Meta-analytic evidence supports a gene-environment (G×E) interaction between life stress and the serotonin transporter polymorphism (5-HTTLPR) on depression, but few studies have examined factors that influence detection of this effect, despite years of inconsistent results. We propose that the "candidate environment" (akin to a candidate gene) is key. Theory and evidence implicate major stressful life events (SLEs)-particularly major interpersonal SLEs-as well as chronic family stress. Participants (N = 400) from the Youth Emotion Project (which began with 627 high school juniors oversampled for high neuroticism) completed up to five annual diagnostic and life stress interviews and provided DNA samples. A significant G×E effect for major SLEs and S-carrier genotype was accounted for significantly by major interpersonal SLEs but not significantly by major non-interpersonal SLEs. S-carrier genotype and chronic family stress also significantly interacted. Identifying such candidate environments may facilitate future G×E research in depression and psychopathology more broadly.

The current study compared two competing theories of the stress generation model of depression (stress causation vs. stress continuation) using interview-based measures of episodic life stress, as well as interpersonal and noninterpersonal chronic life stress. We also expanded on past research by examining anxiety disorders as well as depressive disorders. In addition, we examined the role of neuroticism and extraversion in these relationships. Participants were 627 adolescents enrolled in a two-site, longitudinal study of risk factors for depressive and anxiety disorders. Baseline and follow-up assessments were approximately one year apart. Results supported the stress causation theory for episodic stress generation for anxiety disorders, with neuroticism partially accounting for this relationship. The stress causation theory was also supported for depression, but only for more moderate to severe stressors; neuroticism partially accounted for this relationship as well. Finally, we found evidence for interpersonal and noninterpersonal chronic life stress continuation in both depressive and anxiety disorders. The present findings have implications regarding the specificity of the stress generation model to depressive disorders, as well as variables involved in the stress generation process.

Though there is a considerable amount of research supporting the association between stressful life events and major depression, there is a paucity of research concerning a range of other life stress constructs, non-depressive disorders, the role of stable personality traits, and gender differences. This study addresses these deficits by: (a) focusing on the association between interpersonal and non-interpersonal chronic life stress (CLS) and both depressive and anxiety disorders; (b) examining the roles of neuroticism and low extraversion in these associations; and (c) assessing gender differences. Participants were 603 adolescents from a study examining risk factors for emotional disorders. Depression and social phobia were associated with interpersonal CLS (IP-CLS), with neuroticism partially accounting for these associations. Low extraversion partially accounted for the association between social phobia and IP-CLS. Depression was also associated with non-interpersonal CLS (NI-CLS), but only in females. This study provides preliminary evidence for the importance of personality variables in explaining shared associations between stress and depression. Additionally, the stress-social phobia relationship is highlighted with no evidence supporting an association between other anxiety disorders and CLS.

Many studies have reported concurrent relationships between depressive symptoms and various personality, cognitive, and personality-cognitive vulnerabilities, but the degree of overlap among these vulnerabilities is unclear. Moreover, whereas most investigations of these vulnerabilities have focused on depression, their possible relationships with anxiety have not been adequately examined. The present study included 550 high school juniors and examined the cross-sectional relationships among neuroticism, negative inferential style, dysfunctional attitudes, sociotropy, and autonomy, with a wide range of anxiety and depressive symptoms, as well as the incremental validity of these different putative vulnerabilities when examined simultaneously. Correlational analyses revealed that all five vulnerabilities were significantly related to symptoms of both anxiety and depression. Whereas neuroticism accounted for significant unique variance in all symptom outcomes, individual cognitive and personality-cognitive vulnerabilities accounted for small and only sometimes statistically significant variance across outcomes. Importantly, however, for most outcomes the majority of symptom variance was accounted for by shared aspects of the vulnerabilities rather than unique aspects. Implications of these results for understanding cognitive and personality-cognitive vulnerabilities to depression and anxiety are discussed.

Neuroticism has been hypothesized to be a non-specific risk factor for both anxiety and unipolar mood disorders whereas some cognitive and personality-cognitive vulnerabilities have been hypothesized to be more specific to depression. Using a retrospective design with a sample of 575 high school juniors, we tested three competing models of the associations among these variables. Both neuroticism and the cognitive and personality-cognitive vulnerabilities had significant zero-order associations with rates of past diagnoses of both anxiety and unipolar mood disorders. Neuroticism had significant unique associations with past anxiety disorders and comorbid anxiety and unipolar mood disorders whereas the other vulnerabilities did not. In addition, gender interacted with neuroticism but not with the other vulnerabilities in associating with past diagnoses of mood disorders, showing that neuroticism is more highly associated with past unipolar mood diagnoses in males than in females. Finally, the cognitive and personality-cognitive vulnerabilities overlapped with substantial portions of the variance that neuroticism shared with diagnoses. These results suggest that, at least for retrospective associations with past anxiety and unipolar mood disorders, the cognitive and other personality-cognitive vulnerabilities are non-specific facets of neuroticism.

Altered functioning of the hypothalamic-pituitary-adrenal (HPA) axis is a robust correlate of major depression in adults, and to a lesser extent, in adolescents. Premorbid differences in HPA axis function have been found to prospectively predict the onset of adolescent depression. To what extent might our knowledge of HPA axis function in adolescents with, or at risk for, depression, help guide efforts to prevent depression in this age group? We review evidence regarding the role of the HPA axis in the development of adolescent depression, and examine whether and which HPA axis measures might be useful in guiding prevention efforts as (a) as a criterion by which to select youth at risk for depression, (b) as a predictor of which youth will be most responsive to prevention efforts, and (c) as an indicator of whether prevention/intervention efforts are working. We conclude that our current understanding of the HPA axis, and its measurement, in adolescent depression are not sufficiently precise to be of immediate practical use in improving prevention efforts. Incorporating HPA axis measures into prevention studies, however, would be immensely useful in clarifying the role of the HPA axis in adolescent depression, such that future prevention efforts might more confidently rely on HPA axis information.

Since 1990, significant efforts have been made towards developing interventions to prevent depression in youth. Meta-analyses of preventive interventions have consistently yielded small but significant effect sizes in the short-term prevention of depression. However, the maintenance of intervention effects over extended follow-ups ranging from 6 months to 3 years has not been consistently demonstrated. In this qualitative review, significant methodological issues that continue to be of concern are discussed. Illustrative studies are described to highlight the accomplishments and limitations of interventions to date. Particular areas in need of attention include the implementation of booster sessions, use of appropriate statistical analyses, examination of multiple outcome variables, augmentation of protective factors, and exploration of mediators and moderators of intervention effects. Future directions for the field of depression prevention are outlined.