Stressful life events and trajectories of depression symptoms in a U.S. military cohort.
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ABSTRACT:
SUBMITTER: Sampson L
PROVIDER: S-EPMC9246834 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundIn a community sample of low-income African American adolescents, we tested the interactive effects of variation in the mu 1 opioid receptor (OPRM1) gene and the occurrence of stressful life events on symptoms of depression.MethodInteractive effects of 24 OPRM1 simple nucleotide polymorphisms (SNP) and adolescent report of stressful life events on depression were tested using multilevel regressions. SNPs were dummy coded to test both additive and dominate forms of coding.ResultsFive OPRM1 SNPs showed significant evidence of interaction with stressful life events to alter depression risk (or symptoms) after adjusting for multiple testing and the correlated nature of the SNPs. Follow-up analyses showed significant differences based on OPRM1 genotype at both lower and higher frequencies of stressful life events, suggesting that participants with a copy of the minor allele on OPRM1 SNPs rs524731, rs9478503, rs3778157, rs10485057, and rs511420 have fewer symptoms in low stress conditions but more symptoms in high stress conditions compared to major allele homozygotes.LimitationsThe genetic variants associated with depression in African American adolescents may not translate to other ethnic groups. This study is also limited in that only one gene that functions within a complex biological system is addressed.ConclusionsThis current study is the first to find an interaction between OPRM1 and life stress that is associated with depression. It also addressed an understudied population within the behavioral genetics literature. Further research should test additional genes involved in the opioid system and expand the current findings to more diverse samples.
| S-EPMC4083691 | biostudies-literature
Project description:Caspi et al. (2003) found an interaction between the serotonin transporter polymorphism gene (5-HTTLPR) and stressful life events on depression. Subsequent attempts to replicate have been inconsistent. The present research included long allele variants modified by SNP rs25531 and tested the interaction on adolescents' trajectories of anxious/depressed symptoms, with consideration of possible age effects. Adolescents (N = 574), of whom 436 were genotyped, were followed from ages 12 to 17. Analyses demonstrated a G × E interaction in predicting the development of anxious/depressed symptoms. Specifically, adolescents with lower serotonin transcriptional efficiency (TE) genotypes whose mothers reported more stressful events were reported to show more anxious/depressed symptoms and greater increases in the development of symptoms of anxiety and depression than were higher TE adolescents, particularly at ages 16 and 17. Interactions did not differ by gender. Findings demonstrate that stress may affect adolescents' likelihood of experiencing anxious/depressed symptoms when they have a low serotonin TE (A/G-modified 5-HTTLPR) genotype and suggest that the vulnerability may be stronger in late than early adolescence.
| S-EPMC3404160 | biostudies-literature
Project description:Despite a growing understanding that early adversity in childhood broadly affects risk for psychopathology, the contribution of stressful life events to the development of symptoms of attention-deficit/hyperactivity disorder (ADHD) is not clear. In the present study, we examined the association between number of stressful life events experienced and ADHD symptoms, assessed using the Attention Problems subscale of the Child Behavior Checklist, in a sample of 214 children (43% male) ages 9.11-13.98 years (M = 11.38, SD = 1.05). In addition, we examined whether the timing of the events (i.e., onset through age 5 years or after age 6 years) was associated with ADHD symptoms. Finally, we examined variation in brain structure to determine whether stressful life events were associated with volume in brain regions that were found to vary as a function of symptoms of ADHD. We found a small to moderate association between number of stressful life events and ADHD symptoms. Although the strength of the associations between number of events and ADHD symptoms did not differ as a function of the age of occurrence of stressful experiences, different brain regions were implicated in the association between stressors and ADHD symptoms in the two age periods during which stressful life events occurred. These findings support the hypothesis that early adversity is associated with ADHD symptoms, and provide insight into possible brain-based mediators of this association.
| S-EPMC6249129 | biostudies-literature
Project description:Objectives: Stressful life events, especially relationship events, are frequent in adult life. We investigated the impact of a variety of stressful life events on symptoms of depression, anxiety, and hostility. Methods: We analyzed data from a large prospective cohort study of men (n = 1,437) in the Boston area (assessed in 1985, 1988, and 1991). Main outcomes were measures of depression, anxiety and hostility symptoms. We used the Elders Life Stress Inventory (ELSI) to measure stressful life events in the past 12 months and examine their association with symptoms of depression, anxiety and hostility. First, we analyzed the association of stressful life events with symptom changes; second, we categorized stressful life events into finance/work, health, relationships, loss, living situations events; and third, we estimated the specific association between relationship events and depression, anxiety and hostility symptoms using multilevel models. Results: The most frequent stressful life events were health, relationship, and financial events. Depression, anxiety, and hostility symptoms were relatively stable among men who did not experience these life events. However, those who reported life events in the past 12 months had a greater increase in symptoms of depression (+0.05; 95% CI: 0.01 to 0.10) and of hostility (+0.05; 95% CI: 0.01 to 0.09) than those who did not. Additionally, we found a significant decrease in hostility (-0.05; 95% CI: -0.08 to -0.01) in those experiencing no life events. Conclusion: Relationship events were more important than any other type of events, and were significantly associated with increased depression and hostility in aging men. Although the effects were small, the results point to a need to understand better the impact of relationships on psychopathology in the aging population.
