Alcohol is a known
carcinogen that may be associated with
colorectal cancer. However, most epidemiologic studies assess alcoholic beverage consumption using self-reported data, leading to potential exposure misclassification.
Biomarkers of alcohol consumption may provide an alternative, complementary approach that reduces misclassification and incorporates individual differences in alcohol metabolism. Therefore, we evaluated the relationship between previously identified alcohol consumption-related metabolites and
colorectal cancer and
adenoma using serum metabolomics data from two studies. Data on
colorectal cancer were obtained from a nested case-control study of 502 US adults (252 cases, 250 controls) within the Prostate, Lung, Colorectal, and
Ovarian Cancer Screening Trial. Data on colorectal
adenoma were obtained from a case-control study of 197 US adults (120 cases, 77 controls) from the Navy Colon
Adenoma Study. Unconditional multivariable logistic regression models were fit to calculate odds ratios (OR) and 95% confidence intervals (CI) for eight alcohol consumption-related metabolites identified in a previous analysis:
ethyl glucuronide; 4-androstene-3beta,17beta-diol disulfate 1; 5-alpha-androstan-3beta,17beta-diol disulfate; 16-hydroxypalmitate;
bilirubin (E,Z or Z,E);
cyclo (-leu-pro); dihomo-
linoleate (20:2n6); and
palmitoleate (16:1n7). We found no clear association between these alcohol consumption-related metabolites and either endpoint. However, we did observe an inverse association between
cyclo (-leu-pro) and colorectal
adenoma that was only observed in the highest metabolite quantile (OR 4th vs. 1st Quantile = 0.30, 95% CI: 0.12-0.78; P-trend = 0.047), but no association for
colorectal cancer. In conclusion, there were no adverse associations between alcohol consumption-related metabolites and
colorectal cancer or
adenoma.