Janna Mantua1, Rebecca M C Spencer2. 1. Neuroscience and Behavior Program, University of Massachusetts, Amherst, MA, USA. 2. Neuroscience and Behavior Program, University of Massachusetts, Amherst, MA, USA; Department of Psychological and Brain Sciences, University of Massachusetts, Amherst, MA, USA. Electronic address: rspencer@psych.umass.edu.
Abstract
BACKGROUND AND AIM: C-reactive protein (CRP) is a general marker of inflammation that has been differentially linked with sleep. Elevated CRP (ie, high inflammation) has been associated with either short/insufficient sleep duration or long sleep duration, both, or neither. Daytime napping has also been tied to increased and decreased inflammation. We attempted to unify these findings by examining the relationship between CRP and sleep duration in conjunction with napping in a healthy young adult cohort. PARTICIPANTS: Participants were young adults (mean age = 29.05 years, n = 2147) from the National Longitudinal Study of Adolescent Health (Add Health) cohort, a nationally representative longitudinal sample. METHODS/ RESULTS: Analysis of covariance (ANCOVA) tests examined whether self-reported sleep duration (short, medium, or long) and nap frequency (none-few days/week; most days/week; every day) interacted in relation to CRP. Standard covariates (ie, age, gender, race/ethnicity, body mass index, physical activity, depression, snoring, systolic blood pressure, clinical symptoms, and household income) were used. There was a linear increase in CRP with increased napping [contrast estimate = 0.265, 95% confidence interval (CI) (0.045-0.485), P = 0.018]. There was also an interaction between sleep duration and napping frequency in relation to CRP (F4,2128 = 2.90, P = 0.021). Inflammation differed between nap groups within the long and short sleep groups. CONCLUSIONS: Our results suggest that increased napping is an independent predictor of inflammation in young adults. These results also provide evidence for interactive effects of inflammation, nocturnal sleep, and daytime naps. Our findings confirm that excess sleep, insufficient sleep, frequent napping, and infrequent napping can all be linked with elevated CRP, but these relationships depend on both nocturnal and daytime sleep patterns. These analyses will guide future work to more specifically examine sleep-inflammation processes and directionality.
BACKGROUND AND AIM: C-reactive protein (CRP) is a general marker of inflammation that has been differentially linked with sleep. Elevated CRP (ie, high inflammation) has been associated with either short/insufficient sleep duration or long sleep duration, both, or neither. Daytime napping has also been tied to increased and decreased inflammation. We attempted to unify these findings by examining the relationship between CRP and sleep duration in conjunction with napping in a healthy young adult cohort. PARTICIPANTS: Participants were young adults (mean age = 29.05 years, n = 2147) from the National Longitudinal Study of Adolescent Health (Add Health) cohort, a nationally representative longitudinal sample. METHODS/ RESULTS: Analysis of covariance (ANCOVA) tests examined whether self-reported sleep duration (short, medium, or long) and nap frequency (none-few days/week; most days/week; every day) interacted in relation to CRP. Standard covariates (ie, age, gender, race/ethnicity, body mass index, physical activity, depression, snoring, systolic blood pressure, clinical symptoms, and household income) were used. There was a linear increase in CRP with increased napping [contrast estimate = 0.265, 95% confidence interval (CI) (0.045-0.485), P = 0.018]. There was also an interaction between sleep duration and napping frequency in relation to CRP (F4,2128 = 2.90, P = 0.021). Inflammation differed between nap groups within the long and short sleep groups. CONCLUSIONS: Our results suggest that increased napping is an independent predictor of inflammation in young adults. These results also provide evidence for interactive effects of inflammation, nocturnal sleep, and daytime naps. Our findings confirm that excess sleep, insufficient sleep, frequent napping, and infrequent napping can all be linked with elevated CRP, but these relationships depend on both nocturnal and daytime sleep patterns. These analyses will guide future work to more specifically examine sleep-inflammation processes and directionality.
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