Patterns of life stress and the development of ruminative brooding in adolescence: A person-centered approach.

Research links life stressors, including acute, chronic, and early life stress, to the development of ruminative brooding. However, singular forms of life stress rarely occur in isolation, as adolescents typically encounter stressors that vary on important dimensions (e.g., types, timings, quantities) across development. The current study employs latent profile analysis (LPA) to identify natural clusters of life stress that, over time, may be differently associated with ruminative brooding. Evaluations of episodic, chronic, and early life stress were conducted with community-recruited mid-adolescents (N = 241, Mage = 15.90 years, 53% female) and their parents using the UCLA Life Stress Interview and lifetime adversity portions of the Youth Life Stress Interview. Analyses identified four distinct patterns: low stress, high peer stress, moderate home / family stress, and multifaceted / high school stress. Adolescents in the high peer stress and moderate home / family stress profiles were at highest risk for developing a brooding style over time. Despite high overall levels of stress, teens in the multifaceted / high school stress profile were at not at elevated risk for developing a brooding style. Findings demonstrate the utility of person-centered approaches to identify patterns of stress exposure that heighten risk for brooding over time.

Distinguishing Transdiagnostic versus Disorder-Specific Pathways between Ruminative Brooding and Internalizing Psychopathology in Adolescents: A Latent Variable Modeling Approach.

Rumination is correlated with diverse types of internalizing problems, but the extent to which it relates to a higher-order internalizing spectrum versus disorder-specific pathology is unclear. Using a quantitative model of the internalizing dimension, we compared the strength of transdiagnostic versus diagnosis-specific pathways from brooding-the most depressogenic component of rumination-to major depressive disorder (MDD) in adolescents. Community-recruited mid-adolescents (N = 241, Mage = 15.90 years, 53% female) completed semi-structured interviews of anxiety and depressive conditions and a self-report brooding measure. Confirmatory factor analysis revealed good fit for a one-factor model of internalizing conditions. Results revealed a large, significant factor correlation between brooding and the internalizing factor (r = 0.55), with some evidence for a more modest specific link between brooding and the unique component of the MDD diagnosis (r = 0.17; approximately one-third as large as the transdiagnostic pathway). These cross-sectional associations were generally consistent across two assessment waves separated by 19 months. We concluded that brooding is better conceptualized as a common characteristic of all internalizing problems in adolescence, rather than a specific feature of MDD. Preregistered hypotheses, data analysis code, and correlation matrices for this study are posted at https://osf.io/dax7u/ .

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.

Negative Emotion Differentiation through a Developmental Lens: Associations with Parental Factors and Age in Adolescence.

Negative emotion differentiation (NED) is the ability to precisely discern negatively-valenced emotional states. Low NED has been linked to numerous negative outcomes. However, little is known about the conditions under which individual differences in NED emerge, particularly during adolescence, a potentially important developmental stage. We examined associations between NED (assessed using intraclass correlations between negative emotion [NE] ratings collected via intensive longitudinal methods), parental variables, and age. Adolescents (N=233, M age=15.90, 53% female) and their parents completed interview measures of depression and self-report questionnaires; adolescents then completed a seven-day ecological momentary assessment. Lower NED was associated with greater parental depression, greater authoritarian parenting style, and lower parental attachment security. Age was negatively and linearly associated with NED. Results held controlling for mean NE and adolescent depression, although authoritarian parenting was non-significant controlling for other developmental variables. Findings suggest healthy parent-child relationships may relate to adolescents' ability to perceive NEs with nuance.

The perils of murky emotions: Emotion differentiation moderates the prospective relationship between naturalistic stress exposure and adolescent depression.

Negative emotion differentiation (NED) refers to the ability to identify and label discrete negative emotions. Low NED has been previously linked to depression and other indices of low psychological well-being. However, this construct has rarely been explored during adolescence, a time of escalating depression risk, or examined in the context of naturalistic stressors. Further, the association between NED and depression has never been tested longitudinally. We propose a diathesis-stress model wherein low NED amplifies the association between stressful life events (SLEs) and depression. A sample of 233 community-recruited midadolescents (Mage 15.90 years, 54% female) completed diagnostic interviews and reported on mood and daily stressors 4 times per day for 7 days. SLEs were assessed using a semistructured interview with diagnosis-blind team coding based on the contextual threat method. Follow-up interviews were conducted 1.5 years after baseline. Low NED was correlated with depression but did not predict prospective changes in depression as a main effect. Confirming predictions and supporting a diathesis-stress model, low NED predicted (a) within-subjects associations between daily hassles and momentary depressed mood, (b) between-subjects associations between SLE severity and depression, and (c) prospective associations between SLE severity and increases in depression at follow-up. Results were specific to negative (vs. positive) emotion differentiation. Results suggest that low NED is primarily depressogenic in the context of high stress exposure. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

The developmental origins of ruminative response style: An integrative review.

