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.

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.

Nodal is required to maintain the uterine environment in an anti-inflammatory state during pregnancy†.

Preterm birth remains the major cause of perinatal mortality and morbidity worldwide, affecting up to 12% of pregnancies and accounting for ~75% of neonatal deaths. However, the mechanisms and causes that underlie it are still largely unknown. One of the major causes of preterm birth is infection or inflammation within the maternal-fetal interface. Our lab has previously shown that a uterine specific deletion of Nodal results in mutant females delivering 2 days prior to term demonstrating an important role for this factor in the maintenance of pregnancy. Here, we have addressed the function of Nodal in the uterus during pregnancy. We demonstrate that Nodal heterozygous mice have an increase in basal levels of pro-inflammatory cytokines IL-1ß, IL-6, IL-12p, TNF-α, and IFN-γ as well as an increase in the number of macrophages in response to the inflammatory agent, lipopolysaccharide (LPS). Using bone marrow-derived macrophages, we demonstrated that pretreatment with recombinant Nodal reduces pro-inflammatory gene expression when these cells are challenged with LPS. Our results demonstrate that Nodal is required to maintain the uterine environment in an anti-inflammatory state by preventing proinflammatory cytokine expression.

Interpersonal childhood adversity and stress generation in adolescence: Moderation by HPA axis multilocus genetic variation.

Research suggests that childhood adversity (CA) is associated with a wide range of repercussions, including an increased likelihood of interpersonal stress generation. This may be particularly true following interpersonal childhood adversity (ICA) and for youth with high hypothalamic-pituitary-adrenal (HPA) axis-related genetic risk. In the current study, we applied a multilocus genetic profile score (MGPS) approach to measuring HPA axis-related genetic variation and examined its interaction with ICA to predict interpersonal stress generation in a sample of adolescents aged 14-17 (N = 241, Caucasian subsample n = 192). MGPSs were computed using 10 single nucleotide polymorphisms from HPA axis-related genes (CRHR1, NRC31, NRC32, and FKBP5). ICA significantly predicted greater adolescent interpersonal dependent stress. Additionally, MGPS predicted a stronger association between ICA and interpersonal dependent (but not independent or noninterpersonal dependent) stress. No gene-environment interaction (G×E) effects were found for noninterpersonal CA and MGPS in predicting adolescent interpersonal dependent stress. Effects remained after controlling for current depressive symptoms and following stratification by race. Findings extend existing G×E research on stress generation to HPA axis-related genetic variation and demonstrate effects specific to the interpersonal domain.

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.

HPA-axis multilocus genetic variation moderates associations between environmental stress and depressive symptoms among adolescents.

Research suggests that genetic variants linked to hypothalamic-pituitary-adrenal (HPA)-axis functioning moderate the association between environmental stressors and depression, but examining gene-environment interactions with single polymorphisms limits power. The current study used a multilocus genetic profile score (MGPS) approach to measuring HPA-axis-related genetic variation and examined interactions with acute stress, chronic stress, and childhood adversity (assessed using contextual threat interview methods) with depressive symptoms as outcomes in an adolescent sample (ages 14-17, N = 241; White subsample n = 192). Additive MGPSs were calculated using 10 single nucleotide polymorphisms within HPA-axis genes (CRHR1, NR3C2, NR3C1, FKBP5). Higher MGPS directly correlated with adolescent depressive symptoms. Moreover, MGPS predicted stronger associations between acute and chronic stress and adolescent depressive symptoms and also moderated the effect of interpersonal, but not noninterpersonal, childhood adversity. Gene-environment interactions individually accounted for 5%-8% of depressive symptom variation. All results were retained following multiple test correction and stratification by race. Results suggest that using MGPSs provides substantial power to examine gene-environmental interactions linked to affective outcomes among adolescents.

Insomnia mediates the longitudinal relationship between anxiety and depressive symptoms in a nationally representative sample of adolescents.

BACKGROUND: Anxiety and depression are commonly comorbid with each other, with anxiety often temporally preceding the development of depression. Although increasingly research has begun to investigate the role of sleep problems in depression, no study has examined insomnia as a mediator in the longitudinal relationship between anxiety and subsequent depression. METHODS: The current study utilizes data from Waves I, II, and IV of the National Longitudinal Study of Adolescent to Adult Health, a nationally representative prospective study conducted over a 14-year period (n = 20,745, 50.5% female, M age at Wave I = 16.20). Participants completed portions of the Center for Epidemiologic Studies Depression Scale at Waves I and IV to assess depressive symptoms, a six-item anxiety measure at Wave I, and three items assessing insomnia, sleep quality, and sleep duration at Wave II. RESULTS: Structural equation modeling indicated that insomnia and unrestful sleep significantly mediated the relationship between anxiety and subsequent depression. The relationship between anxiety and depression was not significantly mediated by sleep duration. CONCLUSIONS: Findings suggest that anxiety may increase risk for the development of later depression through insomnia.

