Am J Psychiatry 165:424, April 2008
doi: 10.1176/appi.ajp.2007.07081351
© 2008 American Psychiatric Association
Issues for DSM-V: Night Eating Syndrome
Albert Stunkard, M.D.,
Kelly Allison, Ph.D., and
Jennifer Lundgren, Ph.D.
Recent demonstration of an effective treatment for night eating syndrome (1) argues for wider recognition of the disorder to benefit the many persons who suffer from it. These include 1.1%–1.5% of the general population, 6%–16% of patients in weight reduction programs, and 8%–42% of candidates for bariatric surgery. Viewed as a delay in the circadian rhythm of food intake, night eating syndrome is defined by two core criteria: evening hyperphagia (ingestion of at least 25% of daily calories after supper) and/or awakenings with ingestions at least three times a week. These criteria have identified persons whose behavior manifests a coherent biobehavioral model of night eating syndrome, supporting its construct validity. Single photon emission computed tomography has shown significant elevation of serotonin transporters in the midbrain of night eaters (2). This elevation may result from a genetic vulnerability transmitted as part of the established heritability of night eating syndrome (3), which is triggered by the stress that night eaters report. Elevations in serotonin transporter levels lead to decreased postsynaptic serotonin transmission and should impair circadian rhythms and satiety. These deficits suggest that improvement in serotonin function should alleviate night eating syndrome, and the selective serotonin reuptake inhibitors do precisely that. Reports of response to paroxetine and fluvoxamine have been accompanied by two larger open-label trials with a strong response to sertraline. Finally, a placebo-controlled, double-blind study of sertraline showed significant improvements in both of the criteria for night eating syndrome (1).
Night eating may be a pathway to obesity; it preceded the onset of obesity in three studies and predicted major weight gain among female night eaters who were already obese (4). Five animal models, each of a different etiology, have also shown a circadian dysrhythmia with hyperphagia and obesity. In addition to its contribution to weight gain, night eating syndrome is a source of distress, making it worthy of treatment for its own sake.
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Footnotes
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Address correspondence and reprint requests to Dr. Stunkard, Center for Weight and Eating Disorders, Department of Psychiatry, University of Pennsylvania School of Medicine, 3535 Market St., Suite 3025, Philadelphia, PA 19104-3309; stunkard{at}mail.med.upenn.edu (e-mail). Editorial accepted for publication October 2007 (doi: 10.1176/appi.ajp.2007.07081351).
The authors report no competing interests.
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References
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- O’Reardon JP, Allison KC, Martino NS, Lundgren JD, Heo M, Stunkard AJ: A randomized, placebo-controlled trial of sertraline in the treatment of night eating syndrome. Am J Psychiatry 2006; 163:893–898[Abstract/Free Full Text]
- Lundgren JD, Newberg A, Allison KC, Wintering N, Ploessl K, Stunkard AJ: 123I-ADAM SPECT imaging of serotonin transporter binding in patients with night eating syndrome: a pilot study. Psychiatry Res (in press)
- Lundgren JD, Allison KC, Stunkard AJ: Familial aggregation in the night eating syndrome. Int J Eat Disord 2006; 39:516–518[CrossRef][Medline]
- Andersen GS, Stunkard AJ, Sørensen TI, Petersen L, Heitmann BL: Night eating and weight change in middle-aged men and women. Int J Obes Relat Metab Disord 2004; 28:1338–1343[CrossRef][Medline]
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