Vulnerability to Stress-Induced Depression Post-job-loss

描述（由申请人提供）：来自乔治华盛顿大学的家庭压力项目和发育与遗传学项目以及亚利桑那大学精神病学系的研究人员提出了一个合作项目，以研究压力和个人脆弱性的相互作用，因为它们有助于失业后抑郁的风险。这项工作的主要目标是开发和测试一个综合理论，即个人脆弱性，包括遗传易感性，如何在面对压力时塑造抑郁反应。这项研究的目的是专门为指导新一代的预防性干预措施，面临失业的高风险个人提供必要的信息。本研究以四个目标为指导。首先，全州范围内最近失业的个人名单将被用来收集一个广泛的社区样本，其中包括432名最近失业的人。这个样本，按性别平衡，包括相当比例的非洲裔美国人，然后将参加家庭访谈，收集有关抑郁症状和抑郁发作的信息;一系列与失业有关的个人、经济和人际关系压力;表型素质包括抑郁史、神经质、消极归因方式和依恋方式。我们还将收集所有参与者的唾液样本进行DNA提取，以研究涉及5-羟色胺转运蛋白（5-HTTLPR）基因功能多态性（SLC 6A 4）的遗传素质对压力诱导的抑郁症的影响。另一个更具探索性的遗传标记系列也将进行基因分型，以提供更多的初步测试，以确定它们是否与压力相互作用，增加患抑郁症的风险。第二，参与者将在失业后的30周内接受随访，以研究压力和脆弱性在影响抑郁症时的动态相互作用。由于风险过程在抑郁反应的过程中可能会有所不同，我们计划进行总共五次评估，以捕捉在此期间症状的动态波动，反映抑郁症的发作，维持和解决。第三，多层次模型将被用来测试一个一般模型，如何暴露于经济和人际压力在几个月后失业沉淀，保持或加剧抑郁反应，以及这些影响是如何影响个人的脆弱性。该模型假设敏感和招聘的影响，这样的个人脆弱性的预测都增加了压力源（招聘）和缓和的影响，压力源（敏感）的轨迹上的抑郁症状在30周的时间。第四，重复随访数据将用于检验有关这些影响的具体机制的假设。我们将测试两个更接近的模型，关于如何应对效能和社会支持和破坏调解个人脆弱性和压力对抑郁症的相互作用。

DESCRIPTION (provided by applicant): Investigators from the Family Stress Program and the Development and Genetics Program at the George Washington University and the Department of Psychiatry at the University of Arizona propose a collaborative project to study the interaction of stress and personal vulnerability as they contribute to risk for depression after job loss. The primary goal of this work is to develop and test an integrated theory of how personal vulnerabilities, including genetic susceptibility, shape depressive response in the face of stress. This study is designed specifically to provide information essential for guiding a new generation of preventive interventions for high-risk individuals facing job loss. The study is guided by four aims. First, statewide lists of recently unemployed individuals will be used to accrue a broad community sample of 432 people who have recently lost their jobs.This sample, balanced by gender and including a substantial proportion of African Americans, will then participate in in-home interviews to collect information on depressive symptoms and depressive episodes; a range of personal, financial, and interpersonal stressors associated with job loss; and phenotypic diatheses including prior history of depression, neuroticism, negative attribution style, and attachment style. We will also collect saliva samples from all participants for DNA extraction, in order to study the effects of genetic diatheses involving a functional polymorphism (SLC6A4) of the serotonin transporter (5-HTTLPR) gene on stress-induced depression. Another more exploratory series of genetic markers will also be genotyped to provide more preliminary tests of whether they interact with stress to increase risk for depression. Second, participants will be followed for 30 weeks after the date of job loss, to study the dynamic interplay of stress and vulnerability as they influence depression. Because risk processes may differ over the course of depressive response, we plan to conduct a total of five assessments in order to capture dynamic fluctuations in symptoms over this period that reflect onset, maintenance, and resolution of depression. Third, multilevel modelling will be used to test a general model of how exposure to economic and interpersonal stressors in the months following job loss precipitates, maintains, or exacerbates depressive response, and how these effects are influenced by personal vulnerabilities. This model hypothesizes both sensitization and recruitment effects, such that personal vulnerabilities are predicted to both increase rates of stressors (recruitment) and to moderate the effects of stressors (sensitization) on trajectories of depressive symptoms over the 30-week period. Fourth repeated followup data will be used to test hypotheses concerning the specific mechanisms responsible for these effects. We will test two more proximal models concerning how coping efficacy and social support and undermining mediate the interaction of personal vulnerabilities and stress on depression.