Nolte Tobias, Guiney Jo, Fonagy Peter, Mayes Linda C, Luyten Patrick
Research Department of Clinical, Educational and Health Psychology, University College London London, UK.
Front Behav Neurosci. 2011 Sep 21;5:55. doi: 10.3389/fnbeh.2011.00055. eCollection 2011.
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.
焦虑症在儿童和成人中都是一种常见但往往使人衰弱的精神病理学形式。虽然在各个研究领域对这些疾病的病因和维持机制的理解日益加深,但直到最近才提出综合的解释。虽然经典的依恋史一直是焦虑症心理模型中的传统核心结构,但当代依恋理论有潜力在多学科发展框架内整合神经生物学和行为学研究结果。本文基于包括社会神经科学、遗传学、神经内分泌学以及焦虑症发展过程中涉及的家庭因素研究等多学科的相关文献,提出了一个基于现代依恋理论的发展模型。最近关于压力调节的研究强调了压力、焦虑和依恋系统激活之间的相互作用。这种相互作用直接影响在早期依恋关系的人际背景中获得的社会认知和心理化能力的发展。早期依恋经历被概念化为遗传、环境和表观遗传因素对焦虑症发展的复杂相互作用的关键组织者——这是一种由恐惧和压力状态的功能失调共同调节导致的多因素病因。这些赋予风险的过程的特征是面对焦虑时的过度激活策略。与过度激活策略相关的累积的应激负荷和随后的“磨损”效应集中在焦虑和压力的神经通路上。依恋经历作为风险因素的潜在调节因素,进一步影响焦虑症的发展,对遗传易感性和相关神经生物学途径有不同的影响。本文概述了对进一步研究和潜在治疗方法的启示。