Baseline brain function in the preadolescents of the ABCD Study.

The Adolescent Brain Cognitive Development (ABCD) Study® is a 10-year longitudinal study of children recruited at ages 9 and 10. A battery of neuroimaging tasks are administered biennially to track neurodevelopment and identify individual differences in brain function. This study reports activation patterns from functional MRI (fMRI) tasks completed at baseline, which were designed to measure cognitive impulse control with a stop signal task (SST; N = 5,547), reward anticipation and receipt with a monetary incentive delay (MID) task (N = 6,657) and working memory and emotion reactivity with an emotional N-back (EN-back) task (N = 6,009). Further, we report the spatial reproducibility of activation patterns by assessing between-group vertex/voxelwise correlations of blood oxygen level-dependent (BOLD) activation. Analyses reveal robust brain activations that are consistent with the published literature, vary across fMRI tasks/contrasts and slightly correlate with individual behavioral performance on the tasks. These results establish the preadolescent brain function baseline, guide interpretation of cross-sectional analyses and will enable the investigation of longitudinal changes during adolescent development.

Lifetime co-morbidity of DSM-IV disorders in the US National Comorbidity Survey Replication Adolescent Supplement (NCS-A).

BACKGROUND: Research on the structure of co-morbidity among common mental disorders has largely focused on current prevalence rather than on the development of co-morbidity. This report presents preliminary results of the latter type of analysis based on the US National Comorbidity Survey Replication Adolescent Supplement (NCS-A). METHOD: A national survey was carried out of adolescent mental disorders. DSM-IV diagnoses were based on the Composite International Diagnostic Interview (CIDI) administered to adolescents and questionnaires self-administered to parents. Factor analysis examined co-morbidity among 15 lifetime DSM-IV disorders. Discrete-time survival analysis was used to predict first onset of each disorder from information about prior history of the other 14 disorders. RESULTS: Factor analysis found four factors representing fear, distress, behavior and substance disorders. Associations of temporally primary disorders with the subsequent onset of other disorders, dated using retrospective age-of-onset (AOO) reports, were almost entirely positive. Within-class associations (e.g. distress disorders predicting subsequent onset of other distress disorders) were more consistently significant (63.2%) than between-class associations (33.0%). Strength of associations decreased as co-morbidity among disorders increased. The percentage of lifetime disorders explained (in a predictive rather than a causal sense) by temporally prior disorders was in the range 3.7-6.9% for earliest-onset disorders [specific phobia and attention deficit hyperactivity disorder (ADHD)] and much higher (23.1-64.3%) for later-onset disorders. Fear disorders were the strongest predictors of most other subsequent disorders. CONCLUSIONS: Adolescent mental disorders are highly co-morbid. The strong associations of temporally primary fear disorders with many other later-onset disorders suggest that fear disorders might be promising targets for early interventions.

Family and high-risk studies of social anxiety disorder.

OBJECTIVE: To present data on the role of familial factors in the etiology of social anxiety disorder. METHOD: Findings presented from a family/high-risk study (the Yale Family Study) and a prospective community study of youth (the Munich Early Developmental Stages of Psychopathology (EDSP) Study). RESULTS: The Yale Family Study demonstrated a substantial degree of familial aggregation of social anxiety disorder and specificity with respect to other anxiety subtypes among adult relatives. The Yale high-risk component and the EDSP Study confirm the association between parental and offspring social anxiety, but did not yield consistent evidence for an association between familial environmental factors and social anxiety. CONCLUSION: Future studies are needed to examine mechanisms for the specificity of social anxiety disorder aggregation, to identify vulnerability factors for its development and to pinpoint environmental conditions that may enhance or suppress expression of underlying vulnerability.

Association between psychiatric disorders and the progression of tobacco use behaviors.

OBJECTIVE: To examine the progression of tobacco use and the patterns of comorbidity of tobacco use and psychiatric disorders. METHOD: The authors conducted analyses of prospective and retrospective reports, collected from 1988 to 1998, of a sample of high- and low-risk youths identified on the basis of the presence or absence of a parental history of substance abuse or dependence. RESULTS: A parental history of substance use disorders was associated with regular tobacco use and nicotine dependence, but not with experimentation for all youths. Individual and composite psychiatric diagnoses were strongly associated with nicotine dependence, but not with regular use or experimentation. While the presence of an affective disorder and drug abuse/dependence generally increased the risk for co-occurring nicotine dependence, analyses based on the temporal onset of disorders showed that it was the initiation of alcohol or drug use that predicted the progression to nicotine dependence. For low-risk youths, oppositional defiant disorder was the single psychiatric risk factor that predicted the transition to nicotine dependence. CONCLUSIONS: This study adds to the accumulating evidence that has implicated comorbid psychiatric disorders in the etiology and subsequent course of nicotine dependence. In addition, family history may represent an important indicator of an increased risk for nicotine dependence.

Mood disorders in children and adolescents: an epidemiologic perspective.

Epidemiologic studies show that major depression is comparatively rare among children, but common among adolescents, with up to a 25% lifetime prevalence by the end of adolescence. Mania is much less common, with no more than a 2% lifetime prevalence by the end of adolescence. Developmental studies that include assessments of both hormonal changes and social changes through the pubertal transition are needed to investigate joint biological and environmental influences on the emergence of the gender difference in depression in puberty. Although subthreshold mood disorder symptoms are common, controversy exists about their clinical significance. This controversy is made more complex by methodologic uncertainties regarding inconsistent symptom reports obtained from parents, teachers, and children and by the pervasive existence of comorbidity. Retrospective reports about age of onset in adult studies suggest that at least 50% of youngsters with major depression and 90% of those with mania continue to have adult recurrences. These recurrences are mediated by adverse role transitions, such as truncated educational attainment and teenage childbearing, that typically occur before the time of initial treatment. Aggressive outreach and early treatment aimed at preventing the occurrence of adverse role effects might help decrease the persistence of child and adolescent mood disorders. Long-term follow-up studies are needed to resolve current uncertainties regarding nosology, methodology, and long-term treatment effects. Innovative epidemiologic research designs aimed at more quickly providing provisional information are also needed to advance understanding of long-term developmental processes.

