Background: Few previous studies of metabolic aberrations and prostate cancer risk have taken into account the fact that men with metabolic aberrations have an increased risk of death from causes other than prostate cancer. The aim of this study was to calculate, in a real-life scenario, the risk of prostate cancer diagnosis, prostate cancer death, and death from other causes.
Methods: In the Metabolic Syndrome and Cancer Project, prospective data on body mass index, blood pressure, glucose, cholesterol, and triglycerides were collected from 285,040 men. Risks of prostate cancer diagnosis, prostate cancer death, and death from other causes were calculated by use of competing risk analysis for men with normal (bottom 84%) and high (top 16%) levels of each factor, and a composite score.
Results: During a mean follow-up period of 12 years, 5,893 men were diagnosed with prostate cancer, 1,013 died of prostate cancer, and 26,328 died of other causes. After 1996, when prostate-specific antigen testing was introduced, men up to age 80 years with normal metabolic levels had 13% risk of prostate cancer, 2% risk of prostate cancer death, and 30% risk of death from other causes, whereas men with metabolic aberrations had corresponding risks of 11%, 2%, and 44%.
Conclusions: In contrast to recent studies using conventional survival analysis, in a real-world scenario taking risk of competing events into account, men with metabolic aberrations had lower risk of prostate cancer diagnosis, similar risk of prostate cancer death, and substantially higher risk of death from other causes compared with men who had normal metabolic levels.
aDepartment of Surgical and Perioperative sciences, Urology and Andrology, Umeå University, Umeå, Sweden; bDepartment of Clinical Sciences in Malmö, Diabetes and Cardiovascular Diseases, Genetic Epidemiology, Lund University, Lund, Sweden; cInstitute of Epidemiology and Medical Biometry, Ulm University, Ulm, Germany; dAgency for Preventive and Social Medicine, Bregenz, Austria; eDepartment of Surgery, Skåne University Hospital, Lund University, Malmö, Sweden; fDepartment of Global Public Health and Primary Care, University of Bergen, Bergen, Norway; gNorwegian Institute of Public Health, Oslo/Bergen, Norway; hDepartment of Public Health and Clinical Medicine, Nutritional Research, Umeå University, Umeå, Sweden; iDepartment of Medical Statistics, Informatics and Health Economics, Innsbruck Medical University, Innsbruck, Austria; jInstitute of Population-based Cancer Research, The Cancer Registry of Norway, Oslo, Norway; and kDepartment of Radiation Sciences, Oncology, Umeå University, Umeå, Sweden.
Submitted 18 March 2014; accepted 1 June 2014; posted 9 September 2014.
The authors report no conflicts of interest.
This work was supported by the World Cancer Research Fund (2007/09); Wereld Kanker Onderzoek Fonds (R2010/247) and the Swedish Cancer Society (2010/628).
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Correspondence: Christel Häggström, Department of Surgical and Perioperative Sciences, Urology and Andrology Umeå University, 901 85 Umeå, Sweden. E-mail: email@example.com.
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