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Differential susceptibility to effects of maternal sensitivity? A study of candidate plasticity genes—CORRIGENDUM
Development and Psychopathology ( IF 3.1 ) Pub Date : 2015-01-05 , DOI: 10.1017/s0954579414001497
Jay Belsky 1 , Daniel A Newman 2 , Keith F Widaman 3 , Phil Rodkin 2 , Michael Pluess 3 , R Chris Fraley 2 , Daniel Berry 2 , Jonathan L Helm 1 , Glenn I Roisman 4
Affiliation  

Development and Psychopathology 27 (2015), 725–746 # Cambridge University Press 2014 doi:10.1017/S0954579414000844 Differential susceptibility to effects of maternal sensitivity? A study of candidate plasticity genes JAY BELSKY, a DANIEL A. NEWMAN, b KEITH F. WIDAMAN, a PHIL RODKIN, b MICHAEL PLUESS, c R. CHRIS FRALEY, b DANIEL BERRY, b JONATHAN L. HELM, a AND GLENN I. ROISMAN d a University of California, Davis; b University of Illinois at Urbana–Champaign; c Kings College London; and d University of Minnesota Abstract Here we tested whether there was genetic moderation of effects of early maternal sensitivity on social–emotional and cognitive–linguistic development from early childhood onward and whether any detected Gene Environment interaction effects proved consistent with differential-susceptibility or diathesis–stress models of PersonEnvironment interaction (N ¼ 695). Two new approaches for evaluating models were employed with 12 candidate genes. Whereas maternal sensitivity proved to be a consistent predictor of child functioning across the primary-school years, candidate genes did not show many main effects, nor did they tend to interact with maternal sensitivity/insensitivity. These findings suggest that the developmental benefits of early sensitive mothering and the costs of insensitive mothering look more similar than different across genetically different children in the current sample. Although acknowledgement of this result is important, it is equally important that the generally null GeneEnvironment results reported here not be overgeneralized to other samples, other predictors, other outcomes, and other candidate genes. The differential-susceptibility hypothesis, which stipulates that some individuals are more susceptible than others to both positive and negative environmental effects, perhaps most especially parenting, has received substantial attention and empirical support in recent years (Belsky, Bakermans- Kranenburg, & van IJzendoorn, 2007; Belsky & Pluess, 2013; Ellis, Boyce, Belsky, Bakermans-Kranenburg, & van IJzendoorn, 2011; Pluess & Belsky, 2009, 2010), including in research on Gene Environment (G E) interaction (Ba- kermans-Kranenburg & van IJzendoorn, 2011; Belsky et al., 2009; Belsky & Pluess, 2009; Berry, Deater-Deckard, McCartney, Wang, & Petrill, 2013). Here we test the specific proposition that a set of 12 candidate “plasticity genes,” se- lected principally on the basis of prior reviews of relevant research (Belsky et al., 2009; Belsky & Pluess, 2009), will moderate the effects of maternal sensitivity on children’s social–emotional and cognitive–linguistic development in a manner consistent with the differential-susceptibility hypothe- sis. Toward this end, we employ two new statistical methods, applying them to longitudinal data collected from the National Institute of Child Health and Human Development Study of Early Child Care and Youth Development (NICHD SECCYD; NICHD Early Child Care Research Network [ECCRN], 2005), in response to questions raised about the adequacy and appro- priateness of existing statistical criteria for evaluating differen- tial susceptibility (Belsky, Pluess, & Widaman, 2013; Roisman et al., 2012; Widaman et al., 2012). The application of appro- priate analytic criteria for differential susceptibility is necessary to minimize Type 1 errors and failures to replicate that have fru- strated previous work on candidate genes and broad phenotypes of human cognition, personality, and social behavior (Charney & English, 2012; Deary, 2012; Wacker, Mueller, Hennig, & Stemmler, 2012). Theories of Socialization and Maternal Sensitivity Extraction and genotyping for the NICHD SECCYD was performed at the Genome Core Facility in the Huck Institutes for Life Sciences at Penn State University under the direction of Deborah S. Grove, Director for Genetic Analysis. Genotyping was principally supported by a Research Board grant from the University of Illinois at Urbana–Champaign (to P.R. and G.I.R.). This work was also supported by NSF Grant BCS-0720538 (to G.I.R. and R.C.F.) and by NICHD Grant R01 HD064687 to Rand Conger, which are gratefully acknowledged. Finally, we dedicate this work to the memory of our friend and coauthor Phil Rodkin. In addition to his major contributions to this manuscript, Phil fully embodied the collaborative and collegial spirit that ultimately birthed this contribution to the literature. Address correspondence and reprint requests to: Jay Belsky, Department of Human Ecology, University of California, Davis, 1331 Hart Hall, One Shields Avenue, Davis, CA 95616; E-mail: jbelsky@ucdavis.edu. A central assumption of many developmental perspectives on socialization, whether based, for example, on theories of at- tachment (Ainsworth, 1973; Sroufe, 2000), social learning (Patterson, 1986), or evolution (Belsky, Steinberg, & Draper, 1991), is that parenting matters when it comes to how children develop. Although a myriad of parenting constructs are mea- sured in socialization research, including, for example, author- itative parenting (Baumrind, 1967, 1991), coercive parenting (Patterson, 1986), and mutually responsive relationships (Ko- chanska, 2002), the focus in the present report is on sensitive parenting, a construct emphasized in attachment theory. Ac-