| S-EPMC7793980 | biostudies-literature
Project description:BackgroundAdolescence is characterized by substantial changes in sleep behavior, heightened exposure to stressful life events (SLEs), and elevated risk for internalizing problems like anxiety and depression. Although SLEs are consistently associated with the onset of internalizing psychopathology, the mechanisms underlying this relationship remain poorly understood, especially at the within-person level. Here, we leverage a high-frequency longitudinal design to examine sleep as a potential mechanism linking SLEs to increases in anxiety and depression symptoms over a one-year period.MethodsThirty female adolescents aged 15-17 years completed 12 monthly in-laboratory assessments of exposure to SLEs and symptoms of anxiety and depression (n = 355 monthly assessments), and wore an actigraphy wristband for continuous monitoring of sleep for the duration of the study (n = 6,824 sleep days). Multilevel models examined concurrent and lagged within-person associations between SLEs, sleep duration and timing regularity, and anxiety and depression symptoms.ResultsWithin-person fluctuations in SLEs were associated with variability in sleep duration both concurrently and prospectively, such that when adolescents experienced greater SLEs than was typical for them, they exhibited more variable sleep duration that same month as well as the following month. In turn, within-person increases in sleep duration variability predicted greater anxiety symptoms in the same month and mediated the association between SLEs and anxiety.ConclusionsThese findings highlight sleep disruptions as a mechanism underlying the longitudinal associations between SLEs and anxiety symptoms, and suggest that interventions promoting sleep schedule consistency may help mitigate risk for stress-related psychopathology in adolescence.
| S-EPMC7494581 | biostudies-literature
Project description:Brain-derived neurotrophic factor (BDNF) polymorphisms have been examined for their contribution toward depression with equivocal results. More homogeneous phenotypes might be used to improve our understanding of genetic liability to depression. The aim of our study was to (a) test for an association between the BDNF Val66Met polymorphism and childhood-onset melancholic depression and (b) to examine the interactive effects of stressful life events (SLE) and the Val66Met polymorphism on the risk of childhood-onset melancholic depression.A total of 583 depressed probands were involved in this study (162 of the melancholic subtype). Diagnoses were derived through the Interview Schedule for Children and Adolescents - Diagnostic Version and life event data were collected using an Intake General Information Sheet.Overall, 27.8% of the participants fulfilled the criteria for melancholy. In the melancholic group, the proportion of females was higher (53.1%), although there were more males in the overall depressed sample. We detected no significant differences in genotype or allele frequency between the melancholic and the nonmelancholic depressed group. The BDNF Val66Met polymorphism and SLE interaction was not significantly associated with the melancholy outcome.In our study, females were more prone to developing the early-onset melancholic phenotype. To our knowledge, this is the first study to investigate the differentiating effect of the genotype and the G×E interaction on the melancholic phenotype in a large sample of depressed young patients. We did not find an association between the melancholic subtype of major depression and the BDNF genotype and SLE interaction in this sample, which is representative of the Hungarian clinic-referred population of depressed youths.
| S-EPMC4714603 | biostudies-literature
Project description:Depressive symptoms are disproportionately high among women and less educated individuals. One mechanism proposed to explain this is the differential vulnerability hypothesis-that these groups experience particularly strong increases in symptoms in response to stressful life events. We identify limitations to prior work and present evidence from a new approach to life stress research using the UK Household Longitudinal Study. Preliminarily, we replicate prior findings of differential vulnerability in between-individual models. Harnessing repeated measures, however, we show that apparent findings of differential vulnerability by both sex and education are artifacts of confounding. Men and women experience similar average increases in depressive symptoms after stressful life events. One exception is tentative evidence for a stronger association among women for events occurring to others in the household. We term this the "female vulnerability to network events" hypothesis and discuss with reference to Kessler and McLeod's related "cost of caring" hypothesis.
