The concept of gene-environment interaction, or G×E, refers to cases where different genetic groups respond differently to the same array of environments for a particular phenotypic trait. In a widely acclaimed study from 2002, researchers found a case of G×E for a gene associated with neuroenzymatic activity (low vs. high), exposure to childhood maltreatment, and the development of antisocial personality disorder (ASPD), or sociopathy. Cases of G×E are generally characterized as evincing a genetic predisposition to the trait under consideration; for example, individuals with low neuroenzymatic activity are generally characterized as having a genetic predisposition to ASPD. Bioethical commentators in turn have asked: Should parents test their embryos or fetuses for this genetic predisposition to ASPD in order to screen against the gene associated with low-MAOA activity? Should the state test all newborns for this genetic predisposition to ASPD in order to identify and treat individuals with the gene associated with low-MAOA activity from birth?
I first show that the concept of a genetic predisposition fundamentally misconstrues the ASPD study. That concept is appropriately applied only to cases of G×E that result in a change of scale, but the ASPD study resulted in a change of rank. For cases of G×E that result in a change of rank, I introduce a new conceptinteractive predisposition. Then, I show how this switch from a genetic predisposition to an interactive predisposition reconfigures old questions and raises new questions in the confines of the ethical discussions about the implications of such studies. For the ASPD study, attempts to screen against the gene associated with low-MAOA activity potentially fall prey to the myth of pre-environmental prediction, and attempts to screen all newborns for the gene associated with low-MAOA activity with an eye towards early intervention will have to face the interventionists dilemma. Moving beyond the ASPD study, traditional cost-benefit analyses involved in deciding whether or not to undertake the genetic testing of a child will have to be reweighed when the disease/disorder of concern results from an interactive predisposition rather than a genetic predisposition.
| Identifer | oai:union.ndltd.org:PITT/oai:PITTETD:etd-10142007-213310 |
| Date | 16 January 2008 |
| Creators | Tabery, James Gregory |
| Contributors | Erik Parens, Lisa Parker, Kenneth Schaffner, Mark Wicclair |
| Publisher | University of Pittsburgh |
| Source Sets | University of Pittsburgh |
| Language | English |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | http://etd.library.pitt.edu/ETD/available/etd-10142007-213310/ |
| Rights | unrestricted, I hereby certify that, if appropriate, I have obtained and attached hereto a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to University of Pittsburgh or its agents the non-exclusive license to archive and make accessible, under the conditions specified below, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report. |
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