Effect of sleep loss on C-Reactive protein, an inflammatory marker of cardiovascular risk
Hans K. Meier-Ewert, MD*,
Paul M. Ridker, MD, MPH ,
Nader Rifai, PhD ,
Meredith M. Regan, ScD ,
Nick J. Price||,
David F. Dinges, PhD¶ and
Janet M. Mullington, PhD#,*
* 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
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Figure 1 Schematic of acute total sleep deprivation (TSD) protocol (left panel) and short-term partial sleep deprivation (PSD) protocol (right panel). Bars represent 24-h periods from 9:00 pm to 9:00 pm for TSD and 5:00 pm to 5:00 pm PSD. Solid bars = sleep periods for the acute TSD subjects (left panel) and for the PSD subjects (right panel). Hatched bars = sleep periods for the 8.2-h control group in the PSD experiment (right panel). bl = baseline; r = recovery; # = frequent blood sampling days.
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Figure 2 Data were log-transformed before analysis. For ease of interpretation, the mean values ± SEM were transformed from the log scale back to the usual scale (mg/dl) in 10 subjects undergoing 88 h of acute total sleep deprivation. Overall p < 0.03 by mixed-models analysis of variance on log-transformed data; each subsequent day is significantly elevated (each p < 0.05) from baseline. The upper portion of the graph represents the boundary separating the low- and mild-risk quintiles of C-reactive protein (CRP) derived from analysis of >5,000 apparently healthy Americans (16). BL = baseline; Dep = deprivation.
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Figure 3 Data were log-transformed before analysis. For ease of interpretation, the mean values ± SEM were transformed from the log scale back to the usual scale (mg/dl) in subjects undergoing 10 consecutive days of short-term partial sleep deprivation (n = 4, squares) and control subjects (n = 5, diamonds). Significance of difference in change from baseline to day 10 between groups (p < 0.08 for interaction) by mixed-models analysis of variance on log-transformed data: the change from baseline to day 10 for the short-term partial sleep deprivation group was significant (p < 0.05), whereas the change from baseline to day 10 in the control subjects was not significant (p = 0.72). The horizontal lines indicate risk boundaries (mild to highest) of C-reactive protein (CRP) quintiles derived from analysis of >5,000 apparently healthy Americans (16).
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