Understanding the effects of neighborhood disadvantage on youth psychopathology.
Understanding the effects of neighborhood disadvantage on youth psychopathology.
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DOI：
10.1017/s0033291721005080
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发表时间：
2023-05
影响因子：
6.9
通讯作者：
Burt, S. Alexandra
中科院分区：
文献类型：
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作者：
Carroll, Sarah L.;Klump, Kelly L.;Burt, S. Alexandra
1942 年，Shaw 和 McKay 报告称，弱势社区预示着青少年的精神病理学。此后的几十年里，数十篇论文证实并扩展了这些早期结果，令人信服地证明，弱势社区环境预示着儿童期和青春期内化和外化疾病发生率的升高。然而，尚不清楚邻里劣势如何增加精神病理学。我们的研究试图通过检查地区剥夺指数（ADI）来填补文献中的这一空白，该指数是人口普查区劣势的综合衡量标准，作为密歇根州立大学双胞胎登记处的两个学龄双胞胎样本（N = 4815 和 1030 对双胞胎）中几种常见精神病理形式的病因学调节因素，后者因邻里劣势而丰富。在这两个样本中，在存在明显劣势的情况下，遗传对注意力缺陷多动问题的影响会加剧，而非共享环境对冷酷无情特征的影响随着劣势的增加而增加。然而，邻里劣势对抑郁、焦虑或躯体症状的病因几乎没有调节作用。这些发现表明，尽管邻里劣势确实似乎是许多（但不是全部）形式的精神病理学的一般病因调节因素，但这种病因调节是表型特异性的。
In 1942, Shaw and McKay reported that disadvantaged neighborhoods predict youth psychopathology. In the decades since, dozens of papers have confirmed and extended these early results, convincingly demonstrating that disadvantaged neighborhood contexts predict elevated rates of both internalizing and externalizing disorders across childhood and adolescence. It is unclear, however, how neighborhood disadvantage increases psychopathology. Our study sought to fill this gap in the literature by examining the Area Deprivation Index (ADI), a composite measure of Census tract disadvantage, as an etiologic moderator of several common forms of psychopathology in two samples of school-aged twins from the Michigan State University Twin Registry (N =4815 and 1030 twin pairs, respectively), the latter of which was enriched for neighborhood disadvantage. Across both samples, genetic influences on attention-deficit hyperactivity problems were accentuated in the presence of marked disadvantage, while nonshared environmental contributions to callous-unemotional traits increased with increasing disadvantage. However, neighborhood disadvantage had little moderating effect on the etiology of depression, anxiety, or somatic symptoms. Such findings suggest that, although neighborhood disadvantage does appear to serve as a general etiologic moderator of many (but not all) forms of psychopathology, this etiologic moderation is phenotype-specific.