The colonic mucosal bacterial community was associated with serum carotenoid concentrations at baseline but was not appreciably changed by dietary intervention.

Dietary fish oils have potential for prevention of colon cancer, and yet the mechanisms of action in normal and tumor colon tissues are not well defined. Here we evaluated the impact of the colonic fatty acid milieu on formation of prostaglandins and other eicosanoids. Distal tumors in rats were chemically induced to model inflammatory colonic carcinogenesis. After 21 weeks of feeding with either a fish oil diet containing an eicosapentaenoic acid:ω-6 fatty acid ratio of 0.4 or a Western fat diet, the relationships between colon fatty acids and prostaglandin E2 (PGE2) concentrations were evaluated. PGE2 is a key pro-inflammatory mediator in the colon tightly linked with the initiation and progression of colon cancer. The fish oil versus the Western fat diet resulted in reduced total fatty acid concentrations in serum but not in colon. In the colon, the effects of the fish oil on fatty acids differed in normal and tumor tissue. There were distinct lipodomic patterns consistent with a lipogenic phenotype in tumors. In tumor tissue, the eicosapentaenoic acid:arachidonic acid ratio, cyclooxygenase-2 expression and the mole percent of saturated fatty acids were significant predictors of inter-animal variability in colon PGE2 after accounting for diet. In normal tissues from either control rats or carcinogen-treated rats, only diet was a significant predictor of colon PGE2. These results show that the fatty acid milieu can modulate the efficacy of dietary fish oils for colon cancer prevention, and this could extend to other preventive agents that function by reducing inflammatory stress.

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Purpose: Fungal-type dysbiosis (FTD) is still an unproven diagnosis. Patients are polysymptomatic, but most have symptoms of irritable bowel. Treatment, using a diet low in fermentable, yeasty and mould-containing foods with or without antifungal drugs, is often rewarding. Patients with FTD show elevated blood ethanol levels after fasting glucose challenge. Because of this most authors suggest a fungal cause. Hydrogen generation is a bacterial fermentation product and would only be expected if a bacterial cause was present. It was therefore decided to correlate ethanol and hydrogen production. Design: Statistical comparison of ethanol producers and non-producers with respect to breath hydrogen and symptomatology. Materials and Methods: The gut fermentation profile was performed by gas-liquid chromatography, and measured ethanol, a number of higher alcohols and short-chain fatty acids. Lactulose breath hydrogen estimations were by gas chromatography. Statistics were calculated using Pearson's rank correlation and the chi-squared test, using Microsoft Excel packages. Results: Two groups were studied. The first produced excess ethanol (n~18) and the second (n~20) did not. Both groups included patients producing hydrogen. There was no statistical correlation between levels of ethanol and hydrogen production. Conclusions: If FTD is solely due to yeasts, our ethanol positive group should not produce hydrogen, solely a bacterial ferment, but the ethanol negative group should. If the conventional view, that yeasts do not produce hydrogen as a fermentation product, is correct, it appears from the commonness of breath hydrogen positives in this series that bacterial fermentation is in some way implicated in FTD.

Data is provided to show the detailed fatty acid and lipidomic composition of normal and tumor rat colon tissues. Rats were fed either a Western fat diet or a fish oil diet, and half the rats from each diet group were treated with chemical carcinogens that induce colon cancer (azoxymethane and dextran sodium sulfate). The data show total fatty acid profiles of sera and of all the colon tissues, namely normal tissue from control rats and both normal and tumor tissues from carcinogen-treated rats, as obtained by gas chromatography with mass spectral detection. Data from lipidomic analyses of a representative subset of the colon tissue samples is also shown in heat maps generated from hierarchical cluster analysis. These data display the utility lipidomic analyses to enhance the interpretation of dietary feeding studies aimed at cancer prevention and support the findings published in the companion paper (Effects of fish oil supplementation on prostaglandins in normal and tumor colon tissue: modulation by the lipogenic phenotype of colon tumors, Djuric et al., 2017 [1]).