Adolescent Social Relationships and Immune, Endocrine, and Metabolic Processes

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DESCRIPTION (provided by applicant): Recent research efforts have identified a connection between psychosocial stress, such as poverty, family violence, or neglect, and disease outcomes (e.g., Dube et al., 2009; Repetti, Taylor, & Seeman, 2002). Several studies have found that individuals who were raised in poor, stressful, and unsupportive environments are at increased risk for developing cardiovascular disease, autoimmune disease, and cancer (Danese et al., 2009; Dube et al., 2009; Keinan-Boker, Vin-Raviv, Liphshitz, Linn, & Barchana, 2009). These findings introduce important questions about the mechanisms through which psychosocial stressors influence the development and progression of chronic diseases. One possibility is that these environments foster chronic activation of the hypothalamic-pituitary-adrenal axis, leading to a progressive desensitization of glucocorticoid receptors and decreased ability of cortisol to regulate the immune system (Miller & Chen, 2010; Miller et al., 2009). Although much of the research on this possibility has emphasized the importance of environmental conditions very early in life (that is, within the first few years) as a sensitive peiod for the activation of a pro-inflammatory phenotype, there is reason to believe that adolescence may be another developmental period of increased vulnerability to environmental conditions that influence risk factors for later disease (Fuligni et al., 2009; Miller & Chen, 2010). Given that adolescent relationship experiences are often considered to be the most important features of adolescence (Lerner & Steinberg, 2009), the proposed research aims focus on the role of adolescents' close relationships as psychosocial predictors of immune, neuroendocrine, and metabolic processes. Using a prospective research design, adolescent social relationships will be examined as predictors of systemic inflammation and metabolic risk over a 2.5 year period. Then, basal cortisol levels and glucocorticoid sensitivity will be examined as mediators of links between social relationships and inflammation and metabolic risk. Finally, in a separate sample, links between adolescent social relationships and adult inflammation and metabolic risk will be examined over a 14 year period, thus capturing insight into the long- term influence of relationships on systemic inflammation and metabolic functioning. In line with the mission of the sponsoring agency, the proposed research will shed light on the ways in which adolescents' social relationships shape the developmental trajectory of immune, neuroendocrine, and metabolic processes that may contribute to long-term health and disease outcomes.