Amianto Federico, Northoff Georg, Abbate Daga Giovanni, Fassino Secondo, Tasca Giorgio A
Regional Expert Centre for Eating Disorders, Neurosciences Department, Psychiatry Section, University of Turin Turin, Italy.
Mind, Brain Imaging and Neuroethics Research Unit, The Royal's Institute of Mental Health Research, University of Ottawa, Ottawa ON, Canada.
Front Psychol. 2016 Jun 14;7:849. doi: 10.3389/fpsyg.2016.00849. eCollection 2016.
The debate concerning the pathogenesis and the maintaining factors of eating disorders, anorexia nervosa in particular, is ongoing especially since therapeutic interventions do not result in satisfactory and enduring rates of remission. This paper presents a model for the pathogenesis of eating disorders, based on the hypothesis of a deficiency in the development of the self. We present the theory in light of new evidence concerning the role of attachment insecurity in the development and maintenance of eating disorders. In particular, we define the self in eating disorders in a comprehensive way by taking into account recent evidence from experimental psychology and neurobiology. The paper considers the development of the self in terms of its synchronic (i.e., experienced in the moment) and diachronic (i.e., experienced as continuous over time) aspects. Both synchronic and diachronic aspects of the self are relevant to the expression of eating disorder symptoms. Further, the maturation of the self is interwoven with the development of attachment functioning from infancy to adolescence. This interplay between these developmental processes of the self and of attachment could be crucial in understanding the pathogenesis of eating disorders. The final part of the paper suggests a neurobiological link between the theory of the self in the eating disorders and the spatiotemporal functioning of the brain. Disturbances in spatiotemporal functioning may represent the neurobiological pathway by which deficiencies in the self is related to attachment functions in individuals with eating disorders.
关于饮食失调，尤其是神经性厌食症的发病机制和维持因素的争论仍在继续，特别是因为治疗干预并未带来令人满意且持久的缓解率。本文基于自我发展存在缺陷的假设，提出了一种饮食失调发病机制的模型。我们根据关于依恋不安全在饮食失调的发展和维持中所起作用的新证据来阐述该理论。特别是，我们通过考虑实验心理学和神经生物学的最新证据，全面地定义了饮食失调中的自我。本文从自我的共时性（即在当下体验到的）和历时性（即随着时间推移体验为连续的）方面来考量自我的发展。自我的共时性和历时性方面都与饮食失调症状的表现相关。此外，自我的成熟与从婴儿期到青春期的依恋功能发展相互交织。自我和依恋的这些发展过程之间的这种相互作用，对于理解饮食失调的发病机制可能至关重要。本文的最后一部分提出了饮食失调中自我理论与大脑时空功能之间的神经生物学联系。时空功能障碍可能代表了自我缺陷与饮食失调个体的依恋功能相关的神经生物学途径。
