The authors investigated the emergence of gender differences in clinical depression and the overall development of depression from preadolescence to young adulthood among members of a complete birth cohort using a prospective longitudinal approach with structured diagnostic interviews administered 5 times over the course of 10 years. Small gender differences in depression (females greater than males) first began to emerge between the ages of 13 and 15. However, the greatest increase in this gender difference occurred between ages 15 and 18. Depression rates and accompanying gender differences for a university student subsample were no different than for a nonuniversity subsample.There was no gender difference for depression recurrence or for depression symptom severity. The peak increase in both overall rates of depression and new cases of depression occurred between the ages of 15 and 18. Results suggest that middle-to-late adolescence (ages 15-18) may be a critical time for studying vulnerability to depression because of the higher depression rates and the greater risk for depression onset and dramatic increase in gender differences in depression during this period.

Descriptive epidemiological studies are reviewed, showing that the female preponderance in depression begins to emerge around age 13. A developmentally sensitive, elaborated cognitive vulnerability-transactional stress model of depression is proposed to explain the "big fact" of the emergence of the gender difference in depression. The elaborated causal chain posits that negative events contribute to initial elevations of general negative affect. Generic cognitive vulnerability factors then moderate the likelihood that the initial negative affect will progress to full-blown depression. Increases in depression can lead transactionally to more self-generated dependent negative life events and thus begin the causal chain again. Evidence is reviewed providing preliminary support for the model as an explanation for the development of the gender difference in depression during adolescence.

Researchers have suggested the presence of a self-serving attributional bias, with people making more internal, stable, and global attributions for positive events than for negative events. This study examined the magnitude, ubiquity, and adaptiveness of this bias. The authors conducted a meta-analysis of 266 studies, yielding 503 independent effect sizes. The average d was 0.96, indicating a large bias. The bias was present in nearly all samples. There were significant age differences, with children and older adults displaying the largest biases. Asian samples displayed significantly smaller biases (d = 0.30) than U.S. (d = 1.05) or Western (d = 0.70) samples. Psychopathology was associated with a significantly attenuated bias (d = 0.48) compared with samples without psychopathology (d = 1.28) and community samples (d = 1.08). The bias was smallest for samples with depression (0.21), anxiety (0.46), and attention-deficit/hyperactivity disorder (0.55). Findings confirm that the self-serving attributional bias is pervasive in the general population but demonstrates significant variability across age, culture, and psychopathology.

Executive function (EF) is essential for successfully navigating nearly all of our daily activities. Of critical importance for clinical psychological science, EF impairments are associated with most forms of psychopathology. However, despite the proliferation of research on EF in clinical populations, with notable exceptions clinical and cognitive approaches to EF have remained largely independent, leading to failures to apply theoretical and methodological advances in one field to the other field and hindering progress. First, we review the current state of knowledge of EF impairments associated with psychopathology and limitations to the previous research in light of recent advances in understanding and measuring EF. Next, we offer concrete suggestions for improving EF assessment. Last, we suggest future directions, including integrating modern models of EF with state of the art, hierarchical models of dimensional psychopathology as well as translational implications of EF-informed research on clinical science.

Stress exposure and reactivity models were examined as explanations for why girls exhibit greater levels of depressive symptoms than boys. In a multiwave, longitudinal design, adolescents' depressive symptoms, alcohol usage, and occurrence of stressors were assessed at baseline, 6, and 12 months later (N=538; 54.5% female; ages 13-18, average 14.9). Daily stressors were coded into developmentally salient domains using a modified contextual-threat approach. Girls reported more depressive symptoms and stressors in certain contexts (e.g., interpersonal) than boys. Sex differences in depression were partially explained by girls reporting more stressors, especially peer events. The longitudinal direction of effects between depression and stressors varied depending on the stressor domain. Girls reacted more strongly to stressors in the form of depression.

Neuroticism's prospective association with common mental disorders (CMDs) has fueled the assumption that neuroticism is an independent etiologically informative risk factor. This vulnerability model postulates that neuroticism sets in motion processes that lead to CMDs. However, four other models seek to explain the association, including the spectrum model (manifestations of the same process), common cause model (shared determinants), state and scar models (CMD episode adds temporary / permanent neuroticism). To examine their validity we reviewed literature on confounding, operational overlap, stability and change, determinants, and treatment effects. None of the models is able to account for (virtually) all findings. The state and scar model cannot explain the prospective association. The spectrum model has some relevance, especially for internalizing disorders. Common causes are most important but the vulnerability model cannot be excluded although confounding of the prospective association by baseline symptoms and psychiatric history is substantial. In fact, some of the findings, such as interactions with stress and the small decay of neuroticism's effect over time, are consistent with the vulnerability model. We describe research designs that discriminate the remaining models and plea for deconstruction of neuroticism. Neuroticism is etiologically not informative yet but useful as an efficient marker of non-specified general risk.

To begin to resolve conflicts among current competing taxonomies of child and adolescent psychopathology, the authors developed an interview covering the symptoms of anxiety, depression, inattention, and disruptive behavior used in the Diagnostic and Statistical Manual of Mental Disorders (4th ed.; DSM-IV; American Psychiatric Association, 1994), the International Statistical Classification of Diseases and Related Health Problems (ICD-10; World Health Organization, 1992), and several implicit taxonomies. This interview will be used in the future to compare the internal and external validity of alternative taxonomies. To provide an informative framework for future hypothesis-testing studies, the authors used principal factor analysis to induce new testable hypotheses regarding the structure of this item pool in a representative sample of 1,358 children and adolescents ranging in age from 4 to 17 years. The resulting hypotheses differed from the DSM-IV, particularly in suggesting that some anxiety symptoms are part of the same syndrome as depression, whereas separation anxiety, fears, and compulsions constitute a separate anxiety dimension.

Evaluated the psychometric properties of a newly created measure of cognitive vulnerability to depression for use with adolescents. Previous measures have shown poor internal consistency reliability and have not completely assessed all hypothesized components of cognitive vulnerability. High school students completed questionnaires assessing cognitive vulnerability to depression, negative life events, depressive symptoms, and general internalizing and externalizing symptoms. The Adolescent Cognitive Style Questionnaire (ACSQ) demonstrated excellent internal consistency reliability and good test-retest reliability. Confirmatory factor analysis showed there were 3 latent factors to the ACSQ. Construct validity was supported by significant correlations with another attributional style questionnaire, as well as with depressive and internalizing symptoms. The interaction of ACSQ with negative events significantly predicted concurrent depressive and internalizing symptoms but not externalizing problems. Last, cognitive vulnerability mediated the gender difference in depressive symptoms. Overall, results suggest that the ACSQ is a highly reliable and valid measure of cognitive vulnerability to depression in adolescence.