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 慢性炎症已成为将低社会经济状况（SES）与 疾病风险；但是，从青少年到成年的炎症风险中SES分布的发展 对基础途径的不确定性尚不确定。这个过渡期 通常涉及社会关系和睡眠行为的正常变化。鉴于心理压力 在炎症途径中都暗示了睡眠中断，从青少年到 成年可能是评估与炎症并阐明SES关联的理想发展时期 可能是这些关联的基础的社会心理和生物行为因素。本研究将利用 两个独立数据集评估SES与炎症的链接多个层次，即通过循环级别 炎症标记和通过炎症途径的基因表达。该研究将确定潜力 社会心理因素（即社会隔离，压力，歧视）和生物行为因素（即，变化 睡眠持续时间和质量）可以解释SES如何产生促炎性状态的风险。 收集了第一项研究的数据是青少年健康纵向研究的一部分 经验，其中n = 350名年轻人从10年/11年级到高中3年。 青少年报道了心理社会经历，通过表观摄影测量睡眠8晚，并提供了 干血点（DBS）样品评估炎症。第二项研究的数据将从 n = 150名潜水员社会经济背景的年轻人在三个时间点的第一年 大学，参与者在过渡到大学期间关于社会心理经历的报告 睡眠持续时间和质量，并提供DBS样本。两个数据集将用于解决三个目标：1） 研究SES与从青少年到的炎症之间的关系 成年，2）确定将SES与炎症联系起来的社会心理经历，3）检查 在SES和炎症之间的关联中睡觉。假设低调将显着 与炎症风险相关，低SES青年会显示出更大的炎症增加 时间。其次，假设低调与不利的社会心理经历有关 这些经验将从SES和炎症之间统计上媒体关联。最后，是 假设低调将与质量较差的睡眠有关，而睡眠的干扰将会 SES与炎症之间的统计媒体关联。这项工作的发现将有助于 文学对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SES青年的健康风险。