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Background: Here, we (a) examined the trajectories of night-time sleep duration, bedtime and midpoint of night-time sleep (MPS) from infancy to adolescence, and (b) explored perinatal risk factors for persistent poor sleep health., Methods: This study used data from 12,962 participants in the Avon Longitudinal Study of Parents and Children (ALSPAC). Parent or self-reported night-time sleep duration, bedtime and wake-up time were collected from questionnaires at 6, 18 and 30 months, and at 3.5, 4-5, 5-6, 6-7, 9, 11 and 15-16 years. Child's sex, birth weight, gestational age, health and temperament, together with mother's family adversity index (FAI), age at birth, prenatal socioeconomic status and postnatal anxiety and depression, were included as risk factors for persistent poor sleep health. Latent class growth analyses were applied first to detect trajectories of night-time sleep duration, bedtime and MPS, and we then applied logistic regressions for the longitudinal associations between risk factors and persistent poor sleep health domains., Results: We obtained four trajectories for each of the three sleep domains. In particular, we identified a trajectory characterized by persistent shorter sleep, a trajectory of persistent later bedtime and a trajectory of persistent later MPS. Two risk factors were associated with the three poor sleep health domains: higher FAI with increased risk of persistent shorter sleep (OR = 1.20, 95% CI = 1.11-1.30, p < .001), persistent later bedtime (OR = 1.28, 95% CI = 1.19-1.39, p < .001) and persistent later MPS (OR = 1.30, 95% CI = 1.22-1.38, p < .001); and higher maternal socioeconomic status with reduced risk of persistent shorter sleep (OR = 0.99, 95% CI = 0.98-1.00, p = .048), persistent later bedtime (OR = 0.98, 95% CI = 0.97-0.99, p < .001) and persistent later MPS (OR = 0.99, 95% CI = 0.98-0.99, p < .001)., Conclusions: We detected trajectories of persistent poor sleep health (i.e. shorter sleep duration, later bedtime and later MPS) from infancy to adolescence, and specific perinatal risk factors linked to persistent poor sleep health domains., (© 2024 The Authors. Journal of Child Psychology and Psychiatry published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.)

Study Objectives: Twin studies have provided data about the relative weight of genetic and environmental factors on sleep variables over the last few decades. However, heritability is a non-intuitive concept and it is often misunderstood even amongst the scientific community. This study aimed to analyze: (1) understanding of the meaning of heritability of insomnia; (2) the accuracy of estimations of heritability in the general population regarding three sleep traits (sleep duration, sleep quality and insomnia); (3) perceptions of the effectiveness of different treatments for insomnia depending on how the disorder is presented (i.e. having an environmental or genetic etiology) and whether the subject's estimate of genetic influence on sleep traits impacted beliefs about the effectiveness of different treatments., Methods: Participants (N = 3658) completed a survey which included: questions about general genetic knowledge; a specific question about the meaning of heritability; estimates of heritability of three different sleep traits; and the effectiveness of different treatments for insomnia depending on how the etiology of this condition was presented., Results: Fewer than 25% of the participants selected the correct description of the heritability of insomnia. Almost half of the sample incorrectly believed that heritability refers to the chance of passing a disorder onto their children. We also found that participants provided different estimates for the effectiveness of different treatments depending on the presumed etiology of the disorder., Conclusion: Most people do not have accurate knowledge about the concept of heritability. People's assumptions about the etiology of a disorder may influence which treatments they consider most effective.

Background: Sleep problems are common in adolescence, and frequently comorbid with both anxiety and depression. Research studies have suggested a bidirectional relationship between sleep and psychopathology, which includes evidence that sleep interventions can alleviate symptoms of anxiety and depression. However, little is known about the nature of sleep problems amongst adolescents with anxiety and depression, and whether specific sleeping difficulties are involved in the longitudinal relationship between sleep, anxiety and depression., Method: The sample was derived from the Avon Longitudinal Study of Parents and Children (ALSPAC), a population-based, prospective, birth cohort study of children born in 1991-1992. Data were explored from a subset of participants who took part in a clinical assessment at age 15, on self-report sleep patterns and quality, and diagnostic outcomes of anxiety and depression (N = 5,033). Subsequent diagnostic and symptom severity data on anxiety and depression at ages 17, 21 and 24 were also examined., Results: Cross-sectional and longitudinal analyses were conducted to explore the relationship between sleep problems, anxiety and depression. Results revealed that adolescents aged 15 with depression experience difficulties with both sleep patterns and sleep quality, whereas adolescents with anxiety only reported problems with sleep quality. A range of sleep variables at age 15 predicted the severity of anxiety and depression symptoms and the diagnoses of anxiety and depressive disorders at age 17, 21 and 24 years., Conclusions: The results provide further insight into the nature of sleep problems amongst adolescents with anxiety and depression, and the prospective relationship between sleep disturbance and future psychopathology. These data suggest that targeting sleep difficulties during adolescence may have long-term mental health benefits., (© 2020 The Authors. Journal of Child Psychology and Psychiatry published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.)

