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Nurses are at a high risk for work-family conflict due to long and irregular work hours and multiple physical and psychosocial stressors in their work environment. Nurses report higher rates of depressive symptoms than the general public, leading to a high rate of burnout, absenteeism, and turnover. Work-family conflict is associated with negative consequences in nurses including physical illnesses and mental disorders.Past research on this topic has not examined the mechanisms for the effect of work family conflict on depression. Studies rarely examine the influence of health behaviors such as sleep in explaining this association. Our study identified significant association of sleep disturbances with both work-family conflict and depressive symptoms in nurses. Our main contribution is reporting the important role of sleep disturbances in translating the effect of work-family conflict on depressive symptoms among nurses.Nurses need to receive training in best practices for maintaining their own sleep and mental health. Organizations should include sleep health education and training in workplace health programs. Evidence-based interventions to promote healthy sleep practices such as cognitive behavioral therapy and complementary and integrative approaches should be evaluated for their effectiveness in addressing the impact of work-family conflict on the mental health of nurses. Healthcare organizations should incorporate mental health services as part of their Employee Assistance Program for nurses and include psychological and sleep disorders screening, counseling, and follow-up.Introduction Depression has been identified as the leading cause of disability worldwide. Nurses report higher rates of depression than the general public. Work-family conflict is challenging for nurses and may lead to depression and poor health. However, the mechanisms for the effect of work-family conflict on depression have not been well understood. Aim The objective is to use a cross-sectional design to examine the role of sleep disturbances in the association between work-family conflict and depressive symptoms in nurses. Methods Questionnaires, measuring working conditions, work-family conflict, sleep disturbances and depressive symptoms were collected from 397 nurses at a not-for-profit community hospital in the north-eastern United States. Results We observed a significant association between work-family conflict and depressive symptoms (β = 2.22, p .001) among nurses. Sleep disturbances partially mediated this association by 40.54%. Discussion Sleep disturbances play an important role in translating work-family conflict into depressive symptoms. Implications Evidence-based interventions to promote healthy sleep practices should be evaluated for their effectiveness in addressing the impact of work-family conflict on mental health. Organizations should include sleep education and training as a component of workplace health promotion and employee assistance programmes to mitigate the effect of work-family conflict and promote overall health in nurses.

Objectives: To evaluate associations between sleep duration at midlife and later life and change in sleep duration over time and cognition in older women. Design: Participants reported sleep duration in 1986 and 2000, and a subgroup of older participants began cognitive testing in 1995 to 2001; follow-up testing was conducted three times, at 2-year intervals. Setting: Prospective Nurses' Health Study cohort. Participants: Female nurses aged 70 and older free of stroke and depression at the initial cognitive assessment (N = 15,385). Measurements: Validated, telephone-based cognitive battery to measure cognitive function; four repeated assessments over 6 years were averaged to estimate overall cognition at older ages, and trajectories of cognitive change were evaluated over follow up. Results: Extreme sleep durations in later life were associated with worse average cognition (P < .001 for the quadratic term for a global score averaging all six cognitive tests). For example, women sleeping 5 h/d or less had worse global cognition than those sleeping 7 h/d, as did women sleeping 9 h/d or more; differences were equivalent to nearly 2 additional years of age. Associations were similar, although slightly attenuated, for sleep duration in midlife. Women whose sleep duration changed by 2 h/d or more over time had worse cognition than women with no change in sleep duration (e.g., for the global score, P < .001 for the quadratic term). Sleep duration was not associated with trajectories of cognitive function over 6 years, which might be attributable to short follow-up for detecting cognitive decline. Conclusion: Extreme sleep durations at midlife and later life and extreme changes in sleep duration over time appear to be associated with poor cognition in older women.

