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      Interpersonal Stress Regulation and the Development of Anxiety Disorders: An Attachment-Based Developmental Framework

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          Abstract

          Anxiety disorders represent a common but often debilitating form of psychopathology in both children and adults. While there is a growing understanding of the etiology and maintenance of these disorders across various research domains, only recently have integrative accounts been proposed. While classical attachment history has been a traditional core construct in psychological models of anxiety, contemporary attachment theory has the potential to integrate neurobiological and behavioral findings within a multidisciplinary developmental framework. The current paper proposes a modern attachment theory-based developmental model grounded in relevant literature from multiple disciplines including social neuroscience, genetics, neuroendocrinology, and the study of family factors involved in the development of anxiety disorders. Recent accounts of stress regulation have highlighted the interplay between stress, anxiety, and activation of the attachment system. This interplay directly affects the development of social–cognitive and mentalizing capacities that are acquired in the interpersonal context of early attachment relationships. Early attachment experiences are conceptualized as the key organizer of a complex interplay between genetic, environmental, and epigenetic contributions to the development of anxiety disorders – a multifactorial etiology resulting from dysfunctional co-regulation of fear and stress states. These risk-conferring processes are characterized by hyperactivation strategies in the face of anxiety. The cumulative allostatic load and subsequent “wear and tear” effects associated with hyperactivation strategies converge on the neural pathways of anxiety and stress. Attachment experiences further influence the development of anxiety as potential moderators of risk factors, differentially impacting on genetic vulnerability and relevant neurobiological pathways. Implications for further research and potential treatments are outlined.

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          Most cited references 270

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          Emotion circuits in the brain.

           J Ledoux (1999)
          The field of neuroscience has, after a long period of looking the other way, again embraced emotion as an important research area. Much of the progress has come from studies of fear, and especially fear conditioning. This work has pinpointed the amygdala as an important component of the system involved in the acquisition, storage, and expression of fear memory and has elucidated in detail how stimuli enter, travel through, and exit the amygdala. Some progress has also been made in understanding the cellular and molecular mechanisms that underlie fear conditioning, and recent studies have also shown that the findings from experimental animals apply to the human brain. It is important to remember why this work on emotion succeeded where past efforts failed. It focused on a psychologically well-defined aspect of emotion, avoided vague and poorly defined concepts such as "affect," "hedonic tone," or "emotional feelings," and used a simple and straightforward experimental approach. With so much research being done in this area today, it is important that the mistakes of the past not be made again. It is also time to expand from this foundation into broader aspects of mind and behavior.
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            Epigenetic programming by maternal behavior.

            Here we report that increased pup licking and grooming (LG) and arched-back nursing (ABN) by rat mothers altered the offspring epigenome at a glucocorticoid receptor (GR) gene promoter in the hippocampus. Offspring of mothers that showed high levels of LG and ABN were found to have differences in DNA methylation, as compared to offspring of 'low-LG-ABN' mothers. These differences emerged over the first week of life, were reversed with cross-fostering, persisted into adulthood and were associated with altered histone acetylation and transcription factor (NGFI-A) binding to the GR promoter. Central infusion of a histone deacetylase inhibitor removed the group differences in histone acetylation, DNA methylation, NGFI-A binding, GR expression and hypothalamic-pituitary-adrenal (HPA) responses to stress, suggesting a causal relation among epigenomic state, GR expression and the maternal effect on stress responses in the offspring. Thus we show that an epigenomic state of a gene can be established through behavioral programming, and it is potentially reversible.
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              Effects of stress throughout the lifespan on the brain, behaviour and cognition.

              Chronic exposure to stress hormones, whether it occurs during the prenatal period, infancy, childhood, adolescence, adulthood or aging, has an impact on brain structures involved in cognition and mental health. However, the specific effects on the brain, behaviour and cognition emerge as a function of the timing and the duration of the exposure, and some also depend on the interaction between gene effects and previous exposure to environmental adversity. Advances in animal and human studies have made it possible to synthesize these findings, and in this Review a model is developed to explain why different disorders emerge in individuals exposed to stress at different times in their lives.
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                Author and article information

                Journal
                Front Behav Neurosci
                Front. Behav. Neurosci.
                Frontiers in Behavioral Neuroscience
                Frontiers Research Foundation
                1662-5153
                02 July 2011
                21 September 2011
                2011
                : 5
                Affiliations
                1simpleResearch Department of Clinical, Educational and Health Psychology, University College London London, UK
                2simpleDevelopmental Neuroscience Unit, Anna Freud Centre, University College London London, UK
                3simpleRoyal Holloway, University of London London, UK
                4simpleYale Child Study Center, Yale University New Haven, CT, USA
                5simpleDepartment of Psychology, University of Leuven Leuven, Belgium
                Author notes

                Edited by: Luke R. Johnson, Uniformed Services University of the Health Sciences, USA

                Reviewed by: René Hurlemann, University of Bonn, Germany; Kwang Choi, Uniformed Services University of the Health Sciences, USA

                *Correspondence: Tobias Nolte, Anna Freud Centre, 12 Maresfield Gardens, London NW3 5SU, UK. e-mail: tobias.nolte@ 123456annafreud.org

                Tobias Nolte and Jo Guiney share joint first authorship.

                Article
                10.3389/fnbeh.2011.00055
                3177081
                21960962
                Copyright © 2011 Nolte, Guiney, Fonagy, Mayes and Luyten.

                This is an open-access article subject to a non-exclusive license between the authors and Frontiers Media SA, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and other Frontiers conditions are complied with.

                Page count
                Figures: 1, Tables: 0, Equations: 0, References: 310, Pages: 21, Words: 21871
                Categories
                Neuroscience
                Hypothesis and Theory

                Neurosciences

                attachment, anxiety disorders, allostasis, hyperactivation, stress, mentalization, anxiety

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