'Hippocrates flagged the value of sleep for good health' was the first line of the Annual Research Review (ARR) by Gregory and Sadeh (2016) in this journal, titled Sleep problems in childhood psychiatric disorders - a review of the latest science. Where Hippocrates has been referred to as the 'Father of Medicine', Professor Avi Sadeh has been respected as a 'Father of Paediatric Sleep Medicine' by those who had the privilege to meet him or read his science. Sadly, Avi Sadeh passed away in the same year this ARR was published. What he left behind was a legacy - including his predecessors (Professor Mary Carskadon), successors and those he inspired, who could be guided by the key findings from his 2016 ARR. These include (a) greater attention to the assessment of sleep in children; (b) sleep research on a wider range of psychiatric disorders; (c) a greater focus on and examination of mechanisms underlying associations; (d) a clearer consideration of developmental questions; and (e) large-scale well-designed treatment studies., (© 2020 Association for Child and Adolescent Mental Health.)

Twin studies have shown that a substantial proportion of the variance for sleep variables is due to genetic factors. However, there is still considerable heterogeneity among research reports. Our main objectives were to: 1) Review the twin literature regarding sleep quality and duration, as well as their behavioural correlates; 2) Estimate the mean heritability of subjective sleep quality and sleep duration; 3) Assess heterogeneity among studies on these topics; and 4) Search for moderator variables. Two parallel meta-analyses were carried out for sleep quality and sleep duration. Seventeen articles were included in the meta-analysis. Mean MZ correlations were consistently higher than DZ correlations. A mean heritability of 0.31 (95% CI: 0.20, 0.41) was found for subjective sleep quality (range: 0-0.43) and 0.38 (95% CI: 0.16, 0.56) for sleep duration (range: 0-1). Heterogeneity indexes were significant for both sleep quality (I 2 = 98.77, p < .001) and sleep duration (I 2 = 99.73, p < .001). The high heterogeneity warrants further research considering possible moderators that may affect heritability., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Study Objectives: This study examines the associations between overall pre-sleep arousal, its cognitive and somatic subscales and insomnia symptoms. Furthermore, the relative contribution of genetic and environmental influences on overall pre-sleep arousal, cognitive pre-sleep arousal, somatic pre-sleep arousal, and insomnia symptoms and the association between these variables is estimated., Methods: The cross-sectional data came from G1219 (wave 5), a twin/sibling study which comprised 862 individuals (aged 22-32 years, 34% males). Pre-sleep arousal was measured using the pre-sleep arousal scale and insomnia symptoms using the insomnia symptoms questionnaire., Results: Both cognitive and somatic pre-sleep arousal were significant, independent factors associated with insomnia symptoms. Overall and somatic pre-sleep arousal showed a significant, substantial genetic influence (47% and 49% respectively) and non-shared environmental influence. For cognitive pre-sleep arousal and insomnia symptoms, non-shared environment appeared to be most important (74% and 61% respectively), and familiality was indicated. A strong, significant association of the genetic influences on overall pre-sleep arousal and insomnia symptoms was found (genetic correlation = .88). Strong, significant genetic correlations were found between cognitive pre-sleep arousal, somatic pre-sleep arousal and insomnia symptoms (genetic correlations .93 to 1). Non-shared environmental influences between these three variables were moderately, significantly correlated (non-shared environmental correlation .22 to .41)., Conclusion: The large overlap of genetic influences between pre-sleep arousal and insomnia symptoms provides novel insight into the associations between these variables. The results indicate that those with cognitive and/or somatic pre-sleep arousal may also have a genetic vulnerability to insomnia symptoms., (© Sleep Research Society 2019. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.)

