To the Editor: The prevalence of night-eating syndrome (morning anorexia, evening hyperphagia, and insomnia) among obese patients ranges from 9% to 27% (1). A concurrent attenuation of the nocturnal elevation in melatonin and leptin blood levels with nighttime awakening and eating has been characterized in obese subjects with night-eating syndrome (2). An open study (3) has suggested that bright-light therapy may reduce body weight in obese subjects, especially those with carbohydrate craving, with or without seasonal affective disorder. We report the first case of which we are aware regarding an overweight patient suffering from night-eating syndrome and nonseasonal depression, both treated with light therapy.
Ms. A, a 51-year-old overweight woman (body mass index=31.2) was seen as an outpatient for the worsening of depressive symptoms over 1 month, despite 2 years of maintenance treatment with paroxetine at a constant dose (40 mg/day). A thorough psychiatric examination by a senior psychiatrist and a record of food consumption (energy and macronutriment content) revealed the following:
1. Nonseasonal major depressive disorder, recurrent episode, moderate, with partial remission between episodes (DSM-IV criteria). Severity was assessed with the Structured Interview Guide for the Hamilton Depression Rating Scale, Seasonal Affective Disorders Version (4) (the usual 21 items of the Hamilton Depression Rating Scale plus eight items assessing atypical symptoms) and with the Beck Depression Inventory (13-item version). Initial scores on the Hamilton scale were 18 on the depression scale and 12 on the scale for atypical symptoms. Ms. A’s Beck Depression Inventory score was 12.
2. Night-eating syndrome, according to the provisional criteria for night-eating syndrome (2): morning anorexia and evening hyperphagia, in which at least 50% of daily energy intake is consumed after the last evening meal (62% after 8:00 p.m.); awakenings at least once a night (at midnight and 3:00 a.m. nightly); and consumption of snacks during awakenings (these snacks were 67.8% carbohydrate and had a carbohydrate-to-protein ratio of 6:1) in order to restore disrupted sleep. These criteria persisted for at least 3 months and were not considered to be side effects of paroxetine treatment.
Bright-light therapy was added to ongoing treatment (paroxetine, 40 mg/day). After 14 daily morning sessions of 10,000-lux white light for 30 minutes, Ms. A no longer fulfilled the DSM-IV criteria for depression, and her scores were significantly lower on the Hamilton scale (depression score=7, atypical symptom score=5) and Beck Depression Inventory (score=5). She no long met the criteria for night-eating syndrome.
One month later, all of Ms. A’s previous night-eating symptoms had returned. She was not depressed (DSM-IV criteria), and her severity scores remained low: depression score=6, atypical symptom score=4, Beck Depression Inventory score=5. Another 12 morning sessions with light therapy completely suppressed her night-eating symptoms.
Exposure to light improved the symptoms of night-eating syndrome in an obese subject, irrespective of comorbid depressive symptoms. These findings should be further tested in controlled studies to establish the possible role of light therapy for obese subjects who suffer from night-eating syndrome, with or without affective disorder.