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We explored patterns of concomitant psychiatric disorders in a large sample of treatment-seeking children and adolescents with autism spectrum disorder (ASD). Participants were 658 children with ASD (age 3–17 years; mean = 7.2 years) in one of six federally-funded multisite randomized clinical trials (RCT) between 1999 and 2014. All children were referred for hyperactivity or irritability. Study designs varied, but all used the Child and Adolescent Symptom Inventory or Early Childhood Inventory to assess Attention Deficit Hyperactivity Disorder (ADHD), Oppositional-Defiant Disorder (ODD), Conduct Disorder (CD), Anxiety Disorders, and Mood Disorders. In addition, several measures in common were used to assess demographic and clinical characteristics. Of the 658 children, 73% were Caucasian and 59% had an IQ >70. The rates of concomitant disorders across studies were: ADHD 81%, ODD 46%, CD 12%, any anxiety disorder 42%, and any mood disorder 8%. Two or more psychiatric disorders were identified in 66% of the sample. Of those who met criteria for ADHD, 50% also met criteria for ODD and 46% for any anxiety disorder. Associations between types of concomitant disorders and a number of demographic and clinical characteristics are presented. In this well-characterized sample of treatment-seeking children with ASD, rates of concomitant psychiatric disorders were high and the presence of two or more co-occurring disorders was common. Findings highlight the importance of improving diagnostic practice in ASD and understanding possible mechanisms of comorbidity. •We observed a high frequency of multiple concomitant DSM-defined disorders.•50% of children who met criteria for ADHD also met criteria for ODD.•46% of children who met criteria for ADHD also met criteria for an anxiety disorder.•Findings highlight the importance of improving diagnostic practices in ASD.

The impact of the Fast Track intervention on externalizing disorders across childhood was examined. Eight hundred-ninety-one early-starting children (69% male; 51% African American) were randomly assigned by matched sets of schools to intervention or control conditions. The 10-year intervention addressed parent behavior-management, child social cognitive skills, reading, home visiting, mentoring, and classroom curricula. Outcomes included psychiatric diagnoses after grades 3, 6, 9, and 12 for conduct disorder, oppositional defiant disorder, attention deficit hyperactivity disorder, and any externalizing disorder. Significant interaction effects between intervention and initial risk level indicated that intervention prevented the lifetime prevalence of all diagnoses, but only among those at highest initial risk, suggesting that targeted intervention can prevent externalizing disorders to promote the raising of healthy children.

Psychiatric disorders are the leading cause of disability worldwide while the pathogenesis remains unclear. Genome-wide association studies (GWASs) have made great achievements in detecting disease-related genetic variants. However, functional information on the underlying biological processes is often lacking. Current reports propose the use of metabolic traits as functional intermediate phenotypes (the so-called genetically determined metabotypes or GDMs) to reveal the biological mechanisms of genetics in human diseases. Here we conducted a two-sample Mendelian randomization analysis that uses GDMs to assess the causal effects of 486 human serum metabolites on 5 major psychiatric disorders, which respectively were schizophrenia (SCZ), major depression (MDD), bipolar disorder (BIP), autism spectrum disorder (ASD), and attention-deficit/hyperactivity disorder (ADHD). Using genetic variants as proxies, our study has identified 137 metabolites linked to the risk of psychiatric disorders, including 2-methoxyacetaminophen sulfate, which affects SCZ (P = 1.7 × 10–5) and 1-docosahexaenoylglycerophosphocholine, which affects ADHD (P = 5.6 × 10–5). Fourteen significant metabolic pathways involved in the 5 psychiatric disorders assessed were also detected, such as glycine, serine, and threonine metabolism for SCZ (P = .0238), Aminoacyl-tRNA biosynthesis for both MDD (P = .0144) and ADHD (P = .0029). Our study provided novel insights into integrating metabolomics with genomics in order to understand the mechanisms underlying the pathogenesis of human diseases.