Exploding head syndrome is a sensory parasomnia characterized by the perception of loud noises and/or a sense of explosion in the head that occurs when transitioning to or from sleep. Despite receiving little attention from both researchers and clinicians, studies suggest that approximately 10%-15% of individuals have episodes, with significant levels of fear occurring in a subset of cases. Using two independent samples, we examine sleep and well-being variables associated with exploding head syndrome. We focused on insomnia symptoms, life stress, anxiety and depression symptoms, and sleep experiences such as sleep paralysis as potential factors associated with exploding head syndrome. Study 1 consisted of 199 female undergraduate students. We found a lifetime prevalence of 37.19%, with 6.54% experiencing at least one episode a month. All variables were associated with exploding head syndrome in univariate analyses, but only insomnia symptoms and sleep paralysis frequency were significantly associated with exploding head syndrome in multiple logistic regression models. Study 2 was an international sample of 1683 participants (age range 18-82, 53.00% female). Lifetime prevalence was 29.59%, with monthly episodes occurring in 3.89% of participants. The same set of variables was investigated as in Study 1, with dissociative experiences during wakefulness and a larger range of sleep experiences also included. Study 2 replicated the results of Study 1. In addition, dissociative experiences during wakefulness and other sleep experiences such as nightmares were associated with exploding head syndrome in multiple logistic regression models. These studies provide valuable first insights into variables associated with exploding head syndrome.Clinical trial information: Study 1 constitutes a planned exploratory outcome of a pilot feasibility study conducted to provide information useful for designing a clinical trial: Name: STOP-pilot. URL: https://clinicaltrials.gov/ct2/show/NCT03062891?term=NCT03062891&rank=1, Registration: NCT03062891.

Study Objectives: Sleep quality is associated with health throughout the life span, which is particularly salient in middle-age and older adulthood. Sleep quality appears to be influenced by both genetic and environmental factors. However, there is still limited information about genetic influences on sleep quality in middle-aged adults, and particularly in those from certain geographical locations. We estimated the magnitude of genetic and environmental influences on sleep quality in a representative sample of middle-aged Spanish twins., Methods: The sample comprised 2150 individuals born between 1939 and 1966, who participate in the Murcia Twin Registry. To estimate the heritability of sleep quality variables, we performed univariate analyses for the global score on the Pittsburgh sleep quality index and for each of its components., Results: We found moderate but significant heritability (34%) for sleep quality. The genetic variance of the components of the Pittsburgh index ranged from 30 to 45 per cent, except for sleep efficiency for which no genetic influence could be detected. In summary, there was a moderate genetic influence on most dimensions of sleep quality in a sample of adult male and female twins. Shared environment influences were not found., Conclusions: This study adds new information regarding the underlying determinants of sleep quality by providing heritability estimates in a middle-aged population-based representative sample from a geographical location that has not been included in studies of this type previously. This could provide a reference point for future research regarding sleep research in middle-age.

