Research on genetic and environmental influences on speech and/or language difficulties (SaLD) is sparse, with inconsistent heritability estimates. We aimed to estimate the prevalence of parental reported SaLD and the relative contributions of genetic and environmental factors for the phenotype using a Swedish population-based twin sample. We hypothesized that there would be a stronger genetic than environmental effect on SaLD.
Data were collected from The Child and Adolescent Twin Study in Sweden. The study sample included 16,774 twin pairs (16,946 males, 16,602 females), of which 5141 were monozygotic, 5861 dizygotic (DZ), and 5772 opposite-sex DZ pairs. The language items in the Autism–Tics, Attention-Deficit Hyperactivity Disorder, and other Comorbidities inventory were used to categorize individuals as having parental-reported SaLD. A classical twin design was used to estimate the relative contribution of genetic and environmental factors to the liability of SaLD.
The prevalence of SaLD was 7.85% (95% confidence interval (CI) [7.57%–8.15%]) and 7.27% (95% CI [6.99%–7.55%]) when excluding individuals with autism and intellectual disability (ID). We also found that SaLD were significantly more prevalent in males than females with a ratio of 2:1. The heritability was estimated to be 75% (95% CI [67%–83%]) for SaLD. Shared environment played a significant role with an estimated contribution of 22% (95% CI [14%–30%]). The heritability estimate was reduced to 70% but with overlapping CI when excluding individuals with autism and ID.
We provide evidence that SaLD is common in the population and under strong genetic influence. Future studies should focus on mapping the genetic architecture of SaLD and related disorders.
Individuals with Attention-Deficit/Hyperactivity Disorder (ADHD) face an elevated risk of criminal convictions compared to those without ADHD. However, understanding this link involves considering sex differences, coexisting psychiatric conditions, and unmeasured familial factors. This study aimed to explore the connection between ADHD and criminal convictions (both violent and non-violent) in males and females, while also assessing the impact of comorbid psychiatric disorders and familial factors.
Using Swedish national registers, we identified individuals born between 1986 and 1997 (635,391 males and 600,548 females). ADHD was defined through clinical diagnosis and prescribed medications, while criminal convictions were determined based on Swedish lower court records. Unmeasured familial factors were accounted for using a sibling design approach.
Findings revealed that individuals with ADHD had a notably higher absolute and relative risk of both violent and non-violent criminal convictions compared to those without ADHD. While criminal convictions were more frequent among males with ADHD, females with ADHD exhibited higher relative risks (HR violent 10.50, non-violent 4.04) than their male counterparts (HR violent 6.03, non-violent 3.57). Additionally, lower socioeconomic status (SES) in individuals with ADHD was associated with increased relative risks for criminal convictions compared to individuals with ADHD who had higher SES. Adjusting for childhood and internalizing psychiatric disorders partially attenuated these associations, while substance use disorders (SUD) substantially attenuated them. SUD also contributed to an elevated absolute risk of criminal convictions in both male and female individuals with ADHD. Accounting for unmeasured shared familial factors slightly reduced the estimates, but the association between ADHD and criminal convictions persisted.
In conclusion, ADHD remains a potent independent risk factor for criminal convictions, with varying effects based on gender. This underscores the importance of tailored crime prevention strategies and early interventions for individuals with ADHD, especially when comorbid SUD is present.
This perspective considers complexities in the relationship between impaired cognitive abilities and autism from a maturational, developmental perspective, and aims to serve as a helpful guide for the complex and growing investigation of cognitive abilities and Autism Spectrum Disorder (ASD). Low Intelligence Quotient (IQ) and ASD are frequently co-occurring. About 37% of 8-year old children and 48% of 4-year old children diagnosed with ASD also have Intellectual Disability, with IQ below 70. And, low IQ in early infancy, including below 1 year of age, carries a 40% greater chance of receiving ASD diagnosis in early childhood. We consider the evidence that may explain this co-occurrence, including the possibility that high IQ may “rescue” the social communication issues, as well as the possible role of critical periods during growth and development. We consider how early low IQ may subsume a part of a subgroup of individuals with ASD, in particular, those diagnosed with autism in very early childhood, and we provide neurobiological evidence in support of this subtype. Moreover, we distinguish the concept of early low IQ from the delay in speech onset in preschool and school-aged children, based on (i) age and (ii) impairments in both verbal and non-verbal domains. The etiology of these early-diagnosed, early low IQ ASD cases is different from later-diagnosed, average or higher-IQ cases, and from children with speech delay onset. Given recent interest in formulating new subtypes of autism, rather than continuing to conceive of ASD as a spectrum, as well as new subtypes that vary in the degree of severity along the spectrum, we identify gaps in knowledge and directions for future work in this complex and growing area.
