Axel Gerdtsson1, Jessica B Poon2, Daniel L Thorek3, Lorelei A Mucci4, Michael J Evans5, Peter Scardino6, Per-Anders Abrahamsson7, Peter Nilsson8, Jonas Manjer9, Anders Bjartell7, Johan Malm10, Andrew Vickers5, Stephen J Freedland11, Hans Lilja12, David Ulmert13. 1. Department of Clinical Sciences (Urology), Lund University, Skåne University Hospital, Malmö, Sweden; Department of Translational Medicine, Lund University, Skåne University Hospital, Malmö, Sweden. 2. Department of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer Center, New York, NY, USA. 3. Division of Nuclear Medicine, Department of Radiology and Radiological Sciences, The Johns Hopkins School of Medicine, Baltimore, MD, USA. 4. Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA. 5. Department of Radiology and Biomedical Imaging, University of California, San Francisco, CA, USA. 6. Department of Surgery (Urology), Memorial Sloan-Kettering Cancer Center, New York, NY, USA. 7. Department of Clinical Sciences (Urology), Lund University, Skåne University Hospital, Malmö, Sweden. 8. Department of Clinical Sciences (Medicine), Lund University, Skåne University Hospital, Malmö, Sweden. 9. Department of Clinical Sciences (Surgery), Lund University, Skåne University Hospital, Malmö, Sweden. 10. Department of Translational Medicine, Lund University, Skåne University Hospital, Malmö, Sweden. 11. Surgery Section, Durham VA Medical Center, Durham, NC, USA; Department of Surgery (Urology), Cedars Sinai Medical Center, Los Angeles, CA, USA. 12. Department of Clinical Sciences (Medicine), Lund University, Skåne University Hospital, Malmö, Sweden; Departments of Laboratory Medicine and Medicine (GU-Oncology), Memorial Sloan-Kettering Cancer Center, New York, NY, USA; Nuffield Department of Surgical Sciences, University of Oxford, Oxford, UK; Institute of Biomedical Technology, University of Tampere, Tampere, Finland; Molecular Pharmacology and Chemistry Program, Memorial Sloan-Kettering Cancer Center, New York, NY, USA. 13. Department of Clinical Sciences (Urology), Lund University, Skåne University Hospital, Malmö, Sweden; Department of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer Center, New York, NY, USA. Electronic address: ulmerth@mskcc.org.
Abstract
BACKGROUND: Previous studies of prostate cancer (PCa) risk and anthropometrics (ie, body measurements) were based on single measurements or obtained over limited time spans. OBJECTIVE: To study the association between anthropometrics measured at multiple time points in life and their relation to later diagnosis, metastasis, or death from PCa. DESIGN, SETTING, AND PARTICIPANTS: This case-control study includes 27 167 Swedish men enrolled in two population-based projects from 1974 to 1996. PCa diagnosis up to December 31, 2006, disease information, gestation time, and anthropometrics at birth, military conscript testing, and adulthood were collected. A total of 1355 PCa cases were matched with 5271 controls. OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: Univariate conditional logistic regression was used to determine whether clinical diagnosis, metastasis, or PCa death was associated with low birth weight (weight <2500 g); with small size for gestational age; or with weight, length, or body mass index (BMI) at birth, adolescence (aged 16-22 yr), or early middle age (aged 44-50 yr). RESULTS AND LIMITATIONS: Apart from weight at adolescence, which was associated with an increased risk of PCa diagnosis (odds ratio [OR] per 5 kg: 1.05; 95% confidence interval [CI], 1.01-1.09; p=0.026), preadulthood measurements were not associated with any PCa end point. Adulthood parameters were not associated with diagnosis. In contrast, weight and BMI at early middle age were significantly associated with metastasis (OR per 5 kg: 1.13; 95% CI, 1.06-1.20; p<0.0001, and OR: 1.09; 95% CI, 1.05-1.14; p<0.0001) and death (OR per 5 kg: 1.11 (95% CI, 1.03-1.19; p=0.005, and OR: 1.08; 95% CI, 1.03-1.13; p=0.003), respectively. It remains unclear whether these results apply to men of nonwhite origin, to populations with active PCa screening programs, or to countries without socialized health care. CONCLUSIONS: The analyses of these large data sets demonstrate that significant effects of body characteristics (with links to metabolic syndrome) measured at early middle age are associated with PCa disease severity, metastatic progression, and outcome. Conversely, measurements at birth and adolescence are not associated with PCa prevalence or outcome. PATIENT SUMMARY: Increased weight and body mass index in adults is associated with a higher risk of prostate cancer metastasis and death.
BACKGROUND: Previous studies of prostate cancer (PCa) risk and anthropometrics (ie, body measurements) were based on single measurements or obtained over limited time spans. OBJECTIVE: To study the association between anthropometrics measured at multiple time points in life and their relation to later diagnosis, metastasis, or death from PCa. DESIGN, SETTING, AND PARTICIPANTS: This case-control study includes 27 167 Swedish men enrolled in two population-based projects from 1974 to 1996. PCa diagnosis up to December 31, 2006, disease information, gestation time, and anthropometrics at birth, military conscript testing, and adulthood were collected. A total of 1355 PCa cases were matched with 5271 controls. OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: Univariate conditional logistic regression was used to determine whether clinical diagnosis, metastasis, or PCa death was associated with low birth weight (weight <2500 g); with small size for gestational age; or with weight, length, or body mass index (BMI) at birth, adolescence (aged 16-22 yr), or early middle age (aged 44-50 yr). RESULTS AND LIMITATIONS: Apart from weight at adolescence, which was associated with an increased risk of PCa diagnosis (odds ratio [OR] per 5 kg: 1.05; 95% confidence interval [CI], 1.01-1.09; p=0.026), preadulthood measurements were not associated with any PCa end point. Adulthood parameters were not associated with diagnosis. In contrast, weight and BMI at early middle age were significantly associated with metastasis (OR per 5 kg: 1.13; 95% CI, 1.06-1.20; p<0.0001, and OR: 1.09; 95% CI, 1.05-1.14; p<0.0001) and death (OR per 5 kg: 1.11 (95% CI, 1.03-1.19; p=0.005, and OR: 1.08; 95% CI, 1.03-1.13; p=0.003), respectively. It remains unclear whether these results apply to men of nonwhite origin, to populations with active PCa screening programs, or to countries without socialized health care. CONCLUSIONS: The analyses of these large data sets demonstrate that significant effects of body characteristics (with links to metabolic syndrome) measured at early middle age are associated with PCa disease severity, metastatic progression, and outcome. Conversely, measurements at birth and adolescence are not associated with PCa prevalence or outcome. PATIENT SUMMARY: Increased weight and body mass index in adults is associated with a higher risk of prostate cancermetastasis and death.
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