Background: Sleep difficulties might be a contributory causal factor in the occurrence of mental health problems. If this is true, improving sleep should benefit psychological health. We aimed to determine whether treating insomnia leads to a reduction in paranoia and hallucinations., Methods: We did this single-blind, randomised controlled trial (OASIS) at 26 UK universities. University students with insomnia were randomly assigned (1:1) with simple randomisation to receive digital cognitive behavioural therapy (CBT) for insomnia or usual care, and the research team were masked to the treatment. Online assessments took place at weeks 0, 3, 10 (end of therapy), and 22. The primary outcome measures were for insomnia, paranoia, and hallucinatory experiences. We did intention-to-treat analyses. The trial is registered with the ISRCTN registry, number ISRCTN61272251., Findings: Between March 5, 2015, and Feb 17, 2016, we randomly assigned 3755 participants to receive digital CBT for insomnia (n=1891) or usual practice (n=1864). Compared with usual practice, the sleep intervention at 10 weeks reduced insomnia (adjusted difference 4·78, 95% CI 4·29 to 5·26, Cohen's d=1·11; p<0·0001), paranoia (-2·22, -2·98 to -1·45, Cohen's d=0·19; p<0·0001), and hallucinations (-1·58, -1·98 to -1·18, Cohen's d=0·24; p<0·0001). Insomnia was a mediator of change in paranoia and hallucinations. No adverse events were reported., Interpretation: To our knowledge, this is the largest randomised controlled trial of a psychological intervention for a mental health problem. It provides strong evidence that insomnia is a causal factor in the occurrence of psychotic experiences and other mental health problems. Whether the results generalise beyond a student population requires testing. The treatment of disrupted sleep might require a higher priority in mental health provision., Funding: Wellcome Trust., (Copyright © 2017 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Background: Feelings of loneliness are common among young adults, and are hypothesized to impair the quality of sleep. In the present study, we tested associations between loneliness and sleep quality in a nationally representative sample of young adults. Further, based on the hypothesis that sleep problems in lonely individuals are driven by increased vigilance for threat, we tested whether past exposure to violence exacerbated this association., Method: Data were drawn from the Environmental Risk (E-Risk) Longitudinal Twin Study, a birth cohort of 2232 twins born in England and Wales in 1994 and 1995. We measured loneliness using items from the UCLA Loneliness Scale, and sleep quality using the Pittsburgh Sleep Quality Index. We controlled for covariates including social isolation, psychopathology, employment status and being a parent of an infant. We examined twin differences to control for unmeasured genetic and family environment factors., Results: Feelings of loneliness were associated with worse overall sleep quality. Loneliness was associated specifically with subjective sleep quality and daytime dysfunction. These associations were robust to controls for covariates. Among monozygotic twins, within-twin pair differences in loneliness were significantly associated with within-pair differences in sleep quality, indicating an association independent of unmeasured familial influences. The association between loneliness and sleep quality was exacerbated among individuals exposed to violence victimization in adolescence or maltreatment in childhood., Conclusions: Loneliness is robustly associated with poorer sleep quality in young people, underscoring the importance of early interventions to mitigate the long-term outcomes of loneliness. Special care should be directed towards individuals who have experienced victimization.

Study Objectives: Sleep quality is associated with different aspects of psychopathology, but relatively little research has examined links between sleep quality and externalizing behaviors or callous-unemotional traits. We examined: (1) whether an association exists between sleep quality and externalizing behaviors; (2) whether anxiety mediates this association; (3) whether callous-unemotional traits are associated with sleep quality., Methods: Data from two studies were used. Study 1 involved 1556 participants of the G1219 study aged 18-27 years (62% female). Questionnaire measures assessed sleep quality, anxiety, externalizing behaviors, and callous-unemotional traits. Study 2 involved 338 participants aged 18-66 years (65% female). Questionnaires measured sleep quality, externalizing behaviors, and callous-unemotional traits. In order to assess objective sleep quality, actigraphic data were also recorded for a week from a subsample of study 2 participants (n = 43)., Results: In study 1, poorer sleep quality was associated with greater externalizing behaviors. This association was partially mediated by anxiety and moderated by levels of callous-unemotional traits. There was no significant relationship between sleep quality and callous-unemotional traits. In study 2, poorer sleep quality, as assessed via self-reported but not objective measures, was associated with higher levels of externalizing behaviors. Furthermore, in study 2, better sleep quality (indicated in both questionnaires and actigraphy measures: lower mean activity, and greater sleep efficiency) was associated with higher levels of callous-unemotional traits., Conclusions: Self-reports of poorer sleep quality are associated with externalizing behaviors, and this association is partially mediated by anxiety. Callous-unemotional traits are not associated with poor sleep and may even be related to better sleep quality. This is an exceptional finding given that poor sleep quality appears to be a characteristic of most psychopathology., (© Sleep Research Society 2017. Published by Oxford University Press [on behalf of the Sleep Research Society].)

Attention-deficit/hyperactivity disorder (ADHD) is associated with poor sleep quality, but there is more to learn about the longitudinal association and aetiology of this association. We investigated the following: (a) Is there an association between childhood ADHD and poor sleep quality in young adulthood? (b) Is this driven by the long-term effects of childhood ADHD or concurrent associations with ADHD in young adulthood? (c) To what extent do genetic and environmental influences explain the overlap between symptoms of ADHD and poor sleep quality? Participants were from the Environmental Risk Longitudinal Twin Study of 2,232 twin children born in the United Kingdom in 1994-1995. We ascertained ADHD diagnoses at ages 5, 7, 10, 12, and 18. We assessed sleep quality using the Pittsburgh Sleep Quality Index at age 18. We used regression models to examine longitudinal associations and bivariate twin modelling to test genetic and environmental influences. Children with ADHD had poorer sleep quality in young adulthood, but only if their ADHD persisted. Adults with ADHD had more sleep problems than those without ADHD, over and above psychiatric comorbidity and maternal insomnia. ADHD and sleep problems in young adulthood were associated because of genetic (55%) and nonshared environmental influences (45%). Should ADHD remit, children with ADHD do not appear to have an increased risk of later sleep problems. Good quality sleep is important for multiple areas of functioning, and a better understanding of why adults with ADHD have poorer sleep quality will further the goal of improving treatments.

