The March 2024 issue of JCPP Advances features two neuroimaging studies that investigate links between early environmental risk factors for mental health problems, brain development and psychopathology in children and young adults. The papers provide new insights into how adverse environments and negative experiences in childhood increase risk for depression and mental health problems, and how this may or may not be mediated, or moderated, by individual differences in the brain.
Due to limitations of categorical definitions of mental illness, there is a need for quantitative empirical investigations of the dimensional structure of psychopathology. Using exploratory bifactor methods, this study investigated a comprehensive and representative structure of psychopathology in children to better understand how psychotic-like experiences (PLEs), autism spectrum disorder (ASD) symptoms, impulsivity, and sensitivity to reward and punishment, may be integrated into extant general factor models of psychopathology.
We used seven child-report and three parent-report instruments capturing diverse mental health symptoms in 11,185 children aged 9–10 from the Adolescent Brain Cognitive DevelopmentSM (ABCD) Study. We built on previous modeling frameworks by conducting both split sample and full sample factor analytic approaches that harnessed recent methodological advances in bifactor exploratory structural equation modeling (B-ESEM) to examine a wide range of psychopathology measures not previously integrated into a single analysis. Validity of psychopathology dimensions was examined by investigating associations with sex, age, cognition, imaging measures, and medical service usage.
All four factor analytic models showed excellent fit and similar structure within informant. PLEs loaded most highly onto a general psychopathology factor, suggesting that they may reflect non-specific risk for mental illness. ASD symptoms loaded separately from attention/hyperactivity symptoms. Symptoms of impulsivity and sensitivity to reward and punishment loaded onto specific factors, distinct from externalizing and internalizing factors. All identified factors were associated with clinically relevant risk factors, providing preliminary evidence for their construct validity.
By integrating diverse child-report and parent-report psychopathology measures for children in the ABCD sample, we deliver data on the quantitative structure of psychopathology for an exceptionally large set of measurements and discuss implications for the field.
Autistic traits are often reported to be elevated in children diagnosed with attention-deficit/hyperactivity disorder (ADHD). However, the distribution of subclinical autistic traits in children with ADHD has not yet been established; knowing this may have important implications for diagnostic and intervention processes. The present study proposes a preliminary model of the distribution of parent-reported ADHD and subclinical autistic traits in two independent samples of Australian children with and without an ADHD diagnosis.
Factor mixture modelling was applied to Autism Quotient and Conners' Parent Rating Scale – Revised responses from parents of Australian children aged 6–15 years who participated in one of two independent studies.
A 2-factor, 2-class factor mixture model with class varying factor variances and intercepts demonstrated the best fit to the data in both discovery and replication samples. The factors corresponded to the latent constructs of ‘autism’ and ‘ADHD’, respectively. Class 1 was characterised by low levels of both ADHD and autistic traits. Class 2 was characterised by high levels of ADHD traits and low-to-moderate levels of autistic traits. The classes were largely separated along diagnostic boundaries. The largest effect size for differences between classes on the Autism Quotient was on the Social Communication subscale.
Our findings support the conceptualisation of ADHD as a continuum, whilst confirming the utility of current categorical diagnostic criteria. Results suggest that subclinical autistic traits, particularly in the social communication domain, are unevenly distributed across children with clinically significant levels of ADHD traits. These traits might be profitably screened for in assessments of children with high ADHD symptoms and may also represent useful targets for intervention.
In the excitement about genomics, it is easy to lose sight of one of the most important findings from behavioural genetics: At least half of the variance of psychopathology is caused by environmental effects that are not shared by children growing up in the same family, which includes error of measurement. However, a 30-year search for the systematic causes of nonshared environment in a line-up of the usual suspects, especially parenting, has not identified the culprits.
I briefly review this research, but primarily consider the conceptual framework of the search for ‘missing’ nonshared environmental effects.
