Wierenga Christina E, Ely Alice, Bischoff-Grethe Amanda, Bailer Ursula F, Simmons Alan N, Kaye Walter H
Department of Psychiatry, University of California San Diego , La Jolla, CA , USA ; Veterans Affairs San Diego Healthcare System , San Diego, CA , USA.
Department of Psychiatry, University of California San Diego , La Jolla, CA , USA.
Front Behav Neurosci. 2014 Dec 9;8:410. doi: 10.3389/fnbeh.2014.00410. eCollection 2014.
The primary defining characteristic of a diagnosis of an eating disorder (ED) is the "disturbance of eating or eating-related behavior that results in the altered consumption or absorption of food" (DSM V; American Psychiatric Association, 2013). There is a spectrum, ranging from those who severely restrict eating and become emaciated on one end to those who binge and overconsume, usually accompanied by some form of compensatory behaviors, on the other. How can we understand reasons for such extremes of food consummatory behaviors? Recent work on obesity and substance use disorders has identified behaviors and neural pathways that play a powerful role in human consummatory behaviors. That is, corticostriatal limbic and dorsal cognitive neural circuitry can make drugs and food rewarding, but also engage self-control mechanisms that may inhibit their use. Importantly, there is considerable evidence that alterations of these systems also occur in ED. This paper explores the hypothesis that an altered balance of reward and inhibition contributes to altered extremes of response to salient stimuli, such as food. We will review recent studies that show altered sensitivity to reward and punishment in ED, with evidence of altered activity in corticostriatal and insula processes with respect to monetary gains or losses, and tastes of palatable foods. We will also discuss evidence for a spectrum of extremes of inhibition and dysregulation behaviors in ED supported by studies suggesting that this is related to top-down self-control mechanisms. The lack of a mechanistic understanding of ED has thwarted efforts for evidence-based approaches to develop interventions. Understanding how ED behavior is encoded in neural circuits would provide a foundation for developing more specific and effective treatment approaches.
进食障碍(ED)诊断的主要定义特征是“进食或与进食相关行为的紊乱,导致食物摄入或吸收改变”(《精神疾病诊断与统计手册》第五版;美国精神病学协会,2013年)。其表现范围很广,一端是那些严重限制饮食并变得消瘦的人,另一端是那些暴饮暴食的人,通常还伴有某种形式的代偿行为。我们如何理解这种极端饮食行为的原因呢?最近关于肥胖和物质使用障碍的研究已经确定了在人类进食行为中起重要作用的行为和神经通路。也就是说,皮质纹状体边缘和背侧认知神经回路可以使药物和食物具有奖赏性,但也会启动可能抑制其使用的自我控制机制。重要的是,有大量证据表明这些系统的改变也发生在进食障碍中。本文探讨了一种假说,即奖赏与抑制平衡的改变导致对显著刺激(如食物)的反应极端改变。我们将回顾最近的研究,这些研究表明进食障碍患者对奖赏和惩罚的敏感性改变,有证据显示在涉及金钱得失和美味食物味道时,皮质纹状体和脑岛区域的活动发生了改变。我们还将讨论进食障碍中一系列极端抑制和调节异常行为的证据,这些研究表明这与自上而下的自我控制机制有关。对进食障碍缺乏机制性理解阻碍了基于证据的干预措施开发工作。了解进食障碍行为在神经回路中的编码方式将为开发更具体、有效的治疗方法奠定基础。