Endogenous N-nitroso compounds, and their precursors, present in bacon, donot initiate or promote aberrant crypt foci in the colon of rats

Processed meat intake is associated with increased risk of colorectal cance r. This association may be explained by the endogenous formation of N-nitro so compounds (NOC). The hypothesis that meat intake can increase fecal NOC levels and colon carcinogenesis was tested in 175 Fischer 344 rats. Initiat ion was assessed by the number of aberrant crypt foci (ACF) in the colon of rats 45 days after the start of a high-fat bacon-based diet. Promotion was assessed by the multiplicity of ACF (crypts per ACF) in rats given experim ental diets for 100 days starting 7 days after an azoxymethane injection. T hree promotion studies were done, each in 5 groups of 10 rats, whose diets contained 7%, 14%, or 28% fat. Tested meats were bacon, pork, chicken, and beef Fecal and dietary NOC were assayed by thermal energy analysis. Results show that feces from rats fed bacon-based diets contained 10-20 times more NOC than feces from control rats fed a casein-based diet (all p < 0.0001 i n 4 studies). In bacon-fed rats, the amount of NOC input (diet) and output (feces) was similar. Rats fed a diet based on beef; pork, or chicken meat h ad less fecal NOC than controls (most p < 0.01). No ACF were detected in th e colon of bacon-fed uninitiated rats. After azoxymethane injection, unproc essed but cooked meat-based diets did not change the number of ACF or the A CF multiplicity compared with control rats. In contrast the bacon-based die t consistently reduced the number of large ACF per rat and the ACF multipli city in the three promotion studies by 12%, 17%, and 20% (all p < 0.01). Re sults suggest that NOC from dietary bacon would not enhance colon carcinoge nesis in rats.