OBJECTIVE: Binge eating disorder (BED) and the night eating syndrome (NES) have been linked to obesity. This review summarizes their characteristics, implications of their diagnoses and treatment outcomes.
METHOD: Selective review of the literature on BED and NES.
RESULTS: BED was proposed as a distinctive disorder on the basis of two large multisite studies in the early 1990s. It is associated with more severe and earlier onset of obesity, earlier onset of dieting and greater psychopathology. It shows large placebo responses and reduction of bingeing in patients on waiting-list controls. Traditional weight reduction programs reduce bingeing at least as well as psychological treatments designed for this purpose. NES is a stress-related eating, sleeping and mood disorder that is associated with disordered neuroendocrine function. It follows a characteristic circadian pattern and has responded to an agent that enhances serotonin function.
CONCLUSIONS: BED responds well to weight reduction programs. It is proposed that this diagnosis be used as a marker for psychological problems that deserve treatment in their own right. NES is an eating, sleep, and mood disorder with distinctive behavioral and neuroendocrine characteristics. Studies of treatment for NES are in their infancy but selective serotonin reuptake inhibitors (SSRI) show promise.
The objective of this paper is to review the current status of two eating disorders: binge eating disorder (BED) and the night eating syndrome (NES). A short report in 1959 challenged the widely held view that obesity is the result of an eating disorder.1 It proposed instead that, among obese persons, disordered eating was confined to a small minority who manifested either of two distinct patterns, then titled the night eating syndrome and the binge eating syndrome.1 These eating patterns received little attention until 1992 when Spitzer et al2,3 marshaled the evidence for what is now called binge eating disorder and in 1999 when Birketvedt et al4 provided a thorough description of the NES. Recent interest in the contribution of these disorders to the cause of obesity makes it timely to review their current status. A Medline search supplemented the authors' continuing survey of the literature on eating disorders.
Binge eating disorder
BED was delineated on the basis of data from 1984 and 1785 subjects derived from 12 eating disorder programs.2,3 The disorder is characterized by ‘recurrent episodes of binge eating associated with subjective and behavioral indicators of impaired control over, and significant distress about, the binge eating without the presence of inappropriate compensatory behaviors,’ including purging, fasting or compulsive exercising.5Table 1 shows the criteria for BED proposed by Spitzer et al, which have been included in an appendix in the Diagnostic and Statistical Manual of Mental Disorders.5
The Spitzer report proposed that, compared to control groups of obese persons, those with BED exhibited: 1) more severe obesity; 2) earlier onset of overweight; 3) earlier onset of, and more frequent, dieting; and 4) greater psychopathology, including depression, substance abuse and emotional problems.3 Extensive research has supported these criteria. Two earlier studies6,7 had noted the relationship between level of body mass index and frequency of bingeing, while two others8,9 confirmed the earlier onset of overweight and dieting among binge eaters. Psychopathology, especially depression, has been consistently reported among binge eaters.10,11,12,13,14,15,16,17,18,19 Axis II disorders, particularly clusters B and C,11,13,15 occur frequently in binge eaters. Four reports8,14,20,21 found weight and shape concerns of persons with BED comparable to those of persons with bulimia nervosa and far more severe than those of obese control groups. Finally, Tanofsky et al22 suggested that men with BED were significantly more likely to manifest substance abuse disorder than were non-binge eaters.
A critical issue in the diagnosis of BED is the nature of the essential feature of the disorder—the binge. After considerable uncertainty, a consensus favors Fairburn and Cooper's23 proposal that a binge comprises at least two elements: one subjective (a sense of loss of control) and the other objective (the actual amount of food consumed). There is general agreement on the subjective aspect of the binge—the feeling of loss of control. By contrast, there is uncertainty about the objective aspect—the size and duration of a binge. This uncertainty is reflected in the imprecise definition of the size of the binge—‘an amount of food that is definitely larger than most people would eat.’5 The duration of a binge is also controversial. In contrast to the purging type of bulimia nervosa, in which a binge is clearly terminated by an episode of purging, in BED there is often no clear termination. Accordingly, duration has been assigned an arbitrary 2 h,5 a clearly unsatisfactory solution. For example, Marcus et al8 have reported that almost 25% of binge episodes in BED lasted an entire day. To cope with this problem investigators have begun to report ‘binge days’ rather than specific episodes of bingeing.23,24,25,26 A feature of BED of particular relevance to obesity is that, in addition to their binges, persons with this disorder show a general tendency to overeat; their binges occur against a background of overeating. In sharp contrast, persons with bulimia nervosa binge against a background of severe dietary restriction.8,27,28
