A substantial portion of interventions designed to support autistic children are also designed to be delivered by caregivers (i.e. are ‘caregiver-mediated’). Brown et al. (Journal of Child Psychology and Psychiatry, 2024) are one of the first groups to critically examine the baseline skills that caregivers bring as they prepare to learn a class of interventions called Naturalistic Developmental Behavioral Interventions (NDBIs), which are designed to support social communication growth in young autistic children. This commentary commends Brown and colleagues for their focus on caregivers, a linchpin within the increasingly prominent caregiver-mediated process of intervention delivery. However, it is imperative that future research understand the potential adverse effects and supports that are needed to bolster caregivers in this crucial role. We present six recommendations for research on caregiver-mediated interventions that build on Brown and colleagues' work and address these needs, which involve: caregiver supports, equitable samples, community settings, adaptive designs, general principles, and implications for NDBI dissemination.
Individuals with attention-deficit/hyperactivity disorder (ADHD) exhibit varied responses to pharmacological treatments (e.g. stimulants and non-stimulants). Accurately and promptly detecting treatment-related improvements, response failure, or deterioration poses significant challenges, as current monitoring primarily relies on subjective ratings. In this commentary, we critically evaluate the evidence supporting the use of QbTest for objectively monitoring ADHD treatment response in clinical practice. We also offer recommendations for future research, advocating for rigorous clinical trials and longitudinal studies to further explore the potential utilisation of QbTest and other tools for monitoring treatment responses in individuals with ADHD.
Although it is widely assumed that avoidant personality disorder (AvPD) originates in childhood, there is little prospective research to substantiate this claim. We therefore aimed to determine whether presumed childhood risk factors predict AvPD traits at 16 years.
A population-based sample (n = 1,077; 50.9% female) from the 2003 and 2004 birth cohorts in Trondheim, Norway was examined biennially from 4 to 16 years. The number of AvPD traits at the age of 16 was assessed with the structured clinical interview for DSM-5 personality disorders and regressed on the intercept and growth in child risk and protective factors until the age of 14.
The prevalence of AvPD at the age of 16 was 3.2% (95% CI: 2.2–4.1). Higher levels and an increased number of social anxiety symptoms over time, as well as increased negative affectivity/neuroticism, predicted a higher number of AvPD traits. When the levels and changes in these factors were adjusted for, less and decreasing extraversion forecasted more AvPD traits, as did declining self-worth, higher levels of parental AvPD traits, and increased onlooking behavior.
Neuroticism, low extraversion, social anxiety symptoms, passive onlooking behavior, and low self-worth predicted a higher number of AvPD traits in adolescence, as did more AvPD traits in parents. Efforts to enhance self-worth, reduce social anxiety, and promote peer interaction among onlooking children may reduce the development of AvPD traits in adolescence.
Many studies show that both callous-unemotional (CU) traits (e.g., low empathy, lack of guilt) and cognitive difficulties increase risk for externalizing psychopathology across development. However, other work suggests that some aggression (e.g., relational, proactive) may rely on intact cognitive function, which could vary based on the presence of CU traits. Moreover, no prior research has adequately accounted for common risk factors shared by CU traits, cognitive difficulties, and externalizing problems, which confounds conclusions that can be drawn about their purported relationships. The current study addressed these knowledge gaps by leveraging rigorous propensity matching methods to isolate associations between CU traits and different dimensions of cognitive function and externalizing problems.
Associations between CU traits, cognitive functioning, and externalizing outcomes were tested within dimensional (n = 11,868) and propensity-matched group-based (n = 1,224) models using data from the Adolescent Brain Cognitive Development Study®, with rigorous statistical control for shared sociodemographic risk factors. Cross-sectional outcomes were parent-reported symptoms of conduct disorder (CD), oppositional defiant disorder (ODD), and attention deficit hyperactivity disorder (ADHD). Longitudinal outcomes were child-reported overt and relational aggression.
CU traits were uniquely related to more parent-reported CD, ODD, ADHD symptoms, as well as more child-reported aggressive behaviors. Effects of cognitive difficulties were domain specific and were not consistent across dimensional and propensity matched models. There was minimal evidence for divergent associations between CU traits and externalizing outcomes as a function of cognition (i.e., no moderation).
Rigorous control for sociodemographic factors within propensity-matched models establish CU traits as a robust and unique risk factor for externalizing psychopathology, over and above difficulties with cognitive functioning.
Background: The mechanisms linking early-life adversity with psychopathology over the life-course are complex. In this prospective study, we collectively examined cognitive, affective, and developmental mediators previously found to individually link childhood threat and deprivation experiences to adolescent psychopathology to identify the most potent mechanisms.
Methods: Data came from a community sample of 227 children (mean child age 11.5 ± 0.5 years, 48.5% female) from the Seattle metro area with recruitment designed to reflect diversity in family income. Candidate mechanisms included self-rated pubertal development and task-measured attention bias to threat, emotion regulation, theory of mind, fear learning, inhibitory control, language ability, reasoning, and reward sensitivity. Using a high-dimensional mediation approach, we determined which mediating pathways linking threat and deprivation to psychopathology persisted after controlling for all candidate mechanisms associated with psychopathology. Models additionally controlled for the child's age, sex, early-childhood emotional and behavioral symptoms, poverty, and maternal depression.
