Although there are considerable data demonstrating the impact of shift work on sleep and alertness, little research has examined the prevalence and consequences of shift work sleep disorder in comparison to the difficulties with insomnia and excessive sleepiness experienced by day workers. The present study was designed to determine the relative prevalence and negative consequences associated with shift work sleep disorder in a representative sample drawn from the working population of metropolitan Detroit. Random-digit dialing techniques were used to assess individuals regarding their current work schedules and a variety of sleep- and non—sleep-related outcomes. Detroit tricounty population. A total of 2,570 individuals aged 18 to 65 years from a representative community-based sample including 360 people working rotating shifts, 174 people working nights, and 2036 working days. Using standardized techniques, individuals were assessed for the presence of insomnia and excessive sleepiness, based on DSM-IV and ICSD criteria. Those individuals with either insomnia or excessive sleepiness and who were currently working rotating or night schedules were classified as having shift work sleep disorder. Occupational, behavioral, and health-related outcomes were also measurd. Individuals who met criteria for shift work sleep disorder had significantly higher rates of ulcers (odds ratio = 4.18, 95% confidence interval = 2.00–8.72), sleepiness-related accidents, absenteeism, depression, and missed family and social activities more frequently compared to those shift workers who did not meet criteria (P < .05). Importantly, in most cases, the morbidity associated with shift work sleep disorder was significantly greater than that experienced by day workers with identical symptoms. These findings suggest that individuals with shift work sleep disorder are at risk for significant behavioral and health-related morbidity associated with their sleep-wake symptomatology. Further, it suggests that the prevalence of shift work sleep disorder is approximately 10% of the night and rotating shift work population.

Summary: Sleep reactivity is the trait‐like degree to which stress exposure disrupts sleep, resulting in difficulty falling and staying asleep. Individuals with highly reactive sleep systems experience drastic deterioration of sleep when stressed, whereas those with low sleep reactivity proceed largely unperturbed during stress. Research shows that genetics, familial history of insomnia, female gender and environmental stress influence how the sleep system responds to stress. Further work has identified neurobiological underpinnings for sleep reactivity involving disrupted cortical networks and dysregulation in the autonomic nervous system and hypothalamic‐pituitary‐adrenal axis. Sleep reactivity is most pathologically and clinically pertinent when in excess, such that high sleep reactivity predicts risk for future insomnia disorder, with early evidence suggesting high sleep reactivity corresponds to severe insomnia phenotypes (sleep onset insomnia and short sleep insomnia). High sleep reactivity is also linked to risk of shift‐work disorder, depression and anxiety. Importantly, stress‐related worry and rumination may exploit sensitive sleep systems, thereby augmenting the pathogenicity of sleep reactivity. With the development of cost‐effective assessment of sleep reactivity, we can now identify individuals at risk of future insomnia, shift‐work disorder and mental illness, thus identifying a target population for preventive intervention. Given that insomniacs with high sleep reactivity tend to present with severe insomnia phenotypes, patient sleep reactivity may inform triaging to different levels of treatment. Future research on sleep reactivity is needed to clarify its neurobiology, characterize its long‐term prospective associations with insomnia and shift‐work disorder phenotypes, and establish its prognostic value for mental illness and other non‐sleep disorders.

