Shorter night-time sleep duration and later sleep timing from infancy to adolescence.

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.

Impact of anxiety and depression across childhood and adolescence on adverse outcomes in young adulthood: a UK birth cohort study.

BACKGROUND: Little is still known about the long-term impact of childhood and adolescent persistent depression and anxiety in adulthood. AIMS: To investigate the impact of persistent anxiety, depression, and comorbid anxiety and depression across childhood and adolescence on the development of multiple adverse outcomes in young adulthood. METHOD: This study used data from 8122 participants in the Avon Longitudinal Study of Parents and Children cohort. The Development and Well-Being Assessment (DAWBA) examined child anxiety and depression symptomatology. The DAWBA generalised anxiety and mood subscales at 8, 10 and 13 years were selected, and a measure of comorbid anxiety and depression symptoms was created at each time point. Further, several mental and physical health, substance misuse and education/employment problems were assessed at 24 years. Latent class growth analyses were used to detect trajectories of anxiety, depression and comorbid anxiety and depression; and logistic regression to examine how persistent anxiety, depression or both were associated with adverse outcomes at 24 years. RESULTS: All three classes with persistent anxiety, depression or both were significantly associated with presenting with any mental health problems and any education/employment problem. Persistent high levels of depression and high levels of comorbid anxiety and depression, but not persistent high anxiety, were significantly associated with any physical health problem. High levels of comorbid anxiety and depression was the only DAWBA domain significantly associated with substance misuse; and overall, this was the domain that exerted the greatest negative impact, as it presented the highest odd ratio values. CONCLUSIONS: Children and adolescents with comorbid anxiety and depression are at the highest risk for having more adverse outcomes at 24 years.

Early neutrophil trajectory following clozapine may predict clozapine response - Results from an observational study using electronic health records.

BACKGROUND: Clozapine has unique effectiveness in treatment-resistant schizophrenia and is known to cause immunological side-effects. A transient spike in neutrophils commonly occurs in the first weeks of clozapine therapy. There is contradictory evidence in the literature as to whether neutrophil changes with clozapine are linked to treatment response. AIMS: The current study aims to further examine the neutrophil changes in response to clozapine and explore any association between neutrophil trajectory and treatment response. METHODS: A retrospective cohort study of patients undergoing their first treatment with clozapine and continuing for at least 2 years identified 425 patients (69% male/31% female). Neutrophil counts at baseline, 3 weeks and 1 month were obtained predominantly by linkage with data from the clozapine monitoring service. Clinical Global Impression- Severity (CGI-S) was rated from case notes at the time of clozapine initiation and at 2 years. Latent class growth analysis (LCGA) was performed to define distinct trajectories of neutrophil changes during the first month of treatment. Logistic regression was then conducted to investigate for association between the trajectory of neutrophil count changes in month 1 and clinical response at 2 years as well as between baseline neutrophil count and response. RESULTS: Of the original cohort, 397 (93%) patients had useable neutrophil data during the first 6 weeks of clozapine treatment. LCGA revealed significant differences in neutrophil trajectories with a three-class model being the most parsimonious. The classes had similar trajectory profiles but differed primarily on overall neutrophil count: with low, high-normal and high neutrophil classes, comprising 52%, 40% and 8% of the sample respectively. Membership of the high-normal group was associated with significantly increased odds of a positive response to clozapine, as compared to the low neutrophil group [Odds ratio (OR) = 2.10, p-value = 0.002; 95% confidence interval (95% CI) = 1.31-3.36]. Baseline neutrophil count was a predictor of response to clozapine at 2 years, with counts of ≥5 × 109/l significantly associated with positive response (OR = 1.60, p-value = 0.03; 95% CI = 1.03-2.49). CONCLUSIONS: Our data are consistent with the hypothesis that patients with low-level inflammation, reflected in a high-normal neutrophil count, are more likely to respond to clozapine, raising the possibility that clozapine exerts its superior efficacy via immune mechanisms.

The role of inflammation in the prospective associations between early childhood sleep problems and ADHD at 10 years: findings from a UK birth cohort study.

