Defeat and Entrapment Mediate the Relationship Between Insomnia Symptoms and Suicidal Ideation in Young Adults.

AIM: In recent years, there has been a growing interest in understanding the relationship between sleep disturbance and suicide. The current study aimed to advance understanding of the psychological processes driving these relationships by examining whether insomnia symptoms are related to suicidal ideation via perceptions of defeat and entrapment. METHODS: Young adults (n = 259; 202 students [78.0%], 45 employed [17.4%], 12 unemployed [4.6%]) completed an anonymous self-report survey that was advertised via social media, university participant pools, and fliers. The survey was described as being related to sleep and mood/mental health. Validated measures were used to assess insomnia symptoms, chronotype, defeat, entrapment, suicidal ideation, and affective covariates. RESULTS: Bivariate associations found insomnia severity to be related to poorer affective outcomes including severity of suicidal ideation. Insomnia and depression were significant independent variables in multiple linear regression with suidical ideation as the dependent variable. The relationship between insomnia and suicidal ideation was mediated by perceptions of defeat and entrapment. CONCLUSION: Taken together, these findings shed light on the psychological mechanisms linking sleep disturbance and suicidal ideation by highlighting the role of defeat and entrapment. These findings have the potential to improve suicide risk assessment and prevention in young adults experiencing difficulties initiating or maintaining sleep.HighlightsDefeat and entrapment mediate relationship between insomnia and suicidal ideationEvidence for Integrated Motivational-Volitional Model of Suicidal Behavior in community sampleUses validated multi-item suicide measure.

Nodding off but can't disconnect: development and validation of the iNOD index of Nighttime Offline Distress.

BACKGROUND: There is a pressing need to update sleep models, education and treatment to better reflect the realities of sleep in a 24/7 connected social world. Progress has been limited to date by available measurement tools, which have largely focused on the frequency or duration of individuals' social media use, without capturing crucial sleep-relevant aspects of this inherently social and interactive experience. METHODS: Survey data from 3008 adolescents (aged 10-18 years) was used to rigorously develop and validate a new self-report measure that quantifies difficulty disengaging from social media interactions at night: the index of Nighttime Offline Distress (iNOD). Exploratory and Confirmatory Factor analyses in a random split sample produced a ten-item two-factor solution, with subscales capturing concerns about Staying Connected and Following Etiquette (Cronbach's alphas = 0.91 and 0.92 respectively). RESULTS: Those with higher scores on these subscales tended to report using social media for longer after they felt they should be asleep (rs = 0.41 and 0.26, respectively), shorter sleep duration (rs = -0.24 and -0.17, respectively) and poorer sleep quality (rs = -0.33 and -0.31, respectively). Results also pointed towards a potentially fragmented process of sleep displacement for those who may struggle to disconnect - and to stay disconnected - from social interactions in order to allow sufficient uninterrupted sleep opportunity. CONCLUSIONS: These findings can inform current models for understanding normal and disordered sleep during adolescence, whilst highlighting specific social concerns as important potential targets for sleep education efforts.

Insomnia symptoms mediate the association between eveningness and suicidal ideation, defeat, entrapment, and psychological distress in students.

Chronotype describes a person's general preference for mornings, evenings, or neither. It is typically conceptualized as a continuous unidimensional spectrum from morningness to eveningness. Eveningness is associated with poorer outcomes across a myriad of physical and mental health outcomes. This preference for later sleep and wake times is associated with increased risk of depression, anxiety, and suicidal ideation in both clinical and community samples. However, the mechanisms underlying the negative consequences of this preference for evenings are not fully understood. Previous research has found that sleep disturbances may act as a mediator of this relationship. The present study aimed to explore the associations between chronotype and affective outcomes in a sample of students. Additionally, it aimed to investigate the potential role of insomnia as a mediator within these relationships. Participants (n = 190) completed an anonymous self-report survey of validated measures online which assessed chronotype, insomnia symptoms, and a range of affective outcomes (defeat, entrapment, suicide risk, stress, and depressive and anxious symptomology). Eveningness was associated with more severe or frequent experiences of these outcomes, with participants that demonstrated a preference for eveningness more likely to report poorer affective functioning and increased psychological distress. Mediation analysis found the relationship between chronotype and these outcome measures was completely or partially mediated by insomnia symptom severity measured by the validated Sleep Condition Indicator insomnia scale. Taken together, these findings add further evidence for the negative consequences of increased eveningness. Additionally, our results show that chronotype and sleep disturbances should be considered when assessing mental well-being. Implementing appropriate sleep-related behavior change or schedule alterations can offer a tool for mitigation or prevention of psychological distress in students that report a preference for later sleep and wake times.