Overlapping genetic influences have been implicated in diurnal preference and subjective sleep quality. Our overall aim was to examine overlapping concurrent and longitudinal genetic and environmental effects on diurnal preference and sleep quality over ~5 years. Behavioral genetic analyses were performed on data from the longitudinal British G1219 study of young adult twins and nontwin siblings. A total of 1556 twins and siblings provided data on diurnal preference (Morningness-Eveningness Questionnaire) and sleep quality (Pittsburgh Sleep Quality Index) at time 1 (mean age = 20.30 years, SD = 1.76; 62% female), and 862 participated at time 2 (mean age = 25.30 years, SD = 1.81; 66% female). Preference for eveningness was associated with poorer sleep quality at both time points (r = 0.25 [95% confidence intervals {CIs} = 0.20-0.30] and r = 0.21 [CI = 0.15-0.28]). There was substantial overlap in the genetic influences on diurnal preference and sleep quality individually, across time (genetic correlations [rAs]: 0.64 [95% CI = 0.59-0.67] and 0.48 [95% CI = 0.42-.053]). There were moderate genetic correlations between diurnal preference and sleep quality concurrently and longitudinally (rAs = 0.29-0.60). Nonshared environmental overlap was substantially smaller for all cross-phenotype associations (nonshared environmental correlations (rEs) = -0.02 to 0.08). All concurrent and longitudinal associations within and between phenotypes were largely accounted for by genetic factors (explaining between 60% and 100% of the associations). All shared environmental effects were nonsignificant. Nonshared environmental influences played a smaller role on the associations between phenotypes (explaining between -0.06% and 40% of the associations). These results suggest that to some extent, similar genes contribute to the stability of diurnal preference and sleep quality throughout young adulthood but also that different genes play a part over this relatively short time frame. While there was evidence of genetic overlap between phenotypes concurrently and longitudinally, the possible emergence of new genetic factors (or decline of previously associated factors) suggests that molecular genetic studies focusing on young adults should consider more tightly specified age groups, given that genetic effects may be time specific., (© 2016 The Author(s).)

Sleep and circadian rhythms are intrinsically linked, with several sleep traits, including sleep timing and duration, influenced by both sleep homeostasis and the circadian phase. Genetic variation in several circadian genes has been associated with diurnal preference (preference in timing of sleep), although there has been limited research on whether they are associated with other sleep measurements. We investigated whether these genetic variations were associated with diurnal preference (Morningness-Eveningness Questionnaire) and various sleep measures, including: the global Pittsburgh Sleep Quality index score; sleep duration; and sleep latency and sleep quality. We genotyped 10 polymorphisms in genes with circadian expression in participants from the G1219 sample (n = 966), a British longitudinal population sample of young adults. We conducted linear regressions using dominant, additive and recessive models of inheritance to test for associations between these polymorphisms and the sleep measures. We found a significant association between diurnal preference and a polymorphism in period homologue 3 (PER3) (P < 0.005, recessive model) and a novel nominally significant association between diurnal preference and a polymorphism in aryl hydrocarbon receptor nuclear translocator-like 2 (ARNTL2) (P < 0.05, additive model). We found that a polymorphism in guanine nucleotide binding protein beta 3 (GNβ3) was associated significantly with global sleep quality (P < 0.005, recessive model), and that a rare polymorphism in period homologue 2 (PER2) was associated significantly with both sleep duration and quality (P < 0.0005, recessive model). These findings suggest that genes with circadian expression may play a role in regulating both the circadian clock and sleep homeostasis, and highlight the importance of further studies aimed at dissecting the specific roles that circadian genes play in these two interrelated but unique behaviours., (© 2014 The Authors. Journal of Sleep Research published by John Wiley & Sons Ltd on behalf of the European Sleep Research Society.)

