Abstract
STUDY OBJECTIVES: To prospectively assess sleep reactivity as a diathesis of insomnia, and to delineate the interaction between this diathesis and naturalistic stress in the development of insomnia among normal sleepers. DESIGN: Longitudinal. SETTING: Community-based. PARTICIPANTS: 2,316 adults from the Evolution of Pathways to Insomnia Cohort (EPIC) with no history of insomnia or depression (46.8 ± 13.2 y; 60% female). INTERVENTIONS: None. MEASUREMENTS AND RESULTS: Participants reported the number of stressful events they encountered at baseline (Time 1), as well as the level of cognitive intrusion they experienced in response to each stressor. Stressful events (OR = 1.13; P < 0.01) and stress-induced cognitive intrusion (OR = 1.61; P < 0.01) were significant predictors of risk for insomnia one year hence (Time 2). Intrusion mediated the effects of stressful events on risk for insomnia (P < 0.05). Trait sleep reactivity significantly increased risk for insomnia (OR = 1.78; P < 0.01). Further, sleep reactivity moderated the effects of stress-induced intrusion (P < 0.05), such that the risk for insomnia as a function of intrusion was significantly higher in individuals with high sleep reactivity. Trait sleep reactivity also constituted a significant risk for depression (OR = 1.67; P < 0.01) two years later (Time 3). Insomnia at Time 2 significantly mediated this effect (P < 0.05). CONCLUSIONS: This study suggests that premorbid sleep reactivity is a significant risk factor for incident insomnia, and that it triggers insomnia by exacerbating the effects of stress-induced intrusion. Sleep reactivity is also a precipitant of depression, as mediated by insomnia. These findings support the stress-diathesis model of insomnia, while highlighting sleep reactivity as an important diathesis. CITATION: Drake CL, Pillai V, Roth T. Stress and sleep reactivity: a prospective investigation of the stress-diathesis model of insomnia.