Date of Award

1-1-2012

Document Type

Campus Access Thesis

Department

Epidemiology and Biostatistics

Sub-Department

Epidemiology

First Advisor

Susan E Steck

Abstract

Laboratory studies have reported an inverse association between flavonoids and prostate cancer cell growth. This association is thought to be due to the anti-inflammatory properties of flavonoids, as well as their ability to induce apoptosis, impair angiogenesis, and inhibit cancer cell proliferation. The current study utilized data from 1,897 African-American (AA) and European-American (EA) prostate cancer patients from the North Carolina-Louisiana Prostate Cancer Project (PCaP). The data were analyzed to determine the association between flavonoid intake and prostate cancer aggressiveness. Intakes of total flavonoids, five subclasses of flavonoids, and the individual flavonoid quercetin were calculated using the NCI Diet History Questionnaire along with the Phenol Explorer database. Men were classified as cases (high aggressive) if they had a Gleason score of 8 or more, or had a PSA greater than 20 ng/ml, or if their Gleason score was 7 and their stage was T3c-T4c. All other men were classified as controls (low and intermediate aggressiveness). Using logistic regression, statistically significant inverse associations between total flavonoid intake and prostate cancer aggressiveness were found. In addition, flavanones and flavones were significantly inversely associated with aggressiveness for AA men. In general, decreasing risks with increasing intakes were found for flavonols and flavanols, although these odds ratios did not reach statistical significance. Associations between flavonoids and aggressiveness were modified by smoking status and age, such that inverse associations were strongest in men younger than age 65 and in current smokers. Orange and grapefruit juice and tea were the main contributors for total flavonoid intake. These results suggest that younger men, current smokers, and AA men may benefit the most from increased flavonoid intake.

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