Objective: Circadian rhythms influence the timing of behavior, neurological diseases, and even death. Rare mutations in homologs of evolutionarily conserved clock genes are found in select pedigrees with extreme sleep timing, and there is suggestive evidence that certain common polymorphisms may be associated with self-reported day/night preference. However, no common polymorphism has been associated with the timing of directly observed human behavioral rhythms or other physiological markers of circadian timing at the population level. Methods: We performed a candidate gene association study with replication, evaluating associations between polymorphisms in homologs of evolutionarily conserved clock genes and the timing of behavioral rhythms measured by actigraphy. For validated polymorphisms, we evaluated associations with transcript expression and time of death in additional cohorts. Results: rs7221412, a common polymorphism near period homolog 1 (PER1), was associated with the timing of activity rhythms in both the discovery and replication cohorts (joint p ¼ 2.1 � 10 � 7 ). Mean activity timing was delayed by 67 minutes in rs7221412 GG versus rs7221412 AA homozygotes. rs7221412 also showed a suggestive time-dependent relationship with both cerebral cortex (p ¼ 0.05) and CD14 þ CD16 � monocyte (p ¼ 0.02) PER1 expression and an interesting association with time of death (p ¼ 0.015) in which rs7221412 GG individuals had a mean time of death nearly 7 hours later than rs7221412 AA/AG . Interpretation: A common polymorphism near PER1 is associated with the timing of human behavioral rhythms, and shows evidence of association with time of death. This may be mediated by differential PER1 expression. These results may facilitate individualized scheduling of shift work, medical treatments, or monitoring of vulnerable patient populations. ANN NEUROL 2012;72:324–334

Light exposure in the early night induces phase delays of the circadian rhythm in melatonin in humans. Previous studies have investigated the effect of timing, intensity, wavelength, history and pattern of light stimuli on the human circadian timing system. We present results from a study of the duration–response relationship to phase-delaying bright light. Thirty-nine young healthy participants (16 female; 22.18±3.62 years) completed a 9-day inpatient study. Following three baseline days, participants underwent an initial circadian phase assessment procedure in dim light (

