Weight History, Brain Activation to Food Cues and Eating Disorder Psychopathology

描述（由申请人提供）：进食障碍（ED）影响约5%的人口，并对精神和身体健康产生各种不良影响。近年来，饮食失调的治疗取得了进展，但进一步的进展将部分取决于提高该领域对饮食失调精神病理学的理解。ED的认知行为治疗（CBT）模型已经获得了大量的支持，但这个框架并没有充分解决两个领域，似乎对饮食失调有重大影响。我们称第一个领域为体重史，它包括发病前的体重，有史以来最高和当前体重（体重抑制，WS）和当前BMI（通常处于非常低的不健康水平）之间的差异。我们已经表明，WS和BMI（及其相互作用）是许多艾德特征的可靠预测因子，这些关系并没有被CBT模型充分解释。第二个领域涉及大脑对可口食物线索的奖励和抑制反应。有证据表明，存在一个连续体，两极由限制性厌食症患者和超重暴食者对食物线索的相反反应所锚定（前者显示出奖励性低激活和抑制性高激活，后者显示出相反）。然而，关于这些异常模式如何导致艾德精神病理学却知之甚少。因为包括两个领域的变量本质上是连续的，并且因为当前应用将研究艾德个体而不管DSM诊断，所以所提出的研究与RDoC建议一致。我们测试的假设，这两个领域将是横截面相关的进食障碍的精神病理学，将预测未来的体重增加，艾德痴呆症和课程，大脑激活的奖励和抑制感兴趣的区域将介导的预测效果的体重历史变量的体重变化和艾德的结果。这些假设将在96名接受任何级别门诊治疗的艾德患者中进行检验。在基线时，将使用体重史和艾德精神病理学的标准化测量对他们进行评估，并将使用旨在测量他们对感兴趣区域中食物图片的奖励和抑制激活的范例进行结构和功能MRI。将在3个月和6个月随访时重复测量体重和艾德勃起功能。拟议的研究有很大的潜力，以确定新的艾德精神病理学的来源，可以转化为新的治疗这些治疗耐药的疾病。

DESCRIPTION (provided by applicant): Eating disorders (EDs) affect approximately 5% of the population and have a variety of adverse effects on mental and physical health. The treatment of disordered eating has progressed in recent years but further progress will depend in part on improving the field's understanding of eating disorder psychopathology. The cognitive-behavioral therapy (CBT) model of EDs has garnered substantial support but this framework does not sufficiently address two domains that appear to have a major impact on disordered eating. We call the first domain Weight History, which consists of premorbid body mass, the discrepancy between highest ever and current body weight (weight suppression, WS) and current BMI (which is often at very low, unhealthy levels). We have shown that WS and BMI (and their interaction) are robust predictors of many ED characteristics and that these relationships are not sufficiently accounted for by the CBT model. The second domain involves brain reward and inhibitory responses to palatable food cues. Evidence indicates that a continuum exists, with the poles anchored by the opposing responses to food cues of restricting anorexic patients and overweight binge eaters (with the former showing reward hypo-activation and inhibitory hyper-activation and the latter showing the reverse). Yet little known about how these abnormal patterns contribute to ED psychopathology. Because the variables comprising both domains are continuous in nature, and because the current application will study ED individuals regardless of DSM diagnosis, the proposed research is consistent with RDoC recommendations. We test the hypotheses that the two domains will be cross-sectionally related to eating disorder psychopathology, will predict future weight gain, ED symptomatology and course and that brain activation in reward and inhibitory regions of interest will mediate the predictive effects of Weight History variables on weight change and ED outcomes. These hypotheses will be tested among 96 ED individuals receiving treatment in any level of outpatient care. At baseline they will be assessed using standardized measures of Weight History and ED psychopathology and will undergo structural and functional MRI using a paradigm aimed at measuring their reward and inhibitory activation to food pictures in regions of interest. The measures of weight and ED symptomatology will be repeated at 3 and 6-month follow-ups. The proposed research has substantial potential to identify new sources of ED psychopathology that can be translated into novel treatments for these treatment-resistant disorders.