A 14‐day in‐house dietary modification of a ‘Western’ diet to an ‘African’ diet changes the microbiota, its metabolome, and biomarkers of colon cancer risk (825.5)

Abstract

Methods Twenty age and sex matched middle aged healthy African Americans were studied on their usual diet and then again after dietary modification to a low meat and fat, high fiber ‘traditional African’ diet, prepared and delivered individually in‐house under close supervision for 2 weeks. Phutu‐ corn meal, Samp‐ dried corn kernels, sugar beans, fruits and vegetables provided 30‐35 Kcal/Kg of energy, 14% protein, 17% fat, 72% carbohydrate, 40 g dietary fiber, and 32 grams resistant starch. The diet was well tolerated overall and their body weights remained stable. Pre‐ and post‐dietary modification fecal and colonic evacuate samples were collected to measure the microbiota and their metabolites and colonoscopies were performed to assess mucosal health and to obtain biopsies for the measurement of inflammatory and proliferative biomarkers (Ki67‐ identified by immunohistochemical staining).Results Following dietary change, significant increases were measured in the expression of functional microbial genes encoding butyrate (BcoA gene, 1.1E+10±1.8E+10 vs. 2.5E+10±9.3E+09 copies/g feces, p= 0.04) and methane synthesis (mcrA gene, 6.5E+5±1.2E+5 vs. 1.6E+6±3.9E+5 copies/g feces, p= 0.01); fecal short chain fatty acids, e.g. butyrate concentrations (3.56±0.96 vs. 8.61± 2.10 µmol/gm feces, p=0.034); expired breath methane levels (12.8±3 vs. 20.3±8.3 ppm, p=0.02); Finally, mucosal Ki67 expression was significantly reduced (p<0.0001).Conclusion In this study, short term dietary change in high colon cancer risk African Americans to a low meat and fat, and high fiber “African” diet promoted saccharolytic fermentation and the production of anti‐neoplastic metabolites such as butyrate in association with a reduction in biomarkers of colon cancer risk. These results support the recommendations for reducing meat and fat and increasing fiber to suppress colon cancer in high‐risk populations.Grant Funding Source: Supported by National Institutes of Health, R01 CA135379 (O’Keefe) and UL1 RR024153 and UL1TR000005