Socioeconomic Status and Inflammation Across the Transition from Adolescence to Adulthood

项目摘要 慢性炎症已经成为连接低社会经济地位(SES)和 疾病风险；然而，从青春期到成年期，SES在炎症风险方面的发展差异 这一点还没有得到很好的理解，潜在的途径仍然存在不确定性。这一过渡期 通常涉及社会关系和睡眠行为的规范变化。鉴于这种心理社会压力 和睡眠障碍都与炎症途径有关，从青春期到 成年期可能是评估SES与炎症的关系并阐明其原因的理想发育期 心理社会和生物行为因素可能是这些联系的基础。本研究将利用 两个独立的数据集，用于评估SES与多个水平的炎症之间的联系，即通过循环水平的 炎症标志物和炎性通路的VIA基因表达。这项研究将确定潜在的 心理社会因素(即社会孤立、压力、歧视)和生物行为因素(即 睡眠时间和质量)，这可能解释了SES如何造成促炎状态的风险。 第一项研究的数据是作为青少年健康和健康纵向研究的一部分收集的 其中N=350名青少年从10/11年级开始接受跟踪调查，进入高中后3年。 青少年报告了心理社会经历，通过活动记录仪测量了8个晚上的睡眠，并提供 取干血斑(DBS)样本以评估炎症反应。第二项研究的数据将从 N=150名具有不同社会经济背景的年轻人，在#年的第一年的三个时间点 在大学，参与者报告了在过渡到大学期间的心理社会经历，报告了他们的 睡眠持续时间和质量，并提供DBS样本。这两个数据集将用于解决三个目标：1) 研究从青春期到青春期的SES与炎症的关系 成年期，2)确定将自闭症与炎症联系起来的心理社会经历，以及3)检查 睡眠中的SES与炎症之间的关联。据推测，低SES将显著 与炎症风险相关，低SES青年将表现出更大的炎症增加 时间到了。其次，假设低SES会与不良的心理社会经历有关，并且 这些经验将在统计上中介SES和炎症之间的联系。最后，它是 假设低SES将与较差的睡眠质量相关，而睡眠中断将 在统计上，SES和炎症之间存在中介关系。这项工作的发现将有助于 文献对SES在健康中生物嵌入的理解，并可用于提供干预信息 旨在降低低社会经济地位青年的健康风险。

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.