Identifying drivers for bedtime social media use despite sleep costs: The adolescent perspective.

OBJECTIVES: Bedtime social media use is associated with poor sleep during adolescence, which in turn contributes to poor mental health, impaired daytime functioning and lower academic achievement. However, the underlying drivers for these bedtime social media habits remain understudied. This study adds an adolescent perspective on motivations for bedtime social media use and perceived impact on sleep. METHODS: Adolescents aged 11-17 years (n = 24) participated in focus group discussions exploring their experiences of using social media, particularly at night. Inductive reflexive thematic analysis produced themes that captured underlying drivers for social media use and associated impact on sleep. RESULTS: Our analyses produced two overarching themes: Missing Out and Norms & Expectations. Adolescents' nighttime social media use was driven by concerns over negative consequences for real-world relationships if they disconnected (often reporting delayed bedtimes, insufficient sleep and daytime tiredness). These concerns included the risk of offline peer exclusion from missing out on online interactions, and the fear of social disapproval from violating norms around online availability and prompt responses. CONCLUSIONS: These findings offer novel insight into why adolescents may choose to prioritize social media over sleep. Researchers and practitioners can respond to the evolving needs of today's adolescents by approaching social media use not as a technology-based activity, but as an embedded social experience underpinned by the same concerns as offline interactions.

Social media use and adolescent sleep patterns: cross-sectional findings from the UK millennium cohort study.

OBJECTIVES: This study examines associations between social media use and multiple sleep parameters in a large representative adolescent sample, controlling for a wide range of covariates. DESIGN: The authors used cross-sectional data from the Millennium Cohort Study, a large nationally representative UK birth cohort study. PARTICIPANTS: Data from 11 872 adolescents (aged 13-15 years) were used in analyses. METHODS: Six self-reported sleep parameters captured sleep timing and quality: sleep onset and wake times (on school days and free days), sleep onset latency (time taken to fall asleep) and trouble falling back asleep after nighttime awakening. Binomial logistic regressions investigated associations between daily social media use and each sleep parameter, controlling for a range of relevant covariates. RESULTS: Average social media use was 1 to <3 hours per day (31.6%, n=3720). 33.7% were classed as low users (<1 hour; n=3986); 13.9% were high users (3 to <5 hours; n=1602) and 20.8% were very high users (5+ hours; n=2203). Girls reported spending more time on social media than boys. Overall, heavier social media use was associated with poorer sleep patterns, controlling for covariates. For example, very high social media users were more likely than comparable average users to report late sleep onset (OR 2.14, 95% CI 1.83 to 2.50) and wake times (OR 1.97, 95% CI 1.32 to 2.93) on school days and trouble falling back asleep after nighttime awakening (OR 1.36, 95% CI 1.10 to 1.66). CONCLUSIONS: This study provides a normative profile of UK adolescent social media use and sleep. Results indicate statistically and practically significant associations between social media use and sleep patterns, particularly late sleep onset. Sleep education and interventions can focus on supporting young people to balance online interactions with an appropriate sleep schedule that allows sufficient sleep on school nights.

Alterations in glutamatergic signaling contribute to the decline of circadian photoentrainment in aged mice.

