Positive affect as a mediator of the longitudinal association between night-time insomnia symptoms and C-reactive protein: a four-year follow-up

Objectives/Introduction: Previous evidence suggests that night-time insomnia symptoms (i.e., difficulties in sleep onset and sleep maintenance) may be associated with increased peripheral inflammatory markers, which is involved in the pathophysiology of mental and somatic illness. The mechanisms underlying this association, however, remain largely unknown. In the context of health psychology, a substantial body of literature suggests that positive affect may have favourable impact on immune and inflammatory response and buffer the proinflammatory effects of stress. With this background, the aim of this study was to assess whether subjective sleep disturbance is longitudinally associated with serum high sensitivity C-reactive protein (hs-CRP), an acute-phase protein which is considered a marker of systemic inflammation, and whether this association is mediated by a decrease in positive affect. Methods: We analysed data from the English Longitudinal Study of Ageing (ELSA) across three waves of data collection. Self-reported sleep disturbance was assessed in 2008–2009, (wave 4), positive affect was assessed in 2010–2011 (wave 5), and serum sh-CRP was assessed in 2012–2013 (wave 6). Path analysis (i.e., structural equation modelling) was conducted adjusting for health-related variables including depressive symptoms, cardiovascular disease, body mass index, smoking, and alcohol intake. Results: The sample included 1894 participants aged 64.11 ± 8.02 years, 51% females. The model showed an excellent fit to the data: χ2 = 9.78 (df = 7, p > 0.05); RMSEA = 0.014 (95% CI 0.000 to 0.034); CFI = 0.997; TLI = 0.994; SRMR = 0.014. Path analysis showed a significant direct effect of sleep disturbance to positive affect (β = 0.15; p < 0.001); positive affect directly predicted hs-CRP (β = 0.04; p < 0.05). Lastly, an indirect effect between sleep disturbance to hs-CRP through the mediating role of positive affect emerged (β = 0.006; p < 0.05); bias-corrected bootstrap confirmed the statistical significance of the indirect effect (p < 0.05). Conclusions: Findings suggest that sleep onset and sleep maintenance difficulties may influence peripheral inflammation via a decrease in positive affect. Replication studies in clinical populations with insomnia disorder are warranted. Our study highlights the need to explore the role of positive affectivity in future population-based studies on sleep disorders and health risk.