遗传和环境因素对3 ~ 5岁儿童易怒发展的影响。

I-Tzu Hung,Argyris Stringaris,Chang Liu,Jody M Ganiban,Kimberly J Saudino
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引用次数: 0

摘要

目的易怒受遗传影响,与内在化和外在化精神病理有关。然而,对学龄前儿童易激惹的病因知之甚少。本研究从等级稳定性和发展轨迹的角度考察了这一点。方法对310对同性双胞胎(单卵= 123;异卵= 187;(51%为女性)在3岁、4岁和5岁时通过父母在儿童行为检查表上的报告进行纵向评估。生物测量Cholesky模型和潜在生长曲线模型分别用于研究遗传和环境对等级稳定性和不稳定性的影响,以及不同年龄(即发育轨迹)的个体易怒水平变化。结果易怒的遗传率在53% ~ 60%之间,其余的变异由非共享环境影响解释。年龄对年龄的稳定性很大程度上是由于遗传的影响。新的遗传和非共享的环境影响在4岁和5岁时出现,表明遗传和环境对不稳定的贡献。在4岁和5岁时,分别约有42%和22%的遗传影响与之前的年龄无关,超过85%的非共享环境影响是年龄特异性的。易怒发展轨迹的个体差异完全是由于非共享的环境影响。结论易激惹的等级稳定性和不同年龄段易激惹水平的个体内变化受不同病因过程的支配,强调从多个角度考察发展的重要性。两种观点都强调了非共享环境因素在早期易怒发展中的作用。干预措施可以受益于利用这些因素来重新定向早期易怒的发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Genetic and Environmental Influences on the Development of Irritability from Ages 3 to 5 Years.
OBJECTIVE Irritability is genetically influenced and is associated with internalizing and externalizing psychopathology. However, little is known about the etiology of the development of irritability in the preschool period. The present study examined this from rank-order stability and developmental trajectories perspectives. METHOD The irritability of 310 same-sex twin pairs (monozygotic = 123; dizygotic = 187; 51% female) was longitudinally assessed at ages 3, 4 and 5 years via parent-reports on the Child Behavior Checklist. Biometric Cholesky models and latent growth curve models were used to examine genetic and environmental influences on both the rank-order stability and instability, and within individual changes in levels of irritability across age (i.e. developmental trajectories), respectively. RESULTS The heritability of irritability ranged from 53% to 60%, with the remaining variances explained by nonshared environmental influences. Age-to-age stability was largely due to genetic influences. Novel genetic and nonshared environmental effects emerged at ages 4 and 5, indicating genetic and environmental contributions to instability. Approximately 42% and 22% of genetic influences at ages 4 and 5, respectively, were independent of prior ages, and over 85% of nonshared environmental influences were age-specific. Individual differences in developmental trajectories of irritability were entirely due to nonshared environmental influences. CONCLUSIONS The rank-order stability of irritability and within-individual change in levels of irritability across age are governed by different etiological processes, emphasizing the importance of examining development from multiple perspectives. Both perspectives highlight the role of nonshared environmental factors in early irritability development. Interventions could benefit from leveraging these factors to redirect early irritability development.
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