The COVID-19 pandemic negatively affected child and adolescent mental health and at the end of the pandemic (April 2022) child mental health had not returned to pre-pandemic levels. We investigated whether this observed increase in mental health problems has continued, halted, or reversed after the end of the pandemic in children from the general population and in children in psychiatric care.
We collected parent-reported and child-reported data at two additional post-pandemic time points (November/December 2022 and March/April 2023) in children (8–18 years) from two general population samples (N = 818–1056 per measurement) and one clinical sample receiving psychiatric care (N = 320–370) and compared these with data from before the pandemic. We collected parent-reported data on internalizing and externalizing problems with the Brief Problem Monitor and self-reported data on Anxiety, Depressive symptoms, Sleep-related impairments, Anger, Global health, and Peer relations with the Patient-Reported Outcomes Measurement Information System (PROMIS®).
In the general population, parents reported no changes in externalizing problems but did report higher internalizing problems post-pandemic than pre-pandemic (p < 0.001). Children also reported increased mental health problems post-pandemic, especially in anxiety and depression, to a lesser extent in sleep-related impairment and global health, and least in anger (all ps < 0.01). In the clinical sample, parents reported higher internalizing (p < 0.001), but not externalizing problems post-pandemic compared to the start of the pandemic. Children reported greatest increases in problems in anxiety, depression, and global health, to a lesser extent on sleep-related impairment, and least on anger (all ps < 0.05).
Child mental health problems in the general population are substantially higher post-pandemic compared to pre-pandemic measurements. In children in psychiatric care mental health problems have increased during the pandemic and are substantially higher post-pandemic than at the start of the pandemic. Longitudinal and comparative studies are needed to assess what the most important drivers of these changes are.
Previous research has demonstrated heterogeneous adaptive outcomes across the autism spectrum; however, the current literature remains limited in elucidating turning points and associated factors for longitudinal variability (chronogeneity). To address these empirical gaps, we aimed to provide a finer-grained characterization of trajectories of adaptive functioning from early childhood to adolescence in autism.
Our sample (N = 406) was drawn from an inception cohort of children diagnosed Autistic at ages 2–5. Adaptive functioning was assessed with Vineland Adaptive Behavior Scales (VABS, 2nd Edition) across 6 visits from the time of diagnosis by age 18. Parallel-process latent growth curve modeling were used to estimate domain-level VABS trajectories, followed by latent class growth analysis to identify trajectory subgroups. Child characteristics at diagnosis, family demographics, and participation outcomes at adolescence were compared across subgroups.
Piecewise latent growth models best described VABS trajectories with two turning points identified at around ages 5-6 and 9–10, respectively reflecting transitions into school age and early adolescence. We parsed four VABS trajectory subgroups that vary by level of functioning and change rate for certain domains and periods. Around 16% of the sample exhibited overall adequate functioning (standard score >85) with notable early growth and social adaptation during adolescence. About 21% showed low adaptive functioning (standard score ≤70), with decreasing slopes by age 6 followed by improvements in communication and daily-living skills by age 10. The other two subgroups (63% in total) were characterized by adaptive functioning between low and adequate levels, with relatively stable trajectories entering school age. These subgroups differed most in their cognitive ability at diagnosis, household income, and social participation in adolescence.
We identified key individual and family characteristics and time windows associated with distinct adaptive functioning trajectories, which have important implications for providing timely and tailored supports to Autistic people across developmental stages.
Early negative life events (NLE) have long-lasting influences on neurodevelopment and psychopathology. Reduced orbitofrontal cortex (OFC) thickness was frequently associated with NLE and depressive symptoms. OFC thinning might mediate the effect of NLE on depressive symptoms, although few longitudinal studies exist. Using a complete longitudinal design with four time points, we examined whether NLE during childhood and early adolescence predict depressive symptoms in young adulthood through accelerated OFC thinning across adolescence.
We acquired structural MRI from 321 participants at two sites across four time points from ages 14 to 22. We measured NLE with the Life Events Questionnaire at the first time point and depressive symptoms with the Center for Epidemiologic Studies Depression Scale at the fourth time point. Modeling latent growth curves, we tested whether OFC thinning mediates the effect of NLE on depressive symptoms.
