Demos Kathryn E, Sweet Lawrence H, Hart Chantelle N, McCaffery Jeanne M, Williams Samantha E, Mailloux Kimberly A, Trautvetter Jennifer, Owens Max M, Wing Rena R
Department of Psychiatry and Human Behavior, The Warren Alpert Medical School of Brown University, Miriam Hospital, Weight Control and Diabetes Research Center, Providence, RI.
Department of Psychology, University of Georgia, Athens, GA.
Sleep. 2017 Nov 1;40(11). doi: 10.1093/sleep/zsx125.
Despite growing literature on neural food cue responsivity in obesity, little is known about how the brain processes food cues following partial sleep deprivation and whether short sleep leads to changes similar to those observed in obesity. We used functional magnetic resonance imaging (fMRI) to test the hypothesis that short sleep leads to increased reward-related and decreased inhibitory control-related processing of food cues.In a within-subject design, 30 participants (22 female, mean age = 36.7 standard deviation = 10.8 years, body mass index range 20.4-40.7) completed four nights of 6 hours/night time-in-bed (TIB; short sleep) and four nights of 9 hours/night TIB (long sleep) in random counterbalanced order in their home environments. Following each sleep condition, participants completed an fMRI scan while viewing food and nonfood images.A priori region of interest analyses revealed increased activity to food in short versus long sleep in regions of reward processing (eg, nucleus accumbens/putamen) and sensory/motor signaling (ie, right paracentral lobule, an effect that was most pronounced in obese individuals). Contrary to the hypothesis, whole brain analyses indicated greater food cue responsivity during short sleep in an inhibitory control region (right inferior frontal gyrus) and ventral medial prefrontal cortex, which has been implicated in reward coding and decision-making (false discovery rate corrected q = 0.05).These findings suggest that sleep restriction leads to both greater reward and control processing in response to food cues. Future research is needed to understand the dynamic functional connectivity between these regions during short sleep and whether the interplay between these neural processes determines if one succumbs to food temptation.
尽管关于肥胖症中神经对食物线索反应性的文献越来越多,但对于大脑在部分睡眠剥夺后如何处理食物线索,以及短睡眠是否会导致与肥胖症中观察到的类似变化,我们知之甚少。我们使用功能磁共振成像(fMRI)来检验短睡眠会导致对食物线索的奖励相关处理增加和抑制控制相关处理减少这一假设。
在一项受试者内设计中,30名参与者(22名女性,平均年龄 = 36.7岁,标准差 = 10.8岁,体重指数范围20.4 - 40.7)在其家中环境中以随机平衡顺序完成了四个每晚6小时卧床时间(TIB;短睡眠)的夜晚和四个每晚9小时TIB(长睡眠)的夜晚。在每种睡眠条件后,参与者在观看食物和非食物图像时完成了一次fMRI扫描。
先验感兴趣区域分析显示,在奖励处理区域(如伏隔核/壳核)和感觉/运动信号区域(即右中央旁小叶,这种效应在肥胖个体中最为明显),短睡眠相对于长睡眠时对食物的激活增加。与假设相反,全脑分析表明,在抑制控制区域(右额下回)和腹内侧前额叶皮质中,短睡眠期间对食物线索的反应性更高,腹内侧前额叶皮质与奖励编码和决策有关(错误发现率校正q = 0.05)。
这些发现表明,睡眠限制会导致对食物线索的奖励和控制处理都增强。未来需要开展研究,以了解短睡眠期间这些区域之间动态的功能连接,以及这些神经过程之间的相互作用是否决定了一个人是否会屈服于食物诱惑。