Circadian rhythm profiles in women with night eating syndrome

Abstract

Night eating syndrome (NES) is characterized by evening hyperphagia and frequent awakenings accompanied by food intake. Patients with NES display a delayed circadian pattern of food intake but retain a normal sleep-wake cycle. These characteristics initiated the current study, in which the phase and amplitude of behavioral and neuroendocrine circadian rhythms in patients with NES were evaluated. Fifteen women with NES (mean age +/- SD, 40.8 +/- 8.7 y) and 14 control subjects (38.6 +/- 9.5 y) were studied in the laboratory for 3 nights, with food intake measured daily. Blood also was collected for 25 h (every 2 h from 0800 to 2000 h, and then hourly from 2100 to 0900 h) and assayed for glucose and 7 hormones (insulin, ghrelin, leptin, melatonin, cortisol, thyroid-stimulating hormone [TSH] and prolactin). Statistical analyses utilized linear mixed-effects cosinor analysis. Control subjects displayed normal phases and amplitudes for all circadian rhythms. In contrast, patients with NES showed a phase delay in the timing of meals, and delayed circadian rhythms for total caloric, fat, and carbohydrate intake. In addition, phase delays of 1.0 to 2.8 h were found in 2 food-regulatory rhythms-leptin and insulin-and in the circadian melatonin rhythm (with a trend for a delay in the circadian cortisol rhythm). In contrast, circulating levels of ghrelin, the primary hormone that stimulates food intake, were phase advanced by 5.2 h. The glucose rhythm showed an inverted circadian pattern. Patients with NES also showed reduced amplitudes in the circadian rhythms of food intake, cortisol, ghrelin, and insulin, but increased TSH amplitude. Thus, patients with NES demonstrated significant changes in the timing and amplitude of various behavioral and physiological circadian markers involved in appetite and neuroendocrine regulation. As such, NES may result from dissociations between central (suprachiasmatic nucleus) timing mechanisms and putative oscillators elsewhere in the central nervous system or periphery, such as the stomach or liver. Considering these results, chronobiologic treatments for NES such as bright light therapy may be useful. Indeed, bright light therapy has shown efficacy in reducing night eating in case studies and should be evaluated in controlled clinical trials.

Figure 1

Raw group-average data and fitted cosinor curves in patients with night eating syndrome (NES; - - -) and control subjects (—) for total calorie (A), carbohydrate (B), fat (C), and protein (D) intake. Circadian rhythms of total calorie, carbohydrate, and fat intake were phase delayed and decreased in amplitude in patients with NES compared with controls.

Figure 2

Raw group-average data and fitted cosinor curves in patients with night eating syndrome (NES; - - -) and control subjects (—) for melatonin (A), thyroid-stimulating hormone (TSH; B), prolactin (C), and cortisol (D). Melatonin circadian rhythms were phase delayed, while cortisol, TSH, and prolactin did not show significant phase differences from controls. Cortisol rhythms were diminished in amplitude in patients with NES compared with controls, while TSH showed increased amplitude.

Figure 3

Raw group-average data and fitted cosinor curves in patients with night eating syndrome (NES; - - -) and control subjects (—) for hormones involved in food intake and metabolism: ghrelin (A), leptin (B), glucose (C), and insulin (D). Insulin was phase delayed and reduced in amplitude, while leptin showed delays without changes in amplitude in patients with NES, even though the overall levels across time points were higher in patients with NES. Glucose showed an inverted circadian rhythm. Ghrelin was out of phase with these rhythms showing a large phase advance and diminished amplitude in patients with NES.