Childhood sexual abuse (CSA) and emotional maltreatment are salient risk factors for the development of major depressive disorder (MDD) in women. However, the type- and timing-specific effects of emotional maltreatment experienced during adolescence on future depressive symptomatology in women with CSA have not been explored. The goal of this study was to fill this gap.

In total, 203 women (ages 20–32) with current depressive symptoms and CSA (MDD/CSA), remitted depressive symptoms and CSA (rMDD/CSA), and current depressive symptoms without CSA (MDD/no CSA) were recruited from the community and completed self-report measures. Depressive symptoms were assessed using the Beck Depression Inventory (BDI-II) and a detailed maltreatment history was collected using the Maltreatment and Abuse Chronology of Exposure (MACE). Differences in maltreatment exposure characteristics, including multiplicity and severity of maltreatment, as well as the chronologies of emotional maltreatment subtypes were compared among groups. A random forest machine-learning algorithm was utilized to assess the impact of exposure to emotional maltreatment subtypes at specific ages on current depressive symptoms.

MDD/CSA women reported greater prevalence and severity of emotional maltreatment relative to rMDD/CSA and MDD/no CSA women [F(2,196) = 9.33, p < 0.001], specifically from ages 12 to 18. The strongest predictor of current depressive symptoms was parental verbal abuse at age 18 for both MDD/CSA women (variable importance [VI] = 1.08, p = 0.006) and MDD/no CSA women (VI = 0.68, p = 0.004).

Targeting emotional maltreatment during late adolescence might prove beneficial for future intervention efforts for MDD following CSA.

Life stress and blunted reward processing each have been associated with the onset and maintenance of major depressive disorder. However, much of this work has been cross-sectional, conducted in separate lines of inquiry, and focused on recent life stressor exposure, despite the fact that theories of depression posit that stressors can have cumulative effects over the lifespan. To address these limitations, we investigated whether acute and chronic stressors occurring over the lifespan interacted with blunted reward processing to predict increases in depression over time in healthy youth.

Participants were 245 adolescent girls aged 8–14 years old (Mage = 12.4, s.d. = 1.8) who were evaluated at baseline and two years later. The reward positivity (RewP), an event-related potential measure of reward responsiveness, was assessed at baseline using the doors task. Cumulative lifetime exposure to acute and chronic stressors was assessed two years later using the Stress and Adversity Inventory for Adolescents (Adolescent STRAIN). Finally, depressive symptoms were assessed at both baseline and follow-up using the Children's Depression Inventory.

As hypothesized, greater lifetime acute stressor exposure predicted increases in depressive symptoms over two years, but only for youth exhibiting a blunted RewP. This interaction, however, was not found for chronic stressors.

Lifetime acute stressor exposure may be particularly depressogenic for youth exhibiting a blunted RewP. Conversely, a robust RewP may be protective in the presence of greater acute lifetime stressor exposure.

Life events (LEs) are a risk factor for first onset and relapse of psychotic disorders. However, the impact of LEs on specific symptoms – namely reality distortion, disorganization, negative symptoms, depression, and mania – remains unclear. Moreover, the differential effects of negative v. positive LEs are poorly understood.

The present study utilizes an epidemiologic cohort of patients (N = 428) ascertained at first-admission for psychosis and followed for a decade thereafter. Symptoms were assessed at 6-, 24-, 48-, and 120-month follow-ups.

We examined symptom change within-person and found that negative events in the previous 6 months predicted an increase in reality distortion (β = 0.07), disorganized (β = 0.07), manic (β = 0.08), and depressive symptoms (β = 0.06), and a decrease in negative symptoms (β = −0.08). Conversely, positive LEs predicted fewer reality distortion (β = −0.04), disorganized (β = −0.04), and negative (β = −0.13) symptoms, and were unrelated to mood symptoms. A between-person approach to the same hypotheses confirmed that negative LEs predicted change in all symptoms, while positive LEs predicted change only in negative symptoms. In contrast, symptoms rarely predicted future LEs.

These findings confirm that LEs have an effect on symptoms, and thus contribute to the burden of psychotic disorders. That LEs increase positive symptoms and decrease negative symptoms suggest at least two different mechanisms underlying the relationship between LEs and symptoms. Our findings underscore the need for increased symptom monitoring following negative LEs, as symptoms may worsen during that time.

Individuals diagnosed with borderline personality disorder (BPD) often describe their lives as stressful and unpredictable. However, it is unclear whether the adversity faced by those with BPD is a product of stress reactivity or stress generation. Here, we examined the dynamic, prospective associations between BPD and stressful life events over 3 years. Given the heterogeneity present in BPD, we sought to understand which empirically derived dimensions of this heterogeneous disorder explain stress reactivity v. stress generation.

Participants included 355 individuals diagnosed with BPD and followed longitudinally at three annual assessments. Auto-regressive cross-lagged panel models were used to examine prospective associations between stressful life events and three latent dimensions implicated in BPD: negative affect, disinhibition, and antagonism.

Antagonism and disinhibition, but not negative affect, prospectively predicted dependent stressful life events (events the individual may have some role in). Evidence for decompensation under stress was more tenuous, with independent stressful life events (those presumably outside the individual's control) predicting increases in negative affect.

Our longitudinal study of a well-characterized clinical sample found more evidence for stress generation than for stress-induced decompensation in BPD. Stress generation in BPD is driven by externalizing dimensions: antagonism and disinhibition. These results highlight the utility of empirically derived dimensions for parsing heterogeneity present in BPD, leading to improvements in diagnostic evaluation, clinical prediction, and individualized approaches to treatment planning.

Investigations of drinking behavior across military deployment cycles are scarce, and few prospective studies have examined risk factors for post-deployment alcohol misuse.

