The NES was first described in 1955 by Stunkard as an eating disorder that is characterized by morning anorexia, evening or nocturnal hyperphagia in a fully conscious state, and insomnia.1 It often occurs during periods of stress and results in obesity with poor weight reduction efforts.2 The NES, recognized as a combination of a mood disorder, a sleep disorder, and an eating disorder, is associated with a circadian pattern delay in eating that results in disrupted sleep patterns1,3 Circadian rhythm control is directed by the suprachiasmatic nucleus of the hypothalamus, an area of the brain that may be responsible for NES symptoms.4 With NES, the biological rhythms of eating and sleep are dissociated with the primary circadian disruption occurring as a delay of energy intake; that is, eating is suppressed in the morning and increased in the evening and night. However, the circadian sleep cycles are not disturbed but there is a relative delay of 2 to 6 hours between the eating patterns and sleep rhythms.3 Therefore, insomnia, sleep onset and sleep maintenance, is characteristically associated with NES.

Although about half of the night awakenings in NES are associated with food intake, bingeing does not occur. The NES pattern of food intake is associated with the consumption of only about 30% of the daily energy intake occurring before 6:00 PM, with a rapid increase in food consumption during the hours of 10:00 PM until 6:00 AM. These night snacks are of a moderate size (271 kcal) but consist of a high-carbohydrate content and a high carbohydrate-to-protein nutrient ratio.1

Provisional criteria for NES includes morning anorexia, evening hyperphagia (>50% of consumed daily energy intake occurs after the evening meal), awakenings at least once a night, consumption of snacks during awakenings, and repetition of criteria for 3 months or more, and these individuals do not meet criteria for bulimia nervosa or BED.2 However, the criteria for NES have been modified several times and have not yet been validated; therefore, it is currently diagnosed as an eating disorder, not otherwise specified in the Diagnostic and Statistical Manual of Mental Disorders of the American Psychological Association.5,6

PREVALENCE

Prevalence of NES in the general population is 1.5%; however, it increases with increasing weight. In obesity clinics, the prevalence increases to 10%, and in individuals undergoing bariatric surgery, the prevalence is as high as 25%.1 Although NES does occur in nonobese individuals, it is more common in obese people, especially those seeking weight loss treatment.2 It is most prevalent in severely obese men.7 In addition, an early age at onset of this disorder has been associated with a chronic course.5

The prevalence and demographic correlates of NES were examined using data from 2 national surveys, the National Health and Nutrition Examination Survey III and the Continuing Survey of Food Intakes by Individuals.8 The results of these 2 surveys similarly demonstrated that night eating is most common during the weekend, with prevalence estimates that varied by age group. Adolescents most often met the criteria for night eating, whereas the elderly were among the least likely to meet NES criteria. In National Health and Nutrition Examination Survey data, men were more likely than women and black Americans more likely than other ethnicities to exhibit night eating.8 The researchers suggested that some variation between surveys could be attributed to differences in symptom criteria for NES diagnosis or may have been the result of social and cultural affects on eating patterns.

BEHAVIORAL CHARACTERISTICS AND NEUROENDOCRINE PATTERNS

In the past, individuals with obesity have been considered a homogenous group; however, behaviorally, there is considerable variability within this population.9 Two of these subcategories, BED and NES, have been investigated for mood and eating behavior differences and similarities.9 The NES, the less studied of the 2 disorders, has had continued modification of its descriptive and diagnostic criteria since its first description by Stunkard in 1955. Initially, morning anorexia, evening hyperphagia, emotional distress, and insomnia were characteristics of the disorder.9 In 1996, the consumption of more than 50% of calories after 7:00 PM was added to these criteria. Later, sleep disturbance and evening tension or distress were included.9 However, the core behavioral symptom of NES remains night eating.8

Birketvedt et al2 studied behavioral and neuroendocrine characteristics of NES. The behavioral observation part of the study, which consisted of 10 obese participants and 10 matched controls, was conducted at an outpatient weight and eating disorders clinic. The timing of energy intake, mood level, and sleep disturbances of the participants was assessed for 1 week. Behaviorally, Birketvedt et al2 demonstrated differences in the patterns of diurnal eating between the groups, although the daily amount of food intake differed only moderately. Night eaters consumed 56% of their total energy intake between 8:00 PM and 6:00 AM, whereas the control group participants consumed only 15% of their total energy intake during the same period. The content of the food eaten during the night demonstrated higher carbohydrate content (70.3%) than the 46.6% content of foods consumed during the day.2 Finally, after 4:00 PM, the mood of the night eaters fell hourly in comparison with the control group, whose mood remained unchanged.

