Previous research on the protective effects of school holidays on adolescent suicidal and non-suicidal self-injury (NSSI) has relied on hospital records which underestimate self-harm prevalence and has not been explored in the post pandemic environment. This study utilised ambulance attendance data to explore whether protective effects of school holidays on suicidal and NSSI behaviours were present pre- and post-COVID-19 restrictions. Using data from the National Ambulance Surveillance System, weekly ambulance attendances for suicidal and NSSI behaviours among adolescents (12-17) and young adults (18-25) in Victoria, Australia, were analysed. Trends in rates per 10,000 population pre- (2015-2019) and post-COVID-19 restrictions (2022-2023) were modelled using seasonal autoregressive integrated moving average with exogenous variables, stratified by age and gender. There were 20,635 suicidal and NSSI related ambulance attendances among adolescents and 36,510 among young adults. Pre-COVID-19 there was a significant decline in weekly rate of attendances per 10,000 population for adolescent females during the December/January (-0.35, p < .001), June/July (-0.46, p = .007) and September/October (-0.41, p = .004) holidays. Similar declines were seen in adolescent males during the December/January (-0.12, p = .003), April/May (-0.22, p = .001), June/July (-0.26, p = .003) and September/October (-0.15, p = .027) holidays. No significant effects were observed for young adults or post-pandemic. Seasonal trends in adolescent suicidal and NSSI harms were evident prior to COVID-19, but were no longer present post-pandemic. Understanding these changes is crucial for informing targeted mental health interventions and support for adolescents.

Evidence on the association between loneliness and psychotic experiences in adolescents remains limited. Moreover, loneliness has typically been assessed at a single time point, which fails to capture its dynamic nature. We hypothesized that persistent loneliness, assessed across repeated measures, would be associated with psychotic experiences and other mental health problems. Using longitudinal data from 3,171 participants in the Tokyo Teen Cohort, we applied the g-formula. We analyzed how loneliness patterns at ages 12 and 14 were associated with psychotic experiences, depression, anxiety, and diminished well-being at age 16, accounting for time-fixed and time-varying confounders. Missing data were handled using multiple imputation by chained equations. Persistent loneliness was associated with increased risk and greater severity of psychotic experiences (RD 7.1%, 95% CI: 0.8-14.3; RR 2.44, 95% CI: 1.16-4.11; β 0.28, 95% CI: 0.10-0.48). Incident loneliness at age 14 showed similar associations. No association was found for adolescents whose loneliness had remitted by age 14 (RD -1.3%, 95% CI: -3.6 to 1.2; RR 0.73, 95% CI: 0.31-1.26; β 0.01, 95% CI: -0.04 to 0.08). Sensitivity analyses using marginal structural models yielded results that were largely unchanged. Findings were generally similar for other mental health problems. Associations were consistent across genders, although the association with well-being appeared particularly important for girls. The dynamics of loneliness are associated with a wide range of mental health problems in adolescents. The risk may not be permanent and could be mitigated if loneliness remits. Further research examining interventions that target loneliness is warranted.

Self-harm is defined as self-injury or self-poisoning, irrespective of the presence of suicidal intent. It includes both non-suicidal self-injury and attempted suicide. The lifetime prevalence of self-harm is approximately 20% in young people. The initial assessment for self-harm should contain an evaluation of risk, a safety plan and a therapeutic element, which should be focused on understanding the nature of self-harm, instilling hope and linking young people with follow-up treatment. Dialectical Behaviour Therapy should be offered to young people with severe self-harm. School-based interventions, such as the Youth Aware of Mental Health programme, could prevent self-harm in young people.

The placebo effect is established in clinical trials, but for paediatric research, questions remain about how to best manage its influence. Within the autism field, data on these issues is sparse. This is particularly important in the oxytocin field where placebo responses are thought to play an important role. This study reports on data from the single-blind, placebo lead-in phase of a randomised controlled trial (RCT) to investigate the placebo response and its relationship to treatment response in autistic children. Eighty-seven autistic children aged 3-12 years (M = 7.27; SD = 2.69; 85.1% male) were consecutively recruited into a multi-site RCT evaluating the efficacy of oxytocin for improving social responsiveness. Participants underwent a 3-week, single-blind placebo lead-in before randomisation into a 12-week double-blind treatment phase (oxytocin, n = 45; placebo, n = 42). The Social Responsiveness Scale, 2nd Edition (SRS-2) Total Raw Score was used to measure change from baseline to post-placebo lead-in. A ≥10-point improvement defined placebo responders. Nearly half the sample (n = 42, 48.3%) were identified as placebo responders during the lead-in phase, showing a clinically significant degree of change on the SRS-2. Caregiver treatment guess did not significantly impact the placebo response (p = .534). Placebo response was associated with greater symptom severity (r's > -.23; p-values < .037) and higher cognitive ability (r = -.35, p = .004). Smaller placebo responses during the lead-in phasewere associated with larger responses during active treatment in participants receiving oxytocin (r = -.36, p = .017). Placebo responses during the lead-in phase were observed across all caregiver-reported measures (Cohen's d = .19-.65). This study provides important information about placebo effects and placebo lead-in designs for clinical trials in the autism field. We show widespread clinically significant improvement during placebo lead-in, utility of identifying placebo responders for informing clinical trial analyses, similarities in symptom measure effect sizes for placebo effects, and a lack of influence of caregiver beliefs on placebo responses.

