Adolescent Social Relationships and Immune, Endocrine, and Metabolic Processes

描述(由申请人提供)：最近的研究发现，贫困、家庭暴力或忽视等心理社会压力与疾病后果之间存在联系(例如，Dube等人，2009；Repetti，Taylor，&Seeman，2002)。几项研究发现，在贫穷、压力和缺乏支持的环境中长大的人患心血管疾病、自身免疫性疾病和癌症的风险更高(丹尼斯等人，2009；Dube等人，2009；Keinan-Boker，Vin-Raviv，Liphshitz，Linn和Barchana，2009)。这些发现提出了关于心理社会应激源影响慢性病的发展和进展的机制的重要问题。一种可能性是，这些环境助长了下丘脑-垂体-肾上腺轴的慢性激活，导致糖皮质激素受体逐渐脱敏，皮质醇调节免疫系统的能力下降(Miller&Chen，2010；Miller等人，2009)。虽然许多关于这种可能性的研究都强调了生命早期(即最初几年内)环境条件作为促炎表型激活的敏感期的重要性，但仍有理由相信青春期可能是另一个发育期，更容易受到影响后来疾病风险因素的环境条件的影响(Fuligni等人，2009；Miller&Chen，2010)。鉴于青少年的人际关系经历通常被认为是青春期最重要的特征(Lerner&Steinberg，2009)，拟议的研究旨在关注青少年亲密关系作为免疫、神经内分泌和新陈代谢过程的心理社会预测因子的作用。使用前瞻性研究设计，青少年的社会关系将作为系统性炎症和代谢风险的预测因子在2.5年内进行检验。然后，基础皮质醇水平和糖皮质激素敏感性将作为社会关系与炎症和代谢风险之间联系的中介进行检查。最后，在一个单独的样本中，将在14年的时间内检查青少年社会关系与成人炎症和代谢风险之间的联系，从而洞察人际关系对全身炎症和代谢功能的长期影响。根据赞助机构的使命，这项拟议的研究将阐明青少年的社会关系如何塑造免疫、神经内分泌和代谢过程的发展轨迹，这些过程可能有助于长期的健康和疾病结果。

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.