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Modeling and estimating the feedback mechanisms among depression, rumination, and stressors in adolescents.

ABSTRACT: The systemic interactions among depressive symptoms, rumination, and stress are important to understanding depression but have not yet been quantified. In this article, we present a system dynamics simulation model of depression that captures the reciprocal relationships among stressors, rumination, and depression. Building on the response styles theory, this model formalizes three interdependent mechanisms: 1) Rumination contributes to 'keeping stressors alive'; 2) Rumination has a direct impact on depressive symptoms; and 3) Both 'stressors kept alive' and current depressive symptoms contribute to rumination. The strength of these mechanisms is estimated using data from 661 adolescents (353 girls and 308 boys) from two middle schools (grades 6-8). These estimates indicate that rumination contributes to depression by keeping stressors 'alive'-and the individual activated-even after the stressor has ended. This mechanism is stronger among girls than boys, increasing their vulnerability to a rumination reinforcing loop. Different profiles of depression emerge over time depending on initial levels of depressive symptoms, rumination, and stressors as well as the occurrence rate for stressors; levels of rumination and occurrence of stressors are stronger contributors to long-term depression. Our systems model is a steppingstone towards a more comprehensive understanding of depression in which reinforcing feedback mechanisms play a significant role. Future research is needed to expand this simulation model to incorporate other drivers of depression and provide a more holistic tool for studying depression.

SUBMITTER: Hosseinichimeh N

PROVIDER: S-EPMC6160072 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Project description:BACKGROUND:Despite research supporting moderate heritability of depression, efforts to replicate candidate gene associations to depression have yielded inconsistent results. We tested whether Val66Met and 5-HTTLPR exhibit utility as genetic markers of depression risk, testing for replicable associations to cognitive and interpersonal endophenotypes of depression (rumination and co-rumination), and further exploring developmental and sex moderation. METHOD:In Study I, 228 youth (ages 8-14) of mothers with or without a history of MDD during the child's lifetime were recruited from the community. Replication tests were carried out in Study II, a sample of 87 youth with similar recruitment. RESULTS:In Study I, the Val66Met single-nucleotide polymorphism (SNP) was associated with rumination in adolescents, but not children, such that adolescents homozygous for the Val allele reported higher rumination levels. Further, a cumulative genetic score (CGS) (Val66Val and 5-HTTLPR) predicted higher levels of co-rumination, specifically among adolescent girls. Both genetic associations maintained significance after covarying for current depressive symptomology, and the other endophenotype. Finally, both genetic associations exhibited similar effect sizes in Study II, although results did not reach statistical significance. CONCLUSIONS:RESULTS replicate a previously reported association between the brain derived neurotrophic factor (BDNF) Val allele and rumination in adolescents, and provide preliminary support for a CGS predictive of co-rumination in adolescent girls. The current study indicates that candidate genes may demonstrate utility as consistent genetic markers of depression risk when focused on specific phenotypes, and supports the need to explore potential differential effects of developmental stage and sex. However, given the small sample sizes and possibility of chance findings, these results should be interpreted with caution pending replication.

Project description:BackgroundAdolescent-onset depression often results in a chronic and recurrent course, and is associated with worse outcomes relative to adult-onset depression. Targeting habitual depressive rumination, a specific known risk factor for relapse, may improve clinical outcomes for adolescents who have experienced a depressive episode. Randomized controlled trials (RCTs) thus far have demonstrated that rumination-focused cognitive behavioral therapy (RFCBT) reduces depressive symptoms and relapse rates in patients with residual depression and adolescents and young adults with elevated rumination. This was also observed in a pilot RCT of adolescents at risk for depressive relapse. Rumination can be measured at the self-report, behavioral, and neural levels- using patterns of connectivity between the Default Mode Network (DMN) and Cognitive Control Network (CCN). Disrupted connectivity is a putative important mechanism for understanding reduced rumination via RFCBT. A feasibility trial in adolescents found that reductions in connectivity between DMN and CCN regions following RFCBT were correlated with change in rumination and depressive symptoms.MethodThis is a phase III two-arm, two-stage, RCT of depression prevention. The trial tests whether RFCBT reduces identified risk factors for depressive relapse (rumination, patterns of neural connectivity, and depressive symptoms) in adolescents with partially or fully remitted depression and elevated rumination. In the first stage, RFCBT is compared to treatment as usual within the community. In the second stage, the comparator condition is relaxation therapy. Primary outcomes will be (a) reductions in depressive rumination, assessed using the Rumination Response Scale, and (b) reductions in resting state functional magnetic resonance imaging connectivity of DMN (posterior cingulate cortex) to CCN (inferior frontal gyrus), at 16 weeks post-randomization. Secondary outcomes include change in symptoms of depression following treatment, recurrence of depression over 12 months post-intervention period, and whether engagement with therapy homework (as a dose measure) is related to changes in the primary outcomes.DiscussionRFCBT will be evaluated as a putative preventive therapy to reduce the risk of depressive relapse in adolescents, and influence the identified self-report, behavioral, and neural mechanisms of change. Understanding mechanisms that underlie change in rumination is necessary to improve and further disseminate preventive interventions.Trial registrationClinicalTrials.gov Identifier: NCT03859297 , registered 01 March 2019.

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Modeling and estimating the feedback mechanisms among depression, rumination, and stressors in adolescents.

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