Macarena Lozano-Lorca1,2, Inmaculada Salcedo-Bellido3,4,5, Rocío Olmedo-Requena1,2,6, Gemma Castaño-Vinyals6,7,8,9, Pilar Amiano6,10, Nitin Shivappa11,12, James R Hébert11,12, Beatriz Pérez-Gómez6,13, Esther Gracia-Lavedan6,7,8, Inés Gómez-Acebo6,14, Ana Molina-Barceló15, Rocío Barrios-Rodríguez1,2,6, Juan Alguacil6,16, Guillermo Fernández-Tardón17,18, Nuria Aragonés6,19, Trinidad Dierssen-Sotos6,14, Dora Romaguera7,20,21, Marina Pollán6,13, Manolis Kogevinas6,7,9,22, José-Juan Jiménez-Moleón23,24,25. 1. Universidad de Granada. Departamento de Medicina Preventiva y Salud Pública, Granada, Spain. 2. Instituto de Investigación Biosanitaria ibs.GRANADA, Granada, Spain. 3. Universidad de Granada. Departamento de Medicina Preventiva y Salud Pública, Granada, Spain. isalcedo@ugr.es. 4. Instituto de Investigación Biosanitaria ibs.GRANADA, Granada, Spain. isalcedo@ugr.es. 5. Consortium for Biomedical Research in Epidemiology & Public Health, CIBERESP, Madrid, Spain. isalcedo@ugr.es. 6. Consortium for Biomedical Research in Epidemiology & Public Health, CIBERESP, Madrid, Spain. 7. Instituto de Salud Global de Barcelona (ISGlobal), Barcelona, Spain. 8. Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra (UPF), Barcelona, Spain. 9. IMIM (Hospital del Mar Medical Research Institute), Barcelona, Spain. 10. Public Health Division of Gipuzkoa, Donostia-San Sebastian, Spain. 11. Cancer Prevention and Control Program, University of South Carolina, Columbia, SC, USA. 12. Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC, USA. 13. Department of Epidemiology for Chronic Diseases, National Center of Epidemiology, Instituto de Salud Carlos III, Madrid, Spain. 14. Department of Preventive Medicine and Public Health, University of Cantabria-IDIVAL, 39011, Santander, Spain. 15. Cancer and Public Health Area, FISABIO-Public Health, Valencia, Spain. 16. Centro de Investigación en Recursos Naturales, Salud y Medio Ambiente (RENSMA), Universidad de Huelva, Huelva, Spain. 17. Health Research Institute of the Principality of Asturias (ISPA), Oncology Institute, University of Oviedo, Oviedo, Asturias, Spain. 18. Department of Medicine, University of Oviedo, Oviedo, Spain. 19. Epidemiology Section, Division of Public Health, Department of Health, Madrid, Spain. 20. Instituto de Investigación Sanitaria Illes Balears (IdISBa), Palma de Mallorca, Spain. 21. Consortium for Biomedical Research in Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Madrid, Spain. 22. Universitat Pompeu Fabra (UPF), Barcelona, Spain. 23. Universidad de Granada. Departamento de Medicina Preventiva y Salud Pública, Granada, Spain. jjmoleon@ugr.es. 24. Instituto de Investigación Biosanitaria ibs.GRANADA, Granada, Spain. jjmoleon@ugr.es. 25. Consortium for Biomedical Research in Epidemiology & Public Health, CIBERESP, Madrid, Spain. jjmoleon@ugr.es.
Abstract
BACKGROUND: The etiology of prostate cancer (PCa) is not well-known, and the role of diet is not well established. We aimed to evaluate the role of the inflammatory power of the diet, measured by the Dietary Inflammatory Index (DII®), on the risk of PCa. METHODOLOGY: A population-based multicase-control (MCC-Spain) study was conducted. Information was collected on sociodemographic characteristics, personal and family antecedents, and lifestyles, including diet from a Food Frequency Questionnaire. The inflammatory potential of the diet was assessed using the energy-adjusted Dietary Inflammatory Index (E-DII) based on 30 parameters (a higher score indicates a higher inflammatory capacity of the diet). Tertiles of E-DII were created using the cut-off points from the control group. The International Society of Urology Pathology (ISUP) was grouped as ISUP 1, ISUP 2, or ISUP 3-5. Unconditional logistic regression models were used to estimate adjusted odds ratios (aOR) and 95% confidence intervals (CI) for the association between E-DII score and PCa risk. RESULTS: A total of 928 PCa cases and 1278 population controls were included. Among PCa cases, the mean value of the E-DII score was 0.18 (SD: 1.9) vs. 0.07 (SD: 1.9) in the control group (p = 0.162). Cases with a more pro-inflammatory diet (3rd tertile) had the highest risk of PCa, aORT3vsT1 = 1.30 (95% CI 1.03-1.65) (p-trend = 0.026). When stratifying by ISUP, this risk association was observed only for ISUP 2 and ISUP 3-5, aORT3vsT1 = 1.46 (95% CI 1.02-2.10) and 1.60 (95% CI 1.10-2.34), respectively. CONCLUSION: A positive association was observed between consuming a pro-inflammatory diet and PCa in the MCC-Spain population, specifically for an ISUP grade greater or equal than 2.
BACKGROUND: The etiology of prostate cancer (PCa) is not well-known, and the role of diet is not well established. We aimed to evaluate the role of the inflammatory power of the diet, measured by the Dietary Inflammatory Index (DII®), on the risk of PCa. METHODOLOGY: A population-based multicase-control (MCC-Spain) study was conducted. Information was collected on sociodemographic characteristics, personal and family antecedents, and lifestyles, including diet from a Food Frequency Questionnaire. The inflammatory potential of the diet was assessed using the energy-adjusted Dietary Inflammatory Index (E-DII) based on 30 parameters (a higher score indicates a higher inflammatory capacity of the diet). Tertiles of E-DII were created using the cut-off points from the control group. The International Society of Urology Pathology (ISUP) was grouped as ISUP 1, ISUP 2, or ISUP 3-5. Unconditional logistic regression models were used to estimate adjusted odds ratios (aOR) and 95% confidence intervals (CI) for the association between E-DII score and PCa risk. RESULTS: A total of 928 PCa cases and 1278 population controls were included. Among PCa cases, the mean value of the E-DII score was 0.18 (SD: 1.9) vs. 0.07 (SD: 1.9) in the control group (p = 0.162). Cases with a more pro-inflammatory diet (3rd tertile) had the highest risk of PCa, aORT3vsT1 = 1.30 (95% CI 1.03-1.65) (p-trend = 0.026). When stratifying by ISUP, this risk association was observed only for ISUP 2 and ISUP 3-5, aORT3vsT1 = 1.46 (95% CI 1.02-2.10) and 1.60 (95% CI 1.10-2.34), respectively. CONCLUSION: A positive association was observed between consuming a pro-inflammatory diet and PCa in the MCC-Spain population, specifically for an ISUP grade greater or equal than 2.