The search has focused on exogenous events like parenting, but nonshared environment might not be caused by anything we would call an event. Instead, it might reflect endogenous processes such as noisy biological systems (such as somatic mutations and epigenetics) or, at a psychological level, idiosyncratic subjective perceptions of past and present experiences, which could be called nonshared environmental experience to distinguish it from exogenous events. Although real, nonshared environment might be random in the philosophy of science sense of being unpredictable, even though it can have stable effects that predict subsequent behaviour.
I wade into the weeds of randomness and suggest that this so-called ‘gloomy prospect’ might not be so gloomy.
Empirical evidence regarding the development of sensory responsivity in young children at high likelihood to develop autism spectrum disorder (ASD) remains relatively limited. It is unclear how sensory responsivity behaviors may change over time and impact later developmental outcomes. The goals of this study were to (a) characterize developmental trajectories of sensory responsivity across infancy (∼12 months), toddlerhood (∼24 months), and school age (6–11 years) in children at high and low familial likelihood for ASD; and (b) determine if sensory responsivity in infancy predicts adaptive and cognitive functioning at school age among children with ASD.
Generalized linear mixed effects models were used to examine scores from the Sensory Experiences Questionnaire in three groups of children including high-likelihood children later diagnosed with ASD (HL-ASD; n = 30), high-likelihood children without ASD (HL-Neg; n = 150), and low-likelihood control children not meeting ASD diagnostic criteria (LL-Neg; n = 94). Hierarchical linear regression was then used to examine the association between sensory responsivity scores in infancy and functional adaptive and cognitive outcomes at school age for children at high likelihood of ASD.
Development of sensory responsivity from infancy to later childhood is best estimated by the effects of chronological age and Group for Sensory Seeking and Hypo responsivity and the additional effect of the interaction of Group and chronological age for Total and Hyper responsivity. Early elevated Hypo responsivity and Sensory Seeking scores are negatively associated with later adaptive behavior but not cognitive level.
Overall, higher degrees of Sensory Seeking and Hypo sensory responsivity are detectable in autistic children's behavioral repertoires by 12 months of age and associate with reduced adaptive functioning in middle childhood. These results point to the potential importance of early detection and treatment implications of early sensory behaviors.
Evidence for substance use-related problems in individuals with mild intellectual disability is sparse and mainly limited to selected psychiatric populations. We evaluated the risk of substance use-related problems in individuals with mild intellectual disability compared to the general population. Additionally, we have performed secondary sibling comparison analyses to account for familial confounding.
We conducted a population-based cohort study of individuals born in Sweden between 1973 and 2003. A total of 18,307 individuals with mild intellectual disability were compared to 915,350 reference individuals from the general population and 18,996 full siblings of individuals with mild intellectual disability. Information on mild intellectual disability and substance use-related problems was obtained from several Swedish national and regional school and healthcare registers. Substance use-related problems were measured via corresponding diagnostic and legal codes and included alcohol use disorder, drug use disorder, alcohol-related somatic disease, conviction for a substance-related crime, and substance-related death.
Individuals with mild intellectual disability had a higher risk of any substance use-related problem compared to the general population (HR, 1.81; 95% CI, 1.72–1.91), both in males (HR, 1.76; 95% CI, 1.65–1.89) and females (HR, 1.89; 95% CI, 1.74–2.05). The risks of substance use-related problems were particularly elevated among individuals with mild intellectual disability and psychiatric comorbidities (HR, 2.21–8.24). The associations were attenuated in the sibling comparison models.
Individuals with mild intellectual disability, especially those with psychiatric comorbidity, are at an elevated risk of substance use-related problems. Familial factors shared by full siblings contribute considerably to the association between mild intellectual disability and substance use-related problems.
Children of parents with a severe mental illness have an increased risk of developing a lifetime mental illness. We aimed to compare the effects of a preventive family-based intervention, VIA Family, with treatment as usual (TAU) on these children's global functioning.
