Study Objectives Prior research suggests that some individuals have a predisposition to experience insomnia following acute stressors (i.e., sleep reactivity). The present study was a proof of concept and specifically aimed to provide additional empirical evidence that the link between stressful life events and the onset of acute insomnia is moderated by sleep reactivity. Methods 1,225 adults with a history of good sleep (Mage = 53.2 years, 68% female, 83% white) were recruited nationwide for an online study on sleep health. Participants completed surveys to assess sleep reactivity (baseline), sleep patterns (daily sleep diary), and stressful life events (weekly survey). All daily and weekly measures were completed for a one-year period. Sleep diary data were used to identify sleep initiation/maintenance difficulties, including whether they met criteria for acute insomnia at any point during the one-year interval. Results Participants with high sleep reactivity compared to low sleep reactivity were at 76% increased odds of developing acute insomnia during the one-year interval. In general, greater weekly stressful life events were associated with greater insomnia during the subsequent week. Those participants with high sleep reactivity demonstrated a stronger relationship between weekly stressful life events and insomnia, such that they reported the greatest levels of insomnia following weeks where they experienced a greater number of stressful life events. Conclusions These results further support the sleep reactivity model of insomnia, and specifically, provide evidence that sleep reactivity predicts the incidence of acute insomnia in a sample of participants with no history of insomnia.

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Introduction Insomnia and depression are highly comorbid and have been shown to be independently associated with lower levels of physical activity. It is not clear, however, if being less physically active is a risk factor for or consequence of depression and insomnia. The factors that explain the associations between insomnia, depression, and physical activity are likely complex and overlapping. For example, insomnia may predict inactivity by impacting one’s energy levels, leaving them too tired to exercise. Insomnia may also interfere with one’s motivation to exercise due to low mood, as insomnia is associated with the development of depressive symptoms. The purpose of the present study was to explore whether depression mediated the link between insomnia and low levels of physical activity. Methods A national online survey was conducted from April-June 2020. Participants completed surveys to assess demographics, mood, sleep, and physical activity. Depressive symptoms were estimated with the Center for Epidemiologic Studies Depression Scale (CES-D). Insomnia symptoms were estimated with the Insomnia Severity Index (ISI). Physical activity levels were estimated with the International Physical Activity Questionnaire (IPAQ). Analyses were conducted using multiple linear regression, with separate models for depression, insomnia, and the combination of the two, on levels of physical activity. Results 3,952 adults (Mage = 46.9 years) completed the survey. According to the unadjusted models, greater insomnia symptoms were associated with greater depressive symptoms (b = 0.4523, SE = 0.019593, p < .001), and lower levels of physical activity (b = -38.741, SE = 18.236, p = 0.0337). The relationship between insomnia and physical activity was no longer significant, however, when controlling for depression (b = -6.140, SE = 19.274, p = 0.75). According to the mediation analyses, there was an indirect effect of insomnia on physical activity that was explained by differences in depressive symptoms (Sobel Test = -4.895, SE = 6.518, p < .001). Conclusion Our findings support previous research indicating associations between symptoms of insomnia and depression and physical activity. Future research should examine if these same results hold using a longitudinal design. Support (if any) Vargas: K23HL141581

Introduction Individuals who report greater perceived vulnerability to disease (e.g., experience emotional discomfort to situations where pathogen transmission is likely) also have the tendency to endorse more anxiety. Insomnia is also associated with greater anxiety. This study assessed (1) whether perceived vulnerability to disease was associated with increased anxiety related to COVID-19 and (2) whether this association was moderated or mediated by insomnia symptoms. Methods 1199 primarily female (n = 845), white (n = 982) participants (mage = 30.52) completed an online survey including the Sleep Disorder Symptom Checklist- 25 (SDS-CL-25), Perceived Vulnerability to Disease (PVD) scale, and a rating of COVID-19 anxiety (scale = 0–100; m = 55.81, sd = 25.39). Insomnia symptoms were calculated using the sum of SDS-CL-25 items 3–6 (m = 7.55, sd = 3.58). The PVD subscales germ aversion (GA; m = 4.18, sd = 1.22) and perceived vulnerability to infection (PVI; m = 3.69, sd = 1.39) were also computed. Results Regressions were used to test if insomnia mediated the impact of GA and PVI on COVID-19 anxiety. The relations between COVID-19 anxiety and insomnia (b = 1.30, t(1197) = 6.47), GA (b =3.60, t(1197) = 6.09), and PVI (b =3.73, t(1197) = 7.20) were significant (p’s < .001). Mediation analyses using the mediation package in R (bootstrap estimation = 1000 samples) showed direct effects of GA (b = 3.26, 95% CI = 2.04 – 4.42, p < .001) and PVI (b = 3.16, 95% CI = 2.00 – 4.22, p < .001) and mediation effects of insomnia (b =.44, 95% CI = .19 - .73, p < .001; b =.58, 95% CI = .33 - .86, p < .001, respectively). According to the moderation analyses, the association between PVD and COVID-19 anxiety did not significantly vary at different levels of insomnia. Conclusion Results suggest insomnia symptoms partially mediate the relationship between perceived vulnerability to disease and COVID-19 anxiety. These associations are likely bidirectional, and therefore, more work in this area is needed, especially with regard to how improved sleep may attenuate risk factors for anxiety. Support (if any) K23HL141581 (PI: Vargas)

Cognitive Behavioral Therapy for Insomnia (CBT-I) is a multi-component treatment for insomnia that targets difficulties with initiating and/or maintaining sleep and is delivered over the course of six to eight sessions. The primary focus of CBT-I is to address the perpetuating factors (according to the three-factor model of insomnia) that contribute to the development of chronic insomnia. Chronic insomnia is the most prevalent sleep disorder, occurring in approximately 6–10% of the population, and is a risk factor for multiple medical and psychiatric disorders. Despite its prevalence and morbidity, the widespread dissemination of CBT-I is not commensurate with insomnia’s overall public health impact. This is particularly surprising given its large evidence base and recent recommendation as the first line intervention for insomnia. The primary goal of this article is to provide a primer or brief introduction to CBT-I that is intended to be accessible to all clinicians and researchers, including non-sleep experts. Core components of CBT-I (i.e., Sleep Restriction Therapy, Stimulus Control Therapy, Sleep Hygiene, and Cognitive Therapy), relapse prevention strategies, multicultural considerations, adjuvants to traditional interventions, treatment adherence issues, efficacy, and further training options are described. A session-by-session outline is also provided.