During the neuroendocrine portion of the study, plasma melatonin, leptin, insulin, blood glucose, and cortisol levels were measured during a 24-hour period. Cortisol, leptin, and melatonin are regulatory hormones with circadian rhythm patterns that regulate physiological and metabolic functions.10 Individuals with NES demonstrated a reduction of the usual nocturnal rise in plasma melatonin and leptin levels, and had higher plasma cortisol levels than controls.2 It is during the normal nocturnal rise of melatonin that sleep is initiated; subsequently, melatonin continues to be produced proportionally to the length of darkness.11 Melatonin, produced rhythmically from the pineal gland, is suppressed during stress by corticotropin-releasing factor. Cortisol, also released in response to chronic stress, makes the body less sensitive to leptin. Leptin is a protein hormone secreted from adipose tissue that signals the brain of satiety, suppresses appetite, and helps to maintain sleep.11 Leptin levels were found to be higher among overweight night eaters than normal weight night eaters. Blood glucose and insulin levels were consistent between the groups.2 On the basis of these findings, the researchers concluded that night eating occurred in NES, an eating disorder, to restore sleep patterns. Through the ingestion of carbohydrate-rich night snacks, night eaters may increase the availability of tryptophan, and thus promote sleep.2

To evaluate the interaction between the biological circadian rhythm patterns of leptin and melatonin with the stress-related biological responses of the hypothalamic-pituitary-adrenal axis, Birketvedt et al10 investigated the neuroendocrine patterns of 5 females with NES. In comparison with matched controls, individuals with NES demonstrated a disturbance in the response of the hypothalamic-pituitary-adrenal axis as well as attenuation of corticotropin and cortisol response as a result of a stimulation dose of intravenous corticotropin-releasing hormone.10 Although the sample was small (N = 10), the researchers concluded that NES is associated with an attenuated corticotropin response as reflected by elevated cortisol levels that disrupt sleep and appetite patterns.10 These responses may explain the circadian alterations of melatonin and leptin associated with NES and the subsequent behavior manifestations of this disorder.10

Recently, Allison et al12 evaluated the appetite-regulating hormones between individuals with NES (n = 15) and a matched control group (n = 14). Although the total energy intake did not differ between the groups, the NES group ate more at night. Ghrelin, which increases before meals in normal persons and is suppressed by eating, was found to be lower in individuals with NES in the early morning hours.12 The lower ghrelin levels associated with night awakenings in the NES group suggested that the food ingestions suppressed ghrelin, and in the NES, the lower ghrelin levels were a consequence not a cause of NES.12 In addition, insulin levels were significantly higher and glucose levels were marginally elevated in the NES group than in the control group. The researchers concluded that these neurohormonal differences in NES occurred as a result of alterations in food timing and not as a result of night eating.12

DIFFERENTIAL DIAGNOSES

In contrast to NES, BED has been considerably researched with specific diagnostic characteristics that include (a) consumption of large amounts of food in a discrete time frame; (b) a lack of control regarding food consumption during this period; and (c) a lack of compensatory behavior after the binge period.9 In a study that examined the psychological and behavioral characteristics of NES and BED, participants from an outpatient university-based weight loss center were recruited.9 The 41 females and 42 males enrolled in this study were classified into 4 groups that consisted of NES only (n = 23), BED only (n = 13), both NES and BED (n = 13), or no diagnosis of an eating disorder (n = 34). The NES group scored significantly lower on anxiety than either the BED group or the group with both NES and BED; the NES and BED combination group had the highest body mass index levels and the highest anxiety scores among the 4 groups. This finding is contradictory to previous findings that individuals with NES experience higher levels of anxiety than other obese individuals.9 The results of this study also demonstrated that individuals with NES had an earlier onset of obesity than individuals with no eating disorder diagnosis. The researchers suggested that these findings may indicate that individuals with both NES and BED experience greater psychological distress as a result of a prolonged struggle with weight issues and may use eating as a coping method.9

In addition to BED, 2 primary sleep disorders, nocturnal sleep-related eating disorder and nocturnal eating/drinking syndrome, are differential diagnoses to consider with NES. The nocturnal sleep-related eating disorder is associated with somnambulism about 80% of the time; therefore, unlike NES, there is a lack of awareness of the nocturnal eating and amnesia for the event the next day.5 The second disorder to consider in the differential diagnosis of NES, nocturnal eating/drinking syndrome, is characterized as a sleep disorder with recurrent awakenings; however, the individual is unable to return to sleep without eating or drinking. In contrast to nocturnal sleep-related eating disorder, the individual does maintain full awareness during the event and has no associated amnesia following the awakening.