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.

Depressive Symptoms and the Anticipation and Experience of Uplifting Events in Everyday Life.

OBJECTIVE: Despite proliferation of laboratory-based studies examining reward functioning in depression, few studies have examined these processes in everyday life. We addressed this shortcoming by exploring experience and anticipation of uplifting experiences under ecologically valid conditions METHOD: One hundred fifty-seven young adults, oversampled for depressive symptoms, completed a 14-day diary tracking mood in relation to recent and anticipated positive events RESULTS: Consistent with studies supporting "mood-brightening" effects in depression, participants with greater baseline dysphoria showed stronger associations between elevated daily uplifts and lower daily depressive symptoms, particularly when events were interpersonal in nature. Baseline dysphoria was associated with lower daily anticipation of positive next-day experiences; however, when dysphoric individuals did anticipate positive experiences, they experienced greater reductions in depressed mood CONCLUSION: Results suggest that despite reward processing deficits found in laboratory studies, dysphoric individuals show improvements in mood in conjunction with anticipation and consumption of uplifting events in daily life.

Genetic moderation of the association between adolescent romantic involvement and depression: Contributions of serotonin transporter gene polymorphism, chronic stress, and family discord.

Studies support a link between adolescent romantic involvement and depression. Adolescent romantic relationships may increase depression risk by introducing chronic stress, and genetic vulnerability to stress reactivity/emotion dysregulation may moderate these associations. We tested genetic moderation of longitudinal associations between adolescent romantic involvement and later depressive symptoms by a polymorphism in the serotonin transporter linked polymorphic region gene (5-HTTLPR) and examined contributory roles of chronic stress and family discord. Three hundred eighty-one youth participated at ages 15 and 20. The results indicated that 5-HTTLPR moderated the association between age 15 romantic involvement and age 20 depressive symptoms, with strongest effects for short homozygotes. Conditional process analysis revealed that chronic stress functioned as a moderated mediator of this association, fully accounting for the romantic involvement-depression link among short/short genotypes. Also, romantic involvement predicted later depressive symptoms most strongly among short-allele carriers with high family discord. The results have important implications for understanding the romantic involvement-depression link and the behavioral and emotional correlates of the 5-HTTLPR genotype.

Protein deficiency and intestinal nematode infection in pregnant mice differentially impact fetal growth through specific stress hormones, growth factors, and cytokines.

BACKGROUND: Protein deficiency (PD) and intestinal nematode infections commonly co-occur during pregnancy and impair fetal growth, but the complex network of signals has not been explored. OBJECTIVE: Our objective was to assess those stress hormones, growth factors, and cytokines affected by maternal PD and nematode infection and associated with fetal growth. METHODS: Using a 2 × 2 factorial design, CD-1 mice, fed protein-sufficient (PS; 24%) or protein-deficient (PD; 6%) isoenergetic diets, were either uninfected or infected every 5 d with Heligmosomoides bakeri, beginning on gestational day (GD) 5. Biomarker concentrations were measured on GD 18 in maternal serum (m), fetal serum (f), and amniotic fluid (af) by using Luminex. RESULTS: Maternal PD lowered fetal body mass (PS/uninfected 1.25 ± 0.02 g, PS/infected 1.19 ± 0.02 g vs. PD/uninfected 1.11 ± 0.02 g, PD/infected 0.97 ± 0.02 g; P = 0.02), fetal lung (P = 0.005), and liver (P = 0.003) but not brain mass, whereas maternal infection lowered fetal length (PS/uninfected 2.28 ± 0.02 cm, PD/uninfected 2.27 ± 0.03 cm vs. PS/infected 2.21 ± 0.03 cm, PD/infected 2.11 ± 0.02 cm; P = 0.05) and kidney mass (P = 0.04). PD elevated stress hormones (m-adrenocortiotropic hormone, f-corticosterone, af-corticosterone) and reduced insulin-like growth factor 1 in all compartments (P ≤ 0.01), but these were unassociated with fetal mass or length. Fetal mass was positively associated with f-leptin (R(2) = 0.71, P = 0.0001) and negatively with fetal cytokines [tumor necrosis factor-α: R(2) = 0.62, P = 0.001; interleukin-4 (IL-4): R(2) = 0.63, P = 0.0004]. In contrast, maternal infection lowered f-prolactin (P = 0.02) that was positively associated with fetal length (R(2) = 0.43; P = 0.03); no other biomarker was affected by infection. Regression analyses showed associations between organ growth, cytokines, and growth factors: 1) thymus, spleen, heart, and brain with m-IL-10; 2) brain and kidney with f-vascular endothelial growth factor, af-monocyte chemotactic protein 1, af-interferon-γ, and af-eotaxin; and 3) liver and lung with f-leptin and af-corticosterone (all P ≤ 0.02). CONCLUSIONS: PD and nematode infection impaired fetal mass and linear growth, respectively. Fetal mass, length, and individual organ masses were regulated by different hormones, growth factors, and cytokines.