Sleep changes throughout the lifespan, with particularly salient alterations occurring during the first few years of life, as well as during the transition from childhood to adolescence. Such changes are partly the result of brain maturation; complex changes in the organisation of the circadian system; as well as changes in daily routine, environmental demands and responsibilities. Despite the automaticity of sleep, given that it is governed by a host of complex mechanisms, there are times when sleep becomes disturbed. Sleep disturbances in childhood are common and may stem from behavioural difficulties or abnormalities in physiological processes-and, in some cases manifest into diagnosable sleep disorders. As well as occurring exclusively, childhood sleep disturbances often co-occur with other difficulties. The purpose of this chapter is to outline the neurobiology of typical sleep/wake processes, and describe changes in sleep physiology and architecture from birth to adulthood. Furthermore, common childhood sleep disorders are described as are their associations with other traits, including all of the syndromes presented in this handbook: ASDs, ADHD, schizophrenia and emotional/behavioural difficulties. Throughout, we attempt to explain possible mechanisms underlying these disorders and their associations.

Sleep is a critical behavior shared by most higher animals. Sleep disturbances are comorbid with numerous psychiatric disorders, most notably symptoms of depression. Twin studies have suggested that genetic influences partially underlie the variation seen for numerous sleep-related traits across individuals. Recently, two Genome-Wide Association Studies (GWAS) conducted for sleep traits have revealed new candidate genes for sleep-related measures. We attempted to replicate the two most significant associations from these two studies, CACNA1C (a l-type calcium channel) with sleep latency and quality and ABCC9 (an ATP-sensitive potassium channel) with sleep duration, using the G1219 British population sample. We genotyped single-nucleotide polymorphisms (SNPs) for each of the two different sleep GWAS loci. Linear regression analyses were conducted to assess main effects of these SNPs on their corresponding sleep measures, as well as for depressive symptoms. We successfully replicated an association of a genetic variant in the CACNA1C gene (rs16929277) with sleep quality using an additive model of inheritance. A significant association of the ABCC9 gene (rs11046209) with sleep duration was seen only in a recessive models based upon a rare homozygous genotype (n = 2). There was also a significant association between a different ABCC9 gene variant (rs11046205) and depressive symptoms. These findings add further support for the involvement of calcium channels in the mechanisms regulating sleep function and suggest a possible role of the ABCC9 gene in depression., (Copyright © 2013 Wiley Periodicals, Inc.)

Over the past 50 years, well over 100 twin studies have focussed on understanding factors contributing to variability in normal sleep-wake characteristics and sleep disturbances. Whilst we have gained a great deal from these studies, there is still much to be learnt. Twin studies can be used in multiple ways to answer questions beyond simply estimating heritability. This paper provides a comprehensive review of some of the most important findings from twin studies relating to sleep to date, with a focus on studies investigating genetic and environmental influences contributing to i) objective and subjective measures of normal sleep characteristics (e.g., sleep stage organisation, sleep quality); as well as sleep disturbances and disorders such as dyssomnias (e.g., insomnia, narcolepsy) and parasomnias (e.g., sleepwalking, bruxism); ii) the persistence of sleep problems from childhood to adulthood, and the possibility that the aetiological influences on sleep change with age; iii) the associations between sleep disturbances, emotional, behavioural and health-related problems; and iv) processes of gene-environment correlation and interaction. We highlight avenues for further research, emphasising the need to further consider the aetiology of longitudinal associations between sleep disturbances and psychopathology; the genetic and environmental overlap between sleep and numerous phenotypes; and processes of gene-environment interplay and epigenetics., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Research has consistently demonstrated that environmental influences are important for explaining the variability in sleep quality observed in the general population. Although there is substantial evidence assessing associations between sleep quality and a host of environmental variables, it is possible that their effects are mediated by genetic influence. A monozygotic twin differences design was used to assess the specific contribution of nonshared environmental influences on sleep quality, whilst controlling for genetic and shared environmental effects in a sample of 380 monozygotic twins (mean age 19.8 years, SD = 1.26, range = 18-22 years). Participants completed the Pittsburgh Sleep Quality Index and questionnaires assessing several candidate "environmental" measures. When controlling for genetic and shared environmental effects, within monozygotic twin-pair differences in sleep quality were associated with within monozygotic twin-pair differences in general health for males (β = 1.56, p < 0.001) and relationship satisfaction for females (β = 1.01, p < 0.05). For the remaining environmental measures the results suggest that these seemingly "environmental" influences are actually in part dependent on genetics and/or the shared environment. These findings give insight into how specific environments affect sleep and the possible mechanisms behind these associations.

