Department of Psychiatry, McKnight Brain Institute, University of Florida, 100 Newell Drive, PO Box 100256, Gainesville, FL 32610, USA.
Curr Pharm Des. 2011;17(12):1149-57. doi: 10.2174/138161211795656855.
Obesity has become a serious epidemic and one of the leading global health problems. However, much of the current debate has been fractious, and etiologies of obesity have been attributed to eating behavior (i.e. fast food consumption), personality, depression, addiction or genetics. One of the interesting new hypotheses for explaining the development of obesity involves a food addiction model, which suggests that food is not eaten as much for survival as pleasure and that hedonic overeating is relevant to both substance-related disorders and eating disorders. Accumulating evidence has shown that there are a number of shared neural and hormonal pathways as well as distinct differences in these pathways that may help researchers discover why certain individuals continue to overeat despite health and other consequences, and becomes more and more obese. Functional neuroimaging studies have further revealed that pleasant smelling, looking, and tasting food has reinforcing characteristics similar to drugs of abuse. Many of the brain changes reported for hedonic eating and obesity are also seen in various types of addictions. Most importantly, overeating and obesity may have an acquired drive similar to drug addiction with respect to motivation and incentive craving. In both cases, the desire and continued satisfaction occur after early and repeated exposure to stimuli. The acquired drive for eating food and relative weakness of the satiety signal would cause an imbalance between the drive and hunger/reward centers in the brain and their regulation. In the current paper, we first provide a summary of literature on food addition from eight different perspectives, and then we proposed a research paradigm that may allow screening of new pharmacological treatment on the basis of functional magnetic resonance imaging (fMRI).
肥胖已成为严重的流行疾病和全球主要健康问题之一。然而，目前的许多争论都是分裂的，肥胖的病因归因于饮食行为（即快餐消费）、个性、抑郁、成瘾或遗传。解释肥胖发展的一个有趣的新假设涉及食物成瘾模型，该模型表明，人们吃食物不仅仅是为了生存，而是为了获得快乐，享乐性暴饮暴食与物质相关障碍和饮食障碍都有关。越来越多的证据表明，存在许多共享的神经和激素途径，以及这些途径中的明显差异，这可能有助于研究人员发现为什么某些人尽管存在健康和其他后果，仍然继续暴饮暴食，变得越来越肥胖。功能神经影像学研究进一步表明，令人愉悦的气味、外观和味道的食物具有类似于滥用药物的强化特征。享乐性进食和肥胖所报告的许多大脑变化也见于各种类型的成瘾。最重要的是，与药物成瘾相比，暴饮暴食和肥胖可能具有类似的获得性驱动力，涉及动机和激励性渴望。在这两种情况下，欲望和持续的满足感都是在早期和反复暴露于刺激之后产生的。对食物的获得性驱动力和饱腹感信号的相对减弱，会导致大脑中的驱动和饥饿/奖励中心之间的不平衡及其调节。在当前的论文中，我们首先从八个不同的角度提供了关于食物成瘾的文献综述，然后我们提出了一个研究范式，该范式可以基于功能磁共振成像（fMRI）筛选新的药物治疗方法。
