دانلود مقاله ISI انگلیسی شماره 122431
ترجمه فارسی عنوان مقاله

چگونگی رژیم افراطی اجباری: یک فرضیه جدید برای نقش اضطراب در توسعه و نگهداری عصب بی هوازی

عنوان انگلیسی
How extreme dieting becomes compulsive: A novel hypothesis for the role of anxiety in the development and maintenance of anorexia nervosa
کد مقاله سال انتشار تعداد صفحات مقاله انگلیسی
122431 2017 7 صفحه PDF
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : Medical Hypotheses, Volume 108, October 2017, Pages 144-150

پیش نمایش مقاله
پیش نمایش مقاله  چگونگی رژیم افراطی اجباری: یک فرضیه جدید برای نقش اضطراب در توسعه و نگهداری عصب بی هوازی

چکیده انگلیسی

The US National Institute of Mental Health’s Research Domain Criteria (NIMH RDoC) advocates the study of features common to psychiatric conditions. This transdiagnostic approach has recently been adopted into the study of anorexia nervosa (AN), an illness that can be considered compulsive in nature. This has led to the development of an account of AN that identifies key roles for the heightened reinforcement of starvation, leading to its excessive repetition, and goal-directed system dysfunction. Considering models of illness in other compulsive disorders, we extend the existing account to explain the emergence of reinforcement and goal-directed system abnormalities in AN, proposing that anxiety is central to both processes. As such we emphasise the particular importance of the anxiolytic effects of starvation, over other reinforcing outcomes, in encouraging the continuation of starvation within a model that proposes a number of mechanisms by which anxiety operates in the development and maintenance of AN. We suggest the psychopathology of AN mediates the relationship between the anxiolytic effects of starvation and excessive repetition of starvation, and that compulsive starvation has reciprocal effects on its determinants. We thus account for the emergence of symptoms of AN other than compulsive starvation, and for the relationship between different features of the disorder. By extending and adapting an existing explanation of AN, we provide a richer aetiological model that invites new research questions and could inform novel approaches to prevention and treatment.