Recent studies have demonstrated that use of light‐emitting (LE) electronic devices in the evening close to bedtime negatively affects physiology and behavior, especially that of sleep and circadian rhythms (Bonnefond et al. 2006; Van den Bulck 2007; Cajochen et al. 2011; Munezawa et al. 2011; Arora et al. 2013, 2014; Czeisler 2013; Foley et al. 2013; Wood et al. 2013; Gamble et al. 2014; Heath et al. 2014; Chang et al. 2015; Carter et al. 2016; Czeisler and Shanahan 2016). Rapid technological advances and market pressures have led to near ubiquitous use of LE‐devices (e.g., desktop, laptop, and tablet computers, cell/smart phones, televisions, and video games) in the modern home and workplace; and such devices are now integral to many daily functions including communication, commerce, recreation, and access to news and information. Greater utility, availability, and portability of LE‐devices have additionally led to widespread LE‐device use in the evening and incorporation into the bedtime routine. A recent National Sleep Foundation survey found that 90% of Americans reported use of LE‐devices within an hour of their bedtimes, and greater use was associated with worse sleep outcomes at all ages (Gradisar et al. 2013). That and other studies have shown that adolescents and young adults are particularly likely to use LE‐devices before bedtime, often multiple LE‐devices at the same time, and the amount of LE‐device use in the evening is associated with multiple negative outcomes including delayed bedtimes, longer sleep latencies, sleep interruption from the LE‐devices during the night, shorter sleep durations, increased daytime sleepiness, and even obesity (Van den Bulck 2007; Munezawa et al. 2011; Arora et al. 2013, 2014; Foley et al. 2013; Gradisar et al. 2013; Gamble et al. 2014; Pourzanjani et al. 2015; Carter et al. 2016; Czeisler and Shanahan 2016). Light exposure per se is thought to cause many of the negative effects from evening use of LE‐devices. Retinal photoreceptors transmit light information to the master circadian clock in the hypothalamus, the suprachiasmatic nucleus (SCN), which regulates secretion of the pineal hormone melatonin together with rhythms in physiology and behavior including sleep, metabolism, immunity, alertness, and performance (Goel et al. 2013; Scheiermann et al. 2013; Qian and Scheer 2016). In the evening hours around bedtime, light exposure suppresses melatonin secretion and causes a phase delay shift in circadian rhythm timing such that melatonin secretion is reset to begin at a later time on subsequent nights (an effect similar to jet lag from extending daylight exposure later due to westward travel) (Khalsa et al. 2003; St Hilaire et al. 2012). This in turn can induce misalignment between the timing of the circadian rhythm of sleep propensity and the timing of sleep, reducing the duration, and quality of sleep (Czeisler et al. 1980; Dijk and Czeisler 1994). Misalignment can also cause delays in bedtime which, especially in children and adolescents, are associated with worse outcomes including behavioral risk factors and mental health problems such as depression (Gangwisch et al. 2010; Lemola et al. 2015; McGlinchey and Harvey 2015). There are also acute effects of light exposure that increase physiological and subjective levels of alertness (Lockley et al. 2006; Cajochen 2007; Rahman et al. 2014), which may impact when an individual feels tired and chooses to go to sleep when they are exposed to light in the evening. Furthermore, the effects of light on sleep, alertness, and circadian physiology are even greater from light exposures that are brighter, longer in duration, timed later in the evening, and contain short‐wavelength light (Lewy et al. 1980; Zeitzer et al. 2000; Brainard et al. 2001; Thapan et al. 2001; Khalsa et al. 2003; Lockley et al. 2006; Cajochen 2007; Santhi et al. 2012; St Hilaire et al. 2012; Lucas et al. 2014; Rahman et al. 2014). Because LE‐devices are often used for extended periods close to bedtime and their screens are typically illuminated by light‐emitting diodes (LED) that are rich in short‐wavelength light (Chang et al. 2015; Gringras et al. 2015) to which the human circadian system is particularly sensitive (Brainard et al. 2001; Thapan et al. 2001; Lockley et al. 2003; Ruger et al. 2013), their use is likely to increase alertness and impact sleep. Our group reported findings from a laboratory‐controlled, within‐subject, counter‐balanced, and randomized study in which the effects of light exposure from five consecutive evenings of reading on a LE‐tablet computer were compared to five consecutive evenings reading from printed books prior to a strictly imposed 10 pm bedtime, followed by an 8‐h scheduled sleep episode in total darkness (Chang et al. 2015). Compared to the evenings with printed books, the LE‐tablet reading condition caused significant melatonin suppression, circadian phase delay shifts, longer sleep latencies, reduced rapid eye movement (REM) sleep, increased alertness prior to bedtime, and lower next‐morning alertness. Those findings provided direct evidence that the light exposure from a tablet computer negatively affected sleep, circadian rhythms, and alertness under controlled laboratory conditions. In that study, the duration of evening reading sessions was set to four hours, bedtimes were fixed at 22:00, and in the LE‐tablet condition the device was placed at a fixed distance from participants and activities were restricted to reading electronic books (eBooks). Other studies that tested the effects of LE‐devices have similarly controlled aspects of the duration, timing, illuminance, and screen content of light exposures (Cajochen et al. 2011; Wood et al. 2013; Heath et al. 2014; van der Lely et al. 2015; Gronli et al. 2016). Now that the effects of LE‐devices on sleep, circadian rhythms, and alertness have been established even when bedtimes are held at a fixed time under controlled laboratory conditions, it is critical to evaluate the impact of LE‐devices on self‐selected bedtimes, sleep, alertness, and circadian rhythms in a randomized trial under controlled laboratory conditions. Increased evening alertness, melatonin suppression, and delayed circadian rhythm timing are likely key factors contributing to epidemiological findings showing associations between evening LE‐device use and later bedtimes (Foley et al. 2013; Gamble et al. 2014; Hysing et al. 2015). Additionally, such devices have numerous capabilities (e.g., internet, email, social media, games, videos, calendar, live streaming). Personal engagement with the diverse available activities may contribute to the selection of later bedtimes, thereby further prolonging evening light exposure from the device, and potentially leading to similar or even greater effects on sleep and circadian rhythms as those already observed under conditions with fixed bedtimes and light exposures. Therefore, in a follow‐up investigation to Chang et al. (Chang et al. 2015) we utilized a similar study design under controlled laboratory conditions, while allowing participants to self‐select their nightly bedtimes and LE‐tablet activities. We aimed to test whether under these unrestricted conditions, evening use of LE‐tablets compared to reading printed materials would affect self‐selection of bedtimes, and influence melatonin secretion, sleep, circadian timing, and alertness.