| S-EPMC9136473 | biostudies-literature
Project description:Assaultive violence events are associated with increased risk for adverse psychiatric outcomes, including post-traumatic stress (PTS), depression, and generalized anxiety. Prior research has indicated that economic, legal, and social stressors that could follow assaultive events may explain the increased risk for adverse psychiatric outcomes, yet longitudinal studies have not adequately examined this pathway. In the current study, we aimed to address this limitation.Participants (N = 1360) were part of a longitudinal population-based study of adults living in Detroit. At three waves, participants indicated their exposure to assaultive violence and economic, legal, and social stressors, and completed inventories of PTS, depression, and generalized anxiety. Longitudinal mediation models were used to test the hypothesized pathway from assaultive violence to each psychiatric outcome.The hypothesized models evidenced good fit with the data and, in each, the paths from Wave 1 (W1) assaultive violence to W2 stressors, and from W2 stressors to W3 symptoms were significant (range of Standardized Estimates: 0.09-0.15, all p < 0.01). Additionally, the indirect paths from W1 assaultive violence to W3 symptoms were significant (range of Standardized Estimates: 0.01-0.02, all p < 0.05).The findings illustrate that the economic, legal, and social stressors that could follow assaultive violence increase risk for a range of psychiatric symptoms. Although future research is needed, the results suggest that investment in interventions that prevent and mitigate assaultive violence survivors' exposure to such stressors may be an effective way to prevent mental illness in the aftermath of violent assaults.
| S-EPMC5675529 | biostudies-literature
Project description:BackgroundAlthough stressful life events (SLEs) predict subsequent risk of developing a major depressive episode (MDE), limited information exists on whether or not race and gender alters the predictive role of SLE on risk of MDE over a long-term period. The current study explored race and gender differences in the long-term predictive role of SLE at baseline (1986) on subsequent risk of MDE 25 years later (2011) in a nationally representative cohort in the United States.MethodsUsing a life course epidemiological approach, this longitudinal study borrowed data from the Americans' Changing Lives (ACL) Study 1986-2011. Main predictor of interest was baseline SLE over the last 3?years measured at 1986. Main outcome was risk of MDE [Composite International Diagnostic Interview (CIDI)] 25 years later (2011). Covariates included demographics, socioeconomics, depressive symptoms [Center for Epidemiological Studies-Depression Scale (CES-D)], chronic medical conditions, and health behaviors measured at baseline (1986). Gender and race were the focal moderators. We employed logistic regressions in the pooled sample, and specific to race and gender, to test whether or not SLE?×?race and SLE?×?gender interactions are significant.ResultsIn the pooled sample, baseline SLE (1986) predicted risk of MDE 25 years later (2011). We also found a gender by SLE interaction, suggesting a stronger predictive role of SLE for subsequent clinical depression for men compared to women. Race did not modify the predictive role of SLE on subsequent risk of MDE 25 years later.ConclusionHow SLE predicts MDE 25 years later differs for men and women, with a stronger predictive role for men compared to women. More research is needed to better understand the complex links between gender, sex, stress, and depression.
| S-EPMC4805579 | biostudies-literature
Project description:BackgroundAn interaction between recent stressful life events (SLEs) and a serotonin transporter promoter polymorphism (5-HTTLPR) in depression has been inconsistently reported. Some of this variability may be due to a previous focus on sub-clinical depression, inclusion of individuals at the lower or upper ends of the age-span, or assumptions concerning the degree of dominance of the low expressing allele. Therefore, a large sample of patients with recurrent clinically diagnosed depression and controls screened for absence of depression was utilised to examine the moderating effect of each 5-HTTLPR genetic model on the association between SLEs and severe depressive episodes.MethodA sample of 1236 recurrent unipolar depression cases and 598 age-matched, never psychiatrically ill controls completed the List of Threatening Experiences Questionnaire to assess the number of SLEs experienced in the 6 months prior to the most severe depressive episode (cases) or interview (controls). DNA extracted from blood or cheek swabs was genotyped for the short (s) and long (l) alleles of 5-HTTLPR.ResultsA greater number of SLEs were reported by cases than controls and this held across all genotypic groups. There was no main effect of 5-HTTLPR on depression and no evidence of interaction between total SLEs and any of the 5-HTTLPR genetic models. The results were the same for men and women.LimitationsUtilisation of retrospective self-reported SLEs may have reduced the accuracy of the findings and the cross-sectional design prevents causal inference.ConclusionsThis study failed to find evidence of gene-environment interplay in recurrent clinical depression.
| S-EPMC3272366 | biostudies-literature