Robust physiological circadian rhythms form an integral part of well-being. The aging process has been found to negatively impact systems that drive circadian physiology, typically manifesting as symptoms associated with abnormal/disrupted sleeping patterns. Here, we investigated the age-related decline in light-driven circadian entrainment in male C57BL/6J mice. We compared light-driven resetting of circadian behavioral activity in young (1-2 months) and old (14-18 months) mice and explored alterations in the glutamatergic pathway at the level of the circadian pacemaker, the suprachiasmatic nucleus (SCN). Aged animals showed a significant reduction in sensitivity to behavioral phase resetting by light. We show that this change was through alterations in N-Methyl-D-aspartate (NMDA) signaling at the SCN, where NMDA, a glutamatergic agonist, was less potent in inducing clock resetting. Finally, we show that this shift in NMDA sensitivity was through the reduced SCN expression of this receptor's NR2B subunit. Only in young animals did an NR2B antagonist attenuate behavioral resetting. These results can help target treatments that aim to improve both physiological and behavioral circadian entrainment in aged populations.

Genome-Wide Association Study of Circadian Rhythmicity in 71,500 UK Biobank Participants and Polygenic Association with Mood Instability.

BACKGROUND: Circadian rhythms are fundamental to health and are particularly important for mental wellbeing. Disrupted rhythms of rest and activity are recognised as risk factors for major depressive disorder and bipolar disorder. METHODS: We conducted a genome-wide association study (GWAS) of low relative amplitude (RA), an objective measure of rest-activity cycles derived from the accelerometer data of 71,500 UK Biobank participants. Polygenic risk scores (PRS) for low RA were used to investigate potential associations with psychiatric phenotypes. OUTCOMES: Two independent genetic loci were associated with low RA, within genomic regions for Neurofascin (NFASC) and Solute Carrier Family 25 Member 17 (SLC25A17). A secondary GWAS of RA as a continuous measure identified a locus within Meis Homeobox 1 (MEIS1). There were no significant genetic correlations between low RA and any of the psychiatric phenotypes assessed. However, PRS for low RA was significantly associated with mood instability across multiple PRS thresholds (at PRS threshold 0·05: OR = 1·02, 95% CI = 1·01-1·02, p = 9·6 × 10-5), and with major depressive disorder (at PRS threshold 0·1: OR = 1·03, 95% CI = 1·01-1·05, p = 0·025) and neuroticism (at PRS threshold 0·5: Beta = 0·02, 95% CI = 0·007-0·04, p = 0·021). INTERPRETATION: Overall, our findings contribute new knowledge on the complex genetic architecture of circadian rhythmicity and suggest a putative biological link between disrupted circadian function and mood disorder phenotypes, particularly mood instability, but also major depressive disorder and neuroticism. FUNDING: Medical Research Council (MR/K501335/1).

Association of disrupted circadian rhythmicity with mood disorders, subjective wellbeing, and cognitive function: a cross-sectional study of 91 105 participants from the UK Biobank.

