Move your feet and sleep: A longitudinal dynamic analysis of self-reported exercise, sedentary behavior, and insomnia symptoms.

INTRODUCTION: Insomnia symptoms are associated with poor physical and mental health. Exercise is associated with good sleep while sedentary behavior is associated with poor sleep. This study investigated the longitudinal, dynamic associations among exercise, sedentary behavior, and insomnia symptoms. METHODS: Seven hundred and fifty-six adults (Mage=47.2years, 54.9% female) took part in an online longitudinal study investigating sleep and health across the lifespan. Participants reported duration of moderate-to-strenuous exercise, percentage of day spent sitting, and insomnia symptoms (Insomnia Severity Index [ISI]). The ISI was scored as a total score and two-factor scores: (1) Sleep Disturbance (items 1, 2, 3) and (2) Daytime Dysfunction (items 4, 5, 6, 7). Multilevel modeling was used to examine the typical (i.e., between-persons) and individual (i.e., within-persons) associations among sedentary behavior, exercise, and insomnia symptoms. RESULTS: Sedentary behavior was significantly associated with total ISI scores at both the between-person and within-person levels (ß = 0.036, t = 3.23, p = .001; ß = 0.014, t = 1.99, p = .048). Both between-persons and within-person levels of sedentary behavior were associated with Daytime Dysfunction (ß = 0.028, t = 3.79, p < .001; ß = 0.009, t = 2.08, p = .039). Exercise was associated with total ISI and Daytime Dysfunction scores at the between-persons level but not at the within-persons level (ß = 0.028, t = 2.57, p = .01; ß = -0.002, t = -3.02, p = .003). CONCLUSIONS: Sedentary behavior was a more consistent and robust predictor of insomnia symptoms than exercise. The association between sedentary behavior and insomnia symptoms was dynamic in that when an individual reported being more sedentary than their norm, they also reported more insomnia symptoms. Future analyses should examine potential moderator variables and comorbid conditions.

The natural history of insomnia: evaluating illness severity from acute to chronic insomnia; is the first the worst?

STUDY OBJECTIVES: The 3P and 4P models represent illness severity over the course of insomnia disorder. The 3P model suggests that illness severity is worst during acute onset. The 4P model suggests that illness severity crescendos with chronicity. The present analysis from an archival dataset assesses illness severity with new onset illness (i.e. from good sleep [GS] to acute insomnia [AI] to chronic insomnia [CI]). Illness severity is quantified in terms of total wake time (TWT). METHODS: GSs (N = 934) were followed up to 1 year with digital sleep diaries, and classified as GS, AI, or CI. Data for CIs were anchored to the first of 14 days with insomnia so that day-to-day TWT was represented prior to and following AI onset. A similar graphic (+/-acute onset) was constructed for number of days per week with insomnia. GS data were temporally matched to CI data. Segmented linear mixed regression models were applied to examine the change in slopes in the AI-to-CI period compared to GS-to-AI period. RESULTS: Twenty-three individuals transitioned to AI and then CI. Average TWT rose during the first 2 weeks of AI onset (b = 1.8, SE = 0.57, p = 0.001) and was then stable for 3 months (b = -0.02, SE = 0.04, p = 0.53). Average number of affected days was stable from AI to CI (b = 0.0005, SE = 0.002, p = 0.81). That is, while there was week-to-week variability in the number of days affected, no linear trend was evident. CONCLUSIONS: In our sample of CIs, primarily with middle insomnia, the average severity and number of affected days were worst with the onset of AI (worst is first) and stable thereafter.

The Assessment of Post-COVID Fatigue and Its Relationship to the Severity and Duration of Acute COVID Illness.

