Department of Psychiatry, University of Cambridge, Herchel Smith Building, Addenbrooke's Hospital, CambridgeCB2 0SZ, UK.
Department of Engineering, Computational and Biological Learning Laboratory, University of Cambridge, CambridgeCB2 1PZ, UK.
Psychol Med. 2021 Dec;51(16):2814-2824. doi: 10.1017/S0033291720001440. Epub 2020 May 28.
Anorexia nervosa (AN) and bulimia nervosa (BN) are complex psychiatric conditions, in which both psychological and metabolic factors have been implicated. Critically, the experience of stress can precipitate loss-of-control eating in both conditions, suggesting an interplay between mental state and metabolic signaling. However, associations between psychological states, symptoms and metabolic processes in AN and BN have not been examined.
Eighty-five women ( = 22 AN binge/purge subtype, = 33 BN, = 30 controls) underwent remote salivary cortisol sampling and a 2-day, inpatient study session to examine the effect of stress on cortisol, gut hormones [acyl-ghrelin, peptide tyrosine tyrosine (PYY) and glucagon-like peptide-1] and food consumption. Participants were randomized to either an acute stress induction or control task on each day, and plasma hormones were serially measured before a naturalistic, meal.
Cortisol-awakening response was augmented in AN but not in BN relative to controls, with body mass index explaining the most variance in post-awakening cortisol (36%). Acute stress increased acyl-ghrelin and PYY in AN compared to controls; however, stress did not alter gut hormone profiles in BN. Instead, a group-by-stress interaction showed nominally reduced cortisol reactivity in BN, but not in AN, compared to controls. consumption was lower in both patient groups and unaffected by stress.
Findings extend previous reports of metabolic dysfunction in binge-eating disorders, identifying unique associations across disorders and under stress. Moreover, we observed disrupted homeostatic signaling in AN following psychological stress, which may explain, in part, the maintenance of dysregulated eating in this serious illness.
神经性厌食症（AN）和神经性贪食症（BN）是复杂的精神疾病，心理和代谢因素都与之有关。至关重要的是，压力的体验会导致这两种疾病的失控性进食，这表明精神状态和代谢信号之间存在相互作用。然而，AN 和 BN 中心理状态、症状和代谢过程之间的关联尚未得到检验。
85 名女性（=22 名 AN 暴食/呕吐亚型，=33 名 BN，=30 名对照）接受了远程唾液皮质醇采样和为期 2 天的住院研究，以研究应激对皮质醇、胃肠激素[酰基-ghrelin、肽酪氨酸酪氨酸（PYY）和胰高血糖素样肽-1]和食物消耗的影响。参与者在每天进行急性应激诱导或对照任务，在自然的、不规律的餐食前连续测量血浆激素。
与对照组相比，AN 的皮质醇觉醒反应增强，但 BN 则没有，体重指数解释了觉醒后皮质醇的最大差异（36%）。急性应激增加了 AN 中的酰基-ghrelin 和 PYY，但 BN 中的胃肠激素谱没有改变。相反，组间应激交互作用显示 BN 中皮质醇反应性降低，但在 AN 中则没有，与对照组相比。在这两个患者组中，进食量都较低，且不受应激影响。
这些发现扩展了关于暴食障碍代谢功能障碍的先前报告，确定了跨障碍和应激下的独特关联。此外，我们观察到 AN 在心理应激后出现了稳态信号的中断，这可能部分解释了这种严重疾病中饮食失调的维持。
