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From Nature Versus Nurture, Via Nature and Nurture, to Gene X Environment Interaction in Mental Disorders Anne-Kathrin Wermter, Manfred Laucht, Benno G

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From Nature Versus Nurture, Via Nature and Nurture, to Gene X Environment Interaction in Mental Disorders Anne-Kathrin Wermter, Manfred Laucht, Benno G From nature versus nurture, via nature and nurture, to gene x environment interaction in mental disorders Anne-Kathrin Wermter, Manfred Laucht, Benno G. Schimmelmann, Tobias Banaschweski, Edmund J. S. Sonuga-Barke, Marcella Rietschel, Katja Becker To cite this version: Anne-Kathrin Wermter, Manfred Laucht, Benno G. Schimmelmann, Tobias Banaschweski, Edmund J. S. Sonuga-Barke, et al.. From nature versus nurture, via nature and nurture, to gene x environment interaction in mental disorders. European Child and Adolescent Psychiatry, Springer Verlag (Ger- many), 2009, 19 (3), pp.199-210. 10.1007/s00787-009-0082-z. hal-00548160 HAL Id: hal-00548160 https://hal.archives-ouvertes.fr/hal-00548160 Submitted on 19 Dec 2010 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Eur Child Adolesc Psychiatry (2010) 19:199–210 DOI 10.1007/s00787-009-0082-z REVIEW From nature versus nurture, via nature and nurture, to gene 3 environment interaction in mental disorders Anne-Kathrin Wermter • Manfred Laucht • Benno G. Schimmelmann • Tobias Banaschweski • Edmund J. S. Sonuga-Barke • Marcella Rietschel • Katja Becker Received: 1 July 2009 / Accepted: 27 November 2009 / Published online: 19 December 2009 Ó Springer-Verlag 2009 Abstract It is now generally accepted that complex potentially prevention. In this paper, we provide an over- mental disorders are the results of interplay between view of the state of field with regard to G 9 E in mental genetic and environmental factors. This holds out the disorders. Strategies for G 9 E research are introduced. prospect that by studying G 9 E interplay we can explain G 9 E findings from selected mental disorders with onset individual variation in vulnerability and resilience to in childhood or adolescence are reviewed [such as environmental hazards in the development of mental depressive disorders, attention-deficit/hyperactivity disor- disorders. Furthermore studying G 9 E findings may give der (ADHD), obesity, schizophrenia and substance use insights in neurobiological mechanisms of psychiatric disorders]. Early seminal studies provided evidence for disorder and so improve individualized treatment and G 9 E in the pathogenesis of depression implicating 5-HTTLPR, and conduct problems implicating MAOA. Since then G 9 E effects have been seen across a wide A.-K. Wermter Á K. Becker (&) Department of Child and Adolescent Psychiatry range of mental disorders (e.g., ADHD, anxiety, schizo- and Psychotherapy, Philipps-University of Marburg, phrenia, substance abuse disorder) implicating a wide Hans-Sachs-Str. 6, 35039 Marburg, Germany range of measured genes and measured environments (e.g., e-mail: [email protected] pre-, peri- and postnatal influences of both a physical and a A.-K. Wermter social nature). To date few of these G 9 E effects have e-mail: [email protected] been sufficiently replicated. Indeed meta-analyses have M. Laucht Á T. Banaschweski Á K. Becker raised doubts about the robustness of even the most well Department of Child and Adolescent Psychiatry studied findings. In future we need larger, sufficiently pow- and Psychotherapy, Central Institute of Mental Health, ered studies that include a detailed and sophisticated charac- 122120, 68072 Mannheim, Germany terization of both phenotype and the environmental risk. B. G. Schimmelmann University Hospital of Child and Adolescent Psychiatry, Keywords Gene–environment interaction Á Depressive University of Bern, Effingerstr. 12, 3011 Bern, Switzerland disorders Á ADHD Á Obesity Á Schizophrenia Á Substance use disorders E. J. S. Sonuga-Barke Developmental Brain-Behaviour Laboratory, Department of Psychology, University of Southampton, Southampton S017 1BJ, UK Introduction E. J. S. Sonuga-Barke Department of Experimental Clinical and Health Psychology, Recent progress in the development of powerful new University of Gent, Henri Dunantlaan 2, 9000 Ghent, Belgium techniques for locating and identifying human suscepti- bility genes and genetic variations contributing to common M. Rietschel diseases has created new opportunities to advance our Division of Genetic Epidemiology in Psychiatry, Central Institute of Mental Health, 122120, understanding of the etiology of mental disorders. Two 68072 Mannheim, Germany approaches, linkage and association analyses, have been 123 200 Eur Child Adolesc Psychiatry (2010) 19:199–210 