OBJECTIVES: To determine whether healthy aging is associated with increased sleepiness and whether healthy older adults experience more sleepiness when acutely sleep deprived. DESIGN: A 5-day inpatient circadian rhythm–sleep study consisting of 3 baseline nights followed by an extended 26-hour wake episode under constant conditions. SETTING: Intensive Physiological Monitoring Unit, General Clinical Research Center, Brigham and Women's Hospital. PARTICIPANTS: Thirty-seven healthy participants without medical, psychological, or sleep disorders: 26 young (7 women, 19 men; mean age 21.9±3.3, range 18–29) and 11 “young-old” adults (3 women, 8 men; mean age 68.1±3.6, range 65–76). INTERVENTION: An extended 26-hour wake episode under constant conditions. MEASUREMENTS: Electroencephalographic-verified wakefulness, slow eye movements, sustained attention, subjective sleepiness. RESULTS: During the first 16 hours corresponding to the usual waking day, both groups rated themselves as alert and had similar levels of vigilance and little evidence of sleepiness. As the wake episode continued, the older subjects were less impaired, showing faster reaction times, fewer performance lapses and attentional failures, and less frequent unintentional sleep episodes than the younger subjects. CONCLUSION: This small study suggests that excessive sleepiness is not normal in healthy older adults. Symptoms of excessive sleepiness in this population, including reliance on caffeine to maintain alertness, should be evaluated and treated. Further study is needed to determine whether daytime sleepiness in middle-old (75–84 years) and old-old (≥85) adults is normal or is instead associated with sleep restriction, undiagnosed sleep disorders, medication side effects, mood disorders, or other medical disorders that disrupt sleep.

Older adults have reduced sleep quality compared to younger adults when sleeping at habitual times, and greater sleep disruption when their sleep is at adverse times. The purpose of this analysis was to investigate how subjective measures of sleep relate to objectively-recorded sleep in older subjects scheduled to sleep at all times of day. We analyzed data from 24 healthy older (55–74 years) subjects who took part in a 32-day inpatient study where polysomnography (PSG) was recorded each night and subjective sleep was assessed after each scheduled wake time. The study included baseline nights and a forced desynchrony (FD) protocol when the subjects lived on a 20-hr rest-activity schedule. Our post-sleep questionnaire both included quantitative and qualitative questions about the prior sleep. Under baseline and FD conditions, objective and subjective sleep latency were correlated, subjective sleep duration was related to slow wave sleep and wake after sleep onset, subjective sleep quality was related to Stage 1 and 2 sleep, and sleepiness and refreshment at wake time were related to duration of premature awakening. During FD, most measures of objective and subjective sleep varied with circadian phase, and many additional correlations between objective and subjective sleep were present. Our findings show that when sleeping at habitual times, these healthy older subjects did not perceive their generally poor sleep quality, but under FD conditions where sleep quality changed from day-to-day their subjective sleep ratings were more associated with their objective sleep.

1. The circadian timing system has been implicated in age-related changes in sleep structure, timing and consolidation in humans. 2. We investigated the circadian regulation of sleep in 13 older men and women and 11 young men by forced desynchrony of polysomnographically recorded sleep episodes (total, 482; 9 h 20 min each) and the circadian rhythms of plasma melatonin and core body temperature. 3. Stage 4 sleep was reduced in older people. Overall levels of rapid eye movement (REM) sleep were not significantly affected by age. The latencies to REM sleep were shorter in older people when sleep coincided with the melatonin rhythm. REM sleep was increased in the first quarter of the sleep episode and the increase of REM sleep in the course of sleep was diminished in older people. 4. Sleep propensity co-varied with the circadian rhythms of body temperature and plasma melatonin in both age groups. Sleep latencies were longest just before the onset of melatonin secretion and short sleep latencies were observed close to the temperature nadir. In older people sleep latencies were longer close to the crest of the melatonin rhythm. 5. In older people sleep duration was reduced at all circadian phases and sleep consolidation deteriorated more rapidly during the course of sleep, especially when the second half of the sleep episode occurred after the crest of the melatonin rhythm. 6. The data demonstrate age-related decrements in sleep consolidation and increased susceptibility to circadian phase misalignment in older people. These changes, and the associated internal phase advance of the propensity to awaken from sleep, appear to be related to the interaction between a reduction in the homeostatic drive for sleep and a reduced strength of the circadian signal promoting sleep in the early morning.