BACKGROUND: Several underlying mechanisms potentially account for the link between sleep and attention deficit and hyperactivity disorder (ADHD), including inflammation. However, studies so far have been cross sectional. We investigate (a) the association between early childhood sleep and probable ADHD diagnosis in childhood and (b) whether childhood circulating inflammatory markers mediate these prospective associations. METHODS: Data from the Avon Longitudinal Study of Parents and Children were available for 7,658 10-year-old children. Parent-reported sleep duration, night awakening frequency and regular sleep routines were collected at 3.5 years. The Development and Wellbeing Assessment was administered to capture children with clinically relevant ADHD symptoms, or probable ADHD diagnosis. Blood samples were collected at 9 years, from which two inflammatory markers were obtained [interleukin-6 (IL-6) and C-reactive protein (CRP)]. Logistic regression analyses were applied to investigate the associations between sleep variables at 3.5 years and probable ADHD diagnosis at 10 years. Further, path analysis was applied to examine the potential mediating role of inflammation at 9 years (as measured by CRP and IL-6) in the associations between early sleep and ADHD at 10 years. RESULTS: Less regular sleep routines (OR = 0.51, 95% CI = 0.28-0.93, p = .029), shorter nighttime sleep (OR = 0.70, 95% CI = 0.56-0.89, p = .004) and higher night awakening frequency (OR = 1.27, 95% CI = 1.06-1.52, p = .009) at 3.5 years were associated with higher odds of ADHD at 10 years. Further, IL-6 at 9 years, but not CRP, mediated the association between irregular sleep routines and ADHD (bias-corrected estimate, -0.002; p = .005) and between night awakening and ADHD (bias-corrected estimate, 0.002; p = .003). CONCLUSIONS: Several sleep problems in early childhood constitute a risk factor for probable ADHD diagnosis at 10 years. Further, these associations are partially mediated by IL-6 at 9 years. These results open a new research vista to the pathophysiology of ADHD and highlight sleep and inflammation as potential preventative targets for ADHD.

Maternal postnatal depression and anxiety and the risk for mental health disorders in adolescent offspring: Findings from the Avon Longitudinal Study of Parents and Children cohort.

OBJECTIVE: The impacts of postnatal psychiatric disorders on different types of mental health problems in offspring are unclear. We investigated the prospective associations of maternal postnatal depression, and anxiety, with offspring depression, anxiety, psychotic-like experiences and Borderline Personality Disorder symptoms, in adolescence, and examined whether these were independent of each other. METHODS: Data were obtained from the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort. Maternal postnatal depression and anxiety at 8 weeks were measured using the Edinburgh Postnatal Depression Scale and Crown-Crisp Index, respectively. Offspring mental health outcomes were measured at 10-13 years old, using a variety of questionnaire-based and interview assessments. Logistic regression analyses were used to assess the associations between maternal postnatal risk factors and offspring mental health, and path analysis was used to investigate the pathways of maternal postnatal factors to adolescent offspring outcomes. RESULTS: Data were available for 14,054 mothers with information reported on postnatal depression and 13,892 on postnatal anxiety. Logistic regression analyses found significant associations between maternal postnatal depression and offspring anxiety at 10 years old (odds ratio = 1.039, 95% confidence interval = [1.005, 1.073], p = 0.022) and between maternal postnatal anxiety and offspring psychotic experiences at 12/13 years old (odds ratio = 1.042, 95% confidence interval = [1.008, 1.077], p = 0.016). These significant associations remained after applying path analyses, when we controlled for potential offspring psychopathological overlay. CONCLUSION: These findings suggest that mothers with postnatal depression are more likely to have offspring with anxiety at 10 years old, and that mothers with postnatal anxiety are more likely to have offspring with psychotic experiences at 12/13 years old. Our findings suggest specific pathways in the association between postnatal anxiety/depression and offspring mental health and contribute to the importance of identifying mothers and their offspring with increased vulnerability to adverse outcomes resulting from postnatal mental health disorders.

Prenatal and Postnatal Predictive Factors for Children's Inattentive and Hyperactive Symptoms at 5 Years of Age: The Role of Early Family-related Factors.

