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To the Editor: Night-eating syndrome is characterized by repetitive awakening because of hunger and excessive eating. In humans, food intake appears to be regulated reciprocally by the anorexigenic leptin and the orexigenic ghrelin. The physiological nocturnal leptin surge is blunted in night-eating syndrome . Ghrelin levels are changed in eating disorders, with elevation in anorexia and Prader-Willi syndrome and blunting in obesity (2). In night-eating syndrome, ghrelin levels are unknown so far. We report the course of ghrelin plasma levels during the treatment of night-eating syndrome.

Ms. A, a 27-year-old woman, reported that the first symptoms of night-eating syndrome appeared 1 year before she underwent our psychiatric examination. As in previous reports, administration of a selective serotonin reuptake inhibitor (citalopram, 100 mg/day) was started (3). A complete remission was obtained within 8 weeks. Medication was continued for another 8 weeks before withdrawal. About 8 weeks later, Ms. A described a relapse of night-eating syndrome.

Her plasma ghrelin concentrations were measured by radioimmunoassay (Phoenix Pharmaceuticals, Belmont, Calif.) at three times (before treatment, 8 weeks later [during drug treatment and full remission], and finally, after relapse). Specimens were collected on all three occasions: every 20 minutes between 10 p.m. and 7:00 a.m. by a long catheter.

Mean nocturnal ghrelin concentrations (10 p.m. to 7 a.m.) were 1051 pg/ml before treatment, 977 pg/ml 8 weeks later (during drug treatment and full remission), and 1013 pg/ml after relapse. The body mass index (kg/m2) of Ms. A was about 23.5 at all examinations.

As control subjects we investigated three healthy women, 22, 23, and 32 years old, with body mass indexes of 21.9, 22.4, and 20.8 kg/m2. Their mean ghrelin concentrations were 372, 402, and 338 pg/ml, respectively.

This preliminary observation suggests that nocturnal ghrelin levels are enhanced in night-eating syndrome. Despite the known sleep-promoting capacity of ghrelin, its elevated levels might disrupt sleep because of hunger at night. Similarly, a higher dose of exogenous ghrelin caused nocturnal eating in a normal subject, whereas a lower dose promoted sleep (4). It appears that elevated ghrelin concentration is not state-dependent and may reflect a marker of vulnerability for developing night-eating syndrome.

For this study, written informed consent and human subjects research committee approval were obtained.

References

1. Birketvedt GS, Florholmen J, Sundsfjord J, Osterud B, Dinges D, Warren B, Stunkard AJ: Behavioral and neuroendocrine characteristics of the night-eating syndrome. JAMA 1999; 282:657–663Crossref, MedlineGoogle Scholar

2. Van Der Lely AJ, Tschöp M, Heiman ML, Ghigo E: Biological, physiological, and pharmacological aspects of ghrelin. Endocr Rev 2004; 25:426–457Crossref, MedlineGoogle Scholar

3. O’Reardon JP, Stunkard AJ, Allison KC: Clinical trial of sertraline in the treatment of night eating syndrome. Int J Eat Disord 2003; 35:16–26CrossrefGoogle Scholar

4. Weikel JC, Wichniak A, Ising M, Brunner H, Friess E, Held K, Mathias S, Schmid DA, Uhr M, Steiger A: Ghrelin promotes slow-wave sleep in humans. Am J Physiol Endocrinol Metab 2003; 284:E407-E415Google Scholar