Department of Psychology, Rhodes College, USA.
Department of Psychology, Rhodes College, USA.
Appetite. 2019 Feb 1;133:393-399. doi: 10.1016/j.appet.2018.11.019. Epub 2018 Nov 22.
The stress-eating relationship is mediated by the release of cortisol from the hypothalamic pituitary adrenal (HPA) axis. Variability in stress-induced eating, and consequently, obesity, may be explained in part by individual differences in chronic stress, which disrupts the regulatory effects of the HPA axis on stress-induced eating. A greater understanding of the physiological mechanisms by which chronic stress affects acute stress-induced eating is critical in order to inform efforts to prevent and treat obesity. The current study examined the relationship between physiological responses to acute stress (cortisol and cardiovascular factors) and the drive to eat (ratings of hunger and desire to eat) in female undergraduates with high and low perceived life stress. Participants (n = 64) rated their perceived life stress in an online screening and, on a separate visit, rated their drive to eat before and after a mental stress task. The present report focused on only participants in the lowest (n = 16) and highest (n = 14) quartiles of perceived life stress. Women with high perceived life stress showed greater stress-induced cortisol responses, but no significant changes in blood pressure or heart rate. The heightened cortisol responses were not associated with hunger and desire to eat, but the cardiovascular responses were positively associated with the drive to eat. Women with low perceived life stress showed no relationships between physiological stress markers and the drive to eat. These results suggest that the cortisol stress response is dissociated from the drive to eat in chronically stressed women, although due to the small sample size the data should be regarded as preliminary. Further studies are needed to explore how cortisol and cardiovascular reactivity affect stress-induced eating.
压力性进食的关系是由下丘脑-垂体-肾上腺 (HPA) 轴释放皮质醇介导的。应激诱导进食的可变性，进而导致肥胖，部分原因可能是个体慢性应激的差异，这会破坏 HPA 轴对应激诱导进食的调节作用。为了防止和治疗肥胖，更深入地了解慢性应激影响急性应激诱导进食的生理机制至关重要。本研究探讨了急性应激（皮质醇和心血管因素）生理反应与进食欲望（饥饿感和进食欲望评分）之间的关系，研究对象为感知生活压力高低不同的女大学生。参与者（n=64）在在线筛查中评估他们的感知生活压力，在另一次访问中，在进行心理压力任务前后评估他们的进食欲望。本报告仅关注感知生活压力最低（n=16）和最高（n=14）四分位数的参与者。感知生活压力较高的女性表现出更大的应激诱导皮质醇反应，但血压或心率没有明显变化。皮质醇反应的增强与饥饿感和进食欲望无关，但心血管反应与进食欲望呈正相关。感知生活压力较低的女性在生理应激标志物与进食欲望之间没有关系。这些结果表明，在慢性应激的女性中，皮质醇应激反应与进食欲望分离，尽管由于样本量较小，数据应被视为初步结果。需要进一步研究探讨皮质醇和心血管反应性如何影响应激诱导的进食。