We examined several parent-reported prenatal and postnatal factors as potential risk factors for attention-deficit and hyperactivity disorder (ADHD) symptomatology in 5-year-old children. Our study is based on the CHILD-SLEEP birth cohort. Several parental questionnaires were collected prenatally (32nd pregnancy week) and postnatally (i.e. child aged 3, 8, and 24 months and at 5 years). At 5 years of age, ADHD symptoms were assessed using questionnaires. Our main results showed that being a boy, parental depressive symptoms, more negative family atmosphere or a child's shorter sleep duration, and maternal authoritarian parenting style predicted inattentive/hyperactive symptoms. Maternal and paternal authoritative parenting style predicted less inattentive/hyperactive symptoms. Children with several risk factors together had the highest risk for inattentive/hyperactive symptoms. Our findings emphasise the need for early screening and treatment of parental mental health, and early evidence-based targeted parental support, to enable early intervention in those children at a risk of developing ADHD.

Development of sleep-wake rhythms during the first year of age.

Circadian rhythms refer to biological rhythms that have an endogenous period length of approximately 24 hr. However, not much is known about the variance in the development of the sleep-wake rhythm. The study objectives were (a) to describe the normative variation in the development of a sleep-wake rhythm in infancy, (b) to assess whether slower development is related to sleep quality and (c) to evaluate factors that are related to the slower development of a sleep-wake rhythm. The study is based on a representative birth cohort. Questionnaires at the ages of 3 (n = 1,427) and 8 months (n = 1,302) and actigraph measurement at 8 months (n = 372) were available. Infants with significant developmental delays (n = 11) were excluded. The results are based on statistical testing and multivariate modelling. We found that the average percentage of daytime sleep was 36.3% (standard deviation [SD], 8.5%) at 3 months and 25.6% (SD, 6.6%) at 8 months. At both time-points, infants with slower sleep-wake rhythm development slept more hours per day, had a later sleep-wake rhythm, more difficulties in settling to sleep and longer sleep-onset latency; they also spent a longer time awake during the night. According to actigraph registrations, we found that the infants with slow development of a sleep-wake rhythm slept less and had a later start and end to night-time sleep than the other infants. Infants' sleep-wake rhythm development is highly variable and is related to parent-reported and objectively measured sleep quality and quantity. Interventions to improve the sleep-wake rhythm might improve sleep quality in these infants.

Variation near MTNR1A associates with early development and interacts with seasons.

Melatonin is a circadian regulatory hormone with neuroprotective properties. We have previously demonstrated the association of the genetic variant rs12506228 near the melatonin receptor 1A gene (MTNR1A) with intolerance to shift-work. Furthermore, this variant has been connected to Alzheimer's disease. Because of the previously suggested role of melatonin signalling in foetal neurocognitive and sleep development, we studied here the association of rs12506228 with early development. The study sample comprised 8-month-old infants from the Finnish CHILD-SLEEP birth cohort (n = 1,301). Parental questionnaires assessed socioemotional, communication and motor development, as well as sleep length and night awakenings. The A allele of rs12506228 showed an association with slower socioemotional (p = .025) and communication (p = .0098) development, but no direct association with sleep. However, the association of the Finnish seasons with infant sleep length interacted with rs12506228. Taken together, rs12506228 near MTNR1A, which has been previously linked to adult and elderly traits, is shown here to associate with slower early cognitive development. In addition, these results suggest that the darker seasons associate with longer infant sleep time, but only in the absence of the rs12506228 AA genotype. Because the risk allele has been connected to fewer brain MT1 melatonin receptors, these associations may reflect the influence of decreased melatonin signalling in early development.

Short Sleep Duration and Later Overweight in Infants.

