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.

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 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.

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.

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.

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.

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.

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.

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.

Persistent Childhood and Adolescent Anxiety and Risk for Psychosis: A Longitudinal Birth Cohort Study.

BACKGROUND: Persistent anxiety in childhood and adolescence could represent a novel treatment target for psychosis, potentially targeting activation of stress pathways and secondary nonresolving inflammatory response. Here, we examined the association between persistent anxiety through childhood and adolescence with individuals with psychotic experiences (PEs) or who met criteria for psychotic disorder (PD) at age 24 years. We also investigated whether C-reactive protein mediated any association. METHODS: Data from the Avon Longitudinal Study of Parents and Children (ALSPAC) were available in 8242 children at age 8 years, 7658 at age 10 years, 6906 at age 13 years, and 3889 at age 24 years. The Development and Well-Being Assessment was administered to capture child and adolescent anxiety. We created a composite score of generalized anxiety at ages 8, 10, and 13. PEs and PD were assessed at age 24, derived from the Psychosis-like Symptoms Interview. The mean of C-reactive protein at ages 9 and 15 years was used as a mediator. RESULTS: Individuals with persistent high levels of anxiety were more likely to develop PEs (odds ratio 2.02, 95% CI 1.26-3.23, p = .003) and PD at age 24 (odds ratio 4.23, 95% CI 2.27-7.88, p < .001). The mean of C-reactive protein at ages 9 and 15 mediated the associations of persistent anxiety with PEs (bias-corrected estimate -0.001, p = .013) and PD (bias-corrected estimate 0.001, p = .003). CONCLUSIONS: Persistent high levels of anxiety through childhood and adolescence could be a risk factor for psychosis. Persistent anxiety is potentially related to subsequent psychosis via activation of stress hormones and nonresolving inflammation. These results contribute to the potential for preventive interventions in psychosis, with the novel target of early anxiety.

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.

Anxiety disorders across middle childhood and early adolescence in a UK population-based cohort.

Background: Patterns of development and underlying factors explaining anxiety disorders in children and adolescents are under-researched, despite their high prevalence, impact and associations with other mental disorders. We aimed to a] understand the pattern and persistence of specific anxiety disorders; b] examine differing trajectories of symptoms of specific anxiety disorders and; c] examine socio-demographic and health-related predictors of persistent anxiety disorder-specific symptoms, across middle childhood to early adolescence. Methods: The current study used data from 8122 participants in the Avon Longitudinal Study of Parents and Children birth cohort. The Development and Wellbeing Assessment questionnaire was administered to parents to capture child and adolescent anxiety total scores and DAWBA-derived diagnoses. Separation anxiety, specific phobia, social anxiety, acute stress reaction, and generalized anxiety at 8, 10 and 13 years were selected. Further, we included the following socio-demographic and health-related predictors: sex, birth weight, sleep difficulties at 3.5 years, ethnicity, family adversity, maternal age at birth, maternal postnatal anxiety, maternal postnatal depression, maternal bonding, maternal socio-economic status and maternal education. Results: Different anxiety disorders presented different prevalence and patterns of development over time. Further, latent class growth analyses yielded a trajectory characterized by individuals with persistent high levels of anxiety across childhood and adolescence; for specific phobia (high = 5.8%; moderate = 20.5%; low = 73.6%), social anxiety (high = 3.4%; moderate = 12.1%; low = 84.5%), acute stress reaction (high = 1.9%; low = 98.1%) and generalized anxiety (high = 5.4%; moderate = 21.7%; low = 72.9%). Finally, the risk factors associated with each of the persistent high levels of anxiety disorders were child sleeping difficulties and postnatal maternal depression and anxiety. Conclusions: Our findings show that a small group of children and young adolescents continue to suffer from frequent and severe anxiety. When considering treatment strategies for anxiety disorders in this group, children's sleep difficulties and postnatal maternal depression and anxiety need to be assessed as these may predict a more prolonged and severe course of illness.

Longitudinal Associations Between Cognitive Deficits in Childhood and Psychopathological Symptoms in Adolescence and Young Adulthood.