BACKGROUND: Disruption of sleep and circadian rhythmicity is a core feature of mood disorders and might be associated with increased susceptibility to such disorders. Previous studies in this area have used subjective reports of activity and sleep patterns, but the availability of accelerometer-based data from UK Biobank participants permits the derivation and analysis of new, objectively ascertained circadian rhythmicity parameters. We examined associations between objectively assessed circadian rhythmicity and mental health and wellbeing phenotypes, including lifetime history of mood disorder. METHODS: UK residents aged 37-73 years were recruited into the UK Biobank general population cohort from 2006 to 2010. We used data from a subset of participants whose activity levels were recorded by wearing a wrist-worn accelerometer for 7 days. From these data, we derived a circadian relative amplitude variable, which is a measure of the extent to which circadian rhythmicity of rest-activity cycles is disrupted. In the same sample, we examined cross-sectional associations between low relative amplitude and mood disorder, wellbeing, and cognitive variables using a series of regression models. Our final model adjusted for age and season at the time that accelerometry started, sex, ethnic origin, Townsend deprivation score, smoking status, alcohol intake, educational attainment, overall mean acceleration recorded by accelerometry, body-mass index, and a binary measure of childhood trauma. FINDINGS: We included 91 105 participants with accelerometery data collected between 2013 and 2015 in our analyses. A one-quintile reduction in relative amplitude was associated with increased risk of lifetime major depressive disorder (odds ratio [OR] 1·06, 95% CI 1·04-1·08) and lifetime bipolar disorder (1·11, 1·03-1·20), as well as with greater mood instability (1·02, 1·01-1·04), higher neuroticism scores (incident rate ratio 1·01, 1·01-1·02), more subjective loneliness (OR 1·09, 1·07-1·11), lower happiness (0·91, 0·90-0·93), lower health satisfaction (0·90, 0·89-0·91), and slower reaction times (linear regression coefficient 1·75, 1·05-2·45). These associations were independent of demographic, lifestyle, education, and overall activity confounders. INTERPRETATION: Circadian disruption is reliably associated with various adverse mental health and wellbeing outcomes, including major depressive disorder and bipolar disorder. Lower relative amplitude might be linked to increased susceptibility to mood disorders. FUNDING: Lister Institute of Preventive Medicine.

Attention to beds in natural scenes by observers with insomnia symptoms.

Attention biases to sleep-related stimuli are held to play a key role in the development and maintenance of insomnia, but such biases have only been shown with controlled visual displays. This study investigated whether observers with insomnia symptoms allocate attention to sleep-related items in natural scenes, by recording eye movements during free-viewing of bedrooms. Participants with insomnia symptoms and normal sleepers were matched in their visual exploration of these scenes, and there was no evidence that the attention of those with insomnia symptoms was captured more quickly by sleep-related stimuli than that of normal sleepers. However, the insomnia group fixated bed regions on more trials and, once fixated on a bed, also remained there for longer. These findings indicate that sleep stimuli are particularly effective in retaining visual attention in complex natural scenes.

Chronic photoperiod disruption does not increase vulnerability to focal cerebral ischemia in young normotensive rats.

Photoperiod disruption, which occurs during shift work, is associated with changes in metabolism or physiology (e.g. hypertension and hyperglycaemia) that have the potential to adversely affect stroke outcome. We sought to investigate if photoperiod disruption affects vulnerability to stroke by determining the impact of photoperiod disruption on infarct size following permanent middle cerebral artery occlusion. Adult male Wistar rats (210-290 g) were housed singly under two different light/dark cycle conditions ( n = 12 each). Controls were maintained on a standard 12:12 light/dark cycle for nine weeks. For rats exposed to photoperiod disruption, every three days for nine weeks, the lights were switched on 6 h earlier than in the previous photoperiod. T2-weighted magnetic resonance imaging was performed at 48 h after middle cerebral artery occlusion. Disruption of photoperiod in young healthy rats for nine weeks did not alter key physiological variables that can impact on ischaemic damage, e.g. blood pressure and blood glucose immediately prior to middle cerebral artery occlusion. There was no effect of photoperiod disruption on infarct size after middle cerebral artery occlusion. We conclude that any potentially adverse effect of photoperiod disruption on stroke outcome may require additional factors such as high fat/high sugar diet or pre-existing co-morbidities.

Sleep characteristics modify the association of genetic predisposition with obesity and anthropometric measurements in 119,679 UK Biobank participants.

