LAUSR

STUDY OBJECTIVES To naturalistically measure sleep disturbances following stress exposure (i.e., sleep reactivity) and stress responses following sleep disturbances (i.e., stress reactivity) at the daily level and prospectively examine these reactivity measures as individual risk factors for insomnia. METHODS The study assessed 392 nurses' sleep and stress for 14 days using daily diaries and actigraphy. Self-reported insomnia symptoms were assessed at the end of the 14 days, as well as 6 and 11 months later. RESULTS In multilevel modeling, while negative fixed effects indicated that shorter total sleep time (TST) and lower sleep efficiency led to greater stress and vice versa, significant random effects indicated individual variability in sleep reactivity and stress reactivity. In latent score change modeling, greater sleep reactivity (lower diary-determined sleep efficiency following greater stress) and greater stress reactivity (greater stress following shorter diary-determined TST) at baseline were associated with greater insomnia symptoms at 11 months (b = 10.34, p = .026; b = 7.83, p = .03). Sleep reactivity and stress reactivity also interacted to predict insomnia symptoms, such that sleep reactivity was significantly associated with insomnia symptoms for those with high (+1SD) stress reactivity (b = 17.23, p = .001), but not for those with low (-1SD) stress reactivity (b = 5.16, p = .315). CONCLUSIONS Baseline stress reactivity and sleep reactivity independently as well as jointly predict greater insomnia symptoms 11 months later. The findings delineate processes underlying the stress-diathesis model of insomnia and highlight the utility of longitudinal and naturalistic measures of sleep and stress reactivity.