Trait rumination and response to negative evaluative lab-induced stress: neuroendocrine, affective, and cognitive outcomes

Theoretical models of depression posit that, under stress, elevated trait rumination predicts more pronounced or prolonged negative affective and neuroendocrine responses, and that trait rumination hampers removing irrelevant negative information from working memory. We examined several gaps regarding these models in the context of lab-induced stress. Non-depressed undergraduates completed a rumination questionnaire and either a negative-evaluative Trier Social Stress Test (n = 55) or a non-evaluative control condition (n = 69), followed by a modified Sternberg affective working memory task assessing the extent to which irrelevant negative information can be emptied from working memory. We measured shame, negative and positive affect, and salivary cortisol four times. Multilevel growth curve models showed rumination and stress interactively predicted cortisol reactivity; however, opposite predictions, greater rumination was associated with blunted cortisol reactivity to stress. Elevated trait rumination interacted with stress to predict augmented shame reactivity. Rumination and stress did not significantly interact to predict working memory performance, but under control conditions, rumination predicted greater difficulty updating working memory. Results support a vulnerability-stress model of trait rumination with heightened shame reactivity and cortisol dysregulation rather than hyper-reactivity in non-depressed emerging adults, but we cannot provide evidence that working memory processes are critical immediately following acute stress

Personality subtyping and bulimia nervosa: psychopathological and genetic correlates

Background. There is empirical evidence suggesting that individuals with bulimia nervosa vary considerably in terms of psychiatric co-morbidity and personality functioning. In this study, latent profile analysis was used to attempt to identify clusters of bulimic subjects based on psychiatric co-morbidity and personality.Method. A total of 178 women with bulimia nervosa or a subclinical variant of bulimia nervosa completed a series of self-report inventories of co-morbid psychopathology and personality, and also provided a buccal smear sample for genetic analyses.Results. Three clusters of bulimic women were identified: an affective-perfectionistic cluster, an impulsive cluster, and a low co-morbid psychopathology cluster. The clusters showed expected differences on external validation tests with both personality and eating-disorder measures. The impulsive cluster showed the highest elevations on dissocial behavior and the lowest scores on compulsivity, while the affective-perfectionistic cluster showed the highest levels of eating-disorder symptoms. The clusters did not differ on genetic variations of the serotonin transporter gene.Conclusions. This study corroborates previous findings suggesting that the bulimia nervosa diagnostic category is comprised of three classes of individuals based on co-morbid psychopathology and personality. These differences may have significant etiological and treatment implications

Depression in early adolescence: Contributions from relational aggression and variation in the oxytocin receptor gene

Interpersonal stress arising from relational aggression (RA)—the intentional effort to harm others via rejection and exclusion—may increase risk for depression in youth. Biological vulnerabilities related to the hormone oxytocin, which affects social behavior and stress responses, may exacerbate this risk. In a community sample of 307 youth (52% female; age range = 10–14 years), we tested whether (1) the association between RA and subsequent depressive symptoms was mediated through social problems and (2) a single nucleotide polymorphism (rs53576) in the oxytocin receptor gene (OXTR) moderated this indirect association between RA and depression, where GG homozygotes are predicted to be more sensitive to the effects of social problems than A-allele carriers. Youth-reported RA and depressive symptoms were measured using a structured interview and a questionnaire, respectively. DNA was extracted from saliva collected with Oragene kits. Consistent with the interpersonal theory of depression, the association between relational aggression and subsequent depressive symptoms was mediated by social problems. This indirect effect was further moderated by rs53576 genotype, such that GG homozygotes showed a stronger mediation effect than A-carriers. These results suggest that rs53576 variants confer vulnerability for depression within the context of interpersonal risk factors, such that youth with the GG genotype may be particularly sensitive to the social consequences resulting from RA

The cortisol awakening response (CAR) interacts with acute interpersonal stress to prospectively predict depressive symptoms among early adolescent girls