TREATMENT AND SELF-REGULATION

Treatment of NES has not been extensively reported in the literature. In one trial of relaxation therapy, abbreviated progressive muscle relaxation technique (APRT) was evaluated as an intervention on a group of 20 adults with NES.13 In this study, participants were randomly assigned to a relaxation-training group with APRT (n = 10) or a control group (n = 10). Individuals were assessed presessions and postsessions for stress, anxiety, relaxation, and salivary cortisol. Mood, food diaries, and hunger ratings were also evaluated. The results of this study demonstrated that after 1 week of 20-minute APRT sessions, the individuals with NES assigned to this group reported increased relaxation, decreased anxiety, and reduced stress levels.13 This reported increase in relaxation and reduction in stress and anxiety levels was accompanied by reduced levels of salivary cortisol on day 1 of the intervention. In addition, the APRT group participants reported higher morning hunger and were more likely to eat breakfast; in the evening, lower hunger was reported and less eating occurred at night in the APRT group.13

Stunkard et al3 reported that 23 night eaters described a total of 83 medications that they considered beneficial with the following results reported: (a) 2 of the 25 reported use of antidepressants was considered as moderately effective therapy; (b) none of the 16 reports on hypnotics was considered effective; (c) 23 reported use of herbal preparations, with 3 indicating benefit from kava-kava, 2 reporting benefits with melatonin, and 2 specifying valerian root as helpful; and (d) 4 individuals reported effectiveness using fenfluramine and phentermine (fen-phen). In an open-label trial, 17 of these individuals participated in a 12-week course of sertraline, a selective serotonin reuptake inhibitor, as a medication for the treatment of NES.3 Twelve participants completed the trial with improved outcome measures for night awakenings (P < .01), nocturnal ingestions (P < .01), and reduced energy intake after supper (P < .01). The researchers concluded that NES may be appropriately treated with serotonin reuptake inhibitors, however, randomized controlled trials are needed.3

In 2006, O'Reardon et al14 conducted the first randomized placebo-controlled trial to evaluate the efficacy of sertraline in the treatment of NES. In this 8-week double-blind study, groups were randomly assigned to a flexible dose (50-200 mg) sertraline group (n = 17) or placebo group (n = 17). The results of this study indicated that sertraline effectively reduced the symptoms of NES in 71% of the sertraline group participants. The suprachiasmatic nucleus, the circadian rhythm pacemaker, is affected by serotonergic neuron input and sertraline may restore energy intake patterns in individuals with NES.14

Chromotherapy, a treatment method that uses the visible spectrum of electromagnetic radiation, has been reportedly used in a limited number of case studies for the treatment of NES. It is based on the principles that the body is composed of colors that are responsible for the function of various systems in the body.15 Bright white full-spectrum light was first used during the 1950s for the successful treatment of neonatal jaundice and is still used today for the treatment of some cancers, seasonal affective disorder, bulimia nervosa, insomnia, jet lag, and drug and alcohol dependencies.15 Melatonin, a light-responsive chemical pathway for the synchronization of circadian rhythms and seasonal variations, is produced during darkness. It has a depressant effect and is associated with induction and maintenance of sleep. In contrast, the neurotransmitter serotonin is produced during daylight and has stimulating effects. Bright light therapy improved the symptoms of NES in an open study of an obese subject despite comorbid depressive symptoms.16 In this case study, a 51-year-old women with a body mass index of 31.2 kg and a nonseasonal major depressive disorder was diagnosed with NES on the basis of the following criteria: morning anorexia, evening hyperphagia, and nocturnal awakenings with consumption of snacks (high-carbohydrate content of 67.8% and a high carbohydrate-to-protein ratio of 6:1). In addition to ongoing pharmacologic therapy with a selective serotonin reuptake inhibitor (paroxetine 40 mg daily), 14 morning sessions of 10 000 lux white light for 30 minutes daily were added. At the conclusion of these sessions, the patient no longer met diagnostic criteria for depression or NES.16 However, 1 month after the light therapy concluded, her NES symptoms had returned, although she was not depressed. Another series of 12 morning light sessions was then commenced and her NES symptoms were again suppressed.

A second case study was reported using light therapy in a nonobese male with nonseasonal depression and NES.17 After 14 consecutive treatments of light therapy (10 000 lux for 30 minutes), both NES and depressive symptoms improved. The researchers suggested that NES may be associated with depression in nonobese individuals and that it may be a predictor for the efficacy of light therapy when these disorders occur concomitantly.

SUMMARY

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