Background: Obesity is a multifactorial condition influenced by genetics, lifestyle, and environment.Objective: We investigated whether the association of a validated genetic profile risk score for obesity (GPRS-obesity) with body mass index (BMI) and waist circumference (WC) was modified by sleep characteristics.Design: This study included cross-sectional data from 119,859 white European adults, aged 37-73 y, participating in the UK Biobank. Interactions of GPRS-obesity and sleep characteristics (sleep duration, chronotype, day napping, and shift work) with their effects on BMI and WC were investigated. Results: ß Values are expressed as the change in BMI (in kg/m2) or WC per 1-SD increase in GPRS-obesity. The GPRS-obesity was associated with BMI (ß: 0.57; 95% CI: 0.55, 0.60; P = 6.3 × 10-207) and WC (1.21 cm; 95% CI: 1.15, 1.28 cm; P = 4.2 × 10-289). There were significant interactions of GPRS-obesity and a variety of sleep characteristics with their relation with BMI (P-interaction < 0.05). In participants who slept <7 or >9 h daily, the effect of GPRS-obesity on BMI was stronger (ß: 0.60; 95% CI: 0.54, 0.65 and ß: 0.73; 95% CI: 0.49, 0.97, respectively) than in normal-length sleepers (7-9 h; ß: 0.52; 95% CI: 0.49, 0.55). A similar pattern was observed for shift workers (ß: 0.68; 95% CI: 0.59, 0.77 compared with ß: 0.54; 95% CI: 0.51, 0.58 for non-shift workers) and for night-shift workers (ß: 0.69; 95% CI: 0.56, 0.82 compared with ß: 0.55; 95% CI: 0.51, 0.58 for non-night-shift workers), for those taking naps during the day (ß: 0.65; 95% CI: 0.52, 0.78 compared with ß: 0.51; 95% CI: 0.48, 0.55 for those who never or rarely had naps), and for those with a self-reported evening chronotype (ß: 0.72; 95% CI: 0.61, 0.82 compared with ß: 0.52; 95% CI: 0.47, 0.57 for morning chronotype). Similar findings were obtained by using WC as the outcome.Conclusion: This study shows that the association between genetic risk for obesity and phenotypic adiposity measures is exacerbated by adverse sleeping characteristics.

Perceptual impairment in face identification with poor sleep.

Previous studies have shown impaired memory for faces following restricted sleep. However, it is not known whether lack of sleep impairs performance on face identification tasks that do not rely on recognition memory, despite these tasks being more prevalent in security and forensic professions-for example, in photo-ID checks at national borders. Here we tested whether poor sleep affects accuracy on a standard test of face-matching ability that does not place demands on memory: the Glasgow Face-Matching Task (GFMT). In Experiment 1, participants who reported sleep disturbance consistent with insomnia disorder show impaired accuracy on the GFMT when compared with participants reporting normal sleep behaviour. In Experiment 2, we then used a sleep diary method to compare GFMT accuracy in a control group to participants reporting poor sleep on three consecutive nights-and again found lower accuracy scores in the short sleep group. In both experiments, reduced face-matching accuracy in those with poorer sleep was not associated with lower confidence in their decisions, carrying implications for occupational settings where identification errors made with high confidence can have serious outcomes. These results suggest that sleep-related impairments in face memory reflect difficulties in perceptual encoding of identity, and point towards metacognitive impairment in face matching following poor sleep.

How are normal sleeping controls selected? A systematic review of cross-sectional insomnia studies and a standardized method to select healthy controls for sleep research.

There appears to be some inconsistency in how normal sleepers (controls) are selected and screened for participation in research studies for comparison with insomnia patients. The purpose of the current study is to assess and compare methods of identifying normal sleepers in insomnia studies, with reference to published standards. We systematically reviewed the literature on insomnia patients, which included control subjects. The resulting 37 articles were systematically reviewed with reference to the five criteria for normal sleep specified by Edinger et al. In summary, these criteria are as follows: evidence of sleep disruption, sleep scheduling, general health, substance/medication use, and other sleep disorders. We found sleep diaries, polysomnography (PSG), and clinical screening examinations to be widely used with both control subjects and insomnia participants. However, there are differences between research groups in the precise definitions applied to the components of normal sleep. We found that none of the reviewed studies applied all of the Edinger et al. criteria, and 16% met four criteria. In general, screening is applied most rigorously at the level of a clinical disorder, whether physical, psychiatric, or sleep. While the Edinger et al. criteria seem to be applied in some form by most researchers, there is scope to improve standards and definitions in this area. Ideally, different methods such as sleep diaries and questionnaires would be used concurrently with objective measures to ensure normal sleepers are identified, and descriptive information for control subjects would be reported. Here, we have devised working criteria and methods to be used for the assessment of normal sleepers. This would help clarify the nature of the control group, in contrast to insomnia subjects and other patient groups.