Importance: Cognitive deficits are core features of mental disorders and are important in predicting long-term prognosis. However, it is still unknown whether individual patterns of cognitive deficits predate specific mental disorders. Objective: To investigate the specificity of the associations of attention, working memory, and inhibition in childhood with borderline personality disorder (BPD), psychosis, depression, and hypomania in adolescence and young adulthood. Design, Setting, and Participants: This cohort study obtained data from the Avon Longitudinal Study of Parents and Children in the United Kingdom. All pregnant women resident in Avon, United Kingdom, with an expected date of delivery from April 1, 1991, and December 31, 1992, were eligible. Data analysis was conducted from April 1 to September 30, 2020. The sample initially comprised 13 988 participants who were alive at 1 year of age. For this study, data were available for 6333 individuals reporting on any psychopathological measure at ages 11 to 12 years, 4903 individuals at ages 17 to 18 years, and 2963 individuals at 22 to 23 years. Exposures: Sustained attention, selective attention, and attentional control were assessed with the Test of Everyday Attention for Children at age 8 years, and working memory and inhibition were assessed at age 10 years with the Counting Span Task and the stop-signal paradigm, respectively. Main Outcomes and Measures: Symptoms of BPD were assessed at ages 11 to 12 years, psychotic experiences and depression were examined at ages 17 to 18 years, and hypomania was examined at ages 22 to 23 years. Results: Among 5315 individuals included in the statistical analysis, 2551 (48.0%) were male and 2764 (52.0) were female. Higher sustained attention at 8 years was associated with decreased risk of BPD symptoms at ages 11 to 12 years (adjusted odds ratio [aOR], 0.964; 95% CI, 0.933-0.996; P = .03), better performance on inhibition at age 10 years with decreased risk of psychotic experiences at ages 17 to 18 years (aOR, 0.938; 95% CI, 0.890-0.989; P = .02), higher sustained attention at age 8 years with decreased risk of depressive symptoms at ages 17 to 18 years (aOR, 0.969; 95% CI 0.938-0.9997; P = .048), and better performance in working memory at age 10 years with decreased risk of hypomania symptoms at ages 22 to 23 years (aOR, 0.694; 95% CI, 0.529-0.911; P = .008). After controlling for potential psychopathological overlay, all the associations remained, except for working memory and hypomania. Higher sustained attention at age 8 years was associated with decreased risk of BPD symptoms at ages 11 to 12 years (ß = -0.05; P < .001) and of depression at ages 17 to 18 years (ß = -0.03; P = .04), and better performance in inhibition at age 10 years was associated with decreased risk of psychotic experiences at ages 17 to 18 years (ß = -0.03; P = .04). Conclusions and Relevance: These findings suggest that specific cognitive deficits in childhood are distinctively associated with different psychopathological symptoms in young people. Furthermore, these results suggest the potential of early cognitive interventions in childhood as a way of modifying or attenuating risk for subsequent psychopathological symptoms.

The Effects of Genetic Background for Diurnal Preference on Sleep Development in Early Childhood.

PURPOSE: No previous research has examined the impact of the genetic background of diurnal preference on children´s sleep. Here, we examined the effects of genetic risk score for the liability of diurnal preference on sleep development in early childhood in two population-based cohorts from Finland. PARTICIPANTS AND METHODS: The primary sample (CHILD-SLEEP, CS) comprised 1420 infants (695 girls), and the replication sample (FinnBrain, FB; 962 girls) 2063 infants. Parent-reported sleep duration, sleep-onset latency and bedtime were assessed at three, eight, 18 and 24 months in CS, and at six, 12 and 24 months in FB. Actigraphy-based sleep latency and efficiency were measured in CS in 365 infants at eight months (168 girls), and in 197 infants at 24 months (82 girls). Mean standard scores for each sleep domain were calculated in both samples. Polygenic risk scores (PRS) were used to quantitate the genetic risk for eveningness (PRSBestFit) and morningness (PRS10kBest). RESULTS: PRSBestFit associated with longer sleep-onset latency and later bedtime, and PRS10kBest related to shorter sleep-onset latency in CS. The link between genetic risk for diurnal preference and sleep-onset latency was replicated in FB, and meta-analysis resulted in associations (P<0.0005) with both PRS-values (PRSBestFit: Z=3.55; and PRS10kBest: Z=-3.68). Finally, PRSBestFit was related to actigraphy-based lower sleep efficiency and longer sleep latency at eight months. CONCLUSION: Genetic liability to diurnal preference for eveningness relates to longer sleep-onset during the first two years of life, and to objectively measured lowered sleep efficiency. These findings enhance our understanding on the biological factors affecting sleep development, and contribute to clarify the physiological sleep architecture in early childhood.

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.

Understanding the Relationship Between Sleep Problems in Early Childhood and Borderline Personality Disorder: A Narrative Review.