OBJECTIVE: To provide further knowledge about the longitudinal association between sleep duration and overweight in infants. STUDY DESIGN: The data for this study are from the CHILD-SLEEP birth cohort (n = 1679). The sleep data are based on parent-reported total sleep duration collected at 3, 8, 18, and 24 months. For a subgroup of 8-month old participants (n = 350), an actigraph recording was also made. Growth data were derived from the child health clinic records. A logistic regression model was used to study the association between sleep duration and later weight development. RESULTS: Shorter sleep duration in 3-month-old infants was cross-sectionally associated with lower weight-for-length/height (all P values ≤ .026) and body mass index (all P values ≤ .038). Moreover, short sleep duration at the age of 3 months was associated with greater weight-for-length/height z score at the age of 24 months (aOR 1.56; 95% CI 1.02-2.38) as well as with a predisposition to gain excess weight between 3 and 24 months of age (aOR 2.61; 95% CI 1.75-3.91). No significant associations were found between sleep duration at 8, 18, or 24 months and concurrent or later weight status. Actigraph-measured short night-time sleep duration at the age of 8 months was associated with greater weight-for-length at the age of 24 months (aOR 1.51; 95% CI 1.02-2.23). CONCLUSIONS: Short total sleep duration at the age of 3 months and short night-time sleep duration at the age of 8 months are associated with the risk of gaining excess weight at 24 months of age.

The effects of seasonal affective disorder and alcohol abuse on sleep and snoring functions in a population-based study in Finland.

Seasonal affective disorder (SAD) is a recurrent depressive disorder with a seasonal pattern. In addition to some specific symptoms such as sad mood, low energy or carbohydrate craving, this mood disorder is also characterized by the presence of sleeping problems and alcohol disorders. Interestingly, there is a strong link between alcohol use and sleeping deficits. Although previous studies have focused extensively on the sleep patterns in SAD patients and patients with alcohol use disorder (AUD), no research has yet been conducted on subjects with comorbid SAD and AUD. The aim of this study was to examine the differences in sleep functioning between subjects with SAD, AUD and SAD+AUD. A total of 4554 Finnish subjects from the population-based Health 2011 survey were interviewed, and of these 2430 individuals completed all the questionnaires. We selected those participants who fulfilled the criteria for SAD (n = 298), AUD (n = 359), SAD+AUD (n = 69), controls 1 (no current alcohol use, n = 226) and controls 2 (current alcohol use but not AUD, n = 1445). Controls with a history of alcohol abuse were excluded (n = 33). All the participants completed the EuroQoL five-dimensions questionnaire (EQ-5), the Seasonal Pattern Assessment Questionnaire (SPAQ), the Alcohol Use Disorders Identification Test (AUDIT) and several questions about sleeping, based on the Basic Nordic Sleep Questionnaire (BNSQ). Our results showed that those subjects with SAD+AUD reported the highest levels of subjective sleeping problems compared to controls, SAD and AUD. These findings suggest the relevance of examining the comorbidity of SAD and AUD when studying sleep functioning in these groups of patients.

The effects of maternal risk factors during pregnancy on the onset of sleep difficulties in infants at 3 months old.

Sleep problems in young children are among the most common concerns reported to paediatricians. Sleep is thought to have important regulatory functions, and sleep difficulties in early childhood are linked to several psychosocial and physiological problems. Moreover, several prenatal factors have been found to influence infants' sleep. Among them, most of the studies have been focused on maternal prenatal depression and/or anxiety as potential risk factors for sleep problems in childhood, whereas other relevant psychological factors during pregnancy have not received as much attention. Therefore, we aimed to examine the effect of several psychiatric maternal risk factors during pregnancy (i.e. symptoms of anxiety, depression, insomnia, alcohol use, seasonality, attention deficit and hyperactivity disorder and/or stressful life events) on the onset of some sleep problems related to sleep quality and sleep practices in 3-month-old infants. We examined 1,221 cases from a population-based birth cohort, with subjective measures during pregnancy in mothers, and at 3 months after birth in the infants. The findings showed that all the maternal risk factors during pregnancy, except for symptoms of alcoholism and sleepiness, were related to sleep difficulties in infants. Interestingly, attention deficit and hyperactivity disorder symptomatology in mothers during pregnancy was the only variable that predicted more than two sleeping difficulties (i.e. long sleep-onset latency, co-sleeping with parents and irregular sleeping routines) at 3 months old. Our results highlight the relevance of maternal risk factors during pregnancy, and not only prenatal depression and/or anxiety, as variables to be considered when examining sleep difficulties in infants.

Elevated midline-parietal gamma band noise power in schizophrenia but not in bipolar patients.