Social interactions, emotion and sleep: A systematic review and research agenda.

Sleep and emotion are closely linked, however the effects of sleep on socio-emotional task performance have only recently been investigated. Sleep loss and insomnia have been found to affect emotional reactivity and social functioning, although results, taken together, are somewhat contradictory. Here we review this advancing literature, aiming to 1) systematically review the relevant literature on sleep and socio-emotional functioning, with reference to the extant literature on emotion and social interactions, 2) summarize results and outline ways in which emotion, social interactions, and sleep may interact, and 3) suggest key limitations and future directions for this field. From the reviewed literature, sleep deprivation is associated with diminished emotional expressivity and impaired emotion recognition, and this has particular relevance for social interactions. Sleep deprivation also increases emotional reactivity; results which are most apparent with neuro-imaging studies investigating amygdala activity and its prefrontal regulation. Evidence of emotional dysregulation in insomnia and poor sleep has also been reported. In general, limitations of this literature include how performance measures are linked to self-reports, and how results are linked to socio-emotional functioning. We conclude by suggesting some possible future directions for this field.

Attenuation of phase shifts to light by activity or neuropeptide Y: a time course study.

Circadian rhythms in mammals can be synchronised to photic and non-photic stimuli. Interactions between photic and behavioural stimuli were investigated during the late subjective night, 6 h after activity onset in Syrian hamsters (CT18). Light pulses of 130 lx for 15 min at this time resulted in phase advance shifts. Novel wheel exposure, for a period of 3 h, following photic stimulation was able to attenuate the phase advancing effects of light. A time delay of up to 60 min between photic and behavioural stimuli also resulted in significant attenuation of light-induced phase shifts (P<0.05). A 90-min interval between stimuli resulted in no significant attenuation. Novel wheel exposure mediates its effects via the intergeniculate leaflet, which conveys information to the SCN and utilises neuropeptide Y (NPY) as its primary neurotransmitter. Phase shifts to light pulses given at CT18 were attenuated by NPY administration. Neuropeptide Y injections up to 60 min post-light exposure significantly attenuated phase shifts by 50% on average. However a 90-min interval between light and NPY microinjection did not significantly affect light-induced phase shifts. These results confirm previous work indicating that novel wheel exposure and NPY administration can modulate light-induced phase shifts during the late night. Further, they show for the first time that the time course for this interaction is similar between wheel running and NPY. Most significantly, our work indicates that the time course in vivo in the late night is similar to that shown previously in vitro during the early night.

MDMA alters the response of the circadian clock to a photic and non-photic stimulus.

3,4-Methylenedioxymethamphetamine (MDMA or 'Ecstasy') is a widely used recreational drug that damages serotonin 5-HT neurons in animals and possibly humans. Published literature has shown that the serotonergic system is involved in photic and non-photic phase shifting of the circadian clock, which is located in the suprachiasmatic nuclei. Despite the dense innervation of the circadian system by 5-HT and the known selective neurotoxicity of MDMA, little is known about the effects of MDMA on the circadian oscillator. This study investigated whether repeated exposure to the serotonin neurotoxin MDMA alters the behavioural response of the Syrian hamster to phase shift to the serotonin 5-HT1A/7 receptor agonist 8-hydroxy-2-(di-n-propylamino) tetralin hydrobromide (8-OH-DPAT). This agonist was administered under an Aschoff Type I (CT8) and Aschoff Type II (ZT8) paradigm (5 mg/kg) and was given before and after treatment with MDMA (10, 15 and 20 mg/kg administered on successive days). Pre-treatment with MDMA significantly attenuated phase shifts to 8-OH-DPAT. We also tested the ability of the clock to phase shift to a photic stimulus after treatment with MDMA. A 15-min light pulse (mean lux 125 at CT14 or ZT14) was administered before and after treatment with MDMA. Phase shifts to a photic stimulus were significantly attenuated by pre-treatment with MDMA. Our study demonstrates that repeated exposure to MDMA may alter the ability of the circadian clock to phase shift to a photic and non-photic stimulus in the hamster. Disruption of circadian function has been linked with a variety of clinical conditions such as sleep disorders, mood, concentration difficulties and depression, consequently outlining the potential dangers of long-term ecstasy use.

