Sleep disturbance is increasingly recognized as an important, but understudied, mechanism in the complex and multi-factorial causation of the symptoms and functional disability associated with psychiatric disorders. This review proposes that it is biologically plausible for sleep disturbance to be mechanistically transdiagnostic. More specifically, we propose that sleep disturbance is aetiologically linked to various forms of psychopathology through: its reciprocal relationship with emotion regulation and its shared/interacting neurobiological substrates in (a) genetics - genes known to be important in the generation and regulation of circadian rhythms have been linked to a range of disorders and (b) dopaminergic and serotonergic function - we review evidence for the interplay between these systems and sleep/circadian biology. The clinical implications include potentially powerful and inexpensive interventions including interventions targeting light exposure, dark exposure, the regulation of social rhythms and the reduction of anxiety. We also consider the possibility of developing a ‘transdiagnostic’ treatment; one treatment that would reduce sleep disturbance across psychiatric disorders.

Objective To determine if a treatment for interepisode bipolar disorder I patients with insomnia improves mood state, sleep, and functioning. Method Alongside psychiatric care, interepisode bipolar disorder I participants with insomnia were randomly allocated to a bipolar disorder–specific modification of cognitive behavior therapy for insomnia (CBTI-BP; n = 30) or psychoeducation (PE; n = 28) as a comparison condition. Outcomes were assessed at baseline, the end of 8 sessions of treatment, and 6 months later. This pilot was conducted to determine initial feasibility and generate effect size estimates. Results During the 6-month follow-up, the CBTI-BP group had fewer days in a bipolar episode relative to the PE group (3.3 days vs. 25.5 days). The CBTI-BP group also experienced a significantly lower hypomania/mania relapse rate (4.6% vs. 31.6%) and a marginally lower overall mood episode relapse rate (13.6% vs. 42.1%) compared with the PE group. Relative to PE, CBTI-BP reduced insomnia severity and led to higher rates of insomnia remission at posttreatment and marginally higher rates at 6 months. Both CBTI-BP and PE showed statistically significant improvement on selected sleep and functional impairment measures. The effects of treatment were well sustained through follow-up for most outcomes, although some decline on secondary sleep benefits was observed. Conclusions CBTI-BP was associated with reduced risk of mood episode relapse and improved sleep and functioning on certain outcomes in bipolar disorder. Hence, sleep disturbance appears to be an important pathway contributing to bipolar disorder. The need to develop bipolar disorder–specific sleep diary scoring standards is highlighted. Public Health Significance This study suggests that an intervention to improve sleep and circadian functioning reduces risk of relapse and improves sleep and overall functioning among individuals who meet diagnostic criteria for bipolar disorder.

Objective To examine the unique contribution of behavior therapy (BT) and cognitive therapy (CT) relative to the full cognitive behavior therapy (CBT) for persistent insomnia. Method Participants were 188 adults (117 women; M age = 47.4 years old, SD=12.6) with persistent insomnia (average of 14.5 years duration). They were randomized to eight, weekly, individual sessions consisting of BT (n = 63), CT (n = 65), or CBT (n = 60). Results Full CBT was associated with greatest improvements, the improvements associated with BT were faster but not as sustained and the improvements associated with CT were slower and sustained. The proportion of treatment responders was significantly higher in the CBT (67.3%) and BT (67.4%) relative to CT (42.4%) groups at post treatment, while 6-months later CT made significant further gains (62.3%), BT had significant loss (44.4%) and CBT retained its initial response (67.6%). Remission rates followed a similar trajectory, with higher remission rates at post treatment in CBT (57.3%) relative to CT (30.8%), with BT falling in between (39.4%); CT made further gains from post treatment to follow up (30.9% to 51.6%). All three therapies produced improvements of daytime functioning at both post treatment and follow up, with few differential changes across groups. Conclusions Full CBT is the treatment of choice. Both BT and CT are effective, with a more rapid effect for BT and a delayed action for CT. These different trajectories of changes provide unique insights into the process of behavior change via behavioral versus cognitive routes.