Gamma oscillations are key in coordinating brain activity and seem to be altered in schizophrenia. In previous work, we studied the spatial distribution of a noise power measure (scalp-recorded electroencephalographic activity unlocked to stimuli) and found higher magnitudes in the gamma band related to symptoms and cognition in schizophrenia. In the current study, we sought to replicate those findings and to study its specificity for schizophrenia in a completely independent sample. A principal component analysis (PCA) was used to determine the factorial structure of gamma noise power acquired with an electroencephalographic recording during an odd-ball P300 paradigm in the 250- to 550-ms window in 70 patients with schizophrenia (16 patients with first episode), 45 bipolar patients and 65 healthy controls. Clinical and cognitive correlates of the resulting factors were also assessed. Three factors arose from the PCA. The first displayed a midline-parietal distribution (roughly corresponding to the default mode network), the second was centro-temporal and the third anterior-frontal. Schizophrenia but not bipolar patients showed higher gamma noise power loadings in the first factor in comparison with controls. Scores for this factor were significantly and directly associated with positive and total symptoms in patients and inversely associated with global cognition in all participants. The results of this study replicate those of our previous publication and suggest an elevated midline-parietal gamma noise power specific to schizophrenia. The gamma noise power measure seems to be a useful tool for studying background oscillatory activity during performance of cognitive tasks.

Sensory Gating Deficits in First-Episode Psychosis: Evidence From Neurophysiology, Psychophysiology, and Neuropsychology.

Sensory gating deficits are commonly found in patients with schizophrenia. However, there is still scarce research on this issue. Thirty-eight patients with first-episode psychosis (FEP) were compared to thirty-eight controls. A condition-test paradigm of event-related potentials (ERP), prepulse inhibition (PPI), and some specific tasks of the MATRICS Consensus Cognitive Battery (MCCB) were used (i.e., TMT, BACS-SC, and Fluency for processing speed and CPT-IP for attention and vigilance). The ERP components measured were P50, N1, and P2. The PPI intervals examined were 30, 60, and 120 msec. Regarding the MCCB, processing speed and attention/vigilance cognitive domains were selected. FEP patients showed significant deficits in N1 and P2 components, at 30 and 60 PPI levels and in all the MCCB subtests selected. We obtained significant relationships in N1 with PPI-60, and with one MCCB subtest for processing speed. In addition, this same subtest showed significant association with P2. Therefore, sensory gating functioning is widely impaired since the very early stages of schizophrenia.

Cannabis abuse effects on prepulse inhibition in patients with first episode psychosis in schizophrenia.

Deficits in prepulse inhibition (PPI) and cannabis abuse are consistently found in schizophrenia. The authors studied PPI deficits in first episode psychosis (FEP) with schizophrenia and cannabis abuse influence. Thirty-five patients with FEP and 22 control subjects were examined. Patients were divided into cannabis use disorder (CUD) (N=21) and non-CUD (N=14). Startle measures were as follows: PPI at 30, 60, and 120 msec. Patients with CUD and patients without CUD showed lower PPI at 30 msec than control subjects. At 60 msec, patients with CUD obtained higher %PPI than patients without CUD, and patients without CUD obtained lower levels than control subjects. These findings show that cannabis abuse may improve PPI in patients with FEP at some levels.

Role of Inflammation in Short Sleep Duration Across Childhood and Psychosis in Young Adulthood.

