Magnetoencephalographic correlates of mood and reward dynamics in human adolescents.

Despite its omnipresence in everyday interactions and its importance for mental health, mood and its neuronal underpinnings are poorly understood. Computational models can help identify parameters affecting self-reported mood during mood induction tasks. Here, we test if computationally modeled dynamics of self-reported mood during monetary gambling can be used to identify trial-by-trial variations in neuronal activity. To this end, we shifted mood in healthy (N = 24) and depressed (N = 30) adolescents by delivering individually tailored reward prediction errors while recording magnetoencephalography (MEG) data. Following a pre-registered analysis, we hypothesize that the expectation component of mood would be predictive of beta-gamma oscillatory power (25-40 Hz). We also hypothesize that trial variations in the source localized responses to reward feedback would be predicted by mood and by its reward prediction error component. Through our multilevel statistical analysis, we found confirmatory evidence that beta-gamma power is positively related to reward expectation during mood shifts, with localized sources in the posterior cingulate cortex. We also confirmed reward prediction error to be predictive of trial-level variations in the response of the paracentral lobule. To our knowledge, this is the first study to harness computational models of mood to relate mood fluctuations to variations in neural oscillations with MEG.

Characterizing Life Stress Exposure Among Sexual Minority Adolescents: Temporality, Content, And Mediating Role in Mental Health Disparities.

Though sexual minority adolescents face a wide array of deleterious stressors, few studies have examined the role of specific types of stress exposure (i.e., chronic vs. episodic, interpersonal vs. non-interpersonal) on mental health disparities. This study utilizes a contextual threat-based assessment to (a) compare levels of stress exposure types between sexual minority and non-sexual minority adolescents, and (b) examine stress type as a mediator between sexual orientation and two outcomes: depressive symptoms and emotion dysregulation. Data comes from a longitudinal sample (14-17 years-old, N = 241; 17.6% sexual minority; 54% assigned female at birth; 73.9% White), with two time-points (T1 and T2) utilized. Sexual minority adolescents reported higher chronic interpersonal stress, but no differences in non-interpersonal chronic or episodic stress, relative to non-sexual minority adolescents. Chronic interpersonal stress exposure mediated the link between membership in an oppressed group (i.e., sexual minority teens) and the primary outcomes (emotion dysregulation and depressive symptoms) at both T1 and T2. Findings demonstrate the utility of contextual threat-based assessments within sexual minority research.

Everyday emotion, naturalistic life stress, and the prospective prediction of adolescent depression.

BACKGROUND AND OBJECTIVES: Increasing research underscores low positive emotion (PE) as a vital component of depression risk in adolescence. Theory also suggests that PE contributes to adaptive coping. However, it is unclear whether naturalistic experiences of emotions contribute to long-term depression risk, or whether daily PE levels equip adolescents to cope with later naturalistic stressors, reducing risk for depression. The current study examines whether PE (and negative emotion [NE]) assessed via ecological momentary assessment (EMA) (a) predict prospective increases in depression, and (b) moderate the association between later life stressors and depression. DESIGN: Longitudinal study of community-recruited adolescents, with EMA at baseline. METHOD: Adolescents (n = 232) completed contextual threat life stress interviews, interview and self-report measures of depression at baseline and 1.5 year follow-up. At baseline, they completed a seven-day EMA of emotion. RESULTS: Preregistered analyses showed that daily NE, but not PE, predicted increased depression over time and moderated the association between interpersonal episodic stress and self-reported depression. CONCLUSIONS: Results did not support daily PE as a buffer against depressogenic effects of life stress, but point to daily NE as a marker of depression risk.

The vicious cycle of psychopathology and stressful life events: A meta-analytic review testing the stress generation model.