When Support Seeking Backfires: Co-Rumination, Excessive Reassurance Seeking, and Depressed Mood in the Daily Lives of Young Adults.

Research has linked depression to maladaptive variants of support seeking, including co-rumination (CR) and excessive reassurance seeking (ERS), which may contribute to symptom onset and maintenance. Although both CR and ERS are associated with depression, insufficient research has examined how daily behaviors and experiences interact with trait-level CR and ERS to predict daily mood. Fifty-one undergraduates, over-selected for internalizing symptoms, completed baseline assessments, followed by a 14-day daily diary assessing behaviors, stressors, and mood. Daily problem-related talk was associated with elevations in depressed mood for participants with high (but not low) trait CR, particularly for those with major depression. Trait ERS similarly moderated the association between daily reassurance seeking and depressed mood. CR, ERS, and daily reassurance seeking each predicted greater affective reactivity to daily stressors. Results align with daily processes hypothesized by CR and ERS models, and suggest that both constructs may be best understood within a diathesis-stress framework.

Does relational dysfunction mediate the association between anxiety disorders and later depression? Testing an interpersonal model of comorbidity.

BACKGROUND: Anxiety disorders tend to precede onset of comorbid depression. Several researchers have suggested a causal role for anxiety in promoting depressive episodes, but few studies have identified specific mechanisms. The current study proposes an interpersonal model of comorbidity, where anxiety disorders disrupt interpersonal functioning, which in turn elevates risk for depression. METHODS: At age 15 (T1), 815 adolescents oversampled for maternal depression completed diagnostic interviews, social chronic stress interviews, and self-report measures. At age 20 (T2), participants repeated all measures and reported on self-perceived interpersonal problems. At approximately age 23 (T3), a subset of participants (n = 475) completed a self-report depressive symptoms measure. RESULTS: Consistent with other samples, anxiety disorders largely preceded depressive disorders. Low sociability and interpersonal oversensitivity mediated the association between T1 social anxiety disorder and later depression (including T2 depressive diagnosis and T3 depressive symptoms), controlling for baseline. Interpersonal oversensitivity and social chronic stress similarly mediated the association between generalized anxiety disorder before age 15 and later depression. CONCLUSIONS: Interpersonal dysfunction may be one mechanism through which anxiety disorders promote later depression, contributing to high comorbidity rates.

Protein deficiency alters impact of intestinal nematode infection on intestinal, visceral and lymphoid organ histopathology in lactating mice.

Protein deficiency impairs local and systemic immune responses to Heligmosomoides bakeri infection but little is known about their individual and interactive impacts on tissue architecture of maternal lymphoid (thymus, spleen) and visceral (small intestine, kidney, liver, pancreas) organs during the demanding period of lactation. Using a 2 × 2 factorial design, pregnant CD1 mice were fed a 24% protein sufficient (PS) or a 6% protein deficient (PD) isoenergetic diet beginning on day 14 of pregnancy and were infected with 100 H. bakeri larvae four times or exposed to four sham infections. On day 20 of lactation, maternal organs were examined histologically and serum analytes were assayed as indicators of organ function. The absence of villus atrophy in response to infection was associated with increased crypt depth and infiltration of mast cells and eosinophils but only in lactating dams fed adequate protein. Infection-induced lobular liver inflammation was reduced in PD dams, however, abnormalities in the kidney caused by protein deficiency were absent in infected dams. Bilirubin and creatinine were highest in PD infected mice. Infection-induced splenomegaly was not due to an increase in the lymphoid compartment of the spleen. During lactation, infection and protein deficiency have interactive effects on extra-intestinal pathologies.

Sensitizing effect of early adversity on depressive reactions to later proximal stress: Moderation by polymorphisms in serotonin transporter and corticotropin releasing hormone receptor genes in a 20-year longitudinal study.

Previous research supports gene-environment interactions for polymorphisms in the corticotropin hormone receptor 1 gene (CRHR1) and the serotonin transporter gene linked polymorphic region (5-HTTLPR) in predicting depression, but it has rarely considered genetic influences on stress sensitization processes, whereby early adversities (EA) increase depressive reactivity to proximal stressors later in life. The current study tested a gene-environment-environment interaction (G × E × E; specifically, gene-EA-proximal stress interaction) model of depression in a 20-year longitudinal study. Participants were assessed prospectively for EA up to age 5 and recent chronic stress and depressive symptoms at age 20 and genotyped for CRHR1 single nucleotide polymorphism rs110402 and 5-HTTLPR. EA predicted stronger associations between recent chronic stress and depression, and the effect was moderated by genes. CRHR1 A alleles and 5-HTTLPR short alleles were associated with greater stress sensitization (i.e., greater depressive reactivity to chronic stress for those also exposed to high levels of EA). The results are consistent with the notion that EA exposure results in neurobiological and cognitive-emotional consequences (e.g., altered hypothalamic-pituitary-adrenal axis functioning), leading to emotional distress in the face of recent stressors among those with certain genetic characteristics, although further research is needed to explore explanatory mechanisms.