Objectives: Little is known about the aetiology of the links between sleep disturbance and anxiety and depression symptoms. The aim of this study was to estimate genetic and environmental influences on these associations., Methods: Questionnaires were completed by 1556 young adults from twin and sibling pairs (61.5% female)., Results: Sleep disturbance was moderately correlated with symptoms of anxiety (r=.39) and depression (r=.50). There was substantial overlap between genes influencing sleep disturbance and those influencing symptoms of anxiety (rA=.58) and depression (rA=.68). Overall, the associations between sleep and symptoms of both anxiety and depression were mainly due to genes (explaining 74% and 58% of the covariances respectively), with the remainder due to nonshared environmental factors., Conclusions: Moderate phenotypic and genetic correlations between the phenotypes support the view that sleep disturbance is related to the presence of various psychiatric difficulties, but also warrants independent consideration and treatment., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Research investigating associations between specific genes and individual differences with regards to the quality and timing of sleep has primarily focussed on serotonin-related and clock genes. However, there are only a few studies of this type and most of those to date have not considered the possibility of gene-environment interaction. Here, we describe associations between sleep quality and diurnal preference and three functional polymorphisms: 5HTTLPR, PERIOD3, and CLOCK 3111. Furthermore, we assessed whether associations between genotypes and sleep phenotypes were moderated by negative life events-a test of gene-environment interaction. DNA from buccal swabs was collected from 947 individuals [mean age = 20.3 years (SD = 1.77), age range = 18-27 years; 61.8% female] and genotyped for the three polymorphisms. Participants completed the Pittsburgh Sleep Quality Index and the Morningness-Eveningness Questionnaire. There was a significant main effect of 5HTTLPR on sleep quality, indicating that "long-long" homozygotes experienced significantly poorer sleep quality (mean = 6.35, SD = 3.36) than carriers of at least one "short" allele (mean = 5.67, SD = 2.96; β = -0.34, P = 0.005). There were no main effects of 5HTTLPR on diurnal preference; no main effects of PERIOD3 or CLOCK on sleep quality or diurnal preference; and no significant interactions with negative life events. The main effect of the "long" 5HTTLPR allele contradicts previous research, suggesting that perhaps the effects of this gene are heterogeneous in different populations. Failure to replicate previous research in relation to PERIOD3 and CLOCK concurs with previous research suggesting that the effects of these genes are small and may be related to population composition., (Copyright © 2011 Wiley-Liss, Inc.)

Background: Certain aspects of sleep co-occur with externalizing behaviours in youth, yet little is known about these associations in adults. The present study: (1) examines the associations between diurnal preference (morningness versus eveningness), sleep quality and externalizing behaviours; (2) explores the extent to which genetic and environmental influences are shared between or are unique to these phenotypes; (3) examines the extent to which genetic and environmental influences account for these associations. method: Questionnaires assessing diurnal preference, sleep quality and externalizing behaviours were completed by 1556 young adult twins and siblings., Results: A preference for eveningness and poor sleep quality were associated with greater externalizing symptoms [r=0.28 (95% CI 0.23-0.33) and 0.34 (95% CI 0.28-0.39), respectively]. A total of 18% of the genetic influences on externalizing behaviours were shared with diurnal preference and sleep quality and an additional 14% were shared with sleep quality alone. Non-shared environmental influences common to the phenotypes were small (2%). The association between diurnal preference and externalizing behaviours was mostly explained by genetic influences [additive genetic influence (A)=80% (95% CI 0.56-1.01)], as was the association between sleep quality and externalizing behaviours [A=81% (95% CI 0.62-0.99)]. Non-shared environmental (E) influences accounted for the remaining variance for both associations [E=20% (95% CI -0.01 to 0.44) and 19% (95% CI 0.01-0.38), respectively]., Conclusions: A preference for eveningness and poor sleep quality are moderately associated with externalizing behaviours in young adults. There is a moderate amount of shared genetic influences between the phenotypes and genetic influences account for a large proportion of the association between sleep and externalizing behaviours. Further research could focus on identifying specific genetic polymorphisms common to both sleep and externalizing behaviours.

