The focus of this article is on internalizing problems that are experienced by children and adolescents. We provide an historical perspective, selectively examine the current state of knowledge, consider advances and gaps in what is known, and identify new research directions. Diagnosis, epidemiology, theory, and research first are considered separately for anxiety and depressive disorders. These internalizing problems, however, whether clinical or subclinical, share many common features and show high comorbidity rates. We emphasize the importance of systematic analysis of comorbid anxiety and depression, including their comorbidity with externalizing problems. This could lead to more valid classification of subtypes of internalizing problems and further an understanding of the diverse conditions that constitute internalized distress. We highlight the need to study anxiety and depression within a developmental psychopathology framework, as well as to include both categorical and dimensional assessments of these problems in the same research designs. This will be essential for understanding the complex interplay of biological and environmental processes that contribute to the emergence, progression, and amelioration of internalizing problems over time.

The hypothalamic-pituitary-adrenal (HPA) axis is a primary mechanism in the allostatic process through which early life stress (ELS) contributes to disease. Studies of the influence of ELS on children’s HPA axis functioning have yielded inconsistent findings. To address this issue, the present study considers multiple types of ELS (maternal depression, paternal depression, and family expressed anger), mental health symptoms, and two components of HPA functioning (trait-like and epoch-specific activity) in a long-term prospective community study of 357 children. ELS was assessed during the infancy and preschool periods; mental health symptoms and cortisol were assessed at child ages 9, 11, 13, and 15 years. A 3-level hierarchical linear model addressed questions regarding the influences of ELS on HPA functioning and its co-variation with mental health symptoms. ELS influenced trait-like cortisol level and slope, with both hyper- and hypo-arousal evident depending on type of ELS. Further, type(s) of ELS influenced co-variation of epoch-specific HPA functioning and mental health symptoms, with a tighter coupling of HPA alterations with symptom severity among children exposed previously to ELS. Results highlight the importance of examining multiple types of ELS and dynamic HPA functioning in order to capture the allostatic process unfolding across the transition into adolescence.

This study aimed to (1) identify a stable, trait-like component to cortisol and its circadian rhythm, and (2) investigate individual differences in developmental trajectories of HPA-axis maturation. Multiple salivary cortisol samples were collected longitudinally across four assessments from age 9 (3rd grade) through age 15 (9th grade) in a community sample of children (N=357). Sophisticated statistical models examined cortisol levels and its rhythm over time; effects of age, puberty and gender were primarily considered. In addition to situation-specific and stable short-term or epoch-specific cortisol components, there is a stable, trait-like component of cortisol levels and circadian rhythm across multiple years covering the transition from childhood into adolescence. Youth had higher cortisol and flatter circadian rhythms as they got older and more physically developed. Girls had higher cortisol, stronger circadian rhythms, and greater developmental influences across adolescence. Distinguishing a stable, trait-like component of cortisol level and its circadian rhythm provides the empirical foundation for investigating putative mechanisms underlying individual differences in HPA functioning. The findings also provide important descriptive information about maturational processes influencing HPA-axis development.

Objective Evidence suggests that chronic high levels of behavioral inhibition are a precursor of social anxiety disorder (SAD). This study identified the early risk factors for and developmental pathways to chronic high inhibition among school-age children and its association with SAD by adolescence. Method A community sample of 238 children was followed from birth to Grade 9. Mothers, children, and teachers reported on children's behavioral inhibition from Grades 1 to 9. Lifetime history of psychiatric disorders was available for the subset of 60 (25%) children who participated in an intensive laboratory assessment at Grade 9. Four early risk factors were assessed: female gender; exposure to maternal stress during the infancy and preschool periods and at child age 4.5 years; early manifestation of behavioral inhibition, and elevated afternoon salivary cortisol levels. Results All four risk factors predicted higher and more chronic inhibition from Grade 1 to Grade 9, and together, defined two developmental pathways. The first pathway in female children was partially mediated by early evidence of behavioral inhibition and elevated cortisol levels at age 4.5 years. The second pathway began with exposure to early maternal stress and was also partially mediated by childhood cortisol levels. By Grade 9, chronic high inhibition was associated with a lifetime history of SAD. Conclusions Chronic high levels of behavioral inhibition are associated with SAD by adolescence. The identification of two developmental pathways suggests the potential importance of considering both sets of risk factors in developing preventive interventions for SAD.

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