Nolte, T; Guiney, J; Fonagy, P; Mayes, LC; Luyten, P; (2011) Interpersonal stress regulation and the development of anxiety disorders: an attachment-based developmental framework. Frontiers in Behavioral Neuroscience , 5 , Article 55. 10.3389/fnbeh.2011.00055.

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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 intergrative accounts been proposed. While classical attachment history has been a traditional core construct in phychological 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 attachement theory-based developmental model grounded in relevant literature form multiple disciplines including social neuroscience, genetics, neuroendocrinology, and the study of family factors involved in the development of anxiety disorders. Recent account of stress regulation hav highlighted the interplay between stress, anxiety, and activation of the attachement system. This interplay directly affects the development of social-cognitive and mentalizing capacities that are acquired in the interpersonal context of early attachemnt relationships. Early attachement 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. Attachement 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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