中文翻译:

对母体敏感性影响的差异易感性?候选可塑性基因的研究——更正

发展与精神病理学 27 (2015), 725–746 # Cambridge University Press 2014 doi:10.1017/S0954579414000844 对母体敏感性影响的差异易感性?候选可塑性基因的研究 JAY BELSKY、DANIEL A. NEWMAN、b KEITH F. WIDAMAN、PHIL RODKIN、b MICHAEL PLUESS、c R. CHRIS FRALEY、b DANIEL BERRY、b JONATHAN L. HELM 和 GLENN I。加利福尼亚大学戴维斯分校的 ROISMAN;b 伊利诺伊大学厄巴纳-香槟分校;c 伦敦国王学院;和 d 明尼苏达大学摘要在这里,我们测试了早期母亲敏感性对儿童早期社会情感和认知语言发展的影响是否存在遗传调节,以及是否发现任何检测到的基因环境相互作用影响与差异易感性或素质一致—— PersonEnvironment 交互的压力模型(N ¼ 695)。对 12 个候选基因采用了两种评估模型的新方法。虽然母亲敏感性被证明是整个小学阶段儿童功能的一致预测因子,但候选基因没有显示出许多主要影响,它们也不会与母亲敏感性/不敏感性相互作用。这些发现表明,在当前样本中,在基因不同的儿童中,早期敏感母亲的发育益处和不敏感母亲的成本看起来更相似,而不是不同。尽管承认这一结果很重要,但同样重要的是,此处报告的通常为空的 GeneEnvironment 结果不会过度泛化到其他样本、其他预测因子、其他结果和其他候选基因。差异易感性假说规定某些人比其他人更容易受到正面和负面环境影响的影响,尤其是在养育子女方面,近年来受到了大量关注和实证支持(Belsky、Bakermans-Kranenburg 和 van IJzendoorn, 2007;Belsky & Pluess,2013;Ellis、Boyce、Belsky,Bakermans-Kranenburg, & van IJzendoorn, 2011; Pluess & Belsky, 2009, 2010),包括对基因环境 (GE) 相互作用的研究 (Bakermans-Kranenburg & van IJzendoorn, 2011; Belsky et al., 2009; Belsky & Pluess, 2009; Berry, Deater-Deckard, McCartney、Wang 和 Petrill,2013 年)。在这里,我们测试了一组 12 个候选“可塑性基因”的具体命题,主要根据相关研究的先前评论(Belsky 等人,2009 年;Belsky & Pluess,2009 年)选择,将缓和以与差异易感性假设一致的方式评估母亲对儿童社会情感和认知语言发展的敏感性。为此,我们采用了两种新的统计方法,将它们应用于从国家儿童健康与人类发展研究所早期儿童保育和青年发展(NICHD SECCYD;NICHD 早期儿童保育研究网络 [ECCRN],2005 年)收集的纵向数据,以回答有关充分性和评估差异敏感性的现有统计标准的适当性(Belsky、Pluess 和 Widaman,2013 年;Roisman 等人,2012 年;Widaman 等人,2012 年)。应用适当的差异易感性分析标准是必要的,以最大限度地减少 1 型错误和复制失败,这些错误和失败使先前关于候选基因和人类认知、人格和社会行为的广泛表型的工作受挫(Charney & English,2012 ;Deary,2012 年;Wacker、Mueller、Hennig 和 Stemmler,2012 年)。NICHD SECCYD 的社会化和母体敏感性提取和基因分型理论在宾夕法尼亚州立大学哈克生命科学研究所的基因组核心设施中进行,由遗传分析主任 Deborah S. Grove 指导。基因分型主要由伊利诺伊大学厄巴纳香槟分校的研究委员会资助(给 PR 和 GIR)。这项工作也得到了 NSF Grant BCS-0720538(给 GIR 和 RCF)和 NICHD Grant R01 HD064687 给 Rand Conger 的支持,在此表示感谢。最后,我们将这项工作献给我们的朋友和合著者 Phil Rodkin。除了他对这份手稿的主要贡献之外,Phil 还充分体现了最终促成了这一对文学贡献的协作和大学精神。地址通信和转载请求: Jay Belsky, Department of Human Ecology, Department of California, Davis, 1331 Hart Hall, One Shields Avenue, Davis, CA 95616; 电子邮件:jbelsky@ucdavis.edu。许多社会化发展观点的核心假设,无论是基于依恋理论(Ainsworth,1973;Sroufe,2000)、社会学习(Patterson,1986)还是进化(Belsky、Steinberg 和 Draper, 1991 年),是说当涉及到孩子的成长方式时,养育子女很重要。尽管在社会化研究中测量了无数的养育结构,例如,包括权威养育(Baumrind,1967,1991)、强制养育(Patterson,1986)和相互响应的关系(Kochanska,2002) ,本报告的重点是敏感的养育方式,依恋理论强调的一种结构。交流-
更新日期:2015-01-05
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