Fecal steroids and colorectal cancer

Abstract

The fecal steroid profiles of healthy subjects were compared with those of colorectal cancer (CRC) patients. The multicomponent profiles did not differ qualitatively in that CRC patients, like control subjects, had similar fecal steroids. The major bile acids detected in fecal extracts were lithocholic acid (LCA) and deoxycholic acid (DCA). The major sterol of animal origin was cholesterol and its bacterial metabolite coprostanol, whereas the major plant sterols were ß‐sitosterol, stigmasterol, campesterol, and their corresponding bacterial metabolites. CRC patients excreted higher amounts of total major bile acids (LCA and DCA) than did the control group, but this difference was not significant. However, the LCA‐to‐DCA ratio was much higher in the CRC group [(1.43, p < 0.01) compared with the control group (0.72)]. The control group excreted significantly higher amounts of total neutral sterols (p < 0.001), sterols of animal origin (p < 0.001), and plant sterols (p < 0.001) compared with the CRC group; the plant sterols represented a much lower proportion of excreted total neutral sterols in the CRC group (p > 0.001) compared with the control group. We propose the following hypotheses. 1) The LCA‐to‐DCA ratio may be an important discriminant market for CRC susceptibility. 2) The fecal LCA‐to‐DCA ratio may depend on the differential hepatic synthesis of their respective precursors chenodeoxycholic acid (CDCA) and cholic acid. 3) Hepatic synthesis of CDC A may be increased by more efficient conservation of dietary cholesterol because it has been shown that cholesterol of exogenous origin is the main precursor of this bile acid. 4) Cholesterol absorption may be augmented in CRC patients because of the low intake of plant sterols, which are known to suppress cholesterol absorption.