Socioeconomic Status and Inflammation Across the Transition from Adolescence to Adulthood

从青春期到成年过渡期间的社会经济地位和炎症

• 批准号: 10537820
• 负责人: Sarah Elizabeth Rocha
• 金额: $ 3.87万
• 依托单位: UNIVERSITY OF CALIFORNIA LOS ANGELES
• 依托单位国家: 美国
• 财政年份: 2022
• 资助国家: 美国
• 起止时间: 2022-09-01 至 2025-08-31
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10537820
• 关键词: Address; Adolescence; Adolescent; Adult; Anti-Inflammatory Agents; Biological; Biological Markers; Blood; Characteristics; Chronic; Data; Data Set; Development; Discrimination; Economics; Education; Enrollment; Face; Family; Fibrinogen; Foundations; Gene Expression; Genes; Goals; Health; Immune; Income; Inflammation; Inflammatory; Intervention; Investigation; Knowledge; Link; Literature; Loneliness; Longevity; Longitudinal Studies; Measurement; Measures; Mediating; Mission; National Institute of Child Health and Human Development; Outcome; Participant; Pathway interactions; Personal Satisfaction; Positioning Attribute; Process; Psychosocial Factor; Psychosocial Stress; Reporting; Research; Risk; Role; Route; Sampling; Sleep; Sleep disturbances; Social Change; Social isolation; Social status; Socioeconomic Status; Spottings; Stress; Time; Uncertainty; Work; Youth; actigraphy; adolescent health; biobehavior; cardiovascular disorder risk; circulating biomarkers; college; cost; cytokine; disorder risk; eleventh grade; experience; health disparity; high school; higher education; improved; inflammatory marker; interest; low socioeconomic status; physical conditioning; psychologic; psychosocial; psychosocial stressors; sleep behavior; sleep quality; social; social relationships; socioeconomic development; socioeconomics; young adult

Project Summary Chronic inflammation has emerged as a potential pathway linking low-socioeconomic status (SES) with disease risk; however, the development of SES disparities in inflammatory risk from adolescence to adulthood is not well understood and there remains uncertainty over the underlying pathways. This transitional period often involves normative changes in social relationships and sleep behavior. Given that psychosocial stress and sleep disruption have both been implicated in inflammatory pathways, the transition from adolescence to adulthood may be an ideal developmental period to assess SES associations with inflammation and elucidate the psychosocial and biobehavioral factors that may underlie these associations. The present study will utilize two independent datasets to assess SES links with inflammation at multiple levels, i.e., via circulating levels of inflammatory markers and via gene expression of inflammatory pathways. The research will identify potential psychosocial factors (i.e., social isolation, stress, discrimination) and biobehavioral factors (i.e., changes in sleep duration and quality) that may explain how SES creates risk for a pro-inflammatory state. Data from the first study were collected as a part of a longitudinal study of adolescent health and experiences, in which N=350 youth were followed from the 10th/11th grade into 3-years post-high school. Adolescents reported on psychosocial experiences, measured sleep via actigraphy for 8 nights, and provided dried blood spot (DBS) samples to assess inflammation. Data from the second study will be collected from N=150 young adults of diverse socioeconomic backgrounds at three time points throughout the first year of college, in which participants report on psychosocial experiences during the transition to college, report on their sleep duration and quality, and provide a DBS sample. The two datasets will be used to address three aims: 1) investigate the relationship between SES and inflammation across the transition from adolescence to adulthood, 2) identify psychosocial experiences that link SES with inflammation and 3) examine the role of sleep in the association between SES and inflammation. It is hypothesized that low-SES will be significantly associated with inflammatory risk, and that low-SES youth will show greater increases in inflammation over time. Secondly, it is hypothesized that low-SES will be associated with adverse psychosocial experiences and that these experiences will statistically mediate associations between SES and inflammation. Finally, it is hypothesized that low-SES will be associated with poorer quality sleep, and that disruptions to sleep will statistically mediate associations between SES and inflammation. Findings from this work will contribute to the literature’s understanding of the biologic embedding of SES in health and can be used to inform interventions aimed at reducing health risk for low-SES youth.

项目摘要 慢性炎症已成为连接低社会经济地位（SES）与 疾病风险;然而，从青春期到成年期，SES的发展在炎症风险方面存在差异 还没有很好地理解，对潜在的途径仍然存在不确定性。这一过渡时期 通常涉及社会关系和睡眠行为的规范性变化。考虑到心理压力 和睡眠中断都与炎症通路有关，从青春期到 成年期可能是评估SES与炎症关系的理想发育期， 这些关联背后的社会心理和生物行为因素。本研究将利用 两个独立的数据集，以评估SES与炎症在多个层面的联系，即，通过循环水平的 炎症标志物和通过炎症途径的基因表达。该研究将确定潜在的 心理社会因素（即，社会孤立、压力、歧视）和生物行为因素（即，变化 睡眠持续时间和质量），这可能解释了SES如何产生促炎状态的风险。 第一项研究的数据是作为青少年健康纵向研究的一部分收集的， 经验，其中N=350青年从10/11年级到3年后高中。 青少年报告了心理社会经验，通过活动记录仪测量了8个晚上的睡眠，并提供了 干血斑（DBS）样品以评估炎症。第二项研究的数据将收集自 N=150名具有不同社会经济背景的年轻人，在第一年的三个时间点 大学，其中参与者报告在过渡到大学期间的心理社会经验，报告他们的 睡眠持续时间和质量，并提供DBS样本。这两个数据集将用于实现三个目标：1） 调查SES和炎症之间的关系，从青春期过渡到 成年期，2）确定将SES与炎症联系起来的社会心理体验，3）检查 在SES和炎症之间的关联中睡眠。据推测，低社会经济地位将显着 与炎症风险相关，低SES青年将表现出更大的炎症增加， 时间其次，假设低社会经济地位与不良的社会心理经历有关， 这些经历将在统计学上介导SES和炎症之间的关联。最后是 假设低SES与睡眠质量较差有关，睡眠中断将 统计学上介导SES和炎症之间的关联。这项工作的结果将有助于 文献对SES在健康中的生物嵌入的理解，可用于告知干预措施 旨在降低低社会经济地位青年的健康风险。