Marie-Pierre St-Onge1, Ayanna Campbell2, Brooke Aggarwal2, Jasmine L Taylor3, Tanya M Spruill4, Arindam RoyChoudhury5. 1. Sleep center of excellence, Department of Medicine, Columbia University Irving Medical Center, New York, NY; Institute of Human Nutrition, Vagelos College of Physicians & Surgeons, Columbia University Irving Medical Center, New York, NY. Electronic address: ms2554@cumc.columbia.edu. 2. Sleep center of excellence, Department of Medicine, Columbia University Irving Medical Center, New York, NY. 3. Institute of Human Nutrition, Vagelos College of Physicians & Surgeons, Columbia University Irving Medical Center, New York, NY; Tulane Medical Center, New Orleans, LA. 4. Department of Population Health, NYU School of Medicine, New York, NY. 5. Division of Biostatistics and Epidemiology, Department of Healthcare Policy and Research, Weill Cornell Medicine, Cornell University, New York, NY.
Abstract
BACKGROUND: Studies assessing the impact of sleep restriction (SR) on blood pressure (BP) are limited by short study length, extreme SR (<4 hours a night), and lack of attention to psychological distress as a possible mediator. METHODS: A community-based cohort was assembled with 237 women (age 34.1 ± 13.5 years; body mass index 25.4 ± 5.4 kg/m2), and a randomized, crossover, intervention study was conducted in 41 women (24 completed: age 30.2 ± 6.5 years; body mass index 24.3 ± 2.8 kg/m2) to determine the causal effect of SR on BP. Sleep was maintained as usual (HS) or reduced by 1.5 hours a night (SR) for 6 weeks. In the cohort, associations between sleep and psychosocial factors were evaluated using multivariable models adjusted for demographic and clinical confounders. In the intervention study, in-office BP was measured weekly; ambulatory BP was measured at end point. Psychological factors were assessed at baseline and end point. Mixed-model analyses with total sleep time (TST, main predictor), week and fraction of time spent in physical activity (covariates), and subject (random effect) were performed. RESULTS: Among the community cohort, higher perceived stress, stressful events and distress, and lower resilience were associated with shorter sleep, worse sleep quality, and greater insomnia symptoms (P < .05). In the intervention, systolic BP increased as TST decreased (TST × week interaction, [coefficient ± standard error] -0.0097 ± 0.0046, P = .036). Wake ambulatory diastolic blood pressure (-0.059 ± 0.022, P = .021) and mean arterial pressure (-0.067 ± 0.023, P = .018) were higher after SR versus HS. Psychological distress variables were not affected by TST and did not mediate the effects of SR on BP. CONCLUSIONS: These results suggest that SR influences CVD risk in women via mechanisms independent of psychological stressors.
RCT Entities:
BACKGROUND: Studies assessing the impact of sleep restriction (SR) on blood pressure (BP) are limited by short study length, extreme SR (<4 hours a night), and lack of attention to psychological distress as a possible mediator. METHODS: A community-based cohort was assembled with 237 women (age 34.1 ± 13.5 years; body mass index 25.4 ± 5.4 kg/m2), and a randomized, crossover, intervention study was conducted in 41 women (24 completed: age 30.2 ± 6.5 years; body mass index 24.3 ± 2.8 kg/m2) to determine the causal effect of SR on BP. Sleep was maintained as usual (HS) or reduced by 1.5 hours a night (SR) for 6 weeks. In the cohort, associations between sleep and psychosocial factors were evaluated using multivariable models adjusted for demographic and clinical confounders. In the intervention study, in-office BP was measured weekly; ambulatory BP was measured at end point. Psychological factors were assessed at baseline and end point. Mixed-model analyses with total sleep time (TST, main predictor), week and fraction of time spent in physical activity (covariates), and subject (random effect) were performed. RESULTS: Among the community cohort, higher perceived stress, stressful events and distress, and lower resilience were associated with shorter sleep, worse sleep quality, and greater insomnia symptoms (P < .05). In the intervention, systolic BP increased as TST decreased (TST × week interaction, [coefficient ± standard error] -0.0097 ± 0.0046, P = .036). Wake ambulatory diastolic blood pressure (-0.059 ± 0.022, P = .021) and mean arterial pressure (-0.067 ± 0.023, P = .018) were higher after SR versus HS. Psychological distress variables were not affected by TST and did not mediate the effects of SR on BP. CONCLUSIONS: These results suggest that SR influences CVD risk in women via mechanisms independent of psychological stressors.
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