Emerging data suggests that COVID-19 is associated with fatigue well beyond the acute illness period. The present analysis aimed to: (1) characterize the prevalence and incidence of high fatigue at baseline and follow-up; (2) examine the impact of COVID-19 diagnosis on fatigue level following acute illness; and (3) examine the impact of acute COVID-19 symptom severity and duration on fatigue at follow-up. Subjects (n = 1417; 81.0% female; 83.3% White; X¯age = 43.6 years) completed the PROMIS-Fatigue during the initial wave of the pandemic at baseline (April-June 2020) and 9-month follow-up (January-March 2021). A generalized linear model (binomial distribution) was used to examine whether COVID-19 positivity, severity, and duration were associated with higher fatigue level at follow-up. Prevalence of high fatigue at baseline was 21.88% and 22.16% at follow-up, with 8.12% new cases at follow-up. Testing positive for COVID-19 was significantly associated with higher fatigue at follow-up. COVID-19 symptom duration and severity were significantly associated with increased fatigue at follow-up. COVID-19 symptom duration and severity during acute illness may precipitate longer-term fatigue, which could have implications for treatment planning and future research. Future studies should further evaluate the relationship between symptom severity, duration, and fatigue.

Efficacy and safety of lemborexant in subjects previously treated with placebo for 6 months in a randomized phase 3 study.

OBJECTIVE/BACKGROUND: To examine the effects of lemborexant (LEM) 5 mg (LEM5) or LEM 10 mg (LEM10) following extended placebo treatment. This post-hoc analysis used subject-reported sleep outcomes data from a phase 3 trial. PATIENTS/METHODS: The subjects in these post-hoc analyses were randomized to placebo for 6 months (Time Period [TP]1) in Study E2006-G000-303 (SUNRISE-2; NCT02952820). Following placebo exposure, subjects were re-randomized to LEM5 or LEM10 for another 6 months (TP2). Subject-reported sleep outcomes derived from sleep diaries included sleep onset latency (sSOL), wake after sleep onset (sWASO), sleep efficiency (sSE), and total sleep time (sTST). Magnitude and change rate in parameters were assessed for 7 days before/after initial randomization to placebo and 7 days before/after re-randomization to LEM (6 months later). Month 6 placebo non-responders were assessed for LEM response in TP2 using predetermined responder definitions. Safety was monitored throughout the study. RESULTS: Overall, 321 subjects received placebo; 258 re-randomized subjects received LEM5 (n = 133) and LEM10 (n = 125). Subjective sleep outcomes improved during TP1 with approximately 62 subjects (∼20%) exhibiting a sustained placebo response. Upon re-randomization to LEM, all measures showed an additional incremental benefit, most prominently in sSOL and sTST. Among Month 6 placebo non-responders, 11%-15% subsequently responded to LEM as assessed at Month 12. The safety profile was similar between treatment periods and treatment groups. CONCLUSIONS: These data suggest that even when insomnia symptoms have improved over time with placebo treatment, additional and sustained clinical gains in sleep outcomes are possible with active treatment using lemborexant.

Elevated estradiol during a hormone simulated pseudopregnancy decreases sleep and increases hypothalamic activation in female Syrian hamsters.

Sleep disruptions are a common occurrence during the peripartum period. While physical and environmental factors associated with pregnancy and newborn care account for some sleep disruptions, there is evidence that peripartum fluctuations in estrogens may independently impact sleep. However, the impact of these large fluctuations in estrogens on peripartum sleep is unclear because it is difficult to tease apart the effects of estrogens on sleep from effects associated with the growth and development of the fetus or parental care. We therefore used a hormone-simulated pseudopregnancy (HSP) in female Syrian hamsters to test the hypothesis that pregnancy-like increases in estradiol decrease sleep in the absence of other factors. Adult female Syrian hamsters were ovariectomized and given daily hormone injections that simulate estradiol levels during early pregnancy, late pregnancy, and the postpartum period. Home cage video recordings were captured at seven timepoints and videos were analyzed for actigraphy. During "late pregnancy," total sleep time and sleep efficiency were decreased in hormone-treated animals during the white light period compared to pretest levels. Likewise, during "late pregnancy," locomotion was increased in the white light period for hormone-treated animals compared to pretest levels. These changes continued into the "postpartum period" for animals who continued to receive estradiol treatment, but not for animals who were withdrawn from estradiol. At the conclusion of the experiment, animals were euthanized and cFos expression was quantified in the ventral lateral preoptic area (VLPO) and lateral hypothalamus (LH). Animals who continued to receive high levels of estradiol during the "postpartum" period had significantly more cFos in the VLPO and LH than animals who were withdrawn from hormones or vehicle controls. Together, these data suggest that increased levels of estradiol during pregnancy are associated with sleep suppression, which may be mediated by increased activation of hypothalamic nuclei.

