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.

We know CBT-I works, now what?

Nearly one-third of the population reports new onset or acute insomnia in a given year. Similarly, it is estimated that approximately 10% of the population endorses sleep initiation and maintenance problems consistent with diagnostic criteria for chronic insomnia. For decades, acute and chronic insomnia have been considered variations of the same condition or disorder, only really differentiated in terms of chronicity of symptoms (days/weeks versus months). Whether or not acute and chronic insomnia are part of the same phenomena is an important question, one that has yet to be empirically evaluated. The goal of the present theoretical review was to summarize the definitions of acute and chronic insomnia and discuss the role that hyperarousal may have in explaining how the pathophysiology of acute and chronic insomnia is likely different (i.e., what biopsychological factors precipitate and/or perpetuate acute insomnia, chronic insomnia, or both?).

Social distancing was universally implemented to reduce the spread of the COVID-19 virus. Long-term social distancing can lead to increased feelings of social isolation or dissatisfaction with one’s daily interpersonal interactions, which can subsequently result in reduced psychological health (e.g., greater depression). The present study quantified this association, and the extent to which it was moderated by measures of sleep and physical activity, by surveying 3658 adults (mean age = 46.0 years) from across the United States. Participants answered questions related to their social experiences, sleep, physical activity, and depressive symptoms during the early stages of the pandemic (March–June 2020). Results showed that social isolation and social dissatisfaction were associated with greater depressive symptoms. As predicted, self-reported sleep quality and physical activity moderated these associations, such that lower sleep quality and physical activity exacerbated their effect on depressive symptoms.

Introduction: Little is known about the relative magnitude of placebo responses on objective and subjective measures of sleep continuity. To address this issue, the pre-post effects of placebos on objective and subjective measures (i.e., polysomnography [PSG] and sleep diaries) were evaluated meta-analytically. The guiding hypothesis was that large responses would be observed on sleep diary measures and small responses would be observed on PSG measures. Methods: PubMed searches, 1967–2016, yielded 329 possible articles, 17 of which met the inclusion and exclusion criteria for the present analysis (including 879 subjects with PSG data, 1,209 subjects with diary data, and six studies with both PSG and sleep diary data). Average change and weighted effect sizes (ESs) were computed via modeling for sleep latency (SL), wake after sleep onset (WASO) and total sleep time (TST). Results: Pre-to-post change on PSG measures were: SL −13.7 min., ES = −0.37; WASO −14.3 min., ES = −0.36; and TST 29.8 min., ES = 0.50. Pre-to-post change on sleep diary measures were: SL −13.5 min., ES = −0.36; WASO −13.3 min., ES = −0.20; and TST 25.5 min., ES = 0.36. The modeled average objective subjective difference per sleep continuity measure was less than 5 minutes. The modeled average objective subjective difference per sleep continuity measure (in effect sizes) was less than 0.17. Discussion: The observed outcomes of this analysis suggest that placebos produce comparable effects on objective and subjective measures of sleep continuity. Thus, objective measures do not appear to protect against placebo responses. This being the case and given the importance of the subjective experience of illness severity and recovery, such data suggests that prospectively sampled sleep continuity data (sleep diaries) may be the optimal data for clinical trials, particularly when only one measure is possible.