Importance: Short sleep duration over a prolonged period in childhood could have a detrimental impact on long-term mental health, including the development of psychosis. Further, potential underlying mechanisms of these associations remain unknown. Objective: To examine the association between persistent shorter nighttime sleep duration throughout childhood with psychotic experiences (PEs) and/or psychotic disorder (PD) at age 24 years and whether inflammatory markers (C-reactive protein [CRP] and interleukin 6 [IL-6]) potentially mediate any association. Design, Setting, and Participants: This cohort study used data from the Avon Longitudinal Study of Parents and Children. Data analysis was conducted from January 30 to August 1, 2023. Exposures: Nighttime sleep duration was collected at 6, 18, and 30 months and at 3.5, 4 to 5, 5 to 6, and 6 to 7 years. Main Outcomes and Measures: PEs and PD were assessed at age 24 years from the Psychosislike Symptoms Interview. CRP level at ages 9 and 15 years and IL-6 level at 9 years were used as mediators. Latent class growth analyses (LCGAs) were applied to detect trajectories of nighttime sleep duration, and logistic regressions were applied for the longitudinal associations between trajectories of nighttime sleep duration and psychotic outcomes at 24 years. Path analyses were applied to test CRP and IL-6 as potential mediators. Results: Data were available on 12 394 children (6254 female [50.5%]) for the LCGA and on 3962 young adults (2429 female [61.3%]) for the logistic regression and path analyses. The LCGA identified a group of individuals with persistent shorter nighttime sleep duration across childhood. These individuals were more likely to develop PD (odds ratio [OR], 2.50; 95% CI, 1.51-4.15; P < .001) and PEs (OR, 3.64; 95% CI, 2.23-5.95; P < .001) at age 24 years. Increased levels of IL-6 at 9 years, but not CRP at 9 or 15 years, partially mediated the associations between persistent shorter sleep duration and PD (bias-corrected estimate = 0.003; 95% CI, 0.002-0.005; P = .007) and PEs (bias-corrected estimate = 0.002; 95% CI, 0-0.003; P = .03) in young adulthood. Conclusions and Relevance: Findings of this cohort study highlight the necessity of addressing short sleep duration in children, as persistence of this sleep problem was associated with subsequent psychosis. This study also provides preliminary evidence for future targeted interventions in children addressing both sleep and inflammatory responses.

Sleep and Mental Health Problems in Children and Adolescents.

Previous reviews have described the links between sleep and mental health extensively. In this narrative review, we focus on literature published during the last decade investigating the links between sleep and mental health difficulties in childhood and adolescence. More specifically, we focus on the mental health disorders listed in the most recent edition of the Diagnostic and Statistical Manual of Mental Disorders. We also discuss possible mechanisms underlying these associations. The review ends with a discussion of possible future lines of enquiry.

Rates and associations of relapse over 5 years of 2649 people with bipolar disorder: a retrospective UK cohort study.

BACKGROUND: Evidence regarding the rate of relapse in people with bipolar disorder (BD), particularly from the UK, is lacking. This study aimed to evaluate the rate and associations of clinician-defined relapse over 5 years in a large sample of BD patients receiving routine care from a UK mental health service. METHOD: We utilised de-identified electronic health records to sample people with BD at baseline. Relapse was defined as either hospitalisation, or a referral to acute mental health crisis services, between June 2014 and June 2019. We calculated the 5-year rate of relapse and examined the sociodemographic and clinical factors that were independently associated with relapse status and the number of relapses, over the 5-year period. RESULTS: Of 2649 patients diagnosed with BD and receiving care from secondary mental health services, 25.5% (n = 676) experienced at least one relapse over 5 years. Of the 676 people who relapsed, 60.9% experienced one relapse, with the remainder experiencing multiple relapses. 7.2% of the baseline sample had died during the 5-year follow-up. Significant factors associated with experiencing any relapse, after adjustment for relevant covariates, were history of self-harm/suicidality (OR 2.17, CI 1.15-4.10, p = 0.02), comorbidity (OR 2.59, CI 1.35-4.97, p = 0.004) and psychotic symptoms (OR 3.66, CI 1.89-7.08, p < 0.001). Factors associated with the number of relapses over 5 years, after adjustment for covariates, were self-harm/suicidality (ß = 0.69, CI 0.21-1.17, p = 0.005), history of trauma (ß = 0.51, CI = 0.07-0.95, p = 0.03), psychotic symptoms (ß = 1.05, CI 0.55-1.56, p < 0.001), comorbidity (ß = 0.52, CI 0.07-1.03, p = 0.047) and ethnicity (ß = - 0.44, CI - 0.87 to - 0.003, p = 0.048). CONCLUSIONS: Around 1 in 4 people with BD in a large sample of people with BD receiving secondary mental health services in the UK relapsed over a 5-year period. Interventions targeting the impacts of trauma, suicidality, presence of psychotic symptoms and comorbidity could help to prevent relapse in people with BD and should be considered in relapse prevention plans.