A higher burden of NLE, a thicker OFC at the age of 14, and an accelerated OFC thinning across adolescence predicted young adults' depressive symptoms. We did not identify an effect of NLE on OFC thickness nor OFC thickness mediating effects of NLE on depressive symptoms.
Using a complete longitudinal design with four waves, we show that NLE in childhood and early adolescence predict depressive symptoms in the long term. Results indicate that an accelerated OFC thinning may precede depressive symptoms. Assessment of early additionally to acute NLEs and neurodevelopment may be warranted in clinical settings to identify risk factors for depression.
Three papers in the December issue (2023) of JCPP Advances focus on children of parents with depression or anxiety. They highlight the value of using prospective longitudinal data to improve the understanding about the development of children of parents with depression or anxiety from early childhood to young adulthood. They contribute to an advanced understanding of long-term outcomes, causality and resilience for children of parents with depression or anxiety.
Evidence suggests that cognitive bias modification of interpretations (CBM-I) is effective in modifying interpretation biases and has a small effect on reducing anxiety in children and adolescents. However, most evidence to date is based on studies which report anxiety or general distress using ad-hoc Likert-type or Visual Analogue Scales, which are useful but do not reliably index symptoms of clinical importance. This meta-analysis aimed to establish the effects of CBM-I for children and adolescents on both anxiety and depression using psychometrically validated symptom measures, as well as state negative affect and negative and positive interpretation bias.
We identified studies through a systematic search. To be eligible for inclusion, studies needed to target interpretation biases, not combine CBM-I with another intervention, randomly allocate participants to CBM-I or a control condition, assess a mental health outcome (i.e., anxiety or depression symptoms using validated measures or state measures of negative affect) and/or interpretation bias and have a mean age less than 18 years.
We identified 36 studies for inclusion in the meta-analysis. CBM-I had a small and non-significant unadjusted effect on anxiety symptoms (g = 0.16), no effect on depression symptoms (g = −0.03), and small and non-significant unadjusted effects on state negative affect both at post-training (g = 0.16) and following a stressor task (g = 0.23). In line with previous findings, CBM-I had moderate to large unadjusted effects on negative and positive interpretations (g = 0.78 and g = 0.52). No significant moderators were identified.
CBM-I is effective at modifying interpretation bias, however there were no effects on mental health outcomes. The substantial variability across studies and paucity of studies using validated symptom measures highlight the need to establish randomized controlled trial protocols that evaluate CBM-I in clinical youth samples to determine its future as a clinical intervention.
Antipsychotics are increasingly prescribed to children and adolescents worldwide, but little is known about reasons for prescribing. We aimed to examine patterns of paediatric antipsychotic prescribing in Australian primary care services in 2011 and 2017, including diagnoses, sociodemographic characteristics, off-label prescribing, and psychotropic co-prescribing.
Retrospective analysis of electronic health records (EHRs) using a large Australian general practice database (MedicineInsight). Diagnoses of mental disorders were extracted from EHRs and associated with antipsychotic prescriptions within the same calendar year for three age-groups: 0–9, 10–14, and 15–18-year-olds.
In 2017, children/adolescents with mental health diagnoses were more likely to be prescribed antipsychotics (2.9% of 27,412 patients) than in 2011 (2.0% of 8418 patients; absolute difference +0.9, 95% CI + 0.5, +1.4). The likelihood was greater for patients with bipolar disorders (21.6% vs. 41.5%), eating disorders (1.1% vs. 7.2%), and autism without behavioural problems (3.7% vs. 6.1%). Depression/anxiety (adjusted 26.8% of patients 2011; 30.8% 2017) was the most common diagnosis associated with antipsychotics in both years. Most antipsychotics were prescribed off-label (69.8% 2011; 79.7% 2017; absolute difference +9.8, 95% CI + 1.54, +18.4). Off-label prescribing increased most among those aged 15–18-years, females, and patients living in outer regional/remote/very remote communities and the most disadvantaged areas. The three most frequently prescribed antipsychotics in both years were risperidone, quetiapine, and olanzapine. Psychotropic co-prescribing among patients receiving antipsychotic prescriptions was approximately 69% in both years.
Prescribing antipsychotics for mental health diagnoses to children/adolescents attending Australian general practices was more frequent in 2017 than 2011, and most commonly associated with depression/anxiety diagnoses. In both years, most prescribing was off-label. The majority of patients were co-prescribed other classes of psychotropics along with antipsychotics.
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