Alice Jessie Clark1,2, Paula Salo3,4, Theis Lange5, Poul Jennum6,7, Marianna Virtanen3, Jaana Pentti3, Mika Kivimäki8,9, Naja Hulvej Rod1,2, Jussi Vahtera3,10. 1. Section of Social Medicine, Department of Public Health, University of Copenhagen, Copenhagen, Denmark. 2. The Copenhagen Stress Research Center, University of Copenhagen, Copenhagen, Denmark. 3. Finnish Institute of Occupational Health, Helsinki and Turku, Finland. 4. Department of Psychology, University of Turku, Turku, Finland. 5. Section of Biostatistics, Department of Public Health, University of Copenhagen, Copenhagen, Denmark. 6. The Danish Center for Sleep Medicine, Department of Clinical Neurophysiology, Glostrup University Hospital, Copenhagen, Denmark. 7. Center for Healthy Aging, University of Copenhagen, Copenhagen, Denmark. 8. Department of Public Health, University of Helsinki, Helsinki, Finland. 9. Department of Epidemiology and Public Health, University College London, London, UK. 10. Department of Public Health, University of Turku and Turku University Hospital, Turku, Finland.
Abstract
STUDY OBJECTIVES: Impaired sleep has been linked to increased risk of cardiovascular disease (CVD), but the underlying mechanisms are still unsettled. We sought to determine how onset of impaired sleep affects the risk of established physiological CVD risk factors (i.e., hypertension, diabetes, and dyslipidemia). METHODS: In a longitudinal cohort study with 3 survey waves (2000, 2004, 2008) from the Finnish Public Sector study we used repeated information on sleep duration and disturbances to determine onset of impaired sleep. Information on development of CVD risk factors, as indicated by initiation of medication for hypertension, diabetes, and dyslipidemia was derived from electronic medical records within 8 years of follow-up. Data on 45,647 participants was structured as two data-cycles to examine the effect of change in sleep (between two waves) on incident CVD events. We applied strict inclusion and exclusion criteria to determine temporality between changes in sleep and the outcomes. RESULTS: While we did not find consistent effects of onset of short or long sleep, we found onset of disturbed sleep to predict subsequent risk of hypertension (hazard ratio = 1.22, 95% CI: 1.04-1.44) and dyslipidemia (HR = 1.17, 95% CI: 1.07-1.29) in fully adjusted analyses. CONCLUSIONS: Results suggest that onset of sleep disturbances rather than short or long sleep mark an increase in physiological risk factors, which may partly explain the higher risk of CVD observed among impaired sleepers. COMMENTARY: A commentary on this paper appears in this issue on page 1629.
STUDY OBJECTIVES: Impaired sleep has been linked to increased risk of cardiovascular disease (CVD), but the underlying mechanisms are still unsettled. We sought to determine how onset of impaired sleep affects the risk of established physiological CVD risk factors (i.e., hypertension, diabetes, and dyslipidemia). METHODS: In a longitudinal cohort study with 3 survey waves (2000, 2004, 2008) from the Finnish Public Sector study we used repeated information on sleep duration and disturbances to determine onset of impaired sleep. Information on development of CVD risk factors, as indicated by initiation of medication for hypertension, diabetes, and dyslipidemia was derived from electronic medical records within 8 years of follow-up. Data on 45,647 participants was structured as two data-cycles to examine the effect of change in sleep (between two waves) on incident CVD events. We applied strict inclusion and exclusion criteria to determine temporality between changes in sleep and the outcomes. RESULTS: While we did not find consistent effects of onset of short or long sleep, we found onset of disturbed sleep to predict subsequent risk of hypertension (hazard ratio = 1.22, 95% CI: 1.04-1.44) and dyslipidemia (HR = 1.17, 95% CI: 1.07-1.29) in fully adjusted analyses. CONCLUSIONS: Results suggest that onset of sleep disturbances rather than short or long sleep mark an increase in physiological risk factors, which may partly explain the higher risk of CVD observed among impaired sleepers. COMMENTARY: A commentary on this paper appears in this issue on page 1629.
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