Importance Digital cognitive behavioral therapy (dCBT) is a scalable and effective intervention for treating insomnia. Most people with insomnia, however, seek help because of the daytime consequences of poor sleep, which adversely affects quality of life. Objectives To investigate the effect of dCBT for insomnia on functional health, psychological well-being, and sleep-related quality of life and to determine whether a reduction in insomnia symptoms was a mediating factor. Design, Setting, and Participants This online, 2-arm, parallel-group randomized trial comparing dCBT for insomnia with sleep hygiene education (SHE) evaluated 1711 participants with self-reported symptoms of insomnia. Participants were recruited between December 1, 2015, and December 1, 2016, and dCBT was delivered using web and/or mobile channels plus treatment as usual; SHE comprised a website and a downloadable booklet plus treatment as usual. Online assessments took place at 0 (baseline), 4 (midtreatment), 8 (posttreatment), and 24 (follow-up) weeks. Programs were completed within 12 weeks after inclusion. Main Outcomes and Measures Primary outcomes were scores on self-reported measures of functional health (Patient-Reported Outcomes Measurement Information System: Global Health Scale; range, 10-50; higher scores indicate better health); psychological well-being (Warwick-Edinburgh Mental Well-being Scale; range, 14-70; higher scores indicate greater well-being); and sleep-related quality of life (Glasgow Sleep Impact Index; range, 1-100; higher scores indicate greater impairment). Secondary outcomes comprised mood, fatigue, sleepiness, cognitive failures, work productivity, and relationship satisfaction. Insomnia was assessed with the Sleep Condition Indicator (range: 0-32; higher scores indicate better sleep). Results Of the 1711 participants included in the intention-to-treat analysis, 1329 (77.7%) were female, mean (SD) age was 48.0 (13.8) years, and 1558 (91.1%) were white. Use of dCBT was associated with a small improvement in functional health compared with SHE (adjusted difference [95% CI] at week 4, 0.90 [0.40-1.40]; week 8, 1.76 [1.24-2.28]; week 24, 1.76 [1.22-2.30]) and psychological well-being (adjusted difference [95% CI] at week 4, 1.04 [0.28-1.80]; week 8, 2.68 [1.89-3.47]; week 24, 2.95 [2.13-3.76]), and with a large improvement in sleep-related quality of life (at week 4, −8.76 [−11.83 to −5.69]; week 8, –17.60 [−20.81 to −14.39]; week 24, −18.72 [−22.04 to −15.41]) (allP < .01). A large improvement in insomnia mediated these outcomes (range mediated, 45.5%-84.0%). Conclusions and Relevance Use of dCBT is effective in improving functional health, psychological well-being, and sleep-related quality of life in people reporting insomnia symptoms. A reduction in insomnia symptoms mediates these improvements. These results confirm that dCBT improves both daytime and nighttime aspects of insomnia, strengthening existing recommendations of CBT as the treatment of choice for insomnia. Trial Registration isrctn.org identifier:ISRCTN60530898

To determine the presence of a hypothesized trait vulnerability to sleep disturbance and hyperarousal. Polysomnographic assessment of sleep in response to stress during a first night in the laboratory and subsequent physiologic arousal. One hundred and four individuals (46% men, mean age = 40.4 ± 12.9 years) drawn from a population-based sample. Individuals were exposed to a first night in the laboratory. Participants completed a Likert-scale questionnaire, consisting of 27 items, that assesses sleep disturbance in response to commonly experienced stressful situations. Factor analytic techniques identified a single 9-item factor that was representative of the construct of “stress-related” vulnerability to sleep disturbance. Reliability of the resulting 9-item scale was high (Cronbach's α = .83). Individuals with higher scores on this scale, the Ford Insomnia Response to Stress Test (FIRST; median split), had a lower sleep efficiency (P = .001), as well as an increased latency to stage 1 sleep (P = .001) and persistent sleep (P = .002) on the first night of nocturnal polysomnography. Moreover, these high-scoring individuals showed increased arousal as evidenced by an elevated sleep latency on the Multiple Sleep Latency Test compared to individuals with low FIRST scores. Importantly, after controlling for current and past insomnia, the differences between individuals scoring high and low on the FIRST in terms of nocturnal sleep and daytime arousal remained significant. Other stages of sleep (stage 2, slow-wave, and rapid eye movement sleep) were not different between the groups. These results showing a relationship between FIRST scores and nocturnal polysomnography and Multiple Sleep Latency Test scores have 3 potential implications: (1) the data demonstrate a characteristic that relates to vulnerability to stress-related sleep disturbance as manifested by a first night in the laboratory; (2) the elevated latencies on the Multiple Sleep Latency Test in these individuals, despite significantly disturbed sleep, support the notion of physiologic hyperarousal in these individuals and suggests they may be predisposed to developing chronic primary insomnia; and (3) the vulnerability identified may underlie vulnerability to transient sleep disturbance associated with other sleep-disruptive factors.

Sleep hygiene recommendations are widely disseminated despite the fact that few systematic studies have investigated the empirical bases of sleep hygiene in the home environment. For example, studies have yet to investigate the relative effects of a given dose of caffeine administered at different times of day on subsequent sleep. This study compared the potential sleep disruptive effects of a fixed dose of caffeine (400 mg) administered at 0, 3, and 6 hours prior to habitual bedtime relative to a placebo on self-reported sleep in the home. Sleep disturbance was also monitored objectively using a validated portable sleep monitor. Results demonstrated a moderate dose of caffeine at bedtime, 3 hours prior to bedtime, or 6 hours prior to bedtime each have significant effects on sleep disturbance relative to placebo (p < 0.05 for all). The magnitude of reduction in total sleep time suggests that caffeine taken 6 hours before bedtime has important disruptive effects on sleep and provides empirical support for sleep hygiene recommendations to refrain from substantial caffeine use for a minimum of 6 hours prior to bedtime.