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Attention deficit hyperactivity disorder, or ADHD, is one of the most common developmental disorders, with an average of 9 per cent of U.S. children between the ages of five and seventeen diagnosed each year. It is also one of the most controversial. Since the 1950s, when hyperactivity in children was first diagnosed, psychiatrists, educators, parents and politicians have debated the causes, treatment and implications of the disorder.

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.

\"Attention-Deficit Hyperactivity Disorder is a long-term disorder affecting many children and adults. It is also a highly controversial psychiatric disorder; in its cause, its diagnosis, and the effect of diagnosis on the patient. This controversy is exacerbated by the commonly recommended treatment for the condition - Ritalin. The Science of ADHD addresses the scientific status of ADHD in an informed and accessible way, without recourse to emotional or biased viewpoints. The very latest studies are used to present a reasoned account of ADHD and its treatment. The Science of ADHD is highly multidisciplinary, covering the areas of genetics, neuroscience, psychology and treatment. The ever increasing scientific evidence is described and discussed, informing the reader of the limitations of the science, but also the benefits that scientific enquiry can bring to understanding what goes on in the ADHD brain\"--Provided by publisher.

Attention-deficit hyperactivity disorder (ADHD), like other psychiatric disorders, represents an evolving construct that has been refined and developed over the past several decades in response to research into its clinical nature and structure. The clinical presentation and course of the disorder have been extensively characterised. Efficacious medication-based treatments are available and widely used, often alongside complementary psychosocial approaches. However, their effectiveness has been questioned because they might not address the broader clinical needs of many individuals with ADHD, especially over the longer term. Non-pharmacological approaches to treatment have proven less effective than previously thought, whereas scientific and clinical studies are starting to fundamentally challenge current conceptions of the causes of ADHD in ways that might have the potential to alter clinical approaches in the future. In view of this, we first provide an account of the diagnosis, epidemiology, and treatment of ADHD from the perspective of both the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders and the eleventh edition of the International Classification of Diseases. Second, we review the progress in our understanding of the causes and pathophysiology of ADHD on the basis of science over the past decade or so. Finally, using these discoveries, we explore some of the key challenges to both the current models and the treatment of ADHD, and the ways in which these findings can promote new perspectives.

Clear, careful explanations offer insight into what ADHD is, what causes it, how people live with it, and the latest information about treatment and prevention. Features include: primary and secondary source quotations, annotated bibliographies, and lists of organizations to contact for additional information.

Attention deficit hyperactivity disorder (ADHD) is a childhood-onset neurodevelopmental disorder with a prevalence of 1·4–3·0%. It is more common in boys than girls. Comorbidity with childhood-onset neurodevelopmental disorders and psychiatric disorders is substantial. ADHD is highly heritable and multifactorial; multiple genes and non-inherited factors contribute to the disorder. Prenatal and perinatal factors have been implicated as risks, but definite causes remain unknown. Most guidelines recommend a stepwise approach to treatment, beginning with non-drug interventions and then moving to pharmacological treatment in those most severely affected. Randomised controlled trials show short-term benefits of stimulant medication and atomoxetine. Meta-analyses of blinded trials of non-drug treatments have not yet proven the efficacy of such interventions. Longitudinal studies of ADHD show heightened risk of multiple mental health and social difficulties as well as premature mortality in adult life.

\"Self-help guide and resource for preteens with attention deficit disorder (ADD) or attention deficit-hyperactivity disorder (ADHD). Includes strategies to manage disorder and practical ways to improve organization, focus, studying, and homework skills. Also tips for making friends, controlling emotions, and being healthy\"-- Provided by publisher.

Attention-deficit hyperactivity disorder (ADHD) is associated with later depression and there is considerable genetic overlap between them. This study investigated if ADHD and ADHD genetic liability are causally related to depression using two different methods. First, a longitudinal population cohort design was used to assess the association between childhood ADHD (age 7 years) and recurrent depression in young-adulthood (age 18-25 years) in N = 8310 individuals in the Avon Longitudinal Study of Parents and Children (ALSPAC). Second, two-sample Mendelian randomization (MR) analyses examined relationships between genetic liability for ADHD and depression utilising published Genome-Wide Association Study (GWAS) data. Childhood ADHD was associated with an increased risk of recurrent depression in young-adulthood (OR 1.35, 95% CI 1.05-1.73). MR analyses suggested a causal effect of ADHD genetic liability on major depression (OR 1.21, 95% CI 1.12-1.31). MR findings using a broader definition of depression differed, showing a weak influence on depression (OR 1.07, 95% CI 1.02-1.13). Our findings suggest that ADHD increases the risk of depression later in life and are consistent with a causal effect of ADHD genetic liability on subsequent major depression. However, findings were different for more broadly defined depression.