Animal models of human insomnia.

Insomnia disorder (chronic sleep continuity disturbance) is a debilitating condition affecting 5%-10% of the adult population worldwide. To date, researchers have attempted to model insomnia in animals through breeding strategies that create pathologically short-sleeping individuals or with drugs and environmental contexts that directly impose sleeplessness. While these approaches have been invaluable for identifying insomnia susceptibility genes and mapping the neural networks that underpin sleep-wake regulation, they fail to capture concurrently several of the core clinical diagnostic features of insomnia disorder in humans, where sleep continuity disturbance is self-perpetuating, occurs despite adequate sleep opportunity, and is often not accompanied by significant changes in sleep duration or architecture. In the present review, we discuss these issues and then outline ways animal models can be used to develop approaches that are more ecologically valid in their recapitulation of chronic insomnia's natural aetiology and pathophysiology. Conditioning of self-generated sleep loss with these methods promises to create a better understanding of the neuroadaptations that maintain insomnia, including potentially within the infralimbic cortex, a substrate at the crossroads of threat habituation and sleep.

On the relationship between EEG spectral analysis and pre-sleep cognitive arousal in insomnia disorder: towards an integrated model of cognitive and cortical arousal.

According to the hyperarousal model, insomnia is characterised by increased arousal in the cortical, cognitive, and physiological domains. However, the interaction between these arousal domains is poorly understood. The present observational case-control study aimed to investigate cortical arousal during the night, pre-sleep cognitive arousal and the relationship between these two domains. A total of 109 patients with insomnia disorder (ID) and 109 age-and gender matched healthy controls were investigated on two sleep laboratory nights. Electroencephalographic (EEG) spectral power during non-rapid eye movement (NREM) and REM sleep was analysed as a measure of cortical arousal. In addition, patients completed the Pre-Sleep Arousal Scale (PSAS), which consists of two subscales, one for cognitive arousal (PSAS-CA) and one for self-reported somatic arousal (PSAS-SA). The relationship between the subscale scores and EEG spectral power was calculated by multi- and univariate analyses of variance. During NREM and REM sleep, patients with ID showed significantly increased spectral power in the EEG gamma band. In addition, patients with ID showed significantly increased scores on both subscales of the PSAS. The PSAS-CA score was significantly associated with increased NREM and REM gamma power, whereas PSAS-SA was associated with decreases in NREM and REM gamma power. Consistent with our hypothesis, patients with ID showed increased cortical and cognitive arousal. Moreover, there was an association between these two arousal domains, which may indicate that cortical arousal during the night is (at least in part) elicited by pre-sleep worry and rumination.

Sleep continuity, timing, quality, and disorder are associated with suicidal ideation and suicide attempts among college students.

Objective: To evaluate sleep continuity, timing, quality, and disorder in relation to suicidal ideation and attempts among college students. Participants: Eight hundred eighty-five undergraduates aged 18-25 in the southwestern United States. Methods: Participants completed questionnaires on sleep, suicide risk, mental health, and substance use. Differences in sleep variables were compared by lifetime and recent suicidal ideation and suicide attempts using covariate-adjusted and stepwise regression models. Results: A total of 363 (41.0%) individuals reported lifetime suicidal ideation, of whom 172 (47.4%) reported suicidal ideation in the last 3 months and 97 (26.7%) had attempted suicide in their lifetime. Sleep disturbances were prevalent among those with lifetime suicidal ideation or a lifetime suicide attempt. Insomnia was identified as the best predictor of recent suicidal ideation, but this relationship did not survive adjustment for covariates. Conclusions: Sleep continuity, quality, and sleep disorders are broadly associated with suicidal thoughts and behaviors among college students.

