Stress, eating and the reward system
Stress, eating and the reward system
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DOI：
10.1016/j.physbeh.2007.04.011
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发表时间：
2007-07-24
影响因子：
2.9
通讯作者：
Epel, Elissa S.
中科院分区：
文献类型：
--
作者：
Adam, Tanja C.;Epel, Elissa S.
越来越多的人报告对生活中的压力感到担忧。与此同时，肥胖是一个不断升级的全球性健康问题。越来越多的证据表明，应激相关的下丘脑-垂体-肾上腺（HPA）轴的慢性刺激和由此产生的过量糖皮质激素暴露可能在内脏型肥胖的发展中起着潜在的作用。由于在压力下充分调节能量和食物摄入对生存很重要，因此HPA轴不仅是适当压力反应的“指挥者”，而且与食欲的内分泌调节密切相关，这并不奇怪。在这里，我们试图将动物和人类的文献联系起来，以梳理不同类型的心理压力如何影响饮食。我们提出了一个基于奖励的压力饮食的理论模型。该模型强调皮质醇和奖赏回路在激发热量密集的食物摄入中的作用，并阐明了压力和进食之间关系中潜在的神经内分泌介质。成瘾文献表明，大脑奖励回路可能是压力引起的食物摄入的关键角色。压力和可口的食物可以刺激内源性阿片样物质的释放。反过来，阿片样物质的释放似乎是生物体强大的防御机制的一部分，通过降低HPA轴的活性，从而减弱应激反应，保护免受应激的有害影响。通过应激诱导的HPA刺激、摄入高度可口的食物或两者来重复刺激奖励途径，可能导致神经生物学适应，从而促进暴饮暴食的强迫性。皮质醇可以通过神经内分泌/肽介质如瘦素、胰岛素和神经肽Y（NPY）影响食物的奖励值。而糖皮质激素拮抗胰岛素和瘦素急性，在慢性压力下，精细平衡的系统失调，可能有助于增加食物摄入和内脏脂肪积累。虽然这些机制在人类中才刚刚开始阐明，但慢性压力的主导、不成功的限食尝试以及它们对增加美味食物的奖励价值的独立且可能的协同作用似乎可能会加剧肥胖流行病。(C)2007年由Elsevier Inc.出版
An increasing number of people report concerns about the amount of stress in their life. At the same time obesity is an escalating health problem worldwide. Evidence is accumulating rapidly that stress related chronic stimulation of the hypothalamic-pituitary-adrenal (HPA) axis and resulting excess glucocorticoid exposure may play a potential role in the development of visceral obesity. Since adequate regulation of energy and food intake under stress is important for survival, it is not surprising that the HPA axis is not only the 'conductor' of an appropriate stress response, but is also tightly intertwined with the endocrine regulation of appetite. Here we attempt to link animal and human literatures to tease apart how different types of psychological stress affect eating. We propose a theoretical model of Reward Based Stress Eating. This model emphasizes the role of cortisol and reward circuitry on motivating calorically dense food intake, and elucidating potential neuroendocrine mediators in the relationship between stress and eating. The addiction literature suggests that the brain reward circuitry may be a key player in stress-induced food intake. Stress as well as palatable food can stimulate endogenous opioid release. In turn, opioid release appears to be part of an organisms' powerful defense mechanism protecting from the detrimental effects of stress by decreasing activity of the HPA axis and thus attenuating the stress response. Repeated stimulation of the reward pathways through either stress induced HPA stimulation, intake of highly palatable food or both, may lead to neurobiological adaptations that promote the compulsive nature of overeating. Cortisol may influence the reward value of food via neuroendocrine/peptide mediators such as leptin, insulin and neuropeptide Y (NPY). Whereas glucocorticoids are antagonized by insulin and leptin acutely, under chronic stress, that finely balanced system is dysregulated, possibly contributing to increased food intake and visceral fat accumulation. While these mechanisms are only starting to be elucidated in humans, it appears the obesity epidemic may be exacerbated by the preponderance of chronic stress, unsuccessful attempts at food restriction, and their independent and possibly synergistic effects on increasing the reward value of highly palatable food. (C) 2007 Published by Elsevier Inc.