Stress generation theory initially posited that depression elevates risk for some stressful events (i.e., dependent events) but not others (i.e., independent events). This preregistered meta-analytic review examined whether stress generation occurs transdiagnostically by examining 95 longitudinal studies with 38,228 participants (537 total effect sizes) from over 30 years of research. Our multilevel meta-analyses found evidence of stress generation across a broad range of psychopathology, as evidenced by significantly larger prospective effects for dependent (overall psychopathology: r = .23) than independent (overall psychopathology: r = .10) stress. We also identified unique patterns of effects across specific types of psychopathology. For example, effects were larger for depression than anxiety. Furthermore, effects were sometimes larger in studies with younger participants, shorter time lags between assessments, checklist measures of stress, and for interpersonal stressors. Finally, a multilevel meta-analytic structural equation model suggested that dependent stress exacerbates psychopathology symptoms over time (ß = .04), possibly contributing to chronicity. Interventions targeting the prevention of stress generation may mitigate chronic psychopathology. Conclusions of this study are limited by the predominance of depression effect sizes in the literature and our review of only English language articles. On the other hand, the findings are strengthened by rigorous inclusion criteria, lack of publication bias, and absence of moderating effects by publication year. The latter underscores the replicability of the stress generation effect over the last 30 years. Taken together, the review provides robust evidence that stress generation is a cross-diagnostic phenomenon that contributes to a vicious cycle of increasing stress and psychopathology. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Risk and protective factors for stress generation: A meta-analytic review.

The stress generation hypothesis suggests that some individuals contribute more than others to the occurrence of dependent (self-generated), but not independent (fateful), stressful life events. This phenomenon is commonly studied in relation to psychiatric disorders, but effects are also driven by underlying psychological processes that extend beyond the boundaries of DSM-defined entities. This meta-analytic review of modifiable risk and protective factors for stress generation synthesizes findings from 70 studies with 39,693 participants (483 total effect sizes) from over 30 years of research. Findings revealed a range of risk factors that prospectively predict dependent stress with small-to-moderate meta-analytic effects (rs = 0.10-0.26). Negligible to small effects were found for independent stress (rs = 0.03-0.12), and, in a critical test for stress generation, most effects were significantly stronger for dependent compared to independent stress (ßs = 0.04-0.15). Moderation analyses suggest effects of maladaptive interpersonal emotion regulation behaviors and repetitive negative thinking are stronger for interpersonal (versus non-interpersonal) stress; effects of repetitive negative thinking and excessive standards for self may be inflated by overreliance on self-report measures that fail to isolate psychological distress from objective experience. Findings have key implications for advancing stress generation theory and informing targets for intervention.

Genome-wide association studies of alcohol dependence, DSM-IV criterion count and individual criteria.

Genome-wide association studies (GWAS) of alcohol dependence (AD) have reliably identified variation within alcohol metabolizing genes (eg, ADH1B) but have inconsistently located other signals, which may be partially attributable to symptom heterogeneity underlying the disorder. We conducted GWAS of DSM-IV AD (primary analysis), DSM-IV AD criterion count (secondary analysis), and individual dependence criteria (tertiary analysis) among 7418 (1121 families) European American (EA) individuals from the Collaborative Study on the Genetics of Alcoholism (COGA). Trans-ancestral meta-analyses combined these results with data from 3175 (585 families) African-American (AA) individuals from COGA. In the EA GWAS, three loci were genome-wide significant: rs1229984 in ADH1B for AD criterion count (P = 4.16E-11) and Desire to cut drinking (P = 1.21E-11); rs188227250 (chromosome 8, Drinking more than intended, P = 6.72E-09); rs1912461 (chromosome 15, Time spent drinking, P = 1.77E-08). In the trans-ancestral meta-analysis, rs1229984 was associated with multiple phenotypes and two additional loci were genome-wide significant: rs61826952 (chromosome 1, DSM-IV AD, P = 8.42E-11); rs7597960 (chromosome 2, Time spent drinking, P = 1.22E-08). Associations with rs1229984 and rs18822750 were replicated in independent datasets. Polygenic risk scores derived from the EA GWAS of AD predicted AD in two EA datasets (P < .01; 0.61%-1.82% of variance). Identified novel variants (ie, rs1912461, rs61826952) were associated with differential central evoked theta power (loss - gain; P = .0037) and reward-related ventral striatum reactivity (P = .008), respectively. This study suggests that studying individual criteria may unveil new insights into the genetic etiology of AD liability.