1. The circadian pacemaker regulates the timing, structure and consolidation of human sleep. The extent to which this pacemaker affects electroencephalographic (EEG) activity during sleep remains unclear. 2. To investigate this, a total of 1.22 million power spectra were computed from EEGs recorded in seven men (total, 146 sleep episodes; 9 h 20 min each) who participated in a one-month-long protocol in which the sleep-wake cycle was desynchronized from the rhythm of plasma melatonin, which is driven by the circadian pacemaker. 3. In rapid eye movement (REM) sleep a small circadian variation in EEG activity was observed. The nadir of the circadian rhythm of alpha activity (8.25-10.5 Hz) coincided with the end of the interval during which plasma melatonin values were high, i.e. close to the crest of the REM sleep rhythm. 4. In non-REM sleep, variation in EEG activity between 0.25 and 11.5 Hz was primarily dependent on prior sleep time and only slightly affected by circadian phase, such that the lowest values coincided with the phase of melatonin secretion. 5. In the frequency range of sleep spindles, high-amplitude circadian rhythms with opposite phase positions relative to the melatonin rhythm were observed. Low-frequency sleep spindle activity (12.25-13.0 Hz) reached its crest and high-frequency sleep spindle activity (14.25-15.5 Hz) reached its nadir when sleep coincided with the phase of melatonin secretion. 6. These data indicate that the circadian pacemaker induces changes in EEG activity during REM and non-REM sleep. The changes in non-REM sleep EEG spectra are dissimilar from the spectral changes induced by sleep deprivation and exhibit a close temporal association with the melatonin rhythm and the endogenous circadian phase of sleep consolidation.

Circadian and sleep/wake dependent processes underlying variations in subjective alertness and cognitive performance were assessed in a constant routine protocol and in a protocol in which the sleep/wake cycle was uncoupled from the output of the endogenous circadian pacemaker. In the latter protocol, the contribution of a sleep/wake dependent process and a circadian process to alertness and performance were separated by folding the data at either the period of the sleep/wake cycle or at the period of the endogenous circadian body temperature rhythm. This analysis revealed that prior wakefulness within a range of 0-18 h significantly reduced alertness and performance and that the circadian rhythm of core body temperature paralleled the circadian rhythm of alertness and performance. During the first 16 h of the constant routine protocol, which coincided with the subjects' habitual period of wakefulness, alertness and performance remained at a stable level. The latter finding was explained by assuming that during our usual waking day the circadian system counteracts the detrimental effects of increasing duration of prior wakefulness.

Previous studies have led to the beliefs: (1) that short-term memory is best during the night when the body temperature is at its nadir, and (2) that the circadian rhythms of short-term memory and subjective alertness are driven by oscillators independent from each other and from the body temperature cycle. Unfortunately, these conclusions, which would have major implications for understanding the organization of the human circadian timing system, are largely based on field and laboratory studies, which in many cases sampled data infrequently and/or limited data collection to normal waking hours. In order to investigate these points further, we have monitored behavioural variables in two different protocols under controlled laboratory conditions: (1) during a period of 36-60 h of sustained wakefulness; and (2) during forced desynchrony between the body temperature and sleep/wake cycles, allowing testing of non-sleep-deprived subjects at all circadian phases. Contrary to earlier findings, we report here that the circadian rhythm of short-term memory varies in parallel with the circadian rhythms of subjective alertness, calculation performance, and core body temperature under both these experimental conditions. These results challenge the notion that short-term memory is inversely linked to the body temperature cycle and suggest that the human circadian pacemaker, which drives the body temperature cycle, is the primary determinant of endogenous circadian variations in subjective alertness and calculation performance as well as in the immediate recall of meaningful material.