Plasma carotenoids and tocopherols in relation to prostate-specific antigen (PSA) levels among men with biochemical recurrence of prostate cancer.

BACKGROUND - Although men presenting with clinically localized prostate cancer (PrCA) often are treated with radical prostatectomy or radiation therapy with curative intent, about 25-40% develop biochemically recurrent PrCA within 5 years of treatment, which has no known cure.

Studies suggest that carotenoid and tocopherol intake may be associated with PrCA risk and progression. We examined plasma carotenoid and tocopherol levels in relation to prostate-specific antigen (PSA) levels among men with PSA-defined biochemical recurrence of PrCA.

METHODS - Data analyzed were from a 6-month diet, physical activity and stress-reduction intervention trial conducted in South Carolina among biochemically recurrent PrCA patients (n=39). Plasma carotenoids and tocopherol levels were measured using high-performance liquid chromatography (HPLC). Linear regression was used to estimate least-square means comparing PSA levels of men with high versus low carotenoid/tocopherol levels, adjusting for covariates.

RESULTS - After adjusting for baseline PSA level, plasma cis-lutein/zeaxanthin level at 3 months was related inversely to PSA level at 3 months (P=0.0008), while α-tocopherol (P=0.01), β-cryptoxanthin (P=0.01), and all-trans-lycopene (P=0.004) levels at 3 months were related inversely to PSA levels at 6-months. Percent increase in α-tocopherol and trans-β-carotene levels from baseline to month 3 were associated with lower PSA levels at 3 and 6 months. Percent increase in β-cryptoxanthin, cis-lutein/zeaxanthin and all-trans-lycopene were associated with lower PSA levels at 6 months only.

CONCLUSIONS - Certain plasma carotenoids and tocopherols were related inversely to PSA levels at various timepoints, suggesting that greater intake of foods containing these micronutrients might be beneficial to men with PSA-defined PrCA recurrence.

Cancer Epidemiol. 2015 Jul 9. pii: S1877-7821(15)00136-8. doi: 10.1016/j.canep.2015.06.008. [Epub ahead of print]

Antwi SO1, Steck SE2, Zhang H3, Stumm L4, Zhang J5, Hurley TG6, Hebert JR6.

1 Division of Epidemiology, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, United States.
2 Epidemiology and Biostatistics Arnold School of Public Health, 915 Greene St, Columbia, SC 29208, United States; Cancer Prevention and Control Program, Arnold School of Public Health, 915 Greene St, Columbia, SC 29208, United States.
3 Epidemiology, Biostatistics, and Environmental Health, University of Memphis, 3825 Desoto Avenue, 224 Robison Hall, Memphis, TN 38152, United States.
4 Epidemiology, James Madison University, 800 Madison Drive, Harrisonburg, VA 22807, United States.
5 Epidemiology and Biostatistics Arnold School of Public Health, 915 Greene St, Columbia, SC 29208, United States.
6 Epidemiology and Biostatistics Arnold School of Public Health, 915 Greene St, Columbia, SC 29208, United States; Cancer Prevention and Control Program, Arnold School of Public Health, 915 Greene St, Columbia, SC 29208, United States.