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The possible mechanisms involved in continuities and discontinuities in psychopathology between childhood and adult life are considered in relation to the findings from systematic, prospective, long-term longitudinal studies. Findings on schizophrenia, neurodevelopmental disorders, emotional disturbances, antisocial behaviour and substance abuse are used as conditions illustrating the key issues. The overarching themes are then discussed in relation to heterotypic continuity and psychopathologic progression, early age at onset and a range of possible mediating mechanisms--including genetic mediation, "kindling" effects, environmental influences, coping mechanisms and cognitive processing of experiences. Some of the key research challenges that remain concern the testing of competing hypotheses on mediating processes, the changes involved in adolescence, the transition from prodromal phase to overt schizophrenia and the emergence of adolescent-limited antisocial behaviour. Greater use needs to be made of genetic research strategies and of the testing of possible cognitive processing mediation effects.

Past research suggests that young children are incapable of reporting information about their own behavior problems. To test this, we examined the validity and the usefulness of children's self-reports in the E-Risk Study, a nationally representative birth cohort of 2,232 children. We used the Berkeley Puppet Interview to obtain children's self-reports of conduct problems when they were 5-years old and the Dominic-R when they were 7-years old. We also collected information about the children and their families by interviewing mothers, sending questionnaires to teachers, and rating examiners' observations during home visits. Results indicate that when children's self-reports are gathered with structured and developmentally appropriate instruments, they are shown to be valid measures: conduct problems reported by the children themselves were associated with known correlates including individual characteristics (e.g., IQ), related behaviors (e.g., hyperactivity), and family variables (e.g., economic disadvantages). Observed correlations closely matched effect sizes reported in the literature using adults' reports of children's behavioral problems. In addition, children's self-reports can be useful: both measures distinguished children meeting DSM-IV criteria for research diagnoses of conduct disorder. Children's reports also contributed unique information not provided by adults. For research and clinical purposes, young children's self-reports can be viewed as a valuable complement to adults' ratings and observational measures of children's behavior problems.

If maternal expressed emotion is an environmental risk factor for children's antisocial behavior problems, it should account for behavioral differences between siblings growing up in the same family even after genetic influences on children's behavior problems are taken into account. This hypothesis was tested in the Environmental Risk Longitudinal Twin Study with a nationally representative 1994-1995 birth cohort of twins. The authors interviewed the mothers of 565 five-year-old monozygotic (MZ) twin pairs and established which twin in each family received more negative emotional expression and which twin received more warmth. Within MZ pairs, the twin receiving more maternal negativity and less warmth had more antisocial behavior problems. Qualitative interviews were used to generate hypotheses about why mothers treat their children differently. The results suggest that maternal emotional attitudes toward children may play a causal role in the development of antisocial behavior and illustrate how genetically informative research can inform tests of socialization hypotheses.

Recent studies have shown that the association between maternal depression and child outcome can be moderated by children's experience of childcare (e.g., daycare) during early childhood (0–5 years). We also know that maternal depression in the child's early years has long-term associations with child development. However, the moderating role of childcare quality on long-term associations between maternal depression and child outcome has not been thoroughly investigated. This article examined longitudinal associations between probable maternal depression (PMD) during early childhood (0–5 years) and childcare quality on children's emotional and behavioral development at the age of 7–8 years (N = 207). Childcare quality was evaluated through observations within the settings. PMD during early childhood was assessed using complementary information from interviews conducted with the mother and current maternal symptoms were assessed using the Center for Epidemiologic Studies Depression Scale. Internalizing and externalizing behaviors were reported by the mother, father and the child at age 7–8 years. Results indicate that when mothers reported clinically relevant depression in early childhood, 7-8-year-old children demonstrate fewer behavioral problems if they attended a higher quality childcare setting. The moderating role of childcare quality remained after considering current maternal depression symptoms. Therefore, it is important to ensure high-quality childcare during early childhood to optimize child development. [ABSTRACT FROM AUTHOR]

As studies of measured gene–environment interactions (G × E) in developmental psychopathology gain momentum, methods for systematically and quantitatively summarizing effects across multiple studies are urgently needed. Meta-analyses of G × E findings are critical for evaluating the overall statistical and theoretical significance of any given G × E based on cumulative and systematically combined knowledge. Although meta-analytic methods for the combination of study findings based on single effect measures such as odds ratios and mean differences are well established, equivalent methods for the meta-analysis of studies investigating interactions are not well developed. This article describes one simple approach to the meta-analysis of G × E effects using, as a contemporaneous example, the interaction of the monoamine oxidase A (MAOA) gene and the impact of childhood maltreatment on risk for developing antisocial behavior. [ABSTRACT FROM PUBLISHER]