Barbra A Dickerman1, Sarah C Markt1, Markku Koskenvuo2, Christer Hublin3, Eero Pukkala4,5, Lorelei A Mucci1, Jaakko Kaprio6,7,8. 1. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 2. Department of Public Health, University of Helsinki, P.O. Box 41, Mannerheimintie 172, 00014, Helsinki, Finland. 3. Finnish Institute of Occupational Health, Center of Expertise for the Development of Work and Organizations, Helsinki, Finland. 4. Finnish Cancer Registry, Institute for Statistical and Epidemiological Cancer Research, Unioninkatu 22, 00130, Helsinki, Finland. 5. School of Health Sciences, University of Tampere, 33014, Tampere, Finland. 6. Department of Public Health, University of Helsinki, P.O. Box 41, Mannerheimintie 172, 00014, Helsinki, Finland. jaakko.kaprio@helsinki.fi. 7. Department of Health, National Institute for Health and Welfare, P.O. Box 30, Mannerheimintie 166, 00300, Helsinki, Finland. jaakko.kaprio@helsinki.fi. 8. Institute for Molecular Medicine (FIMM), University of Helsinki, P.O. Box 20, Tukholmankatu 8, 00014, Helsinki, Finland. jaakko.kaprio@helsinki.fi.
Abstract
PURPOSE: Sleep disruption and shift work have been associated with cancer risk, but epidemiologic evidence for prostate cancer remains limited. We aimed to prospectively investigate the association between midlife sleep- and circadian-related parameters and later prostate cancer risk and mortality in a population-based cohort of Finnish twins. METHODS: Data were drawn from the Older Finnish Twin Cohort and included 11,370 twins followed from 1981 to 2012. Over the study period, 602 incident cases of prostate cancer and 110 deaths from prostate cancer occurred. Cox regression was used to evaluate associations between midlife sleep duration, sleep quality, chronotype, and shift work with prostate cancer risk and prostate cancer-specific mortality. Within-pair co-twin analyses were employed to account for potential familial confounding. RESULTS: Compared to "definite morning" types, "somewhat evening" types had a significantly increased risk of prostate cancer (HR 1.3; 95 % CI 1.1, 1.6). Chronotype significantly modified the relationship between shift work and prostate cancer risk (p-interaction <0.001). We found no significant association between sleep duration, sleep quality, or shift work and prostate cancer risk in the overall analyses and no significant association between any sleep- or circadian-related parameter and risk in co-twin analyses. Neither sleep- nor circadian-related parameters were significantly associated with prostate cancer-specific mortality. CONCLUSION: The association between sleep disruption, chronotype, and shift work with prostate cancer risk and mortality has never before been studied in a prospective study of male twins. Our findings suggest that chronotype may be associated with prostate cancer risk and modify the association between shift work and prostate cancer risk. Future studies of circadian disruption and prostate cancer should account for this individual-level characteristic.
PURPOSE: Sleep disruption and shift work have been associated with cancer risk, but epidemiologic evidence for prostate cancer remains limited. We aimed to prospectively investigate the association between midlife sleep- and circadian-related parameters and later prostate cancer risk and mortality in a population-based cohort of Finnish twins. METHODS: Data were drawn from the Older Finnish Twin Cohort and included 11,370 twins followed from 1981 to 2012. Over the study period, 602 incident cases of prostate cancer and 110 deaths from prostate cancer occurred. Cox regression was used to evaluate associations between midlife sleep duration, sleep quality, chronotype, and shift work with prostate cancer risk and prostate cancer-specific mortality. Within-pair co-twin analyses were employed to account for potential familial confounding. RESULTS: Compared to "definite morning" types, "somewhat evening" types had a significantly increased risk of prostate cancer (HR 1.3; 95 % CI 1.1, 1.6). Chronotype significantly modified the relationship between shift work and prostate cancer risk (p-interaction <0.001). We found no significant association between sleep duration, sleep quality, or shift work and prostate cancer risk in the overall analyses and no significant association between any sleep- or circadian-related parameter and risk in co-twin analyses. Neither sleep- nor circadian-related parameters were significantly associated with prostate cancer-specific mortality. CONCLUSION: The association between sleep disruption, chronotype, and shift work with prostate cancer risk and mortality has never before been studied in a prospective study of male twins. Our findings suggest that chronotype may be associated with prostate cancer risk and modify the association between shift work and prostate cancer risk. Future studies of circadian disruption and prostate cancer should account for this individual-level characteristic.
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