Identifying the Irritability Dimension of ODD: Application of a Modified Bifactor Model Across Five Large Community Samples of Children

The importance of irritability, as measured among the symptoms of oppositional defiant disorder (ODD), has dramatically come to the fore in recent years. New diagnostic categories rely on the distinct clinical utility of irritability, and models of psychopathology suggest it plays a key role in explaining developmental pathways within and between disorders into adulthood. However, only a few studies have tested multidimensional models of ODD, and the results have been conflicting. Further, consensus has not been reached regarding which symptoms best identify irritability. The present analyses use 5 large community data sets with 5 different measures of parent-reported ODD, comprising 16,280 youth in total, to help resolve these questions. Across the samples, ages ranged from 5 to 18, and included both boys and girls. Confirmatory factor analyses demonstrated that a modified bifactor model showed the best fit in each data set. The structure of the model included 2 correlated specific factors (irritability and oppositional behavior) in addition to a general ODD factor. In 4 models, the best fit was obtained using the items “being touchy,” “angry,” and “often losing temper” as indicators of irritability. Given the structure of the models and the generally high correlation between the specific dimensions, the results suggest that irritability may not be sufficiently distinct from oppositional behavior to support an entirely independent diagnosis. Rather, irritability may be better understood as a dimension of psychopathology that can be distinguished within ODD, and which may be related to particular forms of psychopathology apart from ODD

Guidelines for evaluating the comparability of down-sampled GWAS summary statistics

Hervorming Sociale Regelgevin

A Hierarchical Taxonomy of Psychopathology Can Transform Mental Health Research

For more than a century, research on psychopathology has focused on categorical diagnoses. Although this work has produced major discoveries, growing evidence points to the superiority of a dimensional approach to the science of mental illness. Here we outline one such dimensional system—the Hierarchical Taxonomy of Psychopathology (HiTOP)—that is based on empirical patterns of co-occurrence among psychological symptoms. We highlight key ways in which this framework can advance mental-health research, and we provide some heuristics for using HiTOP to test theories of psychopathology. We then review emerging evidence that supports the value of a hierarchical, dimensional model of mental illness across diverse research areas in psychological science. These new data suggest that the HiTOP system has the potential to accelerate and improve research on mental-health problems as well as efforts to more effectively assess, prevent, and treat mental illness.FSW – Publicaties zonder aanstelling Universiteit Leide

Quantitative genetic studies of antisocial behaviour

This paper will broadly review the currently available twin and adoption data on antisocial behaviour (AB). It is argued that quantitative genetic research can make a significant contribution to further the understanding of how AB develops. Genetically informative study designs are particularly useful for investigating several important questions such as whether: the heritability estimates vary as a function of assessment method or gender; the relative importance of genetic and environmental influences varies for different types of AB; the environmental risk factors are truly environmental; and genetic vulnerability influences susceptibility to environmental risk. While the current data are not yet directly translatable for prevention and treatment programmes, quantitative genetic research has concrete translational potential. Quantitative genetic research can supplement neuroscience research in informing about different subtypes of AB, such as AB coupled with callous–unemotional traits. Quantitative genetic research is also important in advancing the understanding of the mechanisms by which environmental risk operates

Characterizing the ADHD phenotype for genetic studies

The genetic study of ADHD has made considerable progress. Further developments in the field will be reliant in part on identifying the most appropriate phenotypes for genetic analysis. The use of both categorical and dimensional measures of symptoms related to ADHD has been productive. The use of multiple reporters is a valuable feature of the characterization of psychopathology in children. It is argued that the use of aggregated measures to characterize the ADHD phenotype, particularly to establish its pervasiveness, is desirable. The recognition of the multiple comorbidities of ADHD can help to isolate more specific genetic influences. In relation to both reading disability and conduct disorder there is evidence that genes may be involved in the comorbid condition that are different from pure ADHD. To date, progress with the investigation of endophenotypes for ADHD has been disappointing. It is suggested that extending such studies beyond cognitive underpinnings to include physiological and metabolic markers might facilitate progress

Risk variants and polygenic architecture of disruptive behavior disorders in the context of attention-deficit/hyperactivity disorder

Contains fulltext : 231701.pdf (publisher's version ) (Open Access)Attention-Deficit/Hyperactivity Disorder (ADHD) is a childhood psychiatric disorder often comorbid with disruptive behavior disorders (DBDs). Here, we report a GWAS meta-analysis of ADHD comorbid with DBDs (ADHD + DBDs) including 3802 cases and 31,305 controls. We identify three genome-wide significant loci on chromosomes 1, 7, and 11. A meta-analysis including a Chinese cohort supports that the locus on chromosome 11 is a strong risk locus for ADHD + DBDs across European and Chinese ancestries (rs7118422, P = 3.15×10(-10), OR = 1.17). We find a higher SNP heritability for ADHD + DBDs (h(2)(SNP) = 0.34) when compared to ADHD without DBDs (h(2)(SNP) = 0.20), high genetic correlations between ADHD + DBDs and aggressive (r(g) = 0.81) and anti-social behaviors (r(g) = 0.82), and an increased burden (polygenic score) of variants associated with ADHD and aggression in ADHD + DBDs compared to ADHD without DBDs. Our results suggest an increased load of common risk variants in ADHD + DBDs compared to ADHD without DBDs, which in part can be explained by variants associated with aggressive behavior