Biobehavioral Prediction of Illness Trajectory in Bulimic Syndromes

暴食症候群疾病轨迹的生物行为预测

• 批准号: 9325086
• 负责人: Pamela K. Keel
• 金额: $ 43.9万
• 依托单位: FLORIDA STATE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2016
• 资助国家: 美国
• 起止时间: 2016-08-05 至 2021-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9325086
• 关键词: Accounting; Address; Age; Anorexia Nervosa; Basic Science; Behavioral; Binge Eating; Binge eating disorder; Biological; Body Image; Body fat; Bulimia; Categories; Cessation of life; Chronic Disease; Clinical; Communities; Comprehension; DSM-V; Development; Diet; Dimensions; Disease; Distress; Eating; Eating Disorders; Evaluation; Food; Individual; Individual Differences; Intake; Intervention; Lead; Leptin; Maintenance; Measures; Mediating; Mediation; Mediator of activation protein; Modeling; Motivation; Outcome; Participant; Patient Self-Report; Physiological; Population; Positive Valence; Public Health; Research; Research Domain Criteria; Research Personnel; Rewards; Risk; Satiation; Series; Severities; Severity of illness; Syndrome; Testing; Text; Translating; Weight; Work; base; behavioral pharmacology; biobehavior; brief intervention; disability; disorder control; effective therapy; follow-up; food consumption; glucagon-like peptide 1; improved; innovation; loss of control over eating; novel; productivity loss; prospective; prospective test; public health relevance; purge; reinforcer; response; restraint; satisfaction; suicidal morbidity; willingness; young woman

Bulimic syndromes (BN-S) are characterized by large out-of-control binge episodes, span the three DSM-5 eating disorder categories of anorexia nervosa-binge purge subtype (ANbp), bulimia nervosa (BN), and binge eating disorder (BED), and vary considerably in illness severity and course. Our long-term objectives are to identify biobehavioral predictors of illness trajectory in BN-S so that treatments may be developed to address key factors influencing the severity and course of binge eating. The specific aims of this study are to test a model in which weight suppression (WS) leads to deficient circulating leptin, which contributes to blunted postprandial glucagon-like peptide 1 (GLP-1) response, which causes alterations in the RDoC core constructs of approach motivation and sustained responsiveness to reward, which then contribute to BN-S severity and maintenance. WS (the difference between an individual's highest weight and current weight) has emerged as one key predictor of severity and maintenance of BN-S, and investigators have posited a biobehavioral mechanism for this association. Yet, no study has evaluated how the biological consequences of WS may contribute to alterations in RDoC core constructs proposed to contribute to binge eating. Our model posits that the same set of physiological consequences of WS contribute to binge eating by 1) increasing drive/motivation to consume food (approach motivation), and 2) decreasing ability for food consumption to lead to a state of satiation/satisfaction (sustained responsiveness to reward). Approach motivation will be measured both behaviorally as breakpoint on progressive ratio tasks for food and non-food reinforcers and by self-report. Sustained responsiveness to reward (satiation) will be measured both behaviorally as food intake in an ad lib meal and by self-report. Participants (N=320) with BN-S and non-eating disorder controls, ranging in BMI from 16 to 35 kg/m2, will be assessed for WS, leptin, GLP-1 response to a fixed meal, approach motivation, ability to achieve satiation in an ad lib meal, self-report measures of core constructs, and binge eating at baseline, 6-, and 12-month follow-up, to produce the first study of biobehavioral predictors of illness trajectory in BN-S transdiagnostically. Examining the integration of approach motivation and satiation through the same set of physiological mechanisms represents a major innovation as it translates cutting-edge research in basic science to understand clinical phenomena in BN-S. If differences in illness trajectory across ANbp, BN, and BED are attributable to the underlying dimension of WS, this will fundamentally alter conceptualization of BN-S from three eating disorder categories to one eating disorder. If findings support biobehavioral distinctions across the BMI range, this would provide important information in what treatments would work in whom. Moreover, our focus on factors that are modifiable via behavioral and pharmacological interventions increases the public health significance of this work by facilitating novel treatment approaches to ameliorate distress, disability, and death in syndromes accounting for an important segment of those suffering from eating disorders.

暴食综合征(BN-S)的特点是大量失控的狂欢发作，跨越三个DSM-5 进食障碍类型神经性厌食症-狂欢净化亚型(ANBP)、神经性暴食症(BN)和狂欢 饮食紊乱(卧床)，在疾病严重程度和病程上有很大差异。我们的长期目标是 确定BN-S疾病轨迹的生物行为预测因素，以便开发治疗方法 影响暴食严重程度和病程的关键因素。这项研究的具体目的是测试一个 体重抑制(WS)导致循环瘦素不足，从而导致迟钝的模型 餐后高血糖素样多肽1(GLP-1)反应，导致RDoC核心结构改变 接近动机和对奖励的持续反应，然后有助于BN-S严重程度和 维修。WS(个人最高体重和当前体重之间的差值)已经出现为 BN严重性和维持性的关键预测因子之一-S，研究人员假设了一种生物行为 此关联的机制。然而，还没有研究评估WS的生物学后果可能 有助于RDoC核心结构的改变，建议有助于暴饮暴食。我们的模型假设 WS的同一组生理后果通过1)增加动力/动力而导致暴饮暴食 消费食物(接近动机)，以及2)食物消费能力下降导致 满足感/满意度(对奖励的持续反应)。方法动机将在以下两个方面进行衡量 作为食物和非食物增强剂累进比例任务的行为断点和自我报告。 对奖励(饱足)的持续反应将在行为上作为临时食物摄入量来衡量 进餐和自我报告。有BN-S和非进食障碍对照组的参与者(N=320)，体重指数从 16至35公斤/平方米，将评估WS，Leptin，GLP-1对固定膳食的反应，接近动机，能力 在即席餐中达到饱腹感，自我报告核心结构的测量，并在基线时暴饮暴食，6-， 并进行了12个月的随访，首次对BN-S的疾病轨迹进行了生物行为预测研究 变态诊断。通过相同的集合考察方法动机和满足感的整合 生理机制代表着一项重大创新，因为它将基础科学中的尖端研究转化为 了解BN-S的临床现象。如果ANBP、BN和BED之间的疾病轨迹差异是 由于WS的深层维度，这将从根本上改变BN-S的概念化 三种进食障碍分类为一种进食障碍。如果研究结果支持生物行为的差异 体重指数范围，这将提供关于哪些治疗方法对谁有效的重要信息。而且，我们的 关注可通过行为和药物干预改变的因素会增加公众 这项工作的健康意义通过促进新的治疗方法来改善痛苦、残疾和 在饮食失调患者中，综合征死亡占很重要的一部分。