Background The aim was to examine the prevalence and consequences of co-occurring insomnia and hypersomnia symptoms in depressed adults drawn from a representative sample of the U.S. population. Method Data from 687 National Comorbidity Survey Replication (NCS-R) respondents meeting criteria for a major depressive episode (MDE) in the past year were included. Respondents completed clinical interviews that assessed 12-month DSM-IV disorders, impairment, mental health treatment, and depressive symptom severity. Outcomes were compared between respondents who experienced insomnia symptoms-only (N=404), hypersomnia symptoms-only (N=44), both insomnia and hypersomnia symptoms (N=184) and no sleep problems (N=55) during an MDE. Results Insomnia and hypersomnia symptoms co-occurred in 27.7% of respondents with past-year MDEs, most frequently in bipolar spectrum disorders and major depressive disorder with dysthymia. Similar to the insomnia-only group, respondents with co-occurring sleep disturbances had more severe depression, and higher rates of past-year impulse control disorders and suicide planning. Similar to the hypersomnia-only group, respondents with co-occurring sleep disturbances had higher rates of past-year drug use disorders and suicide attempts. Compared to the insomnia-only and no sleep problem groups, respondents with both sleep disturbances were more frequently in mental health treatment, seeing a general practitioner, and taking antidepressants. Limitations The NCS-R is cross-sectional and did not evaluate sleep disorder diagnoses. Conclusions Co-occurring insomnia and hypersomnia symptoms were associated with a more severe MDE. Further research is warranted to more fully understand the joint presentation of insomnia and hypersomnia in depression.

Comorbid mood and anxiety disorders are associated with high rates of severe insomnia complaints, which were independently associated with substantial functional impairment.

Insomnia was characterized by regional alterations in relative glucose metabolism across NREM sleep and wakefulness. Significant group-by-state interactions in relative rCMR suggest that insomnia is associated with impaired disengagement of brain regions involved in cognition (left frontoparietal), self-referential processes (precuneus/posterior cingulate), and affect (left middle frontal, fusiform/lingual gyri) during NREM sleep, or alternatively, to impaired engagement of these regions during wakefulness.

Adolescence is a time of marked changes across sleep, circadian rhythms, brain function, and alcohol use. Starting at puberty, adolescents’ endogenous circadian rhythms and preferred sleep times shift later, often leading to a mismatch with the schedules imposed by secondary education. This mismatch induces circadian misalignment and sleep loss, which have been associated with affect dysregulation, increased drug and alcohol use, and other risk-taking behaviors in adolescents and adults. In parallel to developmental changes in sleep, adolescent brains are undergoing structural and functional changes in the circuits subserving the pursuit and processing of rewards. These developmental changes in reward processing likely contribute to the initiation of alcohol use during adolescence. Abundant evidence indicates that sleep and circadian rhythms modulate reward function, suggesting that adolescent sleep and circadian disturbance may contribute to altered reward function, and in turn, alcohol involvement. In this review, we summarize the relevant evidence and propose that these parallel developmental changes in sleep, circadian rhythms, and neural processing of reward interact to increase risk for alcohol use disorder (AUD).

The aim of this study was to explore how interindividual differences in circadian type (morningness) and sleep timing regularity might be related to subjective sleep quality and quantity. Self-report circadian phase preference, sleep timing, sleep quality, and sleep duration were assessed in a sample of 62 day-working adults (33.9% male, age 23–48 yrs). The Pittsburgh Sleep Quality Index (PSQI) measured subjective sleep quality and the Sleep Timing Questionnaire (STQ) assessed habitual sleep latency and minutes awake after sleep onset. The duration, timing, and stability of sleep were assessed using the STQ separately for work-week nights (Sunday–Thursday) and for weekend nights (Friday and Saturday). Morningness-eveningness was assessed using the Composite Scale of Morningness (CSM). Daytime sleepiness was measured using the Epworth Sleepiness Scale (ESS). A morning-type orientation was associated with longer weekly sleep duration, better subjective sleep quality, and shorter sleep-onset latency. Stable weekday rise-time correlated with better self-reported sleep quality and shorter sleep-onset latency. A more regular weekend bedtime was associated with a shorter sleep latency. A more stable weekend rise-time was related to longer weekday sleep duration and lower daytime sleepiness. Increased overall regularity in rise-time was associated with better subjective sleep quality, shorter sleep-onset latency, and higher weekday sleep efficiency. Finally, a morning orientation was related to increased regularity in both bedtimes and rise-times. In conclusion, in daytime workers, a morning-type orientation and more stable sleep timing are associated with better subjective sleep quality.