Rumination has been conceptualized as a stable, trait-level response style involving repetitive and passive focus on the symptoms of distress and the possible causes and consequences of those symptoms. This theoretical review examines developmental risk factors of ruminative response style, incorporating a developmental psychopathology perspective. A model integrating these developmental factors within a conceptual framework is proposed, wherein risk factors for distress (i.e., temperamental negative affectivity, stressful environments, parenting, and genetic vulnerability) lead to engagement in rumination. We propose that when rumination is well-practiced, it will consolidate into a trait-like response style, especially among adolescents who experience cognitive control deficits. Reciprocal relationships and moderators that may contribute to the formation of a ruminative response style are also included. To understand how these factors converge and influence the formation of ruminative response styles, we review patterns of stability and change in physical and cognitive development to demonstrate that individual differences in rumination may emerge and consolidate into enduring, trait-level response styles during early adolescence.

Chronic stress exposure, diurnal cortisol slope, and implications for mood and fatigue: Moderation by multilocus HPA-Axis genetic variation.

Chronic stress exposure has been shown to alter hypothalamic-pituitary-adrenal (HPA) axis functioning, which may mediate its effects on psychopathology and negative health outcomes. The nature of the chronic stress-HPA axis dysregulation is unclear and individuals likely vary in the extent to and manner in which indices of HPA axis regulation, such as diurnal cortisol slope, are influenced by chronic stress. We examined whether HPA-axis-linked genetic variation moderates the association between chronic stress and diurnal cortisol slope, and potential implications for mood and fatigue (possible manifestations of negative clinical outcomes). 211 adolescents (M age 15.89, 54.5% female) completed chronic stress interviews and provided DNA samples. Participants then provided saliva samples at waking and 12 h post-waking for two consecutive weekdays. HPA-axis genetic variation was calculated using a multilocus genetic profile score (MGPS) approach, using ten SNPs from CRHR1, NR3C1, NR3C2, and FKBP5 to generate an additive score of HPA-axis-linked genetic risk. Neither chronic stress nor MGPS directly predicted diurnal slope, but MGPS moderated the association between chronic stress and diurnal slope, with stress predicting a high waking cortisol followed by steep slope among youth with low but not high MGPS scores. MGPS also interacted with chronic stress to predict both negative affect and fatigue, and moderated the indirect effect of chronic stress on mood and fatigue via diurnal slope. Results suggest that diurnal cortisol regulation may be one mechanism by which genetic risk intensifies the association between chronic stress and negative outcomes.

Childhood adversity moderates the influence of proximal episodic stress on the cortisol awakening response and depressive symptoms in adolescents.

Childhood adversity (CA) is known to predict sensitization to proximal stressors. Researchers have suggested that disruptions in hypothalamus-pituitary-adrenal axis functioning may be a biological mechanism. If so, CA may predict altered associations between proximal life stress and markers of cortisol secretion. We examined whether CA moderates associations between recent episodic stress and (a) the cortisol awakening response (CAR), and (b) depressive symptoms, in 241 adolescents aged 14-17 years (cortisol n = 196). Salivary cortisol was sampled at 0, 30, and 60 min postawakening for 2 days. The CAR was calculated as the area under the curve with respect to increase and waking cortisol. CA and episodic stress were assessed using contextual-threat-method-coded objective interviews. CA significantly interacted with episodic stress to predict both the CAR and depression. Among those with low CA, episodic stress predicted increased CAR but did not predict depression. For adolescents with high CA, episodic stress predicted lower CAR and higher depression. These interactions were found only for independent (uncontrollable, fateful) events, and not for dependent (self-generated) stress. Increased allostatic load resulting from CA exposure may interfere with adolescents' ability to optimally regulate their CAR in relation to recent stress, contributing to increased depression risk.

Tics and Tourette syndrome.

Tourette syndrome is a childhood onset neurodevelopmental disorder characterized by multiple motor and vocal tics. Although many youth experience attenuation or even remission of tics in adolescence and young adulthood, some individuals experience persistent tics, which can be debilitating or disabling. Most patients also have 1 or more psychiatric comorbid disorders, such as attention-deficit/hyperactivity disorder or obsessive-compulsive disorder. Treatment is multimodal, including both pharmacotherapy and cognitive-behavioral treatment, and requires disentanglement of tics and the comorbid symptoms.