The cortisol awakening response (CAR) has been shown to prospectively predict depression, but it remains unresolved whether a greater CAR predicts risk independently of subsequent acute stress, or whether greater CAR indicates increased vulnerability to subsequent acute stress. Further, no prior work has evaluated whether the CAR increases vulnerability to certain types of acute stress, but not others, in predicting depression. To address these gaps, we investigated whether the CAR predicted depressive symptoms alone and in interaction with acute interpersonal stress in a one-year longitudinal study of 86 early adolescent girls with no history of diagnosable depression. To index the CAR, adolescents collected saliva at waking and 30-minutes past waking for 3 days; compliance with the sampling protocol was electronically monitored. Diagnostic and objective contextual stress interviews were used to quantify acute stress in the 2-months prior to worst depressive symptom onset during the follow-up. Supporting hypotheses, results indicated that greater CAR predicted greater depressive symptoms, and interacted with acute interpersonal stress in predicting depressive symptoms. Further, the CAR interacted with acute dependent (i.e., at least partially arising from the person’s behavior) interpersonal stress in predicting depressive symptoms. In contrast, the CAR did not interact with acute non-interpersonal stress nor acute interpersonal independent (i.e., fateful) stress in predicting depressive symptoms. These results further refine circumstances in which the CAR is predictive of depressive symptoms among early adolescent girls, and highlight the importance of focusing on etiologically relevant stress when testing interactions between physiological stress indicators and environmental stress

Individual differences in early adolescents’ latent trait cortisol: Interaction of early adversity and 5-HTTLPR

The present study aimed to examine the interaction of 5-HTTLPR and early adversity on trait-like levels of cortisol. A community sample of 117 early adolescent girls (M age = 12.39 years) provided DNA samples for 5-HTTLPR genotyping, and saliva samples for assessing cortisol 3 times a day (waking, 30 min post-waking, and bedtime) over a three-day period. Latent trait cortisol (LTC) was modeled using the first 2 samples of each day. Early adversity was assessed with objective contextual stress interviews with adolescents and their mothers. A significant 5-HTTLPR × early adversity interaction indicated that greater early adversity was associated with lower LTC levels, but only among individuals with either L/L or S/L genotype. Findings suggest that serotonergic genetic variation may influence the impact of early adversity on individual differences in HPA-axis regulation. Future research should explore whether this interaction contributes to the development of psychopathology through HPA axis functioning

Serotonergic Multilocus Genetic Variation Moderates the Association Between Major Interpersonal Stress and Adolescent Depression: Replication and Candidate Environment Specification

Serotonin-linked genetic risk and stressful life event (SLE) interaction research has been criticized for using single genetic variants with inconsistent replicability. A recent study showed that a multilocus genetic profile score (MGPS) capturing additive risk from five serotonin-linked polymorphisms moderated the association between major interpersonal SLEs and depression, but no subsequent replication attempts have been reported. Moreover, major interpersonal SLEs have been suggested as “candidate environments” for this MGPS, but it has never been demonstrated that gene-environment interactions (G × Es) for major interpersonal SLEs are significantly stronger than for other contexts. Adolescents (N = 241) completed contextual-threat life stress interviews and clinical interviews assessing depressive symptoms, and provided DNA. MGPS intensified the major interpersonal stress-depression association; the interaction accounted for 4% of depressive symptom variance. Genetic moderation was statistically unique to major interpersonal stress versus other environments. Extending previous findings, results support an MGPS approach and underscore the cruciality of the G × E candidate environment

Stress in Depression

That life stress precipitates depression is one of the most replicated findings in psychiatric research,but prior to Brown and Harris’s seminal contributions, insufficiently rigorous methods led tounderestimates of the effects of stress and threatened the field. This chapter provides amethodological and historical overview, followed by a review of evidence that recent stresspredicts depression across the life span. It also examines demographic vulnerability factors andresearch on early adversity and depression, closing with future directions. Two themes manifestthroughout. First, stress assessment that uses investigator-rated severity, accounts for severity,establishes temporal precedence, and isolates the few months prior to depression onset remainscritical to progress. Second, identifying the most potent forms of stress for depression is a keyquestion that will facilitate both preventive/intervention efforts and more powerful tests inmechanistic research. Although evidence points to interpersonal forms of stress, few studiesprovide the necessary direct tests

