The Impact of Maternal Depression, Anxiety, and Stress

项目3 -摘要 精神病理学发展中的重要问题将在以下纵向研究中得到解决： 婴儿在出生前暴露在母亲的抑郁、压力和焦虑中。这些妇女及其 丈夫/伴侣将参加拟议的翻译研究中心，围产期压力和 基因影响：婴儿脆弱性的途径。我们有独特的机会利用 在整个妊娠期间收集的广泛的前瞻性数据，包括 抑郁、压力、焦虑、使用抗抑郁药物（核心B）和胎儿活动（项目1） 作为婴儿及其父母中5 HT TLPR多态性的“s”等位基因的基因分型（项目2）。在 认识到拟议数据集的独特方面及其为回答问题提供的机会 新出现的问题，我们建议测试假设，承诺揭示最佳模型的理解 在精神病理学风险传递中最可能的风险因素、介导者和调节者， 怀孕期间抑郁的妇女所生的孩子。Goodman和Gotlib（1999）模型 精神病理学向抑郁母亲的子女的传播描述了多种风险机制 由此，所提出的样本中的所有婴儿都处于抑郁症和其他疾病的增加的风险中。 问题，相对于那些母亲在怀孕期间没有抑郁的孩子，有些是 根据不同的遗传风险水平，预测比其他人有更高的风险， 环境、早期孕产妇护理不足以及父亲的参与。我们建议测试假设 从这个模型中推导出的发展过程中出现的预测（和 连续性/不连续性）的脆弱性的理论和实践为基础的措施， 在婴儿身上可以观察到的精神病理学。婴儿第一年的评估将包括 神经内分泌、行为和心理生理功能的测量。为了将 考虑任何额外的暴露于孕产妇抑郁症，孕产妇保健的质量，和作用， 神父，这些构造也会被测量。我们将根据经验得出一组预测因子中的“最佳”预测因子 婴儿的结果，有理论和经验的联系，暗示高风险的后期发展， 精神病理学对这些角色的理解将用于描述临床应用的指南。 干预措施。

PROJECT 3 - Abstract Important issues in the development of psychopathology will be addressed in a longitudinal study of infants exposed prenatally to their mothers' depression, stress, and anxiety. These women and their husbands/partners will be participants in the proposed translational research center, Perinatal Stress and Gene Influences: Pathways to Infant Vulnerability. We have the unique opportunity to take advantage of the extensive prospective data that will have been collected throughout pregnancy, including measures of depression, stress, anxiety, use-of antidepressant medication (Core B), and fetal activity (Project 1) as well as genotyping for the 's' allele of the 5HT TLPR polymorphism in the infants and their parents (Project 2). In recognition of the unique aspects of the proposed dataset and the opportunities it presents for answering emerging questions, we propose to test hypotheses that promise to reveal the best model for understanding the most likely risk factors, mediators, and moderators in the transmission of risk for psychopathology in children born to women who were depressed during pregnancy. The Goodman and Gotlib (1999) model for the transmission of psychopathology to children of depressed mothers describes multiple mechanisms of risk whereby all of the infants in the proposed sample are at an increased risk for depression and other problems, relative to children whose mothers have not been depressed in pregnancy, and some are predicted to be at higher risk than others as a function of varying levels of genetic risk, adverse fetal environment, inadequate early maternal care, and father involvement. We propose to test hypotheses derived from this model in the prediction of the developmental course in the emergence (and continuity/discontinuity) of theory- and empirically-based measures of vulnerabilities for the development of psychopathology as they can be observed in infants. Assessments through the infants' first year will include measures of neuroendocrine, behavioral, and psychophysiological functioning. In order to take into consideration any added exposure to maternal depression, quality of maternal care, and the role fo the father, these constructs will also be measured. We will empirically derive the "best" set of predictors in a set of infant outcomes that have theoretical and empirical links implicating high risk for the later development of psychopathology. The understanding of such roles will be used to delineate guidelines for clinical interventions.