Genetic background to attention deficit and hyperactivity disorder and attention deficit and hyperactivity disorder symptoms at the age of 5 years: the role of sleep duration.

STUDY OBJECTIVES: We studied the associations between polygenic risk score (PRS) for attention deficit and hyperactivity disorder (ADHD) and (1) ADHD symptoms in 5-year-old children, (2) sleep duration throughout childhood, and (3) the interaction between PRS for ADHD and short sleep duration relative to ADHD symptoms at 5 years. METHODS: This study is based on the population-based CHILD-SLEEP birth cohort (N = 1420 children). PRS was used to quantitate the genetic risk for ADHD. Parent-reported ADHD symptoms at 5 years were obtained from 714 children, using the Strengths and Difficulties Questionnaire (SDQ) and the Five-to-Fifteen (FTF). Our primary outcomes were SDQ-hyperactivity and FTF-ADHD total scores. Parent-reported sleep duration was measured at 3, 8, 18, 24 months, and 5 years in the whole sample and actigraphy-based sleep duration at 2 and 24 months in a subsample. RESULTS: PRS for ADHD associated with SDQ-hyperactivity (ß = 0.214, p = .012) and FTF-ADHD total (ß = 0.639, p = .011), and FTF-inattention and hyperactivity subscale scores (ß = 0.315, p = .017 and ß = 0.324, p = .030), but not with sleep duration at any time point. Significant interactions were found between high PRS for ADHD and parent-reported short sleep throughout childhood in FTF-ADHD total score (F = 4.28, p = .039) and FTF-inattention subscale (F = 4.66, p = .031). We did not find any significant interaction between high PRS for ADHD and actigraphy-based short sleep. CONCLUSIONS: Parent-reported short sleep moderates the association between genetic risk of ADHD and ADHD symptoms in early childhood in the general population, so that children with short sleep, in combination with high genetic risk for ADHD, could be at highest risk for ADHD symptoms.

Sleep and Postpartum Psychosis: A Narrative Review of the Existing Literature.

Sleep problems are extremely common during the postpartum period. The role of sleep in the development of postpartum psychosis (PP) is, however, still under-researched. This narrative review aims to (1) provide a summary of the existing evidence for the associations between sleep problems and PP, (2) discuss the relevant risk factors associated with sleep problems and PP, and (3) suggest future lines of research in this area. Some of the existing literature suggests an association between sleep problems, specifically insomnia, sleep loss and sleep disruption during pregnancy and postpartum, and PP, with the most relevant risk factors including history of bipolar disorder and time of delivery. However, it is still unclear whether the previously mentioned sleep problems are a symptom of, or a trigger for PP. Thus, further research is needed to identify the specific role of sleep problems in PP, using longitudinal designs and more objective measures of sleep. This will allow appropriate detection, intervention and support for women experiencing and/or at risk for PP.

Associations between Sleep and Mental Health in Adolescents: Results from the UK Millennium Cohort Study.

(1) Background: There is a growing interest in investigating the relationship between sleep and mental health development in adolescents. This study aims to further investigate this relationship by identifying the specific associations between several sleep problems in adolescents and several mental health areas, and the role of gender in these associations. (2) Methods: Data from the Millennium cohort survey containing 11,553 individuals at 13-14 years old was included. Nighttime sleep duration and bedtime during weekdays and weekends, night awakening frequency, and sleep onset latency were assessed using self-reported questionnaires. Affective symptom and emotional and behavioural problems were examined with self-reported questionnaires. (3) Results: Regression analyses and path analysis models suggested that frequent night awakening was associated with all the outcomes, and hyperactivity/inattention was the outcome that presented a higher number of significant associations with sleep patterns. Long sleep onset latency and late bedtime at school days were associated with higher risk of emotional and behavioural difficulties. Further, poor sleep seems to manifest more externally in males, while more internally in females. (4) Conclusions: Specific sleep problems should be considered when assessing mental health in adolescence, which would allow more targeted prevention and intervention strategies. Further, special attention should be given to gender differences when addressing sleep and mental health.