Why do African Americans get more colon cancer than native Africans?

被引:112
作者
O'Keefe, Stephen J. D. [1 ]
Chung, Dan
Mahmoud, Nevine
Sepulveda, Antonia R.
Manafe, Mashudu
Arch, Judith
Adada, Haytham
van der Merwe, Tian
机构
[1] Univ Pittsburgh, Div Gastroenterol & Pathol, Pittsburgh, PA 15213 USA
[2] Univ Limpopo, GaRankuwa, South Africa
关键词
COLORECTAL-CANCER; LACTOBACILLUS-PLANTARUM; NUTRITIONAL-STATUS; MEAT CONSUMPTION; DIETARY-INTAKE; N-NITROSATION; RISK; PATTERNS; BACTERIA; FIBER;
D O I
10.1093/jn/137.1.175S
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
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-alpha 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-alpha 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.
引用
收藏
页码:175S / 182S
页数:8
相关论文
共 55 条
[1]  
[Anonymous], 2005, CANC FACTS FIG
[2]  
[Anonymous], 1997, FOOD NUTR PREV CANC
[3]   ENVIRONMENTAL FACTORS AND CANCER INCIDENCE AND MORTALITY IN DIFFERENT COUNTRIES, WITH SPECIAL REFERENCE TO DIETARY PRACTICES [J].
ARMSTRONG, B ;
DOLL, R .
INTERNATIONAL JOURNAL OF CANCER, 1975, 15 (04) :617-631
[4]  
Ashktorab H, 2003, CLIN CANCER RES, V9, P1112
[5]   Demonstration of a direct stimulatory effect of bile salts on rat colonic epithelial cell proliferation [J].
Barone, M ;
Berloco, P ;
Ladisa, R ;
Ierardi, E ;
Caruso, ML ;
Valentini, AM ;
Notarnicola, M ;
Di Leo, A ;
Francavilla, A .
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY, 2002, 37 (01) :88-94
[6]   Colonic food: Pre- and probiotics [J].
Bengmark, S .
AMERICAN JOURNAL OF GASTROENTEROLOGY, 2000, 95 (01) :S5-S7
[7]   Effect of white versus red meat on endogenous N-nitrosation in the human colon and further evidence of a dose response [J].
Bingham, SA ;
Hughes, R ;
Cross, AJ .
JOURNAL OF NUTRITION, 2002, 132 (11) :3522S-3525S
[8]  
BURKITT DP, 1971, CANCER, V28, P3, DOI 10.1002/1097-0142(197107)28:1<3::AID-CNCR2820280104>3.0.CO
[9]  
2-N
[10]  
CHRISTL S U, 1991, Gastroenterology, V100, pA203