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

描述(申请人提供)：饮食失调(EDS)影响大约5%的人口，并对心理和身体健康产生各种不利影响。近年来，进食障碍的治疗取得了进展，但进一步的进展将在一定程度上取决于该领域对进食障碍精神病理学的理解。EDS的认知行为疗法(CBT)模型已经获得了实质性的支持，但这个框架并没有充分解决似乎对饮食紊乱有重大影响的两个领域。我们称之为第一个领域体重历史，它由病前体重、有史以来最高体重和当前体重之间的差异(体重抑制，WS)和当前BMI(通常处于非常低的、不健康的水平)组成。我们已经证明，WS和BMI(及其相互作用)是许多ED特征的稳健预测因子，而CBT模型不能充分解释这些关系。第二个领域涉及大脑对美味食物的奖励和抑制反应。证据表明，存在一个连续体，两极由限制厌食症患者和超重暴食者对食物暗示的相反反应固定(前者表现为奖赏低激活和抑制性高激活，后者表现为相反)。然而，人们对这些异常模式如何导致勃起功能障碍的精神病知之甚少。由于组成这两个领域的变量本质上是连续的，而且当前的应用程序将研究ED患者而不考虑DSM诊断，因此拟议的研究与RDoC的建议是一致的。我们测试了这样的假设，即这两个领域将与进食障碍精神病理学横截面相关，将预测未来的体重增加、ED症状和病程，以及感兴趣的奖赏和抑制区域中的大脑激活将中介体重历史变量对体重变化和ED结果的预测效果。这些假设将在96名在任何级别的门诊接受治疗的ED患者中进行测试。在基线时，将使用体重历史和ED精神病理学的标准化测量对它们进行评估，并将使用旨在测量它们对感兴趣区域中食物图片的奖励和抑制激活的范式进行结构和功能磁共振成像。体重和ED症状的测量将在3个月和6个月的随访中重复。这项拟议的研究有很大的潜力来确定ED精神病理学的新来源，这些来源可以转化为治疗这些耐药障碍的新疗法。

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.