Genetic Epidemiology of Attention Deficit Hyperactivity Disorder (ADHD Index) in Adults

Context: In contrast to the large number of studies in children, there is little information on the contribution of genetic factors to Attention Deficit Hyperactivity Disorder (ADHD) in adults. Objective: To estimate the heritability of ADHD in adults as assessed by the ADHD index scored from the CAARS (Conners’ Adult ADHD Rating Scales). Design: Phenotype data from over 12,000 adults (twins, siblings and parents) registered with the Netherlands Twin Register were analyzed using genetic structural equation modeling. Main outcome measures: Heritability estimates for ADHD from the twin-family study. Results: Heritability of ADHD in adults is estimated around 30 % in men and women. There is some evidence for assortative mating. All familial transmission is explained by genetic inheritance, there is no support for the hypothesis that cultural transmission from parents to offspring is important. Conclusion: Heritability for ADHD features in adults is present, but is substantially lower than it is in children

Does Television Reflect the Evolution of Scientific Knowledge? The Case of Attention Deficit Hyperactivity Disorder Coverage on French Télévision

Biomedical findings mature from uncertain observations to validated facts. Although subsequent studies often refute initial appealing findings, newspapers privilege the latter and often fail to cover refutations. Thus, biomedical knowledge and media reporting may diverge with time. Here we investigated how French television reported on three scientific questions relative to attention deficit hyperactivity disorder (ADHD) from 1995 to 2010: i) is ADHD mainly genetic in origin, ii) does methylphenidate treatment decrease the risk of academic underachievement, and iii) are brain imaging techniques able to reveal ADHD in individual patients? Although scientific evidence regarding these questions has evolved during these 16 years, we observed that nine out of ten TV programs broadcast between 2007 and 2010 still expressed only opinions against the current scientific consensuses. The failure of TV programs to reflect the evolution of the scientific knowledge might be related to a biased selection of medical experts

From nature versus nurture, via nature and nurture, to gene x environment interaction in mental disorders

It is now generally accepted that complex mental disorders are the results of interplay between genetic and environmental factors. This holds out the prospect that by studying G × E interplay we can explain individual variation in vulnerability and resilience to environmental hazards in the development of mental disorders. Furthermore studying G × E findings may give insights in neurobiological mechanisms of psychiatric disorder and so improve individualized treatment and potentially prevention. In this paper, we provide an overview of the state of field with regard to G × E in mental disorders. Strategies for G × E research are introduced. G × E findings from selected mental disorders with onset in childhood or adolescence are reviewed [such as depressive disorders, attention-deficit/hyperactivity disorder (ADHD), obesity, schizophrenia and substance use disorders]. Early seminal studies provided evidence for G × E in the pathogenesis of depression implicating 5-HTTLPR, and conduct problems implicating MAOA. Since then G × E effects have been seen across a wide range of mental disorders (e.g., ADHD, anxiety, schizophrenia, substance abuse disorder) implicating a wide range of measured genes and measured environments (e.g., pre-, peri- and postnatal influences of both a physical and a social nature). To date few of these G × E effects have been sufficiently replicated. Indeed meta-analyses have raised doubts about the robustness of even the most well studied findings. In future we need larger, sufficiently powered studies that include a detailed and sophisticated characterization of both phenotype and the environmental risk<br/