Race/Ethnicity, Psychosocial and Environmental Stressors, and Telomere Length

描述(由申请人提供)：我们建议进行第一次基于社区的研究，研究广泛年龄范围的成年人端粒长度和平衡负荷的种族差异及其与城市应激源的关系。我们假设，城市黑人居民经历的慢性应激源加速了生物衰老和慢性病的发病。有证据表明，白细胞端粒长度(TL)可能是受压力影响的生物年龄的指标；而非稳态负荷是重要身体系统受压力调节的磨损的指标。我们有一个独特的机会来补充健康环境伙伴关系(HEP)计划收集的调查数据，HEP是密歇根大学与底特律社区组织和卫生服务机构之间的合作伙伴关系，通过血液采集和实验室分析端粒长度、端粒相关化合物和平衡负荷，包括生物应激反应、炎症以及心血管和代谢风险的测量。通过将静脉采血添加到HEP调查中，我们可以建立一个数据集，以经济高效的方式包括这些生物测量和详细的心理社会和物理环境措施；增加接触难以接触到的人群的机会；并促进研究结果的传播，以改善社区健康。我们将估计TL和变态负荷对种族的一系列回归，控制年龄、性别和社会经济特征的混杂影响，并探索心理社会或环境应激源在多大程度上调节剩余的种族差异。为了确保发现不是由函数形式驱动的，我们将使用匹配方法重新分析数据。我们还将根据端粒长度、高氧化应激或低端粒酶活性来模拟疾病结果，以探索端粒长度和慢性疾病之间的生物机制途径。我们的研究团队在社会和行为科学、细胞生物学、心理学和生物化学方面拥有卓越的专业知识，以确保最先进的端粒测量、理论驱动和统计合理的社会科学测量和模型，以及对研究结果的适当解释，以提供重要的见解。我们期待研究结果阐明累积应激假说解释疾病社会模式的合理性；端粒长度作为衰老生物衡量标准的可行性；以及应激源可能与端粒长度和疾病过程联系在一起的机制途径。如果这种跨学科合作努力的结果支持研究假设，这可能会在理解健康中种族不平等的生物学机制方面取得重大进展。公共卫生相关性：了解社会因素如何通过生物机制影响健康是理解种族健康差异的基础。通过在跨学科合作中研究个人和社区压力源以及底特律居民的健康，我们希望能阐明这个问题。

DESCRIPTION (provided by applicant): We propose to conduct the first community-based study of racial differences in telomere length and allostatic load in adults of broad age range and their association with urban stressors. We hypothesize that chronic stressors experienced by black urban residents accelerate biological aging and chronic disease onset. Evidence suggests that leukocyte telomere length (TL) may be an indicator of biological age that can be affected by stress; and that allostatic load is an indicator of stress-mediated wear on important body systems. We have a unique opportunity to supplement survey data scheduled to be collected by the Healthy Environments Partnership (HEP) a partnership between the University of Michigan and community-based organizations and health service agencies in Detroit with blood collection and lab analyses of telomere length, telomere-related compounds, and allostatic load, including measures of the biological stress response, inflammation, and cardiovascular and metabolic risk. By appending a venous blood draw to the HEP survey, we can construct a data set including these biomeasures and detailed psychosocial and physical environmental measures in a cost-effective way; enhance access to a hard-to-reach population; and facilitate dissemination of study results to improve community health. We will estimate a series of regressions of TL and allostatic load on race, controlling for the confounding effects of age, gender, and socioeconomic characteristics and exploring the extent to which psychosocial or environmental stressors mediate remaining racial differences. To ensure findings are not driven by functional form we will reanalyze the data using matching methods. We will also model disease outcomes, conditional on telomere length, on high oxidative stress or low telomerase activity to explore biological mechanistic pathways between telomere length and chronic disease. Our investigative team brings exceptional expertise in social and behavioral science, cell biology, psychology and biochemistry to insure state-of-the art telomere measurement, theory-driven and statistically sound social science measures and models, and appropriate interpretation of study findings to provide important insights. We expect study findings to shed light on the plausibility of cumulative stress hypotheses to explain the social patterning of disease; the viability of telomere length as a biomeasure of aging; and the mechanistic pathways through which stressors may be linked to telomere length and disease processes. If findings from this interdisciplinary collaborative effort support study hypotheses, this could constitute a significant advance in the understanding of the biological mechanisms that underlie racial inequality in health. PUBLIC HEALTH RELEVANCE: Learning how social factors work through biological mechanisms to impact health is fundamental to understanding racial health disparities. By studying personal and neighborhood stressors and the health of Detroit residents in an interdisciplinary collaboration, we hope to shed light on this question.