OBJECTIVE: Recent research indicates that sleep problems in childhood precede the development of borderline personality disorder (BPD) symptoms, but the mechanisms by which sleep problems associate with BPD are still unknown. This narrative review aims to provide some potential explanations for how early sleep problems might associate with BPD. METHODS: We used the biosocial developmental model of BPD as a framework to discuss how sleep problems may associate with BPD. Articles were identified via PubMed and Embase, and papers published between January 1991 and April 2021 were extracted. Authors made a series of literature searches using the following keywords: Sleep problems, Insomnia, Nightmares, Hypothalamic-Pituitary-Adrenal Axis (HPA), Prefrontal Cortex, Family Psychopathology, Disrupted Attachment, Child Maltreatment, Impulsivity, Emotion Regulation, Internalizing, Externalizing, Rumination, Childhood, Adolescence, Young people. The inclusion criteria were published in peer-reviewed journals; human studies or reviews; published in English. The exclusion criteria were commentaries; abstracts from conferences; studies with animal samples. A total of 96 articles were included for the purpose of this review. RESULTS: The evidence from this review suggests that some biological factors and core features of BPD act as potential mechanisms mediating the associations between early sleep and subsequent BPD, while some family-related factors might constitute common risk factors for sleep problems and BPD. CONCLUSION: The biosocial developmental model of BPD provides a plausible characterization of how sleep disruption might lead to subsequent BPD. Further research on new developmental and early intervention approaches to understand how sleep in early stages associates with BPD could have significant clinical impact on these patients and could inform targeted therapeutic interventions.

The longitudinal associations between temperament and sleep during the first year of life.

Temperament and sleep in infants are related but also distinct concepts. The longitudinal effects of temperament on sleep in infancy remain unclear, although this information is potentially important for the prevention and treatment of early sleep problems. We examined how various temperament features influence sleep development during the first year of life in a large birth cohort. This study comprised mother-infant dyads with complete longitudinal data on sleep, temperament and sociodemographic measurements at six and 12 months (N = 1436). We observed that higher infant Negative Affectivity was related to several sleep problems, and that many subscales of Negative Affectivity and Orienting/Regulation predicted worse sleep and deterioration in sleep problems from six to 12 months. Few associations between Surgency and sleep were found. Our findings highlight especially Negative Affectivity as a risk factor for persistent and increasing sleep problems, and also the specific importance of the fine-grained aspects of temperament in predicting infant sleep development.

Association of Parent-Reported Sleep Problems in Early Childhood With Psychotic and Borderline Personality Disorder Symptoms in Adolescence.

Importance: Persistent nightmares in childhood have been prospectively associated with psychosis and borderline personality disorder (BPD) in adolescence. However, the extent to which this association is also true for behavioral sleep problems is still unknown, and the potential mechanisms are unexplored. Objective: To examine the prospective associations between several parent-reported sleep problems in early childhood and psychotic and BPD symptoms at 11 to 13 years of age and the potential mediation of the associations by depression at 10 years of age. Design, Setting, and Participants: This cohort study assessed 13 488 participants in the Avon Longitudinal Study of Parents and Children birth cohort who were followed up for more than 13 years. Pregnant women from Avon, United Kingdom, with expected dates of delivery from April 1, 1991, to December 31, 1992, were invited to take part in the study. Data analysis was conducted from May 1 to December 31, 2019. Main Outcomes and Measures: Psychotic experiences at 12 to 13 years of age were assessed using the Psychosis-Like Symptom Interview, and BPD symptoms at 11 to 12 years of age were tested using the UK Childhood Interview for DSM-IV Borderline Personality Disorder. Parent-reported nighttime sleep duration, night awakening frequency, bedtime, and regularity of sleep routines were assessed when the child was 6, 18, and 30 months and 3.5, 4.8, and 5.8 years of age. Results: Data were available on 7155 participants (3718 girls [52%]) who reported on BPD symptoms and 6333 (3280 boys [52%]) who reported on BPD symptoms. Higher night awakening frequency at 18 months of age (odds ratio [OR], 1.13; 95% CI, 1.01-1.26) and less regular sleep routines at 6 months (OR, 0.68; 95% CI, 0.50-0.93), 30 months (OR, 0.64; 95% CI, 0.44-0.95), and 5.8 years (OR, 0.32; 95% CI, 0.19-0.53) of age were significantly associated with psychotic experiences in adolescence, whereas shorter nighttime sleep duration (OR, 0.78; 95% CI, 0.66-0.92) and later bedtime at 3.5 years of age (OR, 1.32; 95% CI, 1.09-1.60) were significantly associated with BPD symptoms. Results of mediation analysis were consistent with all these associations, except for later bedtime at 3.5 years and BPD in adolescence, which had no association. Depression at 10 years of age mediated the associations between frequent night awakenings at 18 months of age (bias-corrected estimate, -0.005; 95% CI, -0.008 to -0.002; P = .002) and irregular sleep routines at 5.8 years of age (bias-corrected estimate, -0.006; 95% CI, -0.010 to -0.003; P = .003) with psychosis. Conclusions and Relevance: The findings suggest that some behavioral sleep problems in childhood are distinctively associated with the onset of psychosis and BPD in adolescence, following different pathways. Furthermore, depression at 10 years of age may mediate only the association with psychosis. These findings contribute to the design of more personalized interventions in psychosis and BPD.