Social anxiety disorder (SAD) is characterized by attentional biases that may contribute to its persistence. While adult models emphasize self-focused and hypervigilant attention, there is limited understanding of how these processes operate in children. This study examined internal and external attentional biases in children with SAD during anticipation of a social stress task-a period when anxiety is typically elevated. Forty-two children with a primary SAD diagnosis and 46 healthy controls (HC), aged 9-14 years, completed a reaction time (RT) task with internal (bodily) and external (visual) probes during anticipation of a speech task, while facing a peer video audience. RTs to probes and eye movements toward audience faces were recorded. RTs did not differ between groups. Exploratory analyses revealed that age correlated negatively with RTs in both groups, suggesting developmental effects on processing speed, although no group differences in this relationship were found. Eye-tracking revealed that children with SAD exhibited more frequent and longer fixations on audience faces during the initial phase of the task compared to HCs. Although RT tasks alone may not detect attentional biases in children with SAD, eye-tracking indicated heightened attention to socially salient cues during anticipation. These findings highlight the importance of multimodal assessment to capture subtle hypervigilance in pediatric SAD.

The landscape of trauma-focused interventions for young children has evolved significantly, though substantial gaps remain. Early childhood trauma exposure occurs during sensitive periods of brain development with potential lifelong consequences. However, these periods also present unique opportunities for intervention to redirect trajectories toward positive outcomes. Rapid neurodevelopmental changes across early childhood necessitate interventions specifically designed for evolving capacities rather than simply "scaled down" versions of adult treatments. A review focused exclusively on evidence-based interventions for young children is needed. This review represents a synthesis of the literature informed by our clinical and research expertise. We review interventions that (1) target trauma symptoms as primary outcomes, (2) were designed for children ages 0-8 years, (3) include substantive caregiver involvement, and (4) have empirical support from published randomized controlled trials or well-designed quasi-experimental studies. Our review revealed a tiered evidence base for young children, with the strongest support for interventions targeting specific age groups: Child-Parent Psychotherapy for infants and toddlers, Preschool PTSD Treatment for preschoolers, and Trauma-Focused CBT for early elementary children. Critical gaps include limited interventions for children under age 3, sparse evidence for interventions targeting noninterpersonal trauma, assessment challenges, particularly with longitudinal measurement across developmental transitions, and insufficient implementation research on disseminating interventions in community settings. By continuing to refine effective trauma interventions for our youngest children, we can alleviate immediate suffering and potentially prevent decades of associated difficulties across the lifespan. Future research priorities should include expanding the evidence base for existing interventions through well-powered trials with diverse samples, developing and testing preventive interventions delivered following potentially traumatic events, adapting established interventions for under-studied trauma types, and implementation research to support widespread adoption in real-world settings.

Prenatal exposure to ambient air pollution has been implicated in adverse neurodevelopment, but evidence from large-scale, long-term studies in Asian populations remains limited. We examined the association between in utero exposure to multiple air pollutants and the risk of neurodevelopmental disorders (NDD) in offspring using a nationwide cohort in South Korea. We conducted a nationwide retrospective cohort study using linked administrative health and environmental data. A total of 1,436,685 children born between January 1, 2010, and December 31, 2014, were identified from the National Health Insurance Service database and followed up through December 31, 2023. Maternal exposure to nitrogen dioxide (NO2), sulfur dioxide (SO2), carbon monoxide (CO), ozone (O3), and particulate matter ≤10 μm (PM10) was estimated by linking residential postal codes to fixed-site monitoring data. NDD diagnoses were identified from healthcare claims. Adjusted hazard ratios (aHRs) with 95% confidence intervals (CIs) were estimated using multivariable Cox proportional hazards models adjusting for maternal sociodemographic, medical, obstetric, and neonatal covariates. During up to 13 years of follow-up, 140,971 children (9.8%) were diagnosed with an NDD. Prenatal exposure to NO2 showed the strongest association: each 0.01-ppm increase was associated with an 18% higher hazard of NDD (aHR 1.18, 95% CI 1.17-1.19; p < .001). SO2 exposure also demonstrated a small but statistically significant association (per 0.001-ppm increase: aHR 1.01, 95% CI 1.01-1.02; p = .008). These associations persisted across major NDD subtypes - including intellectual disabilities, developmental delays, and behavioral or emotional disorders - and remained robust in trimester-specific, stratified, and sensitivity analyses. Prenatal exposure to ambient air pollutants - particularly NO2 and SO2 - is associated with increased long-term risk of NDD in offspring. These findings highlight the neurodevelopmental vulnerability of the prenatal period and underscore the need for strengthened environmental policies to reduce maternal exposure to harmful pollutants.