Objective To examine whether behavioural strategies designed to improve children’s sleep problems could also improve the symptoms, behaviour, daily functioning, and working memory of children with attention deficit hyperactivity disorder (ADHD) and the mental health of their parents.Design Randomised controlled trial.Setting 21 general paediatric practices in Victoria, Australia.Participants 244 children aged 5-12 years with ADHD attending the practices between 2010 and 2012.Intervention Sleep hygiene practices and standardised behavioural strategies delivered by trained psychologists or trainee paediatricians during two fortnightly consultations and a follow-up telephone call. Children in the control group received usual clinical care.Main outcome measures At three and six months after randomisation: severity of ADHD symptoms (parent and teacher ADHD rating scale IV—primary outcome), sleep problems (parent reported severity, children’s sleep habits questionnaire, actigraphy), behaviour (strengths and difficulties questionnaire), quality of life (pediatric quality of life inventory 4.0), daily functioning (daily parent rating of evening and morning behavior), working memory (working memory test battery for children, six months only), and parent mental health (depression anxiety stress scales).Results Intervention compared with control families reported a greater decrease in ADHD symptoms at three and six months (adjusted mean difference for change in symptom severity −2.9, 95% confidence interval −5.5 to −0.3, P=0.03, effect size −0.3, and −3.7, −6.1 to −1.2, P=0.004, effect size −0.4, respectively). Compared with control children, intervention children had fewer moderate-severe sleep problems at three months (56% v 30%; adjusted odds ratio 0.30, 95% confidence interval 0.16 to 0.59; P<0.001) and six months (46% v 34%; 0.58, 0.32 to 1.0; P=0.07). At three months this equated to a reduction in absolute risk of 25.7% (95% confidence interval 14.1% to 37.3%) and an estimated number needed to treat of 3.9. At six months the number needed to treat was 7.8. Approximately a half to one third of the beneficial effect of the intervention on ADHD symptoms was mediated through improved sleep, at three and six months, respectively. Intervention families reported greater improvements in all other child and family outcomes except parental mental health. Teachers reported improved behaviour of the children at three and six months. Working memory (backwards digit recall) was higher in the intervention children compared with control children at six months. Daily sleep duration measured by actigraphy tended to be higher in the intervention children at three months (mean difference 10.9 minutes, 95% confidence interval −19.0 to 40.8 minutes, effect size 0.2) and six months (9.9 minutes, −16.3 to 36.1 minutes, effect size 0.3); however, this measure was only completed by a subset of children (n=54 at three months and n=37 at six months).Conclusions A brief behavioural sleep intervention modestly improves the severity of ADHD symptoms in a community sample of children with ADHD, most of whom were taking stimulant medications. The intervention also improved the children’s sleep, behaviour, quality of life, and functioning, with most benefits sustained to six months post-intervention. The intervention may be suitable for use in primary and secondary care.Trial registration Current Controlled Trials ISRCTN68819261.

\"Do you find yourself constantly asking your child to 'pick up the pace?' Does he or she seem to take longer than others to get stuff done--whether completing homework, responding when spoken to, or getting dressed and ready in the morning? Drs. Ellen Braaten and Brian Willoughby have worked with thousands of kids and teens who struggle with an area of cognitive functioning called 'processing speed,' and who are often mislabeled as lazy or unmotivated ... This ... resource demystifies processing speed and shows how to help kids (ages 5 to 18) catch up in this key area of development\"-- Provided by publisher.

Purpose of Review Autism spectrum disorder (ASD) and attention deficit/hyperactivity disorder (ADHD) are both increasing in prevalence and commonly co-occur with each other. The goal of this review is to outline what has been published recently on the topics of ASD, ADHD, and the comorbid state (ASD+ADHD) with a particular focus on shared phenomenology, differential diagnosis, and treatment considerations. Recent Findings ASD and ADHD have shared genetic heritability and are both associated with shared impairments in social functioning and executive functioning. Quantitative and qualitative differences exist, however, in the phenotypic presentations of the impairments which characterize ASD and ADHD. For ASD interventions to be maximally efficacious, comorbid ADHD needs to be considered (and vice versa). Summary The research on ASD and ADHD suggests some overlap between the two disorders yet enough differences to indicate that these conditions are sufficiently distinct to warrant separate diagnostic categories.