Department of Psychiatry, CB #7175, University of North Carolina, Chapel Hill, NC, 27599-7175, USA,
Drugs. 2015 Jan;75(1):9-32. doi: 10.1007/s40265-014-0327-0.
In the USA, binge eating disorder (BED) is the most common eating disorder, with a lifetime prevalence of ~3.5 % in adult women, 2.0 % in adult men, and 1.6 % in adolescents. BED is characterized by frequent episodes of binge eating that are accompanied by a sense of loss of control over eating and result in marked psychological distress. BED is highly co-morbid with obesity and with depression and other psychiatric conditions, and it is associated with substantial role impairment. Currently, there are no US FDA-approved pharmacological treatments for BED. Animal and human studies implicate underlying dysregulation in dopamine, opioid, acetylcholine, and serotonin neurocircuitry within brain reward regions in the pathogenesis and maintenance of BED. To date, the efficacy of various agents that target these and other neurotransmitter systems involved in motivated feeding behavior, mood regulation, and impulse control have been investigated in the treatment of BED. Several antidepressant and anticonvulsant agents have demonstrated efficacy in reducing binge eating frequency, but only in limited cases have these effects resulted in patients achieving abstinence, which is the primary goal of treatment; they also range from less (fluvoxamine) to more (topiramate) effective in achieving weight loss that is both clinically meaningful and significantly greater than placebo. Collectively, the literature on pharmacological treatment approaches to BED is limited in that very few agents have been studied in multiple, confirmatory trials with adequate follow up, and almost none have been evaluated in large patient samples that are diverse with respect to age, sex, and ethnicity. In addition, prior trials have not adequately addressed, through study design, the high placebo response commonly observed in this patient population. Several novel agents are in various phases of testing, and recent animal studies focusing on glutamate-signaling circuits linking the amygdala to the lateral hypothalamus offer new avenues for exploration and potential therapeutic development. Studies of newly FDA-approved medications for long-term obesity treatment and further explorations of dietary supplements and neutraceuticals with appetite- and mood-altering properties may also be worthwhile.
在美国，暴食障碍（BED）是最常见的饮食障碍，成年女性终身患病率约为 3.5%，成年男性为 2.0%，青少年为 1.6%。BED 的特征是频繁出现暴食发作，同时伴有对进食失去控制的感觉，并导致明显的心理困扰。BED 与肥胖症以及抑郁症和其他精神疾病高度共病，并与严重的角色障碍有关。目前，美国食品和药物管理局（FDA）尚未批准用于治疗 BED 的药物。动物和人类研究表明，大脑奖励区域中多巴胺、阿片类、乙酰胆碱和 5-羟色胺神经回路的潜在失调与 BED 的发病机制和维持有关。迄今为止，各种针对这些和其他参与动机性进食行为、情绪调节和冲动控制的神经递质系统的药物的疗效已在 BED 的治疗中得到了研究。一些抗抑郁药和抗惊厥药已被证明能有效减少暴食发作的频率，但只有在有限的情况下，这些效果能使患者达到戒断，这是治疗的主要目标；它们在实现临床意义重大且显著大于安慰剂的减重方面的有效性也从较低（氟伏沙明）到较高（托吡酯）不等。总的来说，关于 BED 药物治疗方法的文献有限，因为只有少数药物在有足够后续观察的多项、确证性试验中进行了研究，而且几乎没有在年龄、性别和种族多样化的大型患者样本中进行评估。此外，先前的试验在研究设计上没有充分解决该患者群体中常见的高安慰剂反应问题。几种新的药物正在不同的测试阶段，最近的动物研究聚焦于连接杏仁核和外侧下丘脑的谷氨酸信号通路，为探索和潜在的治疗开发提供了新的途径。对新获得美国 FDA 批准的长期肥胖治疗药物的研究以及对具有改变食欲和情绪特性的膳食补充剂和营养保健品的进一步探索也可能是值得的。
