Effect Modification of Selenium Supplementation by Intake and Serum Concentrations of Antioxidants on the Development of Metachronous Colorectal Adenoma

Abstract

Background

Selenium (Se) is a trace element that has been investigated as a potential chemopreventive agent for colorectal cancer. Dietary intake of other antioxidant nutrients may modify the effect of Se.

Objective

We examined the association between intake and serum concentrations of retinol, β-carotene, β-cryptoxanthin, lycopene, lutein/zeaxanthin, and α- and γ-tocopherol and the development of metachronous colorectal adenoma, and if these nutrients modified the effect of Se.

Methods

We conducted a prospective study of 1874 participants from the Se Trial with data for antioxidant intake, as well as a subcohort of 508 participants with serum biomarker concentrations.

Results

Statistically significantly lower odds for the development of metachronous adenoma were observed for those participants in the highest tertile of intake for lutein/zeaxanthin compared to the lowest, with an OR (95% CI) of 0.72 (0.56-0.94). No effect modification for intake of any nutrient was observed. However, circulating concentrations of lycopene exhibited statistically significant effect modification of selenium supplementation (p < 0.06),

Conclusion

These findings show that intake and circulating concentrations of antioxidant nutrients were not consistently associated with reduced odds for the development of metachronous lesions, although blood concentrations of lycopene may modify the effect of selenium supplementation.

Author Contributions

Primary data analysis and manuscript preparation was done by ETJ, with support from KS, MT, and MH. ETJ, PL, HHSC, JM, and KB made significant contributions to study design, data analysis and interpretation, and manuscript preparation. CC and WC generously contributed to this project analyzing blood levels of antioxidants, and by assisting with data interpretation and manuscript preparation.

Disclosure Statement

The authors report there are no competing interests to declare.

Additional information

Funding

This work was supported by the National Institutes of Health under the following grants: National Cancer Institute under P30 CA023074, R01CA151708, P01 CA041108, and R01CA151708.