applied to identify and study genetic effects across a vice versa [64]. The article starts with an overview of the number of mental disorders. These disorders include impact as well as the limitations of G 9 E studies. In attention-deficit/hyperactivity disorder (ADHD), autism general, this is followed by more detailed information spectrum disorders, mood disorders, substance use disor- about G 9 E research findings in some selected mental ders, schizophrenia, eating disorders, obesity, and anxiety disorders with onset in childhood or adolescence. disorders. However, despite initial optimism, few suscep- tibility genes (i.e., predisposing sequence variations) have been replicated with some consistency. Even for replicated The importance of gene–environment interplay findings the effects are very small: taking all risk genotypes in the etiology of mental disorders into account explains only a small fraction of the variation in the expression of a disorder. G 9 E provides a potential explanation of the individual There are several possible explanations for this. One is differences in responses to environmental influences. G 9 E that gene–environment interactions (G 9 E) have so far occurs when the effect of exposure to an environmental been largely ignored in the design and analyses of genetic pathogen on a person’s health is conditional on the genotype studies. This has hampered the detection of significant [19]. For example, children exposed to an environment genetic effects operating in those exposed to one environ- stressor known to increase risk for a certain psychiatric ment and not another [69]. This notion is supported by the disorder (e.g., high family adversity) are at a higher risk for growing body of evidence for the contribution of genetic that disorder if they carry particular gene variants which effects in explaining individual variability in response to all renders them more susceptible to that stressor (see Fig. 1). kinds of environmental hazards [68, 82, 83]. Because of Alternatively children carrying a genotype known to this type of work it is nowadays generally accepted that increase susceptibility for a specific mental disorder may complex mental disorders require an understanding of the only develop that disorder if they are exposed to specific interplay between genetic and environmental factors. This environmental risk factors (see Fig. 2). G 9 E hypothesis is neurobiologically plausible and is According to these models on the one hand, differences supported by a growing body of evidence (e.g., there are in individual genetic make-up are responsible for the dif- formal genetic studies in its favor [51]). However, some ferences between individuals with regard to resilience or researchers remain skeptical and call for more robust rep- vulnerability to the similar environmental pathogens. On lication of initial results [70]. Clearly much more work is the other hand, outcomes among individuals who do not needed to establish (1) the conditions under which G 9 E vary in terms of the susceptibility allele may be determined occur; and (2) the mechanisms that drive the G 9 E as a function of variability in environmental exposure. In effects. Why do some genetic variants have effects only in other words, G 9 E effects index a genetically determined the presence of a particular environmental exposure and/or liability to specific environmental influences. One example Fig. 1 Environmental factors only lead to a disorder in presence of a specific genetic make-up Fig. 2 An individual with a susceptible genetic make-up will only develop a disorder if there are additional environmental pathogens 123 Eur Child Adolesc Psychiatry (2010) 19:199–210 201 with one dichotomous genotype (present or absent) of a possibility of overestimating effects and false positive causative genetic mutation and one dichotomous environ- findings because of multiple testing and/or data dredging. mental exposure (exposure vs. non-exposure) is phenyl- Along with difficulties in statistical power [16, 63, 107], ketonuria (PKU) [46]. The development of PKU needs the susceptibility to artifacts in G 9 E research has to be both homozygote mutations in the causative gene encoding kept in mind. Statistically significant interactions are sen- phenylalanine hydroxylase, and exposure to phenylalanine sitive to alterations in the definition and scaling of the [53]. An example for a complex genetic disorder is the variables being examined: artefactual interactions can be alcohol flush reaction after alcohol ingestion in individuals produced by altering scaling [68]. Another problem is how with a genetic variant leading to lowered activity of the to disentangle G 9 E from
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