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J Am Coll Cardiol, 2004; 43:678-683, doi:10.1016/j.jacc.2003.07.050 © 2004 by the American College of Cardiology Foundation |
* Department of Cardiology, Lahey Clinic Medical Center, Burlington, and Tufts University Medical School, Boston, Massachusetts, USA
Center for Cardiovascular Disease Prevention, Harvard Medical School and Brigham and Women's Hospital, and Leducq Center for Molecular and Genetic Epidemiology of Cardiovascular Disorders, Boston, Massachusetts, USA
Departments of Pathology and Laboratory Medicine, Harvard Medical School and Children's Hospital, and Leducq Center for Molecular and Genetic Epidemiology of Cardiovascular Disorders, Boston, Massachusetts, USA
Biometrics Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
|| Department of Psychiatry, Division of Sleep and Chronobiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
¶ Department of Psychiatry, Division of Sleep and Chronobiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
# Department of Neurology, Harvard Medical School, and Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA
Manuscript received June 1, 2003; revised manuscript received July 14, 2003, accepted July 22, 2003.
* Reprint requests and correspondence: Dr. Janet M. Mullington, Department of Neurology, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, E/DA-779, Boston, Massachusetts 02215, USA.
jmulling{at}bidmc.harvard.edu
OBJECTIVES: We sought to investigate the effects of sleep loss on high-sensitivity C-reactive protein (CRP) levels.
BACKGROUND: Concentrations of high-sensitivity CRP are predictive of future cardiovascular morbidity. In epidemiologic studies, short sleep duration and sleep complaints have also been associated with increased cardiovascular morbidity. Two studies were undertaken to examine the effect of acute total and short-term partial sleep deprivation on concentrations of high-sensitivity CRP in healthy human subjects.
METHODS: In Experiment 1, 10 healthy adult subjects stayed awake for 88 continuous hours. Samples of high-sensitivity CRP were collected every 90 min for 5 consecutive days, encompassing the vigil. In Experiment 2, 10 subjects were randomly assigned to either 8.2 h (control) or 4.2 h (partial sleep deprivation) of nighttime sleep for 10 consecutive days. Hourly samples of high-sensitivity CRP were taken during a baseline night and on day 10 of the study protocol.
RESULTS: The CRP concentrations increased during both total and partial sleep deprivation conditions, but remained stable in the control condition. Systolic blood pressure increased across deprivation in Experiment 1, and heart rate increased in Experiment 2.
CONCLUSIONS: Both acute total and short-term partial sleep deprivation resulted in elevated high-sensitivity CRP concentrations, a stable marker of inflammation that has been shown to be predictive of cardiovascular morbidity. We propose that sleep loss may be one of the ways that inflammatory processes are activated and contribute to the association of sleep complaints, short sleep duration, and cardiovascular morbidity observed in epidemiologic surveys.
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