Daria M McMahon1, James B Burch2, James R Hébert3, James W Hardin1, Jiajia Zhang1, Michael D Wirth4, Shawn D Youngstedt5, Nitin Shivappa4, Steven J Jacobsen6, Bette Caan7, Stephen K Van Den Eeden7. 1. Department of Epidemiology and Biostatistics, University of South Carolina, Columbia. 2. Department of Epidemiology and Biostatistics, University of South Carolina, Columbia; Cancer Prevention and Control Program, University of South Carolina, Columbia; WJB Dorn Department of Veterans Affairs Medical Center, Columbia, SC. 3. Department of Epidemiology and Biostatistics, University of South Carolina, Columbia; Cancer Prevention and Control Program, University of South Carolina, Columbia; Connecting Health Innovations, LLC, Columbia, SC. Electronic address: jhebert@sc.edu. 4. Department of Epidemiology and Biostatistics, University of South Carolina, Columbia; Cancer Prevention and Control Program, University of South Carolina, Columbia; Connecting Health Innovations, LLC, Columbia, SC. 5. College of Nursing and Health Innovation, Arizona State University, Phoenix; Phoenix VA Health Care System, Phoenix, AZ. 6. Department of Research and Evaluation, Kaiser Permanente Southern California, Pasadena. 7. Division of Research, Kaiser Permanente Northern California, Oakland.
Abstract
PURPOSE: The purpose of the study was to examine the relationship between proinflammatory diet and prostate cancer risk. METHODS: Energy-adjusted Dietary Inflammatory Index (E-DII) scores were computed among 40,161 participants in the California Men's Health Study. Over 9.7 ± 3.8 years of follow-up, 2707 incident prostate cancer cases were diagnosed and categorized as low-, intermediate-, or high-risk, based on disease grade and stage. Accelerated failure-time models assessed time to diagnosis of prostate cancer. Cox proportional hazard models estimated hazard ratios (HR) and 95% confidence intervals (95% CI). Nonlinear effects of E-DII were modeled as third-order polynomials. RESULTS: Time to prostate cancer diagnosis did not differ by E-DII quartile. The HR for high-risk prostate cancer increased in the third E-DII quartile (HRQ3 vs. Q1 = 1.36; 95% CI: 1.04-1.76), but not in the fourth (HRQ4 vs. Q1 = 0.99; 95% CI: 0.74-1.32, Ptrend = .74), suggesting a nonlinear dose-response. HR curves for prostate cancer increased exponentially above an E-DII threshold of ≈+3.0. HR curves for high-risk prostate cancer had a much steeper incline above an E-DII threshold of ≈+2.5. Curves were higher among Blacks and Whites relative to other races and among overweight or obese men. No relationship was observed between E-DII scores and intermediate- or low-risk disease. CONCLUSIONS: Relationships between proinflammatory diet and prostate cancer risk may be nonlinear, with an increased risk above an E-DII threshold of ≈+2.5.
PURPOSE: The purpose of the study was to examine the relationship between proinflammatory diet and prostate cancer risk. METHODS: Energy-adjusted Dietary Inflammatory Index (E-DII) scores were computed among 40,161 participants in the California Men's Health Study. Over 9.7 ± 3.8 years of follow-up, 2707 incident prostate cancer cases were diagnosed and categorized as low-, intermediate-, or high-risk, based on disease grade and stage. Accelerated failure-time models assessed time to diagnosis of prostate cancer. Cox proportional hazard models estimated hazard ratios (HR) and 95% confidence intervals (95% CI). Nonlinear effects of E-DII were modeled as third-order polynomials. RESULTS: Time to prostate cancer diagnosis did not differ by E-DII quartile. The HR for high-risk prostate cancer increased in the third E-DII quartile (HRQ3 vs. Q1 = 1.36; 95% CI: 1.04-1.76), but not in the fourth (HRQ4 vs. Q1 = 0.99; 95% CI: 0.74-1.32, Ptrend = .74), suggesting a nonlinear dose-response. HR curves for prostate cancer increased exponentially above an E-DII threshold of ≈+3.0. HR curves for high-risk prostate cancer had a much steeper incline above an E-DII threshold of ≈+2.5. Curves were higher among Blacks and Whites relative to other races and among overweight or obesemen. No relationship was observed between E-DII scores and intermediate- or low-risk disease. CONCLUSIONS: Relationships between proinflammatory diet and prostate cancer risk may be nonlinear, with an increased risk above an E-DII threshold of ≈+2.5.
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