Background: Previous studies revealed that sleep deprivation (SD) impairs risk perception and leads to poor decision-making efficiency. However, how risk perception is related to brain regions’ communication after SD has not been elucidated. In this study, we investigated the neuropsychological mechanisms of SD-impaired risk perception. Methods: Nineteen healthy male adults were recruited and underwent resting-state functional magnetic resonance imaging during a state of rested wakefulness and after nearly 36 h of total SD. They then completed the balloon analog risk task, which was used to measure the risk perception ability of risky decision-making. Regional homogeneity (ReHo) and voxel-wise functional connectivity were used to investigate neurobiological changes caused by SD. Correlation analysis was used to investigate the relationship between changes in ReHo, function, and risk perception. Results: At the behavioral level, risk perception decreased after 36 h of SD. At the neural level, SD induced a significant increase in ReHo in the right postcentral gyrus and was positively correlated with risk perception changes. The functional connectivity between the right postcentral gyrus, left medial temporal gyrus, and right inferior temporal gyrus was enhanced. Critically, increased right postcentral gyrus and right inferior temporal gyrus connectivity positively correlated with changes in risk perception. Conclusions: SD impairs the risk perception associated with altered postcentral connectivity. The brain requires more energy to process and integrate sensory and perceptual information after SD, which may be one possible reason for decreased risk perception ability after SD.

Sleep deprivation leads to reduced inhibitory control in individuals. However, the underlying neural mechanisms are poorly understood. Accordingly, this study aimed to investigate the effects of total sleep deprivation (TSD) on inhibitory control and their neuroelectrophysiological mechanisms from the perspective of the time course of cognitive processing and brain network connectivity, using event-related potential (ERP) and resting-state functional connectivity techniques. Twenty-five healthy male participants underwent 36 h of TSD (36-h TSD), completing Go/NoGo tasks and resting-state data acquisition before and after TSD; their behavioral and electroencephalogram data were recorded. Compared to baseline, participants’ false alarms for NoGo stimuli increased significantly (t = −4.187, p < 0.001) after 36-h TSD. ERP results indicated that NoGo-N2 negative amplitude increased and latency was prolonged (t = 4.850, p < 0.001; t = −3.178, p < 0.01), and NoGo-P3 amplitude significantly decreased and latency was prolonged (t = 5.104, p < 0.001; t = −2.382, p < 0.05) after 36-h TSD. Functional connectivity analysis showed that the connectivity of the default mode and visual networks in the high alpha band was significantly reduced after TSD (t = 2.500, p = 0.030). Overall, the results suggest that the negative amplitude increase in N2 after 36-h TSD may reveal that more attention and cognitive resources are invested after TSD; the significant decrease in P3 amplitude may indicate the impairment of advanced cognitive processing. Further functional connectivity analysis indicated impairment of the brain’s default mode network and visual information processing after TSD.

Emotional eating under negative affect refers to eating responses that occur in brief unpleasant emotional states and are not explained by hunger alone. This narrative review synthesizes representative evidence from experimental, ecological, and neurocognitive studies on emotional eating under negative affect, with emphasis on two interrelated pathways. (1) Emotion regulation: emotional eating may function as a rapid and accessible regulatory strategy through which food, especially highly palatable food, is used to attenuate negative affect. The immediate soothing effects of eating may reinforce later motivation and habitual responses to regulate emotions through food, whereas more adaptive strategies, such as cognitive reappraisal, may reduce the likelihood and intensity of emotion-related eating. (2) Reward processing and biased decision making: negative affect and affective stress contexts may diminish cognitive control and bias food choice toward immediate rewards. This pathway is reflected in increased attentional bias to food cues, stronger weighting of taste and palatability during value weighing, heightened responsivity to highly rewarding foods, and reduced regulatory influence of health and nutrition attributes. These processes may shift food choice toward energy-dense, nutrient-poor, and ultra-processed foods. The nutritional manifestations of emotional eating are not limited to total intake. Changes in intake quantity are heterogeneous, whereas changes in food choice, diet quality, degree of processing, and eating patterns appear more consistent. Repeated emotional eating may therefore contribute to less stable eating patterns and potential nutritional implications, although links with long-term physiological outcomes remain indirect. Future longitudinal and ecological momentary assessment studies are needed to clarify when emotional eating becomes a stable dietary pattern and which individual or contextual factors increase vulnerability.