Baseline sleep characteristics are associated with gains in sleep duration after cognitive behavioral therapy for insomnia.

OBJECTIVE/BACKGROUND: Cognitive behavioural therapy for insomnia (CBT-I) substantially reduces total wake time (TWT) by the end of treatment. In contrast, total sleep time (TST) does not increase above baseline levels for most patients following 4-8 sessions of treatment. In the 6-12 months following CBT-I, without any further intervention, up to 64% of participants substantially increase their TST (by ≥ 30 min). The current study investigated which baseline characteristics are associated with increases in TST after CBT-I. PATIENTS/METHODS: Data were analysed from a randomised controlled trial assessing acute and maintenance CBT-I (N = 80). Linear mixed models were conducted to assess the effect of baseline characteristics on changes in TST up to 24 months after CBT-I. Baseline characteristics included age, sex, marital status, sleep continuity (derived from sleep diaries and polysomnography studies), and mental health and quality of life questionnaires. RESULTS: At baseline, self-reported sleep latency, wake after sleep onset, early morning awakenings, TWT, TST, and sleep efficiency were associated with the greatest changes in TST (p < .03 for interactions), such that patients who reported more wake/less sleep at baseline also reported the largest increases in TST. No other baseline variables were associated with changes in TST after CBT-I, including age, sex, and polysomnography-derived sleep continuity (p > .07 for interactions). CONCLUSIONS: Patients with more severe self-reported sleep difficulties and lower sleep duration at baseline showed greater improvements in TST after CBT-I. Whether more patients could increase their TST, within the context of acute treatment or following treatment, warrants investigation.

Insomnia symptoms predict longer COVID-19 symptom duration.

OBJECTIVE: /Background: The goal of the present study was to assess the prevalence and incidence of insomnia in the United States during the COVID-19 pandemic, and whether, among those that contracted COVID-19, insomnia predicted worse outcomes (e.g., symptoms of greater frequency, duration, or severity). METHODS: A nationwide sample of 2980 adults living in the United States were surveyed online at two points during the COVID-19 pandemic (T1 = April-June 2020; T2 = January-March 2021). Insomnia symptoms were assessed at both time points using the Insomnia Severity Index (ISI). The T2 survey also asked questions regarding COVID-19 testing and symptoms. RESULTS: The prevalence of insomnia (defined as ISI ≥15) was 15% at T1 and 13% at T2. The incidence rate of insomnia (i.e., new cases from T1 to T2) was 5.6%. Participants with insomnia were not more likely to contract COVID-19 relative to those participants without insomnia. Among those participants in our sample that contracted the virus during the study interval (n = 149), there were no significant group differences in COVID-19 symptom outcomes, with one exception, participants with insomnia were more likely to report a longer symptom duration (insomnia = 24.8 sick days, no insomnia = 16.1 sick days). CONCLUSIONS: The present study suggests the prevalence of insomnia in the U.S. population remained high during the COVID-19 pandemic. The data also support that insomnia may be related to experiencing more chronic COVID-19 symptoms. These findings have more general implications for the role of sleep and insomnia on immune functioning.

Social Jetlag and Other Aspects of Sleep Are Linked to Non-Suicidal Self-Injury Among College Students.

