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从遗传易感性到交互易感性:重新思考基因-环境相互作用筛查的伦理意义

From a genetic predisposition to an interactive predisposition: rethinking the ethical implications of screening for gene-environment interactions.

作者信息

Tabery James

机构信息

Department of Philosophy, University of Utah, Salt Lake City, Utah 84112, USA.

出版信息

J Med Philos. 2009 Feb;34(1):27-48. doi: 10.1093/jmp/jhn039. Epub 2009 Feb 4.

Abstract

In a widely acclaimed study from 2002, researchers found a case of gene-environment interaction for a gene controlling neuroenzymatic activity (low vs. high), exposure to childhood maltreatment, and antisocial personality disorder (ASPD). Cases of gene-environment interaction are generally characterized as evincing a genetic predisposition; for example, individuals with low neuroenzymatic activity are generally characterized as having a genetic predisposition to ASPD. I first argue that the concept of a genetic predisposition fundamentally misconstrues these cases of gene-environment interaction. This misconstrual will be diagnosed, and then a new concept--interactive predisposition--will be introduced. I then show how this conceptual shift reconfigures old questions and raises new questions for genetic screening. Attempts to screen embryos or fetuses for the gene associated with low neuroenzymatic activity with an eye toward selecting against the low-activity variant fall prey to the myth of pre-environmental prediction; attempts to screen newborns for the gene associated with low neuroenzymatic activity with an eye toward early intervention will have to face the interventionist's dilemma.

摘要

在2002年一项广受赞誉的研究中,研究人员发现了一个基因-环境相互作用的案例,涉及一个控制神经酶活性的基因(低活性与高活性)、童年期受虐待经历以及反社会人格障碍(ASPD)。基因-环境相互作用的案例通常被认为表明存在遗传易感性;例如,神经酶活性低的个体通常被认为具有患反社会人格障碍的遗传易感性。我首先认为,遗传易感性的概念从根本上误解了这些基因-环境相互作用的案例。这种误解将被剖析,然后引入一个新的概念——交互易感性。接着,我将展示这种概念转变如何重新构建旧问题,并为基因筛查提出新问题。试图筛查胚胎或胎儿中与低神经酶活性相关的基因,以期选择淘汰低活性变体,这陷入了环境前预测的误区;试图筛查新生儿中与低神经酶活性相关的基因,以期进行早期干预,将不得不面对干预主义者的困境。

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