From nature versus nurture, via nature and nurture, to gene x environment interaction in mental disorders
From nature versus nurture, via nature and nurture, to gene x environment interaction in mental disorders
It is now generally accepted that complex mental disorders are the results of interplay between genetic and environmental factors. This holds out the prospect that by studying G × E interplay we can explain individual variation in vulnerability and resilience to environmental hazards in the development of mental disorders. Furthermore studying G × E findings may give insights in neurobiological mechanisms of psychiatric disorder and so improve individualized treatment and potentially prevention. In this paper, we provide an overview of the state of field with regard to G × E in mental disorders. Strategies for G × E research are introduced. G × E findings from selected mental disorders with onset in childhood or adolescence are reviewed [such as depressive disorders, attention-deficit/hyperactivity disorder (ADHD), obesity, schizophrenia and substance use disorders]. Early seminal studies provided evidence for G × E in the pathogenesis of depression implicating 5-HTTLPR, and conduct problems implicating MAOA. Since then G × E effects have been seen across a wide range of mental disorders (e.g., ADHD, anxiety, schizophrenia, substance abuse disorder) implicating a wide range of measured genes and measured environments (e.g., pre-, peri- and postnatal influences of both a physical and a social nature). To date few of these G × E effects have been sufficiently replicated. Indeed meta-analyses have raised doubts about the robustness of even the most well studied findings. In future we need larger, sufficiently powered studies that include a detailed and sophisticated characterization of both phenotype and the environmental risk
199-210
Wermter, Anne-Kathrin
893b113a-4cc9-4ba8-bb26-bd5af33e3442
Laucht, Manfred
e8020abe-ffa1-432d-85b2-3314fbf428df
Schimmelmann, Benno G.
200f2b11-35f9-4461-8a55-319008fdc1da
Banaschewski, Tobias
4627c589-04cc-4f5b-ac2d-05f547f63dfd
Sonuga-Barke, Edmund J.S.
bc80bf95-6cf9-4c76-a09d-eaaf0b717635
Rietschel, Marcella
bfe692f6-8ff2-4137-aa33-b28b65710390
Becker, Katja
53e985be-20dd-4ae3-a66d-7b0e881ae5b7
2010
Wermter, Anne-Kathrin
893b113a-4cc9-4ba8-bb26-bd5af33e3442
Laucht, Manfred
e8020abe-ffa1-432d-85b2-3314fbf428df
Schimmelmann, Benno G.
200f2b11-35f9-4461-8a55-319008fdc1da
Banaschewski, Tobias
4627c589-04cc-4f5b-ac2d-05f547f63dfd
Sonuga-Barke, Edmund J.S.
bc80bf95-6cf9-4c76-a09d-eaaf0b717635
Rietschel, Marcella
bfe692f6-8ff2-4137-aa33-b28b65710390
Becker, Katja
53e985be-20dd-4ae3-a66d-7b0e881ae5b7
Wermter, Anne-Kathrin, Laucht, Manfred, Schimmelmann, Benno G., Banaschewski, Tobias, Sonuga-Barke, Edmund J.S., Rietschel, Marcella and Becker, Katja
(2010)
From nature versus nurture, via nature and nurture, to gene x environment interaction in mental disorders.
European Child & Adolescent Psychiatry, 19 (3), .
(doi:10.1007/s00787-009-0082-z).
Abstract
It is now generally accepted that complex mental disorders are the results of interplay between genetic and environmental factors. This holds out the prospect that by studying G × E interplay we can explain individual variation in vulnerability and resilience to environmental hazards in the development of mental disorders. Furthermore studying G × E findings may give insights in neurobiological mechanisms of psychiatric disorder and so improve individualized treatment and potentially prevention. In this paper, we provide an overview of the state of field with regard to G × E in mental disorders. Strategies for G × E research are introduced. G × E findings from selected mental disorders with onset in childhood or adolescence are reviewed [such as depressive disorders, attention-deficit/hyperactivity disorder (ADHD), obesity, schizophrenia and substance use disorders]. Early seminal studies provided evidence for G × E in the pathogenesis of depression implicating 5-HTTLPR, and conduct problems implicating MAOA. Since then G × E effects have been seen across a wide range of mental disorders (e.g., ADHD, anxiety, schizophrenia, substance abuse disorder) implicating a wide range of measured genes and measured environments (e.g., pre-, peri- and postnatal influences of both a physical and a social nature). To date few of these G × E effects have been sufficiently replicated. Indeed meta-analyses have raised doubts about the robustness of even the most well studied findings. In future we need larger, sufficiently powered studies that include a detailed and sophisticated characterization of both phenotype and the environmental risk
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Published date: 2010
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Local EPrints ID: 71841
URI: http://eprints.soton.ac.uk/id/eprint/71841
ISSN: 1018-8827
PURE UUID: e671134f-c7dc-43b6-bdce-9cfb4551d089
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Date deposited: 05 Jan 2010
Last modified: 13 Mar 2024 20:48
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Author:
Anne-Kathrin Wermter
Author:
Manfred Laucht
Author:
Benno G. Schimmelmann
Author:
Tobias Banaschewski
Author:
Edmund J.S. Sonuga-Barke
Author:
Marcella Rietschel
Author:
Katja Becker
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