INTRODUCTION: Disrupted sleep is associated with non-suicidal self-injury (NSSI) in young adults, but many specific features of sleep continuity and timing have yet to be examined. Additionally, the psychological mechanisms linking sleep to NSSI are unclear. The present study evaluated 14 sleep variables as classifiers of lifetime or recent NSSI and examined potential confounding and mediating factors. METHODS: A sample of 885 college students provided measures of sleep continuity (e.g., duration, timing, fragmentation), nightmares, insomnia, and perceived sleep control. Lifetime and past 3-month NSSI were measured using a self-report version of the Columbia Suicide Severity Ratings Scale. Bidirectional stepwise regression identified significant sleep classifiers and subsequent models examined their associations with NSSI after adjusting for covariates and through potential psychological mediators. RESULTS: Only absolute social jetlag was associated with recent NSSI, even after adjusting for covariates, such that each additional hour difference between weekday and weekend sleep schedules was associated with a 17% greater risk of recent NSSI. Nightmares, weekend sleep efficiency, and perceived sleep control were associated with lifetime NSSI, although only weekend sleep efficiency remained associated after adjusting for covariates. Bootstrap mediations identified negative urgency as a partial mediator for recent and lifetime NSSI, and lack of premeditation and perceived burdensomeness as partial mediators for lifetime NSSI. CONCLUSIONS: The timing and consistency of young adults' sleep schedules may be of greater importance to NSSI among college students than insomnia or insufficient sleep. Future studies of sleep and NSSI should include these measures as potential risk factors. HIGHLIGHTSDifferences between weekday/weekend sleep timing are linked to recent NSSI.Negative urgency partially mediates poor sleep on recent and lifetime NSSI.Sleep shares a multifaceted relationship with NSSI risk in college students.

Do Placebos Primarily Affect Subjective as Opposed to Objective Measures? A Meta-Analysis of Placebo Responses in Insomnia RCTs.

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.

Associations between Insomnia Symptoms and Anxiety Symptoms in Adults in a Community Sample of Southeastern Pennsylvania, USA.

Although insomnia is reliably associated with anxiety symptoms, aspects of insomnia may differentially relate to one anxiety symptom versus another. Therefore, treatment for insomnia comorbidity with anxiety might be individually tailored to optimize treatment response. Working from this hypothesis, we analyzed data from a survey of 1007 community-dwelling adults. Insomnia was measured using the Insomnia Severity Index (ISI), categorizing items as nighttime disturbances, daytime dysfunction, or self-perceived dissatisfaction. Anxiety symptoms were measured with the Generalized Anxiety Disorder 7-item questionnaire (GAD-7). Linear and binomial logistic regression were used and adjusted for covariates. Post hoc forward stepwise analyses determined which components of the insomnia contributed to individual anxiety symptoms. Significant associations between nighttime disturbance (ß = 0.88 [0.44, 1.3]), daytime dysfunction (ß = 1.30 [0.81, 1.80]), dissatisfaction (ß = 1.20 [0.60, 1.7]) and total GAD-7 score were maintained after adjusting for covariates. Nighttime disturbance was associated with excess worrying, restlessness, irritability, and fear of catastrophe. Daytime dysfunction was associated with all symptoms except for fear of catastrophe, and self-perceived dissatisfaction was associated with all symptoms except irritability. Stepwise analyses revealed that daytime dysfunction and dissatisfaction were most consistently related to anxiety symptoms.Greater attention should be paid to daytime dysfunction in patients with insomnia and anxiety, as improving daytime functioning may improve anxiety.

Insomnia.

Insomnia is highly prevalent in clinical practice, occurring in up to 50% of primary care patients. Insomnia can present independently or alongside other medical conditions or mental health disorders and is a risk factor for the development and exacerbation of these other disorders if not treated. In 2016, the American College of Physicians recommended that insomnia be specifically targeted for treatment. The recommended first-line treatment for insomnia, whether the underlying cause has been identified or not, is cognitive behavioural therapy for insomnia (CBT-I). Currently, there is no global consensus regarding which pharmacological treatment has the best efficacy or risk-benefit ratio. Both CBT-I and pharmacological intervention are thought to have similar acute effects, but only CBT-I has shown durable long-term effects after treatment discontinuation. Administering a combined treatment of CBT-I and medication could decrease the latency to treatment response, but might diminish the durability of the positive treatment effects of CBT-I.

Pre-Sleep Cognitive Arousal Is Unrelated to Sleep Misperception in Healthy Sleepers When Unexpected Sounds Are Played during Non-Rapid Eye Movement Sleep: A Polysomnography Study.

