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

项目总结/摘要 不和谐的情境有无数种形式，并有力地预测侵略性和破坏规则 反社会行为1，2.这些预测超越了简单的表型关联，现在有多项研究 表明遗传和环境对反社会行为的影响程度也 作为邻居劣势的函数而变化，例如遗传影响在以下中表达得最强烈： “平均的、可预期的环境”，并在贫困的背景下受阻3 -5。虽然重要，但优先 基因型-环境相互作用（GxE）研究一直局限于其单一的关注邻里 这只是儿童可能遇到的几种不利情况之一。因此， 是否有其他相关形式的不利条件，包括家庭（例如，收入），学校（例如，补贴 午餐费率），和化学品（例如，神经毒素暴露）的缺点，也作为病因调节剂， 反社会行为此外，由于迄今为止没有GxE研究联合检查了多个指标， 不知道它们是否会增加彼此的影响，或者一种形式的不利因素是否会增加 作为现存GxE的主要“活性成分”。拟议研究的目标是填补这些空白， 文献通过检查多种形式的不利因素，作为侵略性和非侵略性的病因调节剂， 攻击性反社会行为。我将使用1,000多对双胞胎的数据 针对不足进行了以下目的：（1）评估邻域的先验发现是否 不利条件还延伸到其他三种主要形式的不利条件：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调节反社会的病因 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 额外的困惑6.这样，我将能够阐明GxE的“活性成分”， 第一次做出反社会行为 通过实现这些目标，我将继续开展一系列研究，致力于了解慢性病是如何 劣势改变发展结果。为了进一步准备进行GxE的学术生涯 研究，我正在寻求额外的培训：（1）获得测量和概念化的专业知识 缺点作为一个多方面的结构，（2）推进我对遗传信息统计的理解 方法，和（3）发展我的手稿和赠款写作技巧。这项培训将有意义地促进 作为一名独立研究人员，我的发展重点是了解劣势对 心理健康结果，无论是独立的，并与个人的遗传倾向。

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.