The public health burden of alcohol is unevenly distributed across the life course, with levels of use, abuse, and dependence increasing across adolescence and peaking in early adulthood. Here, we leverage this temporal patterning to search for common genetic variants predicting developmental trajectories of alcohol consumption. Comparable psychiatric evaluations measuring alcohol consumption were collected in three longitudinal community samples (N = 2,126, obs = 12,166). Consumption-repeated measurements spanning adolescence and early adulthood were analyzed using linear mixed models, estimating individual consumption trajectories, which were then tested for association with Illumina 660W-Quad genotype data (866,099 SNPs after imputation and QC). Association results were combined across samples using standard meta-analysis methods. Four meta-analysis associations satisfied our pre-determined genome-wide significance criterion (FDR < 0.1) and six others met our ‘suggestive’ criterion (FDR <0.2). Genome-wide significant associations were highly biological plausible, including associations within GABA transporter 1, SLC6A1 (solute carrier family 6, member 1), and exonic hits in LOC100129340 (mitofusin-1-like). Pathway analyses elaborated single marker results, indicating significant enriched associations to intuitive biological mechanisms, including neurotransmission, xenobiotic pharmacodynamics, and nuclear hormone receptors (NHR). These findings underscore the value of combining longitudinal behavioral data and genome-wide genotype information in order to study developmental patterns and improve statistical power in genomic studies.

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 rate of depression rises overall between childhood and adolescence, and by early adulthood depression is twice as common in women as in men. However, study results are conflicting as to the relative rates of depression in prepubertal boys and girls, and it is not clear whether the rates in adolescent boys rise, fall, or remain steady. It is also uncertain when in adolescence the female preponderance emerges. A number of studies point to effects of the biological developments of puberty as having an important place in these changes. From a developmental point of view, the fact that the hormonal and physical changes of puberty differ in boys and girls, mean that a “biological explanation” fits in well with the gender differentiation in rates of depression across puberty. In a sample of 3,519 8–16-year-old psychiatric patients, both boys and girls shared increasing levels of depression across this age range, but the rate of increase was faster in girls. There was no difference in the rates of depression between boys and girls before the age of 11, but by the age of 16 girls were twice as likely as boys to have significant depressive symptomatology. When age was controlled for, pubertal status had no effect on depression scores. Thus, these results did not support the idea that the biological changes of puberty are a primary motive force in producing the changes in the sex ratio in depression in adolescence. Therefore, further research on this topic needs not only to address the etiology of depression in young people, but also to search for etiologic factors with differential distributions or effects on boys and girls.

The question of whether to view psychopathology as categorical or dimensional continues to provoke debate. We review the many facets of this argument. These include the pragmatics of measurement; the needs of clinical practice; our ability to distinguish categories from dimensions empirically; methods of analysis appropriate to each and how they relate; and the potential theoretical biases associated with each approach. We conclude that much of the debate is misconceived in that we do not observe pathology directly; rather, we observe its properties. The same pathology can have some properties that are most easily understood using a dimensional conceptualization while at the same time having other properties that are best understood categorically. We suggest replacing Meehl's analogy involving qualitatively distinct species with an alternative analogy with the “duality” of light, a phenomenon with both wave- and particle-like properties.

Since the mid-1980s Ian Goodyer and his colleagues have been engaged in trying to understand the dynamics of the relationship between acute and chronic life stresses and depression in adolescents (Goodyer et al. 1985, 1986). One of the great strengths of their work has been their attention to an array of potential risk factors ranging from the apparently exogenous (such as life events, e.g. Goodyer et al. 1988; Goodyer & Altham, 1991; Goodyer, 1999), through those of uncertain origin (e.g. peer and family relationships and problems, Goodyer et al. 1990), to those that can be regarded as being endogenous to the child (e.g. measures of temperament or endocrine function, Goodyer et al. 1993, 1996, 1998; Herbert et al. 1996). They have then typically attempted to determine how subsets of these factors interact in the generation of disorder (see Goodyer, 2002 for a speculative presentation of his current thinking about the relationships between social adversity and depression). A second characteristic of their research lies in its frequent attention to outcomes over time, as opposed to cross-sectional relationships (e.g. Goodyer et al. 1997a,b). Thirdly, in line with growing evidence that the relationships between environmental stress (and perhaps neuro-anatomical correlates) and depression change as repeated episodes occur (Lewinsohn et al. 1999; Daley et al. 2000), they have distinguished among first, recurrent, remitting and chronic depressive episodes. The group's latest work, presented in this issue (Goodyer et al. 2003), nicely illustrates these characteristics, and their extension to consideration of potential dynamic relations among endocrine parameters in relation to psychopathology.

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.

Studies on adults have suggested important effects of stressful life events in provoking onset of psychiatric disorder. Only a few comparable studies on children exist, and their results are inconsistent in relation to definite timing effects. Meeting some important methodological challenges overlooked in the past research, this study set out to examine whether the onset of psychiatric disorder in children was more likely to occur shortly after a severe event, as compared with other times. The sample consisted of 99 consecutive, newly referred patients, aged 8–16 years, from a child psychiatry service in London. PACE (Psychosocial Assessment of Childhood Experiences), an investigator-based, standardized interview was used to assess the timing and impact of life events over the preceding 18 months. CAPA (Child and Adolescent Psychiatric Assessment), a standardized diagnostic assessment, was used to establish the presence, timing, and consequential impairment of child and adolescent psychiatric symptoms. In a within-subject, over-time design, conditional logistic regression techniques were employed to examine whether risk of onset was greater in the 9 weeks following a high-threat life event than at other times. There was a small but statistically significant association between child-reported events and child-reported onset; the associations with parent-reported onset were inconsistent. Parent-reported events failed to relate to onset by either source. The study offers only quite limited support to the notion of negative life events provoking onset of psychiatric disorder in children and young people. The possible reasons for this are discussed, together with important conceptual and methodological issues to problems of defining onset, and the choice of appropriate designs for data analysis.

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.

Seclusion is a commonly used management technique in some areas of psychiatric practice. However, its theoretical and empirical underpinnings are greatly wanting in many respects. This paper reviews the present state of our knowledge and ignorance about seclusion, and suggests some strategies for much-needed research.

The tremendous increase in interest in childhood and adolescent depression that has occurred since the early 1970s has resulted in a large and contradictory literature. Development of the concept of childhood depression, and the many clinical studies of depression and its concomitants, both psychosocial and biological, are critically reviewed. A number of methodological and theoretical problems are discussed.