Trait positive affect buffers the association between experimental sleep disruption and inflammation. (July 2021)

• Record Type: Journal Article
• Authors: Hunt, Carly A.; Smith, Michael T.; Mun, Chung Jung; Irwin, Michael R.; Finan, Patrick H.
• Is Part Of: Psychoneuroendocrinology. Volume 129(2021)
• Publication Date: 2021-07
• Subjects: Positive affect -- Experimental sleep disruption -- Interleukin-6 -- Tumor necrosis factor -- Stimulated monocyte production; Psychoneuroendocrinology -- Periodicals; Endocrinology -- Periodicals; Neurology -- Periodicals; Psychiatry -- Periodicals; Neuropsychoendocrinologie -- Périodiques; 616.8
• DOI: 10.1016/j.psyneuen.2021.105240
• Languages: English
• ISSNs: 0306-4530

Abstract

Abstract: Background: Sleep disturbances and insufficient sleep are highly prevalent. Both clinical sleep disorders and multiple forms of experimental sleep loss predict heightened inflammation. As such, it is necessary to investigate potential protective factors. Given that trait positive affect (PA) is associated with reduced inflammation, and buffers the proinflammatory effects of stress, it is possible that high trait positive affect might protect individuals from an inflammatory response to sleep disruption. The present study tested this hypothesis in an experimental sleep disruption paradigm with assessment of cellular inflammation. Methods: Data were drawn from good sleeping adults (n = 79) who participated in a randomized, within-subjects crossover experiment comparing the effects of two nights of sleep disruption versus two nights of uninterrupted sleep. Stimulated monocytic production of intracellular proinflammatory cytokines tumor necrosis factor (TNF) and interleukin-6 (IL-6) were assayed using flow cytometric methods and indexed as the percentage of monocytes expressing TNF, IL-6, or co-expressing both. Hypotheses were evaluated using linear mixed effects models. Results: Controlling for negative affect, body mass index, age, and sex, PA significantly moderated the associations between sleep condition and stimulated monocyte production of IL-6 ( b = −1.03, t = −2.02, p = .048) and its co-expression with TNF ( b = −0.93, t = −2.00, p = .049), such that inflammatory responses were blunted among those high in PA with increases principally among those low in PA. The effect on TNF was similar in terms of effect size, but marginally significant. Conclusions: Activation of cellular inflammation in response to sleep disruption is buffered by PA independent of negative affect. Interventions that promote PA might protect persons from the inflammatory activation following sleep loss, with the potential to mitigate the adverse health consequences of sleep disturbance. Highlights: Cellular inflammation increased after experimental sleep disruption only among people low in positive affect. Positive affect is protective independent of negative affect and demographic factors. Negative affect did not modify the effect of sleep disruption on cellular inflammation.