The importance of including developmental and environmental measures in genetic studies of human pathology is widely acknowledged, but few empirical studies have been published. Barriers include the need for longitudinal studies that cover relevant developmental stages and for samples large enough to deal with the challenge of testing gene–environment–development interaction. A solution to some of these problems is to bring together existing data sets that have the necessary characteristics. As part of the National Institute on Drug Abuse-funded Gene-Environment-Development Initiative, our goal is to identify exactly which genes, which environments, and which developmental transitions together predict the development of drug use and misuse. Four data sets were used of which common characteristics include (1) general population samples, including males and females; (2) repeated measures across adolescence and young adulthood; (3) assessment of nicotine, alcohol, and cannabis use and addiction; (4) measures of family and environmental risk; and (5) consent for genotyping DNA from blood or saliva. After quality controls, 2,962 individuals provided over 15,000 total observations. In the first gene–environment analyses, of alcohol misuse and stressful life events, some significant gene–environment and gene–development effects were identified. We conclude that in some circumstances, already collected data sets can be combined for gene–environment and gene–development analyses. This greatly reduces the cost and time needed for this type of research. However, care must be taken to ensure careful matching across studies and variables.

Amulticategory item-response theory model was developed to characterize developmental changes in three items relating to the assessment of puberty in adolescent twin girls and boys. The model allowed for the fixed effects of age on probability of endorsing the responses and for the random effects of individual differences on the timing of pubertal changes relative to chronological age. In girls, the model was applied three-wave data on twin pairs (N = 414 female monozygotic [MZ] and 197 female dizygotic [DZ] pairs) and female twins from boy–girl pairs (N = 300 twins) from the Virginia Twin Study of Adolescent Behavioral Development. In boys, the data comprised 318 MZ and 185 DZ pairs and 297 male twins from boy–girl pairs. A total of 3172 and 2790 individual twin assessments were available in girls and boys, respectively, spanning ages 8–17 years. The availability of twin data allows the contributions of genes, the shared environment and individual unique environmental experiences to be resolved in the relative timing of pubertal changes. Parameters of the mixed model including fixed effects of age and random effects of genes and environment were estimated by Markov Chain Monte Carlo simulations using the BUGS algorithm for Gibbs sampling. The estimated standard deviation of random differences in the timing of puberty relative to age was 0.96 years in girls and 1.01 years in boys. The estimated intraclass correlations for the relative timing of pubertal changes were 0.99 +/−0.01 in MZ girls, 0.52 +/−0.02 in DZ girls, 0.88 +/−0.04 in MZ boys and 0.44+/−0.02 in DZ boys, indicating a very large contribution of genetic factors to the relative timing of pubertal change in both sexes. Additive genetic factors account for an estimated 96.3+/−3.3% of the total variance in random effects in girls and 88.0+/−3.6% in boys. Shared environmental influences account for 3.6+/−3.4% in girls and 0% in boys. In girls, nonshared environmental effects explain 0.1+/−0.1% of the total residual variance. The comparable figure in boys is 12.0+/−;3.6%.

Epidemiology, the study of patterns of disease distribution in time and space, offers a powerful set of theories and methods for understanding and preventing illness. The disruptive behavior disorders (DBDs) can be studied from the point of view of whether or not epidemiological methods could help to understand and prevent them. We suggest that the best approach to the DBDs is one that takes into account both the development of the child and the development of the disorder. Developmental epidemiology is the attempt to use recent advances in developmental psychopathology to help answer questions about how developmental processes increase or decrease vulnerability to DBDs, how risk factors change across childhood, and how the development of the disorder is reflected in rates of onset and patterns of symptomatology. Using examples of primary and secondary prevention studies, we discuss the importance of appropriate sampling strategies and a clearly articulated theoretical background, if intervention trials are to achieve their full utility as tests of a developmental theory of the DBDs.

The goal of the study was to ascertain the factor structure and prevalence of psychiatric disability in children and adolescents in relation to demographic variables and diagnosis. A representative sample of 1420 children (9–13 years) from 11 countries in North Carolina was followed for up to 6 years. Children and caretakers were interviewed with the Child and Adolescent Psychiatric Assessment, which generates DSM-IV diagnoses and includes a measure of disability secondary to psychological symptoms. Three broad areas of disability were identified (relating to family, school, and peers). School disabilities were more common in boys than girls, while the reverse was true of family disability. Effects of age were complex, and partially gender-differentiated. Children from minority ethnic groups had a higher overall prevalence of school disabilities, and were more prone than Whites to the disabling effects of disruptive behavior disorders. Anxiety disorders were as likely to result in disability as depressive disorders, and oppositional defiant disorders were more strongly associated with disability in some areas than was conduct disorder. The areas where disability is manifested are different depending on race, gender, age, and the type of disorder suffered. The implications of these findings for nosology and prevention are discussed.

Children's healthy mental development has never been the focus of long-term, committed public health policy in the way that early physical health and development have been. We discuss four types of societal response to illness—cure, care, control, and prevention—and trace the history of public health in terms of its special responsibility to control and prevent disease. We identify four periods in the history of public health: the Sanitarian era (up to 1850), the Bacterial era (1850–1950), the Behavioral era (1950–present), and the Communitarian era (the next century). Looking at this history from the viewpoint of the developmental psychopathology of the first 2 decades of life, we trace progress in public health responses to children with mental illness, from a philosophy of control by isolation toward one of preventive intervention. We examine primary, or universal, prevention strategies that have been tried, and we suggest some that might be worth reconsidering.

We review recent research on the prevalence, causes, and effects of diagnostic comorbidity among the most common groups of child and adolescent psychiatric disorders; anxiety disorders, depressive disorders, attention deficit hyperactivity disorders, oppositional defiant and conduct disorders, and substance abuse. A meta-analysis of representative general population studies provides estimates of the strength of associations between pairs of disorders with narrower confidence intervals than have previously been available. Current evidence convincingly eliminates methodological factors as a major cause of comorbidity. We review the implications of comorbidity for understanding the development of psychopathology and for nosology.