Sara Haidar


July 2008

Document Type


Degree Name



Dept. of Public Health and Preventive Medicine


Oregon Health & Science University


Background: Each year, prostate cancer affects one in six men and kills one in thirty five. It is the second leading cause of cancer death in men, topped only by lung cancer[superscript 3,4]. Recent studies have shown that chronic inflammation of the prostate may be involved in cancer development, possibly through the disruption of oxidative balance and elevated chemokine levels[superscript 17-24]. In addition, obesity has been associated with both prostate cancer[superscript 25-39] and systemic body inflammation[superscript 40-44]. Objectives: In this cross-sectional study of 661 Caucasian VA patients in Oregon, we determine if there is an association between obesity and prostate inflammation, specifically Type IV asymptomatic prostate inflammation, based on NIH consensus classification[superscript 8,9]. Methods: Using univariate analyses and multivariate logistic regression, we built models to understand the relationship between BMI and prostate inflammation (IV) and adjusted for variables including: age, prostate-specific antigen levels, family history of cancer, digital rectal examination findings, statin-use, and prostate volume. Results: Univariate analysis showed that mean BMI was statistically significantly different between cases (patients with inflammation) and controls (no inflammation) and that when modeled alone, BMI was a significant predictor of inflammation (p-value = 0.03 for both). Backwards stepwise model-building showed that BMI is not an independent predictor of inflammation. On the other hand, prostate volume and family history of cancer were significant predictors of inflammation. Our models showed that the odds of inflammation increased by approximately 70% as prostate volume doubled and were 42% greater for a man with a family history of cancer compared to one with no family history of cancer. Conclusions: In this study, obesity does not appear to be an independent predictor of asymptomatic prostate inflammation. Future studies should attempt to circumvent the shortfalls of our study, namely the temporal limitation inherent in its cross-sectional design and address the question in a broader sense to include other races and ethnicities and other types of prostate inflammation.




School of Medicine



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