Prevalence of alcohol misuse was estimated among 4645 US Army soldiers who participated in a longitudinal survey. Assessment occurred 1–2 months before soldiers deployed to Afghanistan in 2012 (T0), upon their return to the USA (T1), 3 months later (T2), and 9 months later (T3). Weights-adjusted logistic regression was used to evaluate associations of hypothesized risk factors with post-deployment incidence and persistence of heavy drinking (HD) (consuming 5 + alcoholic drinks at least 1–2×/week) and alcohol or substance use disorder (AUD/SUD).

Prevalence of past-month HD at T0, T2, and T3 was 23.3% (s.e. = 0.7%), 26.1% (s.e. = 0.8%), and 22.3% (s.e. = 0.7%); corresponding estimates for any binge drinking (BD) were 52.5% (s.e. = 1.0%), 52.5% (s.e. = 1.0%), and 41.3% (s.e. = 0.9%). Greater personal life stress during deployment (e.g., relationship, family, or financial problems) – but not combat stress – was associated with new onset of HD at T2 [per standard score increase: adjusted odds ratio (AOR) = 1.20, 95% CI 1.06–1.35, p = 0.003]; incidence of AUD/SUD at T2 (AOR = 1.54, 95% CI 1.25–1.89, p < 0.0005); and persistence of AUD/SUD at T2 and T3 (AOR = 1.30, 95% CI 1.08–1.56, p = 0.005). Any BD pre-deployment was associated with post-deployment onset of HD (AOR = 3.21, 95% CI 2.57–4.02, p < 0.0005) and AUD/SUD (AOR = 1.85, 95% CI 1.27–2.70, p = 0.001).

Alcohol misuse is common during the months preceding and following deployment. Timely intervention aimed at alleviating/managing personal stressors or curbing risky drinking might reduce risk of alcohol-related problems post-deployment.

The effect of life stress on suicidal symptoms during adolescence is well documented. Stressful life events can trigger suicidality, but most adolescents are resilient and it is unclear which factors protect against the deleterious impact of stress. Social support is thought to be one such factor. Therefore, we investigated the buffering effect of specific sources of social support (parental and peer) on life stress (interpersonal and non-interpersonal) in predicting suicidal symptoms during adolescence. In order to test the specificity of this stress buffering, we also examined it with regard to dysphoric mood.

Data come from the Adolescent Development of Emotions and Personality Traits (ADEPT) Project, a cohort of 550 adolescent females aged 13.5–15.5 recruited from Long Island. Self-reported social support, suicidality, and dysphoria were assessed at baseline and suicidality and dysphoria were assessed again at 9-month follow-up. Life stress was assessed by interview at the follow-up.

High levels of parental support protected adolescent girls from developing suicidal symptoms following a stressor. This effect was less pronounced for peer support. Also, social support did not buffer the pathogenic effects of non-interpersonal stress. Finally, social support did not buffer the effect of life stress on dysphoric symptoms.

Altogether, our results highlight a distinct developmental pathway for the development of suicidal symptoms involving parental support that differs from the development of dysphoria, and signifies the importance and specificity of social support in protecting against suicidality in adolescent girls.

This study aimed to assess the prevalence, incidence, and persistence of suicidal ideation (SI), and to investigate the psychosocial factors associated with these.

A total of 1,204 community dwelling elderly adults aged 65 years or older were evaluated at baseline, 909 (75%) of whom were followed two years later. The presence of SI was identified using the questions from the community version of the Geriatric Mental State (GMS) diagnostic schedule (GMS B3) at both baseline and follow-up interviews. Baseline measures included demographic status, years of education, rural/urban residence, accommodation, past and current occupation, monthly income, marital status, stressful life events, social support deficits, number of physical illnesses, severity of pain, physical activity, disability, depressive symptoms, anxiety, insomnia, cognitive function, alcohol consumption, and smoking.

Baseline SI prevalence, follow-up incidence (SI rate at follow-up of 805 elderly subjects who did not have SI at baseline), and persistence (SI rate at follow-up of 104 elderly subjects who had SI at baseline) were 11.5%, 9.6%, and 36.5%, respectively. Baseline SI was independently associated with no current employment, lower monthly income, stressful life events, more severe pain, presence of disability, depressive symptoms, and smoking. Incident SI was independently predicted by baseline unmarried status, social support deficit, severe pain, presence of depressive symptoms, and smoking. Persistent SI was independently predicted by baseline stressful life events and depressive symptoms.

Depressive symptoms were independently associated with prevalent, incident, and persistent SI, but other predictors varied according to incidence and persistence outcomes.

Depression requires the presence of either depressed mood or anhedonia, yet little research attention has been focused on distinguishing these two symptoms. This study aimed to obtain the prevalence rates of these two core depression symptoms and to explore the risk factors for each symptom by race/ethnicity.

2423 White, African American, Hispanic and Asian/Pacific Islander (API) women from the Massachusetts area completed the Pregnancy Risk Assessment Monitoring System (PRAMS) from 2007 to 2008.

Socioeconomic variables (SES) accounted for increased rates in depressed mood and anhedonia among African Americans and Hispanics compared with Whites. API women were still 2.1 times more likely to report anhedonia after controlling for SES. Stressors were associated with depressed mood across groups and associated with anhedonia for Whites and Hispanics. Having a female infant was associated with depressed mood for APIs. Being non-US born was associated with anhedonia for Whites, APIs and African Americans, but not Hispanics.

Prevalence rates for depressed mood and anhedonia differ across race/ethnic groups and risks associated with depressed mood and anhedonia depend on the race/ethnic group, suggesting the importance of distinguishing depressed mood from anhedonia in depression assessment and careful inquiry regarding symptom experiences with a diverse patient population.