Alessandra Grotta1, Matteo Bottai2, Hans-Olov Adami3,4, Swann Arp Adams5,6, Olof Akre7, Steven Noel Blair8,9, Daniela Mariosa10, Olof Nyrén11, Weimin Ye12, Pär Stattin13, Rino Bellocco14,15, Ylva Trolle Lagerros16. 1. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Box 281, 171 77, Stockholm, Sweden. alessandra.grotta@ki.se. 2. Institute of Environmental Medicine, Karolinska Institutet, Box 210, 171 77, Stockholm, Sweden. matteo.bottai@ki.se. 3. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Box 281, 171 77, Stockholm, Sweden. hadami@hsph.harvard.edu. 4. Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA. hadami@hsph.harvard.edu. 5. Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC, USA. swann.adams@sc.edu. 6. Statewide Cancer Prevention and Control Program, University of South Carolina, Columbia, SC, USA. swann.adams@sc.edu. 7. Department of Medicine, Karolinska Institutet, Solna, Sweden. olof.akre@ki.se. 8. Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC, USA. sblair@mailbox.sc.edu. 9. Department of Exercise Science, Arnold School of Public Health, University of South Carolina, Columbia, SC, USA. sblair@mailbox.sc.edu. 10. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Box 281, 171 77, Stockholm, Sweden. daniela.mariosa@ki.se. 11. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Box 281, 171 77, Stockholm, Sweden. olof.nyren@ki.se. 12. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Box 281, 171 77, Stockholm, Sweden. weimin.ye@ki.se. 13. Surgery and Perioperative Sciences, Urology and Andrology, Umeå University Hospital, Umeå, Sweden. par.stattin@umu.se. 14. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Box 281, 171 77, Stockholm, Sweden. rino.bellocco@ki.se. 15. Department of Statistics and Quantitative Methods, University of Milano-Bicocca, Milan, Italy. rino.bellocco@ki.se. 16. Unit of Clinical Epidemiology, Department of Medicine, Karolinska Institutet, Solna, Sweden. ylva.trolle@ki.se.
Abstract
PURPOSE: Physical activity and body mass index (BMI) are involved in prostate cancer etiology; possible biologic mechanisms include their effects on hormonal levels. Our aim was to investigate the relationship between physical activity, obesity, and prostate cancer. METHODS: We followed a cohort of 13,109 Swedish men for 13 years and investigated the association of self-reported physical activity and BMI at baseline with prostate cancer incidence. We further analyzed whether BMI could modulate effects of physical activity. Occupational, recreational, and total physical activity were analyzed in relation to overall, localized, and advanced prostate cancer. RESULTS: During the study follow-up, we observed a total of 904 cases of prostate cancer (429 localized, 407 advanced, and 68 unclassified). High levels of occupational physical activity were associated with a nonsignificantly decreased risk of overall (HR 0.81, 95 % CI 0.61-1.07), localized (HR 0.75, 95 % CI 0.51-1.12), and advanced (HR 0.85, 95 % CI 0.55-1.31) prostate cancer. We found no association between high BMI and risk of prostate cancer incidence: We observed, however, a significant interaction between BMI and leisure physical activity. CONCLUSION: No association was confirmed between total physical activity and localized or advanced prostate cancer. The highest, relative to the lowest, level of occupational physical activity tended to be linked to a lower risk of prostate cancer, with a suggested dose-response relationship. We found no association between high BMI and risk of prostate cancer incidence; however, our analyses suggested an interaction between BMI and physical activity during recreational time that merits further investigation in future studies.
PURPOSE: Physical activity and body mass index (BMI) are involved in prostate cancer etiology; possible biologic mechanisms include their effects on hormonal levels. Our aim was to investigate the relationship between physical activity, obesity, and prostate cancer. METHODS: We followed a cohort of 13,109 Swedish men for 13 years and investigated the association of self-reported physical activity and BMI at baseline with prostate cancer incidence. We further analyzed whether BMI could modulate effects of physical activity. Occupational, recreational, and total physical activity were analyzed in relation to overall, localized, and advanced prostate cancer. RESULTS: During the study follow-up, we observed a total of 904 cases of prostate cancer (429 localized, 407 advanced, and 68 unclassified). High levels of occupational physical activity were associated with a nonsignificantly decreased risk of overall (HR 0.81, 95 % CI 0.61-1.07), localized (HR 0.75, 95 % CI 0.51-1.12), and advanced (HR 0.85, 95 % CI 0.55-1.31) prostate cancer. We found no association between high BMI and risk of prostate cancer incidence: We observed, however, a significant interaction between BMI and leisure physical activity. CONCLUSION: No association was confirmed between total physical activity and localized or advanced prostate cancer. The highest, relative to the lowest, level of occupational physical activity tended to be linked to a lower risk of prostate cancer, with a suggested dose-response relationship. We found no association between high BMI and risk of prostate cancer incidence; however, our analyses suggested an interaction between BMI and physical activity during recreational time that merits further investigation in future studies.
Entities:
Keywords:
Body mass index; Cohort study; Epidemiology; Physical activity; Prostate cancer
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