Between 2017 and 2021, we conducted a pragmatic, rater-blinded, two-arm parallel-group superiority trial in Denmark. Families with at least one child aged 6–12 years and at least one biological parent with schizophrenia spectrum disorder, bipolar disorder, or recurrent major or moderate depression were included. We randomly allocated 95 families with their 113 children to VIA Family or TAU (ratio 1:1). VIA Family was individually tailored and based on case management. The intervention included options for psychoeducation, parental support, and treatment for emerging child psychiatric symptoms. Blinded raters assessed children and their families at baseline and after 18 months. The primary outcome was the difference in change between groups at end-of-treatment in daily global functioning measured with the Children's Global Assessment Scale. Secondary outcomes were emotional and behavioral problems and days absent from school. We analyzed data blinded to allocation.
At post-intervention, differences in mean change from baseline between VIA Family and TAU were non-significant (CGAS: −1.20, 95% CI = −6.61; 4.21, p = 0.66), as were the differences on the secondary and exploratory outcomes.
Contrary to our hypothesis, we did not find a superior effect of VIA Family compared with TAU. The short follow-up period and large sample heterogeneity might explain the null findings. Therefore, a possible long-term, preventive treatment effect has yet to be explored.
A child's socioeconomic environment can shape central aspects of their life, including vulnerability to mental disorders. Negative environmental influences in youth may interfere with the extensive and dynamic brain development occurring at this time. Indeed, there are numerous yet diverging reports of associations between parental socioeconomic status (SES) and child cortical brain morphometry. Most of these studies have used single metric- or unimodal analyses of standard cortical morphometry that downplay the probable scenario where numerous biological pathways in sum account for SES-related cortical differences in youth.
To comprehensively capture such variability, using data from 9758 children aged 8.9–11.1 years from the ABCD Study®, we employed linked independent component analysis (LICA) and fused vertex-wise cortical thickness, surface area, curvature and grey-/white-matter contrast (GWC). LICA revealed 70 uni- and multimodal components. We then assessed the linear relationships between parental education, parental income and each of the cortical components, controlling for age, sex, genetic ancestry, and family relatedness. We also assessed whether cortical structure moderated the negative relationships between parental SES and child general psychopathology.
Parental education and income were both associated with larger surface area and higher GWC globally, in addition to local increases in surface area and to a lesser extent bidirectional GWC and cortical thickness patterns. The negative relation between parental income and child psychopathology were attenuated in children with a multimodal pattern of larger frontal- and smaller occipital surface area, and lower medial occipital thickness and GWC.
Structural brain MRI is sensitive to SES diversity in childhood, with GWC emerging as a particularly relevant marker together with surface area. In low-income families, having a more developed cortex across MRI metrics, appears beneficial for mental health.
The concept of neurodiversity draws upon scientific research, and lessons from practice and lived experience to suggest new ways of thinking about neurodevelopmental conditions. Among the formative observations are that characteristics associated with neurodevelopmental conditions are part of a “broader phenotype” of variation across the whole population, and that there appear to be “transdiagnostic” similarities as well as differences in these characteristics. These observations raise important questions that have implications for understanding diversity in neurodevelopmental conditions and in neurocognitive phenotypes across the whole population.
The present work examines broader phenotypes using seven widely used self-report assessments of traits associated with autism, ADHD, dyslexia, Developmental Coordination Disorder/dyspraxia, tic disorders/Tourette's, cortical hyperexcitability associated with subclinical epilepsy, and sensory sensitivities. A representative sample of 995 adults (aged 17–77) in the UK completed self-report measures of neurodiversity, wellbeing, generalized anxiety, and depression, and cognitive abilities (nonverbal intelligence and executive functioning).
We used confirmatory factor analysis to test whether variation and covariation was better characterized (1) by traditional diagnostic labels, or (2) transdiagnostically according to similarities in functions, behaviours, or phenomena. Results indicated that neurodiversity characteristics were best explained using a bifactor model with one general “N” factor and four condition-specific factors.
This was the largest examination to date of the factor structure of broader phenotypes relevant to neurodevelopmental conditions. It provides critical benchmark data, and a framework approach for asking systematic questions about the structure of neurocognitive diversities seen in the whole population and in people with one or more diagnoses.
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