Early life adversities (ELAs) including experiences such as abuse, neglect, and household dysfunction are strongly linked to psychopathology; yet, the developmental pathways connecting ELA to externalizing and internalizing psychopathology remain unclear. While most research has focused on threat and negative affect, positive emotions may represent a critical but understudied mechanism linking ELA to mental health outcomes. Using data from the Adolescent Brain Cognitive Development (ABCD) study, we examined positive affect trajectories across six timepoints spanning childhood through adolescence (ages 9-10 to 12-13). We employed person-centered trajectory-based clustering to identify distinct patterns in positive affect - independent of ELA exposure - followed by multinomial logistic regression to examine associations between cumulative ELA exposure and trajectory membership. Mediation analyses tested whether positive affect trajectories explained links between ELA and psychopathology outcomes. Four distinct positive affect trajectories emerged: High-Stable, Declining, Persistently Low, and Volatile (N = 7,457). Higher ELA scores significantly predicted membership in all non-high-stable trajectories, with the strongest association existing for the Persistently Low group (β = .321, p < .001). Mediation analyses revealed that Persistently Low trajectory group membership significantly mediated the relationship between ELA and internalizing problems (indirect effect = 0.030, 95% CI [0.012, 0.056], p = .007), but not externalizing problems (N = 3,927). This study demonstrates that ELA shapes positive affect development through distinct, heterogeneous pathways rather than uniform effects, with persistently low positive affect representing a specific mechanism linking early adversity to later depression and anxiety. Findings suggest that targeting positive emotional experiences may be a promising intervention strategy for youth exposed to ELA.

From a functionalist perspective, parenting behaviors have adaptive functions and are partly expressions of genetic variation. Maternal genes that have effects on children are often referred to as indirect maternal genetic effects. Indirect genetic effects provide a means for measuring the role of parenting without the need for specifying the relevant parental behaviors. We studied indirect maternal genetic effects to address both the importance and commonality of parenting across the internalizing-externalizing spectrum of behavior problems in childhood. We further addressed how indirect genetic effects impact our understanding of direct genetic effects if not accounted for. Utilizing data from the Norwegian Mother, Father, and Child Cohort Study (MoBa), our analyses involved 42,423 children and their mothers. Both pedigree and genotype data were used to infer genetic relationships. We applied multivariate latent variable models to distinguish indirect maternal genetic effects and direct offspring genetic effects on seven measures of internalizing-externalizing behaviors. Our findings indicate significant maternal genetic influences, explaining 7%-18% of the variance across internalizing-externalizing behaviors. A general maternal effect common across behaviors could adequately account for most of the variability. The analyses further indicate that direct child genetic effects appear smaller and more complex when indirect maternal genetic effects are modeled simultaneously. By summarizing the effects of parenting with indirect maternal genetic effects, we show a substantial contribution of parents with respect to internalizing-externalizing behaviors in childhood. Although parenting is multifaceted, the effects of parenting are general and can succinctly be described as a single common dimension. Further, our study demonstrates that direct genetic effects appear smaller and more complex when maternal genetic effects are accounted for, highlighting the confounding potential of parental effects in understanding the role of genetic differences in child psychopathology.

A major research effort in the past two decades has begun to illuminate how experience 'gets under the skin' - that is - the cellular and molecular processes that are associated with adversity and resilience. We selectively review three areas of this research: epigenetics, especially DNA methylation, telomere length, and inflammatory processes, and consider the implications of this work for better understanding the effects of adversity and pathways of recovery. Because infant mental health practitioners focus on children in the earliest years of life, they are well positioned to favorably alter the developmental trajectories of children experiencing or at risk for maladaptation. In addition to helping us develop more individually effective treatments, we consider other ways in which research advances in cell and molecular biology may be especially important to infant mental health practitioners in the future. Better understanding these processes will enhance effectiveness and potentially enlarge the scope of our practice.