Date

6-2014

Document Type

Thesis

Degree Name

M.P.H.

Department

Dept. of Public Health and Preventive Medicine

Institution

Oregon Health & Science University

Abstract

Objective:

The role of diet in prostate carcinogenesis has been well-documented. However, previous studies have focused primarily on the effect of individual dietary constituents on prostate cancer risk. The goal of the present analysis was to study the effects of the inflammatory potential of the whole diet on risk of prostate cancer. Specifically, we aimed to estimate the effects of consuming a pro-inflammatory diet on prostate cancer risk.

Methods:

We conducted a secondary analysis of data from the Diet and Prostate Cancer Risk case-control study conducted from 2001 to 2006 at the Portland Veterans Affairs Medical Center. We studied the effect of dietary-induced inflammation on prostate cancer risk utilizing data from 118 biopsy-confirmed prostate cancer cases, 230 biopsy-negative controls, and 165 screen-negative (PSA normal) controls. Participants were analyzed in six separate comparisons: (1) cases versus biopsy-negative controls, (2) cases versus screen-negative controls, (3) high-grade prostate cancer cases versus biopsy-negative controls, (4) high-grade prostate cancer cases versus screen-negative controls, (5) low-grade prostate cancer cases versus biopsy-negative controls, and (6) low-grade prostate cancer cases versus screen-negative controls. Dietary inflammation was assessed by calculating each participant’s dietary inflammatory index (DII) score; a measure of dietary inflammatory potential. We assessed correlations between DII score and plasma IL-6 concentration, DII score and plasma CRP concentration, and DII score and prostate volume. Mediation analysis was utilized to estimate the association between DII score and prostate cancer risk and to explore the possibility of mediation by chronic systemic inflammation, as quantified by plasma IL-6 concentration. Multivariable logistic regression analysis was conducted to elucidate the association between DII score, plasma IL-6 concentration, and prostate cancer risk. v

Results:

DII score was not significantly correlated with plasma IL-6 concentration or prostate volume for the entire study population or for cases, biopsy-negative controls, and screen-negative controls separately. DII score was marginally statistically significantly correlated with plasma CRP concentration for case participants. However, we observed no significant correlations between DII score and plasma CRP concentration for the total study population or for biopsy-negative controls when analyzed separately. Plasma IL-6 concentration did not account for the entirety of the association between DII score and prostate cancer in any of the six status comparisons and, therefore, was not a mediator in the aforementioned association. DII score was significantly associated with risk of prostate cancer in the comparison of low-grade prostate cancer cases to screen-negative controls (OR = 1.254, 95% CI = 1.015, 1.549). However, we found no significant associations between DII score and prostate cancer risk in any of the remaining five status comparisons during multivariable logistic regression analysis.

Conclusion:

DII score was associated with prostate cancer risk when comparing low-grade prostate cancer cases to screen-negative controls. However, this association was not observed in the remaining five status comparisons, which suggests that the significant association found in the present analysis should be interpreted with caution. Due to concerns regarding the power of the present study and possible measurement error stemming from the use of the modified diet history questionnaire, further studies are necessary before the association between DII score and prostate cancer risk is conclusively refuted. Furthermore, DII score may be more appropriately applied in observational studies of diseases in which inflammation and the role of diet on inflammatory processes have been well-established, such as in the context of colorectal cancer.

Identifier

doi:10.6083/M45Q4TSC

School

School of Medicine

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