BACKGROUND - Controversies remain over the safety and efficacy of vitamin E (i.e., α-tocopherol) supplementation use for the prevention of prostate cancer (CaP); however, associations of different tocopherol forms and CaP aggressiveness have yet to be examined.
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METHODS - This study examined whether food intake of tocopherols, vitamin E supplement use, and adipose tissue biomarkers of tocopherol were associated with CaP aggressiveness among African-American (AA, n = 1,023) and European-American (EA, n = 1,079) men diagnosed with incident CaP. Dietary tocopherols were estimated from a food frequency questionnaire, supplement use from questionnaire/inventory, and biomarkers from abdominal adipose samples measured using high-performance liquid chromatography. Odds ratios (ORs) and 95% confidence intervals (95%CIs) were estimated from logistic regression comparing high-aggressive CaP to low/intermediate aggressive CaP, adjusting for covariates.
RESULTS - Dietary intakes of α-and δ-tocopherol were related inversely to CaP aggressiveness among EAs [OR (95%CI), highest versus lowest quartile: α-tocopherol, 0.34 (0.17-0.69), Ptrend = 0.006; δ-tocopherol, 0.45 (0.21-0.95) Ptrend = 0.007]. Inverse associations between dietary and supplemental α-tocopherol and CaP aggressiveness were observed among AAs, though these did not reach statistical significance [OR (95%CI), highest versus lowest quartile: dietary α-tocopherol, 0.58 (0.28-1.19), Ptrend = 0.20; supplemental α-tocopherol, 0.64 (0.31-1.21) Ptrend = 0.15]. No significant association was observed between adipose tocopherol levels and CaP aggressiveness [OR (95%CI), highest versus lowest quartiles of α-tocopherol for EAs 1.43 (0.66-3.11) and AAs 0.66 (0.27-1.62)].
CONCLUSIONS - The inverse associations observed between dietary sources of tocopherols and CaP aggressiveness suggests a beneficial role of food sources of these tocopherols in CaP aggressiveness. Prostate © 2015 Wiley Periodicals, Inc.
Prostate. 2015 Jun 5. doi: 10.1002/pros.23025. [Epub ahead of print]
Antwi SO1, Steck SE2,3, Su LJ4, Hébert JR2,3, Zhang H5, Fontham ET6, Smith GJ7, Bensen JT8, Mohler JL7, Arab L9.
1 Division of Epidemiology, Health Sciences Research, Mayo Clinic, Rochester, Minnesota.
2 Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, South Carolina.
3 Cancer Prevention and Control Program, Arnold School of Public Health, University of South Carolina, Columbia, South Carolina.
4 National Cancer Institute, National Institutes of Health, Rockville, Maryland.
5 Department of Epidemiology, Biostatistics, and Environmental Health, University of Memphis, Memphis, Tennessee.
6 School of Public Health, Louisiana State University Health Sciences Center, New Orleans, Louisiana.
7 Department of Urology, Roswell Park Cancer Institute, Buffalo, New York.
8 Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
9 David Geffen School of Medicine at UCLA, Los Angeles, California.