Early Adversity and Depressive Symptoms Among Early Adolescent Girls: The Mediating Role of Exposure to Recent Interpersonal Acute Stress

Early adversity confers risk for depression in part through its association with recent (i.e., proximal) acute stress. However, it remains unresolved whether: a) early adversity predicts increases in recent acute stress over time; b) all – or only certain types – of recent events mediate the relationship between early adversity and depression; and c) early adversity places individuals at greater risk for depression via greater exposure to independent (i.e., fateful) interpersonal events or via greater generation of dependent (i.e., partially self-initiated) interpersonal events (i.e., stress generation) or both. These questions were examined in a 3-wave longitudinal study of early adolescent girls (N = 125; M = 12.35 years [SD = .77]) with no history of diagnosable depression using contextual life stress and diagnostic interviews. Path analyses indicated that increases in past-year acute interpersonal, but not non-interpersonal, stress mediated the link between early adversity and depressive symptoms. The mediating role of interpersonal events was limited to independent ones, suggesting increases in interpersonal event exposure, not interpersonal stress generation, acted as a mediator. Finally, findings support prior evidence that early adversity may not directly predict future depressive symptoms. Implications for understanding the role of recent stress in the association between early adversity and adolescent depression are discussed

Stress sensitization to depression following childhood adversity: Moderation by HPA-axis and serotonergic multilocus profile scores

Childhood adversity appears to sensitize youth to stress, increasing depression risk following stressful life events occurring throughout the lifespan. Some evidence suggests hypothalamic–pituitary–adrenal (HPA) axis-related and serotonergic genetic variation moderates this effect, in a “gene-by-environment-by-environment” interaction (G × E × E). However, prior research has tested single genetic variants, limiting power. The current study uses a multilocus genetic profile score (MGPS) approach to capture polygenic risk relevant to HPA axis and serotonergic functioning. Adolescents (N = 241, Mage = 15.90) completed contextual-threat-based interviews assessing childhood adversity and acute life events, and diagnostic interviews assessing depression. Established MGPSs indexed genetic variation linked to HPA axis (10 single nucleotide polymorphisms [SNPs]) and serotonergic (five SNPs) functioning. Results showed significant MGPS × Childhood Adversity × Recent Life Stress interactions predicting depression for both HPA axis and serotonergic MGPSs, with both risk scores predicting stronger Childhood Adversity × Recent Stress interactions. Serotonergic genetic risk specifically predicted sensitization to major interpersonal stressors. The serotonergic MGPS G × E × E was re-tested in an independent replication sample of early adolescent girls, with comparable results. Findings support the notion that genetic variation linked to these two neurobiological symptoms alters stress sensitization, and that gene-by-environment (G × E) interactions may be qualified by environmental exposures occurring at different points in development

Neuroticism and interpretive bias as risk factors for anxiety and depression

Neuroticism has been associated with depression and anxiety both cross-sectionally and longitudinally. Interpretive bias has been associated with depression and anxiety, primarily in cross-sectional and bias induction studies. The purpose of the current study was to examine the role of interpretive bias as a prospective risk factor and a mediator of the relation between neuroticism and depressive and anxious symptoms in young adults assessed longitudinally. Neuroticism significantly predicted a broad general-distress dimension but not intermediate fears and anhedonia-apprehension dimensions or a narrow social-fears dimension. Neuroticism also significantly predicted negative interpretive bias for social scenarios. Negative interpretive bias for social scenarios did not significantly predict dimension scores, nor did it mediate the relation between neuroticism and general distress or social fears. These results suggest that although neuroticism relates to negative interpretive bias, its risk for symptoms of depression and anxiety is at most weakly conferred through negative interpretive bias