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.

Multiple Infections, Nutrient Deficiencies, and Inflammation as Determinants of Anemia and Iron Status during Pregnancy: The MINDI Cohort.

In pregnant women with multiple infections, nutrient deficiencies, and inflammation (MINDI), the study of anemia and iron status is limited. For this cross-sectional study (n = 213 Panamanian indigenous women), we investigated if hemoglobin, anemia (Hb < 110 g/L), ferritin, serum iron, serum transferrin receptor, and hepcidin were associated with (1) maternal nutritional status and supplementation practices, (2) biomarkers of inflammation, and (3) presence/absence of infections. Hierarchical generalized linear and logistic regression models and dominance analyses identified the relative importance of these predictors. Anemia (38%), which was likely underestimated due to low plasma volume (95%), was associated with lower ferritin, vitamin A, and weight-for-height, suggesting anemia of undernutrition. Inflammation was not associated with Hb or anemia; nevertheless, higher CRP was associated with increased odds of low serum iron and higher ferritin and hepcidin, indicating iron restriction due to inflammation. The length of iron supplementation did not enter models for anemia or iron indicators, but a multiple nutrient supplement was associated with higher ferritin and hepcidin. Moreover, iron supplementation was associated with higher odds of vaginal trichomoniasis but lower odds of caries and bacterial vaginosis. The complex pathogenesis of anemia and iron deficiency in MINDI settings may require other interventions beyond iron supplementation.

Intolerance of uncertainty as a predictor of anxiety severity and trajectory during the COVID-19 pandemic.

BACKGROUND: Efforts to identify risk and resilience factors for anxiety severity and course during the COVID-19 pandemic have focused primarily on demographic rather than psychological variables. Intolerance of uncertainty (IU), a transdiagnostic risk factor for anxiety, may be a particularly relevant vulnerability factor. METHOD: N = 641 adults with pre-pandemic anxiety data reported their anxiety, IU, and other pandemic and mental health-related variables at least once and up to four times during the COVID-19 pandemic, with assessments beginning in May 2020 through March 2021. RESULTS: In preregistered analyses using latent growth models, higher IU at the first pandemic timepoint predicted more severe anxiety, but also a sharper decline in anxiety, across timepoints. This finding was robust to the addition of pre-pandemic anxiety and demographic predictors as covariates (in the full sample) as well as pre-pandemic depression severity (in participants for whom pre-pandemic depression data were available). Younger age, lower self/parent education, and self-reported history of COVID-19 illness at the first pandemic timepoint predicted more severe anxiety across timepoints with strong model fit, but did not predict anxiety trajectory. CONCLUSIONS: IU prospectively predicted more severe anxiety but a sharper decrease in anxiety over time during the pandemic, including after adjustment for covariates. IU therefore appears to have unique and specific predictive utility with respect to anxiety in the context of the COVID-19 pandemic.

Negative emotion differentiation in trauma-exposed community members: Associations with posttraumatic stress disorder symptoms in daily life.

The ability to make fine-grained distinctions between discrete negative emotions-termed negative emotion differentiation (NED)-is important for emotion regulation and psychological well-being. Posttraumatic stress disorder (PTSD) is associated with elevated trauma-related negative emotions (e.g., fear, anger, guilt, shame) and self-reported difficulty identifying feelings, suggesting that low NED may be a feature of PTSD. PTSD is also characterized by overreliance on avoidance as an emotion regulation strategy-a characteristic that could be influenced by low NED. Here, we examined whether NED is reduced in PTSD and the role NED plays in the association between trauma-related avoidance and other PTSD symptoms (traumatic reexperiencing, negative alterations in cognition and mood, alterations in arousal and reactivity). Hypotheses were tested using 3 days of ecological momentary assessment (up to 17 prompts per day) in 80 trauma-exposed participants (39 with PTSD, 41 without PTSD; total completed surveys = 2,158). NED was reduced and self-reported difficulty identifying feelings was elevated in those with PTSD, and both predicted PTSD severity (Clinician-Administered PTSD Scale-5 score) and momentary PTSD symptoms. Furthermore, low NED, but not difficulty identifying feelings, predicted a stronger association between momentary trauma-related avoidance and PTSD symptoms. Results suggest that NED is involved in the emotional processing of trauma by decreasing the negative impact of avoidance behavior on other PTSD symptoms. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

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.