Objectives: Negative life events are associated with sleep disturbances. Further understanding of these associations is beneficial as sleep disturbances are common. We assessed the association between two commonly distinguished types of negative life events (dependent vs. independent) and sleep quality. The extent to which genetic and environmental influences explained the association between dependent negative life events and sleep quality was also assessed. Finally, we examined the presence of gene-environment interaction by assessing whether genetic liability to sleep disturbance varied as a function of dependent negative life events., Methods: Structural equation modelling was used to perform the statistical analyses on questionnaire data collected from 1556 twin and non-twin siblings., Results: Poor sleep quality was more strongly associated with dependent as compared to independent negative life events (r=.34 and .15, respectively). There was substantial overlap in the genetic influences on the association between dependent negative life events and poor sleep quality (rA=.62([.43-.81])), suggesting gene-environment correlation. Environmental overlap was small (rE=.16([.04-.28])). Genetic influences accounted for a large proportion of the association (70%([.47-.92])) with the remaining co-variance due to non-shared environment (30%([.08-.53])). Genetic liability to sleep quality was not moderated by dependent negative life events., Conclusions: Genetic and environmental effects on sleep are not necessarily distinct but to some extent work in concert. This should be considered in future studies assessing the genetic and environmental effects on sleep., (Copyright © 2011 Elsevier B.V. All rights reserved.)

Study Objectives: To examine the extent to which genetic and environmental factors influence components of sleep quality; the degree to which these components co-occur; and genetic and environmental influences on this co-occurrence., Design: Twin study., Setting: Population based twin registry across the U.K., Patients or Participants: Four hundred twenty monozygotic twins, 773 dizygotic twins, and 363 siblings (mode age = 20 years; range 18 to 27 years)., Interventions: N/A., Measurements and Results: The Pittsburgh Sleep Quality Index (PSQI) assessed 7 components of sleep quality which overlap to varying degrees. Genetic influence on individual components ranged from 0% to 47%. The remaining source of variance was non-shared environment, except for "sleep duration", for which shared environmental influences were important. Phenotypic correlations between components ranged from 0.22 to 0.61. Bivariate analyses indicated substantial overlap between genes influencing phenotypes (10 of 15 correlations were > or = 0.69); and in general, genetic influence accounted for roughly half the association (> 40% in 9 of 15 correlations). Non-shared environmental influences were in general less correlated across variables (11 of 15 were < 0.4), but owing to their greater influence on each variable, still accounted for roughly half of each association (> or = 40% in 12 of 15 correlations)., Conclusions: Genetic and non-shared environmental factors are most important in explaining individual differences with regards to different components of sleep quality, although shared environment may influence sleep duration. The pattern of overlap in the genetic and environmental influences accounting for the associations between components of sleep quality is consistent with that seen in other areas of developmental psychopathology of general genes and specific non-shared environmental influences.

The aims of this study were to examine the genetic and environmental influences on diurnal preference and sleep quality, the association between these phenotypes, the genetic and environmental influences on this association, and the magnitude of overlap between these influences. Using a twin design, data on diurnal preference (measured by the Morningness-Eveningness Questionnaire) and sleep quality (measured by the Pittsburgh Sleep Quality Index) were collected from 420 monozygotic twins, 773 dizygotic twins, and 329 siblings (mode age = 20 yrs, range = 18-27 yrs) from a population-based twin registry across the UK. Univariate analyses indicated that dominance genetic influence accounted for 52% and non-shared environment 48% of variance in diurnal preference. For sleep quality, additive genetic influence explained 43% and non-shared environment 57% of the variance. The bivariate analysis indicated a significant association between greater eveningness preference and poorer sleep quality (r = .27). There was substantial overlap in the additive genetic influences on both phenotypes (rA = .57), and overlap in the dominance genetic influences common to both phenotypes was almost absolute (rD = .99). Overlap in non-shared environment was much smaller (rE = .02). Additive genetic influence accounted for 2% of the association, dominance genetic influence accounted for 94%, and non-shared environmental influences accounted for the remaining 4%. The substantial overlap in genetic influence between these phenotypes indicates that similar genes are important for diurnal preference and sleep quality. Therefore, those genes already known to influence one phenotype may be possible candidates to explore with regards to the other phenotype.