Neuroendocrine levels, circadian profiles, and sleep in night eating syndrome: integration of findings

Night eating syndrome (NES) is characterized by evening hyperphagia and awakenings with nocturnal food ingestions. Elucidation of the disturbance in sleep and neuroendocrine physiology that underlies the clinical syndrome is crucial and helps to target treatments. We conducted an inpatient study of 15 overweight women with NES and 14 similar control participants to compare the 25 h levels and circadian patterns of neuroendocrine and caloric intake profiles and polysomnographic features. Polysomnography revealed no differences in timing of sleep, but the NES group had less stage 2, percentage of stage 2, and stage 3 sleep, less total sleep time, and reduced sleep efficiency. In comparison to the controls, in NES participants: energy intake was phase delayed by 1.5 h and nocturnal food intake was significantly higher; insulin was elevated during the night and phase delayed by 2.8 h and glucose was inverted (delayed by 11.6 h); ghrelin was lower during the night and phase advanced by 5.2 h; levels of plasma cortisol,; melatonin, and leptin were not different, but were phase delayed by 0.7 h-1.1 h; TSH was marginally elevated with a 0.7 h phase delay; and prolactin did not differ by amplitude or phase. These results suggest desynchrony between eating and sleep-wake cycles and a possible uncoupling of peripheral and central oscillators involved in appetite and neuroendocrine regulation. These findings provide evidence for NES as a circadian rhythm disorder.