Americans Postgrad. Med. J., September 1, 2007; 83(983): 583 - 589. [Abstract] [Full Text] [PDF]