Early pubertal maturation has been identified as a potential risk factor for internalizing and externalizing problems during adolescence. However, questions about the mechanisms that link early pubertal timing and psychopathology remain. In this article, we describe four hypotheses that explain the effects of early pubertal maturation. The hormonal influence hypothesis predicts that an increase in hormones at puberty leads to increased psychopathology. The maturation disparity hypothesis focuses on the gap between physical, social, and psychological maturation in early maturers that exacts the toll on individuals' adjustment. The contextual amplification hypothesis proposes that experiencing early pubertal transition in a disadvantaged context increases the risk for psychopathology. Finally, the accentuation hypothesis maintains that preadolescent vulnerabilities and challenges during early pubertal transition together increase problems. This article concludes with a consideration of how these hypotheses individually and collectively generate new lines of research linking early pubertal maturation and psychopathology.

Background Families of children with attention deficit hyperactivity disorder (ADHD) report more negative family relationships than families of children without ADHD. Questions remain as to the role of genetic factors underlying associations between family relationships and children’s ADHD symptoms, and the role of children’s ADHD symptoms as an evocative influence on the quality of relationships experienced within such families. Utilizing the attributes of two genetically sensitive research designs, the present study examined associations between biologically related and non-biologically related maternal ADHD symptoms, parenting practices, child impulsivity/activation, and child ADHD symptoms. The combined attributes of the study designs permit assessment of associations while controlling for passive genotype-environment correlation and directly examining evocative genotype-environment correlation (rGE); two relatively under examined confounds of past research in this area. Methods A cross-sectional adoption-at-conception design (Cardiff IVF Study; C-IVF) and a longitudinal adoption-at-birth design (Early Growth and Development Study; EGDS) were used. The C-IVF sample included 160 mothers and children (age 5–8 years). The EGDS sample included 320 linked sets of adopted children (age 6 years), adoptive-, and biologically-related mothers. Questionnaires were used to assess maternal ADHD symptoms, parenting practices, child impulsivity/activation, and child ADHD symptoms. A cross-rater approach was used across measures of maternal behavior (mother reports) and child ADHD symptoms (father reports). Results Significant associations were revealed between rearing mother ADHD symptoms, hostile parenting behavior, and child ADHD symptoms in both samples. Because both samples consisted of genetically-unrelated mothers and children, passive rGE was removed as a possible explanatory factor underlying these associations. Further, path analysis revealed evidence for evocative rGE processes in the longitudinal adoption-at-birth study (EGDS) from biologically-related maternal ADHD symptoms to biologically-unrelated maternal hostile parenting through early disrupted child behavior (impulsivity/activation), with maternal hostile parenting and disrupted child behavior associated with later child ADHD symptoms, controlling for concurrent adoptive mother ADHD symptoms. Conclusions Results highlight the importance of genetically-influenced child ADHD-related temperamental attributes on genetically-unrelated maternal hostility that in turn links to later child ADHD symptoms. Implications for intervention programs focusing on early family processes and the precursors of child ADHD symptoms are discussed.

This 11-year longitudinal study models the trajectories of depressive symptoms among approximately 550 females and males raised in divorced and nondivorced families in the rural Midwest. Using multilevel analyses, we demonstrate that, first, depressive symptoms changed according to a curvilinear pattern, especially for females; they increased during early to midadolescence and then declined in late adolescence to young adulthood. Second, compared with males, females experienced a greater number of depressive symptoms in adolescence and early adulthood. Third, children who experienced parental divorce by age 15 manifested a sharper increase in depressive symptoms compared to those from nondivorced families. Fourth, stressful life events children experienced shortly after parental divorce mediated the effect of parental divorce on depressive symptoms. Fifth and finally, time-varying stressful life events, particularly those related to relationship and personal loss, were significantly associated with the trajectories of depressive symptoms.

The effects of pubertal timing and adolescent dating on trajectories of depressed mood from early adolescence to young adulthood were examined among youths who participated in the National Longitudinal Study of Adolescent Health. Results showed that for both boys and girls, the trajectories of depressed mood between the ages of 12 and 23 took an inverse U-shape with its peak in mid-adolescence. Furthermore, pubertal timing was a significant predictor of depressed mood at age 12. The pubertal timing effect was nonlinear, suggesting that at age 12, early and late maturing youths were at risk of experiencing elevated levels of depressed mood. The adverse effect of off-time maturation gradually dissipated over time. Moreover, in early adolescence, teenagers, particularly girls, were adversely affected by dating, and off-time physical maturation exacerbated the negative effects of dating. However, the interactive effect of dating and pubertal timing gradually decreased with age. Our findings underscore the importance of examining JOURNAL OF RESEARCH ON ADOLESCENCE, 19(1), 47-74 r

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