Measured Gene–Environment Interactions and Mechanisms Promoting Resilient Development
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چکیده
Childhood maltreatment elevates risk for antisocial behavior, depression, and other problems over the life span, but a subset of maltreated individuals avoids maladaptive development and shows resilience. Resilience reflects a dynamic confluence of factors that promotes positive adaptation despite exposure to adverse experiences. Recent replicated findings of gene–environment interactions (abbreviated G E) involving maltreatment have identified two genes, monoamine oxidase A (MAOA) and serotonin transporter (5-HTT), that moderate the association between childhood maltreatment and psychopathology. Accordingly, G E raise new questions about potential biological mechanisms by which some individuals are able to cope adaptively and function relatively well despite experiencing early adversity. We summarize advances toward greater specification of G E mechanisms, including genetic and environmental moderation of G E effects and imaging genomics that provide clues regarding resilience processes in development. KEYWORDS—resilience; gene–environment interaction; maltreatment; MAOA; 5-HTT Each year in the United States, hundreds of thousands of children are victims of abuse and neglect. Although maltreated children are at heightened risk of developing mental and physical health problems, some of these children ‘‘beat the odds’’ and go on to live relatively healthy, productive lives. What biological and environmental processes explain favorable outcomes in some individuals following childhood maltreatment? How can such information be applied to foster resilience in individuals who experience severe adversity? Resilience reflects a dynamic confluence of factors that promotes positive adaptation—defined as either the absence of psychopathology or the presence of competence—despite exposure to adverse life experiences. In recent years, increasing attention has been drawn to the potential role that genetics and neurobiology might play in determining resilience (Cicchetti & Blender, 2006; Kim-Cohen, Moffitt, Caspi, & Taylor, 2004; Luthar & Brown, 2007; Masten & Obradovic, 2006). This shift toward incorporating biological hypotheses in resilience models has been stimulated by the groundbreaking incorporation of gene–environment interactions (hereafter abbreviated G E) in behavioral research by Caspi and Moffitt (2006) and their colleagues. In brief, G E demonstrate that variation in specific genes moderates the impact of environmental risks on psychopathology (or vice versa), such that risk-exposed individuals who carry the ‘‘protective’’ version (or allele) of the gene have significantly reduced levels of psychopathology compared to comparably risk-exposed individuals with the ‘‘vulnerable’’ allele. Here, we review the emerging literature on G E involving childhood maltreatment and discuss potential G E mechanisms in resilient development. We then outline future directions that can advance our understanding of resilience phenomena.
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تاریخ انتشار 2009