BACKGROUND: It is well-established that environmental noise can disrupt sleep, and cause a mismatch between subjective and objective sleep, which is known as "sleep misperception". Naturalistic studies indicate that pre-sleep cognitive arousal and sleep misperception are associated in the context of noise. However, it is not known if this is the case when ecologically valid noises are specifically played during non-rapid eye movement (NREM) sleep, which is susceptible to noise-related disruption. The present study evaluated if pre-sleep cognitive arousal was associated with sleep misperception in healthy normal sleepers, when unexpected ecologically valid common nocturnal noises were played during NREM sleep. METHODS: Eighteen healthy sleepers (Mage = 23.37 years, SDage = 3.21 years) participated. Sleep was measured objectively on three consecutive nights using polysomnography, in a sleep laboratory environment, and subjectively, through participant estimates of total sleep time (TST). Night 1 was a baseline night where no noises were played. On Night 2, noises, which were chosen to be representative of habitual nocturnal noises heard in home environments, were played to participants via in-ear headphones after 5 min of objective sleep. RESULTS: Unexpectedly, habitual pre-sleep cognitive arousal was not associated with subjective-objective TST discrepancy on Night 2. CONCLUSIONS: These results suggest that in healthy sleepers, when ecologically valid noises are played unexpectedly during NREM sleep in an unfamiliar sleep laboratory environment the subjective experience of sleep is not associated with pre-sleep cognitive arousal, or negatively impacted by noise exposure.

The natural history of insomnia: high sleep reactivity interacts with greater life stress to predict the onset of acute insomnia.

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: About 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.

Nocturnal Wakefulness and Suicide Risk in the Australian Population.

Objective: Temporal patterns for suicide over a 24-hour period have shown mixed results among prior studies. However, analyses of 24-hour temporal patterns for wakeful actions including suicidal behavior should adjust for expected sleep requirements that inherently skew such activities to conventional wakeful times. This study analyzed the time-of-day for suicide cases from the Australian population for the year 2017, adjusting for expected sleep patterns. Identification of time-of-day trends using this methodology may reveal risk factors for suicide and potentially modifiable contributors.Methods: The Australian National Coronial Information System database was accessed, and data for completed suicide were extracted for the most recent completed year (2017). Time of suicide was allocated to one of four 6-hourly time bins across 24 hours, determined from time last seen alive and time found subsequently. Prevalence of suicide for each time bin was adjusted for the likelihood of being awake for each bin according to sleep-wake norms published from a large Australian community survey. Observed prevalence of suicide was compared to expected values predicted from likelihood of being awake across each time bin calculated as a standardized incidence ratio (SIR).Results: For the year 2017, there were 2,808 suicides, of which 1,417 were able to be allocated into one of four 6-hourly time bins. When compared to expected values, suicides were significantly more likely to occur in the overnight bin (2301-0500; SIR = 3.93, P < .001).Conclusions: Higher-than-expected rates of suicide overnight associated with nocturnal wakefulness may represent a modifiable risk factor for triggering suicide events.

The Mind After Midnight: Nocturnal Wakefulness, Behavioral Dysregulation, and Psychopathology.

Sufficient sleep with minimal interruption during the circadian/biological night supports daytime cognition and emotional regulation. Conversely, disrupted sleep involving significant nocturnal wakefulness leads to cognitive and behavioral dysregulation. Most studies to-date have examined how fragmented or insufficient sleep affects next-day functioning, but recent work highlights changes in cognition and behavior that occur when someone is awake during the night. This review summarizes the evidence for day-night alterations in maladaptive behaviors, including suicide, violent crime, and substance use, and examines how mood, reward processing, and executive function differ during nocturnal wakefulness. Based on this evidence, we propose the Mind after Midnight hypothesis in which attentional biases, negative affect, altered reward processing, and prefrontal disinhibition interact to promote behavioral dysregulation and psychiatric disorders.