Comorbidity of depression in children and adolescents: models and evidence from a prospective high-risk family study.

Despite abundant research demonstrating the magnitude of comorbidity and its importance in understanding childhood psychopathology, there has been limited empirical research designed to examine the nature and causes of comorbidity among youth. This article reviews the current literature on the magnitude and mechanisms of depressive comorbidity and presents data to exemplify the application of high-risk and longitudinal study designs to investigate patterns and explanations for comorbidity. A prospective family study of offspring at high and low risk for the development of anxiety was used to examine the specificity of familial comorbidity of depression and anxiety and the longitudinal stability of "pure" and comorbid disorders over an 8-year period. Findings suggest some specificity of familial expression, as well as longitudinal specificity, of depression and anxiety. The onset of depression follows the onset of most anxiety subtypes, suggesting the sequential nature of depressive comorbidity. Evaluation of mechanisms for comorbidity is important for the identification of homogeneous syndrome categories that will inform research designed to gain understanding of the pathogenesis of mood or anxiety disorders.

Correspondence among informants on parenting: preschool children, mothers, and observers.

The authors examined the correspondence among preschool children's, mothers', and observers' descriptions of parenting in the mother-child relationship along 3 dimensions (structure, warmth-responsiveness, and hostility). Ninety-four children (mean age = 5 years, 3 months) and their mothers, who represent diverse ethnic and socioeconomic groups, participated in the project. Preschool children were interviewed about their mothers' parenting by means of a developmentally sensitive, age-appropriate research tool for assessing the subjective experience of preschool children. Mothers responded to a self-report measure on their own parenting, and observers rated mothers' parenting behavior during a series of interaction tasks designed to elicit the relevant dimensions of parenting. Results indicated significantly greater correspondence between observer and child report of parenting than that between mother and child and mother and observer reports. Explanations for the inconsistencies among informants and implications of this finding are discussed.

Implications of genetic epidemiology for the prevention of substance use disorders.

Despite advances in characterizing human genotypes, the complex process through which genes exert their influence limits the application of molecular genetics to human diseases. Substance use disorders are necessarily complicated by gene-environment interaction because exposure to an exogenous substance is required for their development. The methods of genetic epidemiology are specifically designed to identify sources of complexity that impede etiologic findings and prevention efforts. The goal of this paper is to illustrate the application of family study methods to identify risk factors for substance abuse and their implications for prevention. The Yale Family Study is a controlled family study of the comorbidity of substance and psychiatric disorders. The sample consists of 223 probands with substance use and/or an anxiety disorders and community controls, 1218 adult first degree relatives and spouses, and 203 offspring (ages 7-17) followed for 8 years. Results indicated familial aggregation of substance disorders in adults and children, independence of familial aggregation of alcoholism and drug dependence, and specificity of familial clustering of some drugs of abuse. Familial factors are more strongly associated with substance dependence than abuse, with an attributable risk of 55%. Premorbid psychiatric disorders--social phobia and bipolar affective disorder in adults, and depression, anxiety, conduct, and oppositional defiant disorders in children--were strongly associated with the subsequent development of substance dependence (attributable risks ranging from 44 to 86%). A family history of substance abuse and premorbid psychopathology are strongly associated with the development of substance use disorders. Implications for primary and secondary prevention are discussed. As specific genetic vulnerability markers for substance use disorders become identified, application of the tools of genetic epidemiology may be employed to identify specific environmental risk factors that may serve as targets for prevention.

The role of context in the development of psychopathology: a conceptual framework and some speculative propositions.

Despite the explosion of studies assessing relations between various contextual factors and various forms of psychological disturbance, about the only firm conclusion one can draw regarding the environment's role in the development of psychopathology is that "bad" things have "bad" effects among some-but not all-people, some-but not all-of the time. We argue that extant research has confused two different roles of context and suggest that (1) environmental factors act as nonspecific stressors in the elicitation of psychopathology by provoking autonomic arousal, with specificity of expressed psychopathology governed by individual differences in endogenous factors; and that (2) context is specific in affecting the course of psychopathology by influencing the extent to which the behavioral, affective, or cognitive components of the pathology are repeated.

Vulnerability factors among children at risk for anxiety disorders.

BACKGROUND: The high-risk strategy is one of the most powerful approaches for identifying premorbid risk factors and reducing etiologic and phenotypic heterogeneity characteristic of the major psychiatric disorders. METHODS: This paper reviews the methods of high-risk research and findings from previous high-risk studies of anxiety. The preliminary results of the 6-8 year follow-up of a high-risk study of 192 offspring of probands with anxiety disorders, substance abuse, and unaffected controls are presented. The key study measures include comprehensive diagnostic interviews, symptom ratings, indirect measures of brain functioning (neuropsychologic, neurologic and psychophysiologic function), developmental measures, and family functioning measures. RESULTS: The major findings reveal that there is specificity of familial aggregation of anxiety disorders among parents and children; children at high risk for anxiety have increased startle reflex, autonomic reactivity, and stress reactivity, higher verbal IQ, and deficits in paired associative learning as compared to other children. CONCLUSIONS: The finding that family environment and parenting do not differ between children at risk for anxiety disorders and other children, when taken together with the strong degree of specificity of transmission of anxiety disorders, suggests that there may be temperamental vulnerability factors for anxiety disorders in general that may already manifest in children prior to puberty.