The role of environmental disadvantage in the etiologic moderation of children's antisocial behavior

项目摘要/摘要 不利的环境有各种各样的形式，有力地预示着攻击性和违规性。 反社会行为1，2。这些预测已经超越了简单的表型关联，现在有了多项研究 这表明基因和环境对反社会行为的影响程度分别也 作为邻里劣势的函数而变化，因此遗传影响在 “平均的、可预期的环境”，在贫困3-5的背景下受阻。虽然很重要，但在 基因-环境互作(GxE)研究由于只关注邻里关系而受到限制 指标，这只是儿童可能经历的几种形式的劣势之一。因此，目前还不清楚 是否存在其他相关形式的不利因素，包括家庭(如收入)、学校(如补贴 午餐时间)和化学物质(例如，神经毒物暴露)的不利因素也是导致 反社会行为。此外，因为到目前为止还没有GxE研究联合检查多个指标 劣势，尚不清楚它们是否会增加彼此的影响，或者是一种形式的劣势 在现有的GxE中作为主要的“活性成分”。拟议研究的目标是填补这些空白 文献通过考察多种形式的不利因素作为侵袭性和非侵袭性的病因调节因素 分别是攻击性反社会行为。我将使用1000多对双胞胎的样本数据 富于劣势以实现以下目的：(1)评估先前的发现是否为邻里 劣势还延伸到其他三种主要形式的劣势：家庭、学校和化学，以及(2) 评估各种形式的不利因素是否协同缓和了反社会的病因 行为。拟议的分析将包括经典的双胞胎生物计量GxE模型和GxE版本的 核心双胞胎家族设计，后者通过控制 更多的混乱6.通过这种方式，我将能够说明GxE在 第一次出现反社会行为。 通过解决这些目标，我将继续开发一系列研究，致力于了解慢性 不利因素会改变发展结果。进一步为从事GxE的学术生涯做准备 在研究方面，我正在寻求额外的培训，以：(1)获得测量和概念化方面的专业知识 劣势作为一个多方面的结构，(2)增进了我对遗传信息统计的理解 方法，以及(3)发展我的手稿和赠款写作技能。这一培训将对 作为一名独立研究员，我的发展重点是了解不利因素对 心理健康结果，既有独立的，也有与个人的遗传倾向相联系的。

Project Summary/Abstract Disadvantaged contexts come in myriad forms and robustly predict both aggressive and rule-breaking antisocial behavior1,2. These predictions go beyond simple phenotypic associations, with multiple studies now indicating that the respective magnitudes of genetic and environmental influences on antisocial behavior also vary as a function of neighborhood disadvantage, such that genetic influences are most strongly expressed in ‘average, expectable environments’ and stymied in the context of poverty3-5. Although important, prior genotype-environment interaction (GxE) research has been limited by its sole focus on neighborhood indicators, which is only one of several forms of disadvantage that children can experience. It is thus unclear whether other, correlated forms of disadvantage, including familial (e.g., income), school (e.g., subsidized lunch rate), and chemical (e.g., neurotoxicant exposure) disadvantage, also serve as etiologic moderators of antisocial behavior. Additionally, because no GxE study to date has jointly examined multiple indicators of disadvantage, it is unknown whether they increment one another’s effects or whether one form of disadvantage serves as a primary ‘active ingredient’ in extant GxE. The goal of the proposed study is to fill these gaps in the literature by examining multiple forms of disadvantage as etiologic moderators of aggressive and non- aggressive antisocial behavior, respectively. I will use data from a sample of more than 1,000 twin pairs enriched for disadvantage to carry out the following aims: (1) evaluate whether prior findings for neighborhood disadvantage also extend to three other key forms of disadvantage: familial, school, and chemical, and (2) evaluate whether the various forms of disadvantage synergistically moderate the etiology of antisocial behavior. The proposed analyses will include both the classical twin biometric GxE model and a GxE version of the nuclear twin family design, the latter of which allows for far stronger causal inferences by controlling for additional confounds6. In this way, I will be able to illuminate the ‘active ingredients’ of disadvantage for GxE in antisocial behavior for the very first time. By addressing these aims, I will continue to develop a line of research dedicated to understanding how chronic disadvantage alters developmental outcomes. To further prepare for an academic career conducting GxE research, I am seeking additional training to: (1) gain expertise in the measurement and conceptualization of disadvantage as a multifaceted construct, (2) advance my understanding of genetically informative statistical methods, and (3) develop my manuscript and grant-writing skills. This training will meaningfully contribute to my development as an independent researcher focused on understanding the effects of disadvantage on mental health outcomes, both independently and in conjunction with individuals’ genetic predispositions.