The effect of 3,4-methylenedioxymethamphetamine ('Ecstasy') on serotonergic regulation of the mammalian circadian clock mechanism in rats: the role of dopamine and hyperthermia.

The recreational drug 3,4-methylenedioxymethamphetamine (MDMA) is known to be a neurotoxin for serotonergic axons ascending from the raphe nucleus including those which terminate on neurons of the suprachiasmatic nuclei (SCN) of the hypothalamus, the putative mammalian circadian clock. Since dopamine release has been implicated in the serotonergic neurotoxicity, we examined the effects of the dopamine synthesis inhibitor alpha-methyl-p-tyrosine (AMPT) and the D2 receptor antagonist haloperidol (HAL) on the long-term effect of MDMA on serotonergic regulation of the SCN neuronal firing rhythm. Co-administration of AMPT or HAL with MDMA eliminated the acute hyperthermic response but had no effect on the MDMA-induced phase shift in the firing rhythm of SCN neurons to the selective 5-HT1A receptor agonist, 8-hydroxy-2-(dipropylamino)-tetralin. It is concluded that neither dopamine metabolism nor hyperthermia account for the altered serotonergic function in the SCN produced by MDMA. Toxic free radical production following MDMA metabolism may be responsible.

The bright-nights and dim-days of the urban photoperiod: implications for circadian rhythmicity, metabolism and obesity.

Artificial light decreases the amplitude of daily rhythms in human lifestyle principally by permitting activity and food intake to occur during hours of darkness, and allowing day-time activity to occur in dim light, indoors. Endogenous circadian timing mechanisms that oscillate with a period of 24 h have evolved to ensure physiology is synchronized with the daily variations in light, food, and social cues of the environment. Artificial light affects the synchronization between these oscillators, and metabolic disruption may be one consequence of this. By dampening the amplitude of environmental timing cues and disrupting circadian rhythmicity, artificial lighting might initiate metabolic disruption and contribute to the association between global urbanization and obesity. The aim of this review is to explore the historical, physiological, and epidemiological relationships between artificial light and circadian and metabolic dysfunction.

What are you looking at? Moving toward an attentional timeline in insomnia: a novel semantic eye tracking study.

STUDY OBJECTIVES: To date, cognitive probe paradigms have been used in different guises to obtain reaction time measurements suggestive of an attention bias towards sleep in insomnia. This study adopts a methodology which is novel to sleep research to obtain a continual record of where the eyes-and therefore attention-are being allocated with regard to sleep and neutral stimuli. DESIGN: A head mounted eye tracker (Eyelink II,SR Research, Ontario, Canada) was used to monitor eye movements in respect to two words presented on a computer screen, with one word being a sleep positive, sleep negative, or neutral word above or below a second distracter pseudoword. Probability and reaction times were the outcome measures. PARTICIPANTS: Sleep group classification was determined by screening interview and PSQI (> 8 = insomnia, < 3 = good sleeper) score. MEASUREMENTS AND RESULTS: Those individuals with insomnia took longer to fixate on the target word and remained fixated for less time than the good sleep controls. Word saliency had an effect with longer first fixations on positive and negative sleep words in both sleep groups, with largest effect sizes seen with the insomnia group. CONCLUSIONS: This overall delay in those with insomnia with regard to vigilance and maintaining attention on the target words moves away from previous attention bias work showing a bias towards sleep, particularly negative, stimuli but is suggestive of a neurocognitive deficit in line with recent research.