Biological Embedding of Early-Life SES

项目总结/摘要 生命早期的社会经济地位（SES）是脆弱性的一个重要决定因素， 成年期的心血管疾病因为这些影响不仅仅是 社会地位的直接影响，他们提出了具有挑战性的机械问题 关于早期社会经济地位是如何在生物学上长期扎根的。这一提议提出 表观遗传编程假说来解释这一过程。它假定社会心理学 与低早期社会经济地位相关的经历通过表观遗传学在基因组中编程 机制，或获得的基因组活动的变化，而不是由于DNA的变化， 顺序在一项420名志愿者的研究中，我们将评估一个假设，即 在低社会经济地位环境中度过的早年经历更大的家庭动荡， 已经形成了警惕的悲观的人生观我们还希望这些经验 已经通过表观遗传修饰嵌入免疫系统， 表现为从青春期开始并持续至 成年这种表型的特征在于促炎转录的激活 控制途径和增加的炎症生物标志物C-反应性 蛋白质和白细胞介素-6。这项工作将揭示生物行为机制的基础 社会经济地位差距，与预防干预的影响。项目叙述 那些在贫困中度过早年时光的人更有可能发展 心脏病和其他疾病，当他们到达成年。本研究 该项目试图查明这一现象背后的机制。它检查 童年早期的贫困会改变免疫系统的功能， 并以一种贯穿一生的方式持续下去， 在成年期易患疾病。

PROJECT SUMMARY/ABSTRACT Socioeconomic status (SES) during early life is an important determinant of vulnerability to cardiovascular disease in adulthood. Because these effects are not simply a result of the more direct influences of social standing in adulthood, they raise challenging mechanistic questions about how early-life SES gets biologically embedded for the long-term. This proposal advances an epigenetic programming hypothesis to explain this process. It posits that psychosocial experiences associated with low early-life SES are programmed in the genome via epigenetic mechanisms, or acquired changes in genomic activity that are not due to changes in DNA sequence. In a study of 420 volunteers, we will evaluate the hypothesis that individuals who spent their early years in low-SES environments were exposed to greater familial turmoil and have developed vigilant, pessimistic outlooks on life. We further expect these experiences to have become embedded in the immune system through epigenetic modifications, and to manifest as a pro-inflammatory phenotype beginning in adolescence and persisting through adulthood. This phenotype will be characterized by activation of pro-inflammatory transcription control pathways and increased concentrations of the inflammatory biomarkers C-reactive protein and interleukin-6. This work will shed light on the biobehavioral mechanisms underlying SES disparities, with implications for preventative interventions. PROJECT NARRATIVE Individuals who spend the early years of their lives in poverty are more likely to develop heart disease and other medical conditions when they reach adulthood. This research project attempts to identify the mechanisms underlying this phenomenon. It examines the idea that poverty in early childhood changes the way the immune system functions, and does so in a fashion that persists across the lifespan and renders a person vulnerable to diseases in adulthood.