Tuesday, April 23, 2024
4/23/2024
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.
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