Stress-induced alterations in HPA-axis reactivity and mesolimbic reward activation in individuals with emotional eating.
Stress-induced alterations in HPA-axis reactivity and mesolimbic reward activation in individuals with emotional eating.
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DOI：
10.1016/j.appet.2021.105707
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发表时间：
2022-01-01
期刊：
影响因子：
5.4
通讯作者：
Holsen LM
中科院分区：
文献类型：
--
作者：
Chang RS;Cerit H;Hye T;Durham EL;Aizley H;Boukezzi S;Haimovici F;Goldstein JM;Dillon DG;Pizzagalli DA;Holsen LM
情绪化进食已经成为暴饮暴食的一个促成因素，有可能导致肥胖或饮食行为紊乱。然而，与情绪化进食相关的潜在生物学机制仍不清楚。本研究检测了有和没有情绪化进食的个体由急性实验室应激源引起的情绪、激素和神经变化。情绪进食者(n=13)和非情绪进食者(n=15)完成了两次主要的研究访问，间隔一周：一次访问包括应激版本的马斯特里赫特急性应激任务(MAST)，另一次包括无应激版本的马斯特里赫特急性应激任务(MAST)。在肥大前和肥大后立即抽血测定血清皮质醇，并对参与者的焦虑程度进行评级。在Mast之后，参与者在功能磁共振成像(FMRI)期间完成了食物激励延迟(FID)任务，随后是一段临时的零食时间。情绪化进食者对压力的反应表现出更高的焦虑(p=0.037)和皮质醇(p=0.001)。在非情绪化进食者对压力肥大的反应中，焦虑或皮质醇没有变化，或者在任何一组人对无压力肥大的反应中都没有变化。与非情绪性进食者相比，情绪性进食者在中脑边缘奖赏区域(尾状核：P=0.014，伏隔核：P=0.022，壳核：P=0.013)对食物奖励的预期激活程度降低。在零食消费方面，不同的群体没有区别。这些数据表明，在其他方面健康的情绪食用者中，神经内分泌和神经对心理社会压力的反应受到干扰，他们表现出HPA轴反应过度活跃，同时奖赏回路中的激活不足。对压力的不同反应可能是发展不适应饮食行为的一个危险因素。
Emotional eating has emerged as a contributing factor to overeating, potentially leading to obesity or disordered eating behaviors. However, the underlying biological mechanisms related to emotional eating remain unclear. The present study examined emotional, hormonal, and neural alterations elicited by an acute laboratory stressor in individuals with and without emotional eating. Emotional (n=13) and non-emotional eaters (n=15) completed two main study visits, one week apart: one visit included a Stress version and the other a No-stress version of the Maastricht Acute Stress Task (MAST). Immediately pre- and post-MAST, blood was drawn for serum cortisol and participants rated their anxiety level. After the MAST, participants completed a Food Incentive Delay (FID) task during functional magnetic resonance imaging (fMRI), followed by an ad libitum snack period. Emotional eaters exhibited elevated anxiety (p=0.037) and cortisol (p=0.001) in response to the Stress MAST. There were no changes in anxiety or cortisol among non-emotional eaters in response to the Stress MAST or in either group in response to the No-stress MAST. In response to the Stress MAST, emotional eaters exhibited reduced activation during anticipation of food reward in mesolimbic reward regions (caudate: p=0.014, nucleus accumbens: p=0.022, putamen: p=0.013), compared to non-emotional eaters. Groups did not differ in snack consumption. These data indicate disrupted neuroendocrine and neural responsivity to psychosocial stress amongst otherwise-healthy emotional eaters, who demonstrated hyperactive HPA-axis response coupled with hypoactivation in reward circuitry. Differential responsivity to stress may represent a risk factor in the development of maladaptive eating behaviors.
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