Results: Blunted reward sensitivity mediated the prospective relationship between threat and internalizing psychopathology, explaining 17.25% (95% CI 1.08%, 69.96%) of this association. Advanced pubertal development was associated with increases in internalizing and externalizing symptoms (standardized associations of 0.16 (95% CI 0.03, 0.29) and 0.17 (95% CI 0.05, 0.29), respectively), but not with adversity. Although deprivation was strongly related to psychopathology, no mechanisms were empirically identified.
Conclusions: In a well-characterized community sample, we isolated reward sensitivity as a robust mediator of the prospective association between early-life threat and adolescent internalizing psychopathology. Interventions aimed at bolstering reward sensitivity may mitigate the impact of early-life threat experiences on internalizing problems.
Adolescence is a critical developmental period for the study of anorexia nervosa (AN), an illness characterized by extreme restriction of food intake. The maturation of the reward system during adolescence combined with recent neurobiological models of AN led to the hypothesis that early on in illness, restrictive food choices would be associated with activity in nucleus accumbens reward regions, rather than caudate regions identified among adults with AN.
Healthy adolescents (HC, n = 41) and adolescents with AN or atypical AN (atypAN, n = 76) completed a Food Choice Task during fMRI scanning. Selection of high-fat foods and choice-related activation in nucleus accumbens and anterior caudate regions-of-interest (ROIs) were compared between individuals with AN/atypAN and HC. Associations were examined between choice-related activation and choice preferences among the AN group. Exploratory analyses examined associations between choice-related activation and psychological assessments among the patient group.
Adolescents with AN or atypAN selected fewer high-fat foods than HC (t = −5.92, p < .001). Counter to predictions, there were no significant group differences in choice-related activation in the ROIs. Among individuals with AN or atypAN, choice-related neural activity in the anterior caudate was significantly negatively associated with high-fat food selections in the task (r = −.32, p = .024). In exploratory analyses, choice-related anterior caudate activation was positively associated with psychological measures of illness severity among patients (p's < .05, uncorrected).
In this large cohort of adolescents with AN/atypAN, there was no evidence of altered reward system engagement during food choice. While there was no group difference in choice-related caudate activation, the associations with choices and psychological measures continue to suggest that this neural region is implicated in illness. Longitudinal analyses will clarify whether neural variability relates to longer-term course.
Antipsychotic medications (AP) are inappropriately prescribed to young people. The goal of this pragmatic trial was to test a four-component approach to improved targeting of antipsychotic prescribing to people aged ≥3 and <18 years.
Clinicians in four health systems were cluster randomized by the number of previous AP orders and service line – specialty mental health and all others. Intervention arm clinicians received a best practice alert and child psychiatrist consultation and feedback. Families received system navigation and expedited access to psychotherapy. Primary outcomes were total days' supply of AP medication and proportion of youth with any AP supply at 6 months. We estimated the log-odds of AP use at 6 months and the relative rate of AP over 6 months. The Safer and Targeted Use of Antipsychotics in Youth (SUAY) trial took place between 3/2018 and 12/2020.
The trial enrolled 733 patients. The odds ratio (OR) comparing use at 6 months was 0.75 (95% CI: 0.52, 1.09). The mean number of days using AP was 118.5 for intervention patients and 128.2 for control patients (relative risk [RR] = 0.92; 95% CI: 0.81–1.04). Exploratory heterogeneity of treatment effects (HTE) was not detected in groups defined by age, gender, provider specialty, and insurance type. HTE by race/ethnicity was present: among youth of color, mean days' supply was 103.2 for intervention arm and 131.2 for the control arm (RR 0.79, 95% CI: 0.67–0.93). Among secondary outcomes, only new psychotherapy referrals differed with 44.3% (n = 154) of intervention participants having a new order for psychotherapy compared to 33.5% (n = 129) in the control arm (OR 1.47: 95% CI: 1.01–2.14).
This intervention did not result in less AP use at 6 months or a reduction in the days' supply of AP medication, although psychotherapy orders increased. The intervention may be effective for some subgroups.
Symptoms related to mood and anxiety disorders (emotional disorders) often present in childhood and adolescence. Some of the genetic liability for mental disorders, and emotional and behavioral difficulties seems to be shared. Yet, it is unclear how genetic liability for emotional disorders and related traits influence trajectories of childhood behavioral and emotional difficulties, and if specific developmental patterns are associated with higher genetic liability for these disorders.
This study uses data from a genotyped sample of children (n = 54,839) from the Norwegian Mother, Father, and Child Cohort Study (MoBa). We use latent growth models (1.5–5 years) and latent profile analyses (1.5–8 years) to quantify childhood trajectories and profiles of emotional and behavioral difficulties and diagnoses. We examine associations between these trajectories and profiles with polygenic scores for bipolar disorder (PGSBD), anxiety (PGSANX), depression (PGSDEP), and neuroticism (PGSNEUR).
Associations between PGSDEP, PGSANX, and PGSNEUR, and emotional and behavioral difficulties in childhood were more persistent than age-specific across early childhood (1.5–5 years). Higher PGSANX and PGSDEP were associated with steeper increases in behavioral difficulties across early childhood. Latent profile analyses identified five profiles with different associations with emotional disorder diagnosis. All PGS were associated with the probability of classification into profiles characterized by some form of difficulties (vs. a normative reference profile), but only PGSBD was uniquely associated with a single developmental profile.
Genetic risk for mood disorders and related traits contribute to both a higher baseline level of, and a more rapid increase in, emotional and behavioral difficulties across early and middle childhood, with some indications for disorder-specific profiles. Our findings may inform research on developmental pathways to emotional disorders and the improvement of initiatives for early identification and targeted intervention.
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