An Integrated Model of Contextual Safety, Social Safety, and Social Vigilance as Psychosocial Contributors to Cardiovascular Disease

项目总结/摘要 尽管心血管疾病（CVD）是美国和世界范围内的主要死亡原因， 世纪，传统的风险因素（例如，糖尿病，高血压，胆固醇）只占50%， CVD结果的差异。四十多年的研究提供了强有力的，可重复的，一致的证据， 心理压力与心血管疾病的结果和假设的行为和生物风险路径有关。因此，在本发明中， 迫切需要了解压力是如何进入“皮下”引起CVD的。这项工作始于 从生态学角度有效地理解压力是如何经历的，并意味着风险。一个主要的当代 理论，广义不安全理论的压力（GUTS），概念化的压力作为一个“默认状态”， 伴随生理后遗症的情绪。强大的数据支持GUTS框架， 环境安全性结构指标、急性应激反应特征和心脏病风险之间的关系 疾病另一个主要的当代模式，社会安全理论（SST），也指出了重要性， 安全的感知指标。SST强调人类社会参与的倾向， 暴露于感知到的社会威胁会驱动生理应激反应和对可用社会威胁的感知。 安全提示缓和了这种压力反应。广泛的工作支持社会安全感， 暴露于社会威胁是CVD相关炎症应激反应模式的贡献者 进展这两种理论都表明，人类处于一种恒定的环境安全评估状态， “警惕”影响一系列的行为，生理和心理反应。的 该提案的总体目标是首次研究一个协调的模型，该模型将应力详细描述为 CVD的生态有效风险决定因素。我将使用NHLBI资助的R 01的现有纵向数据， 通过三个目标实现这一目标。在目标1下，我调查了环境安全， 社会安全性、日常社会警惕性和颈动脉内膜中层厚度（cIMT）的2年变化作为临床前 CVD的标志物。在目标2中，我研究了社会警惕在多大程度上介导了 环境安全、社会安全和cIMT的2年变化。最后，通过探索性目标3，我 描述血压和炎症标志物如何解释环境因素之间的关系， 安全性、社会安全性、日常社会警戒和cIMT的2年变化。经验丰富的导师团队 研究人员将支持我的研究和培训，使我成为一名领先的心理社会机制科学家。 有助于理解CVD的非传统决定因素。通过拟议的培训机会， 我将：1）加深对与心血管健康相关的当代压力模型的概念理解; 2） 发展从压力到疾病的关键途径的方法论理解; 3）获得先进的知识， CVD病因学; 4）加强我的专业发展和研究传播;和4）提高我的 培养技能并申请未来的资助。

PROJECT SUMMARY/ABSTRACT Despite cardiovascular disease (CVD) being the leading cause of death in the U.S. and worldwide for over a century, traditional risk factors (e.g., diabetes, blood pressure, cholesterol) account for only 50% of the variance in CVD outcomes. Over four decades of research provide robust, replicated, consistent evidence that psychological stress is linked to CVD outcomes and hypothesized behavioral and biological paths of risk. Thus, there is a critical need for understanding how stress gets “under the skin” to cause CVD. This work begins with an ecologically valid understanding of how stress is experienced and connotes risk. One major contemporary theory, the Generalized Unsafety Theory of Stress (GUTS), conceptualizes stress as a “default state” of emotion with concomitant physiological sequelae. Robust data supports GUTS framework by demonstrating associations between structural indicators of contextual safety, acute stress reactivity profiles, and risk of heart disease. Another major contemporary model, Social Safety Theory (SST), also points to the importance of perceived indicators of security. SST emphasizes the human propensity for social engagement, positing exposure to perceived social threat drives physiological stress reactivity and perception of available social safety cues moderates such stress responses. Extensive work supports perception of social safety and exposure to social threat as contributors to inflammatory stress response patterns associated with CVD progression. Both theories suggest humans are in a constant state of environmental safety evaluation or “vigilance” influencing a constellation of behavioral, physiological, and psychological reactions. The overarching goal of this proposal is to investigate, for the first time, a harmonized model detailing stress as an ecologically valid risk determinant of CVD. I will use existing longitudinal data from an NHLBI-funded R01 to address this goal through three aims. Under aim 1, I investigate the relationship between environmental safety, social safety, daily social vigilance, and 2-year change in carotid intima-media thickness (cIMT) as a preclinical marker of CVD. With aim 2, I examine the extent to which social vigilance mediates associations between environmental safety, social safety, and 2-year change in cIMT. Finally through exploratory aim 3, I characterize how blood pressure and inflammatory markers account for relationships among environmental safety, social safety, daily social vigilance, and 2-year change in cIMT. A highly experienced mentorship team of investigators will support my research and training to become a leading psychosocial mechanism scientist contributing to understanding nontraditional determinants of CVD. Through the proposed training opportunities, I will: 1) deepen conceptual understanding of contemporary stress models related to cardiovascular health; 2) develop methodological understanding of key pathways from stress to disease; 3) gain advanced knowledge in CVD etiology; 4) enhance my professional development and research dissemination; and 4) improve my grantsmanship skills and apply for future grant support.