Biological Underpinnings of Socioeconomic Differentials in Health and Mortality

健康和死亡率社会经济差异的生物学基础

• 批准号: 9766180
• 负责人: EILEEN M CRIMMINS
• 金额: $ 43.21万
• 依托单位: UNIVERSITY OF SOUTHERN CALIFORNIA
• 依托单位国家: 美国
• 财政年份: 2018
• 资助国家: 美国
• 起止时间: 2018-09-01 至 2023-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9766180
• 关键词: Affect; Age; Aging; Biological; Biological Aging; Biological Markers; Biological Process; Biology; Buffers; C-reactive protein; Characteristics; Chemicals; Childhood; Chronology; Clinical; Cytomegalovirus; DNA Methylation; Deterioration; Diabetes Mellitus; Disadvantaged; Disease; Economically Deprived Population; Elderly; Emotional; Epigenetic Process; Etiology; Event; Gene Expression; Genetic; Genetic Risk; Health; Health and Retirement Study; Health behavior; Heart Diseases; Heart Rate; Immunologics; Impaired cognition; Individual; Length; Life; Life Cycle Stages; Link; Malignant Neoplasms; Measures; Methylation; Mitochondria; Mitochondrial DNA; Modification; Molecular; Morbidity - disease rate; Neurodegenerative Disorders; Organ; Outcome; Pathogenesis; Pathway interactions; Persons; Physiological; Population; Precipitating Factors; Predisposing Factor; Predisposition; Process; Research; Risk; Risk Factors; Skin; Socioeconomic Status; Stress; System; T-Lymphocyte; Testing; Work; age related; base; cost; cytokine; data resource; disability; disadvantaged population; disorder risk; environmental stressor; experience; gene environment interaction; genetic profiling; genome wide methylation; health disparity; immune function; immune system function; indexing; low socioeconomic status; mortality; novel; psychologic; psychosocial; resilience; social; social disparities; socioeconomics; telomere

Abstract This project will use a unique new data resource from the Health and Retirement Study (HRS) to elucidate multiple biological pathways through which life course social disadvantage “gets under the skin” and influences subsequent morbidity and mortality. We will examine the association between social adversity and multiple composite measures related to basic processes of biological aging including clinical indicators of physiological status, immune system functioning, telomere attrition, mitochondrial depletion, DNA methylation, and gene expression in order to understand the mechanisms through which those of low socioeconomic status (SES) “age” at a faster rate than persons with higher SES. The uniqueness of this project resides in the breadth and depth of the biological indicators which characterize some of the basic mechanisms of aging and have not been examined in a nationally representative population with ability to characterize SES differences. We expect that low socioeconomic status (SES), and related stressful life events, adverse psychological states, and poor health behaviors will be associated with worse physiological status, immunological functioning, methylation profile, adverse expression, more mitochondrial depletion, and shorter telomere length at a given chronological age. While low SES and accompanying life circumstances at any age are expected to be associated with late life biology, cumulative social disadvantage beginning in childhood and sustained throughout life is expected to have a multiplicative association in increasing adverse biological markers as we expect some biological processes to be more influenced by childhood circumstances and others by more current circumstances. We will examine the association of emotional, financial, and psychological costs of low SES in early and later life with biological outcomes and hypothesize that the effect of these different aspects of life will vary with timing and domain. We will also identify both genetic and social, psychological and environmental buffering factors that will reduce the association of low SES with adverse biological profiles. The outcome of this project will be the identification of a comprehensive-integrated set of measures that characterize the biological pathway from social adversity to poor health and “explain” at a biological level why socially disadvantaged individuals are at greater risk of aging-related morbidity and mortality outcomes. Identifying multiple social and biological mechanisms that influence the pace of aging will enhance our understanding of the underlying causes of health disparities and the lifecycle processes by which they arise. This work will increase substantially our understanding of how predisposing factors (cellular and molecular changes, deterioration in the immune function, and physiological characteristics) and precipitating factors (socioeconomic status, psychosocial and environmental stressors, and health behaviors) together influence age- related health conditions (age-related morbidity and mortality).

摘要 该项目将使用来自健康和退休研究（HRS）的独特新数据资源来阐明 多种生物途径，通过这些途径，生命过程中的社会不利因素“渗透到皮肤下”， 随后的发病率和死亡率。我们将研究社会逆境与多重 与生物老化的基本过程有关的综合措施，包括生理老化的临床指标 状态、免疫系统功能、端粒磨损、线粒体耗竭、DNA甲基化和基因 表达，以了解那些社会经济地位低（SES）的人“年龄”的机制 比社会经济地位高的人更快。这个项目的独特之处在于它的广度和深度 的生物指标的特点，一些基本的机制老化，并没有得到 在具有全国代表性的人群中进行检查，能够表征SES差异。 我们预计，低社会经济地位（SES）和相关的压力生活事件，不良心理 状态和不良的健康行为将与更差的生理状态，免疫功能， 甲基化谱，不利的表达，更多的线粒体消耗，以及在给定的时间段较短的端粒长度。 实际年龄虽然预计任何年龄段的社会经济地位和随之而来的生活环境都较低， 与晚年生物学有关，从儿童时期开始并持续到整个 预期寿命在增加不利生物标志物方面具有倍增关联，因为我们预期一些 生物过程更多地受到童年环境的影响，而其他过程则受到更现实的影响 情节我们将研究低社会经济地位者的情感、经济和心理成本之间的关系， 早期和后期的生活与生物学结果，并假设这些不同方面的影响，生活将 随时间和域而变化。我们还将确定遗传和社会，心理和环境 缓冲因素，这将减少低SES与不良生物学特征的关联。 该项目的成果将是确定一套全面综合的措施， 描述从社会逆境到健康状况不佳的生物学途径，并在生物学水平上“解释”为什么 处于社会不利地位的个人面临与老龄化有关的发病率和死亡率后果的风险更大。 识别影响衰老速度的多种社会和生物机制将增强我们对衰老的认识。 了解健康差距的根本原因及其产生的生命周期过程。 这项工作将大大增加我们对易感因素（细胞和分子）如何影响人类健康的理解。 变化、免疫功能和生理特征的恶化）和诱发因素 （社会经济地位、心理社会和环境压力源以及健康行为）共同影响年龄- 相关的健康状况（与年龄相关的发病率和死亡率）。