Estimates of the prevalence of BED vary widely, in part because of the varying definitions of a binge. The first studies, by Spitzer et al, based on self-report questionnaires, estimated a prevalence of 29% and 30% of people seeking treatment for their obesity.2,3 Later interview-based studies of treatment-seeking obese persons found a lower prevalence: 8.9%29 and 18.8%.27 In one study, 1450 persons who had identified themselves as binge eaters in a phone screen following a television show yielded only 50 subjects (3.4%) who met interview-based criteria for BED.30 In one community study, the prevalence rate was 2%, of whom less than half were obese.2 In another community study, the prevalence was 1.8%, the majority of whom were obese.31 Among patients undergoing bariatric surgery, the rates for BED were 27%,32 38%,33 43%34 and 47%.35
While anorexia nervosa and bulimia nervosa have historically affected mainly Caucasian women, BED affects minority women more frequently. One study of a biracial cohort of young adults suggested an overall BED prevalence of 1.5%, with similar rates among white women, white men, and black women. Only black men reported a significantly lower occurrence of BED.36 Other studies have found that minority and white women with BED did not differ on measures of disordered eating,37 and that both groups experienced similar levels of clinical impairments in functioning.38
Fairburn et al have proposed that BED is associated with exposure to risk factors in two different domains: psychiatric disorders and obesity.39 While binge eaters in this community sample reported less exposure to risk factors for general psychopathology than those with bulimia nervosa, binge eaters showed more frequent parental depression, greater vulnerability to obesity, more exposure to negative comments about shape, weight, and eating, morbid perfectionism and negative self-evaluation when compared to healthy control subjects. Compared to subjects with other psychiatric disorders, binge eaters were distinguished only by more frequent childhood obesity and awareness of negative comments about shape, weight and eating. Unlike the experience with other psychiatric disorders, Lee et al 40 did not find a familial tendency for BED, nor did they find familial relationships between BED and other eating disorders.
Dieting as a risk factor
Special attention should be directed toward the belief that dieting is a risk factor for BED.41,42 This belief appears to be incorrect. It is based on two propositions. The first proposition is that dieting is a risk factor for bulimia nervosa and, since bingeing occurs, it must also be a risk factor for BED.43,44 This belief has been rejected by the National Task Force on the Prevention and Treatment of Obesity, which has concluded that empirical studies do not support the belief that dieting induces binge eating in obese adults who seek weight reduction.45 The original publications of Spitzer et al2,3 reported that dieting occurred after the onset of binge eating and so could hardly have caused it. Wilson et al20 found that bingeing preceded obesity in 64% of their patients and that no more than 9% had been on a strict diet at the time that they began to binge. Five subsequent reports have confirmed that bingeing preceded dieting in a majority of binge eaters,46,47,48,49,50 while only one paper has reported that dieting preceded bingeing in 46% of binge eaters.51
The other proposition in support of the belief that dieting is a risk factor for BED derives from the use of the ‘Restraint Scale’ of Herman and Polivy. The ‘restraint’ factor of this scale was elevated in bulimic anorexics who were dieting. On this basis Herman and Polivy proposed that ‘restrained eating is a precondition, or even a cause, of binge eating.’41 Not only did they not study BED, but the ‘restraint’ that they cited was a misnomer. A later scale, the Eating Inventory,52 has shown that the so-called ‘restraint’ on the ‘Restraint Scale’ is not restraint at all but rather ‘disinhibition’ of restraint. The restraint factor on the Eating Inventory, on the other hand, measures what is generally accepted as restraint of eating. As expected, persons with BED increased their ‘restraint’ on the Eating Inventory at the same time that their binge eating decreased significantly.53 Far from predicting bingeing, ‘restraint’ on the Eating Inventory predicted successful dieting.54,55 ‘Disinhibition’, another scale on the Eating Inventory, is what predicted binge eating.53,56 There is thus no credible support for either of the two arguments that dieting is a risk factor for BED.
Despite the strong empirical and psychometric evidence that dieting and dietary restraint do not cause bingeing, the idea that they do persists and, in fact, informs the position that BED must be resolved before weight loss is attempted.
Treatment of binge eating disorder
Binge eaters have received three types of treatment: psychotherapy; pharmacotherapy; and, notably, weight reduction programs that have ignored the issue of binge eating.
Cognitive behavior therapy, often delivered in weekly programs over a 20-week period, focuses on the eating disturbance and the associated problematic cognitions and attitudes about eating, body shape and weight. It is consistently associated with reductions in binge eating, ranging from 48 to 98%.24,57,58,59,60,61,62,63,64,65 A second psychological treatment, interpersonal therapy, was associated with a clinically significant reduction (71%) in binge eating, and with maintenance of these effects at a 1 y follow-up.24,58 Despite the reduction in binge eating, significant weight loss did not occur in any of the psychological treatments.10,24,56,59,60,61,62,64
Pharmacotherapy has also reduced the frequency of binge eating. The first, open-label trials found a marked discrepancy in outcomes. Devlin et al reported complete cessation of binge eating in 12 of 16 binge eaters who received a combination of phentermine and fluoxetine.66 Ricca et al, on the other hand, reported that neither fluoxetine nor fluvoxamine alone had any effect on binge eating episodes in a 1 y, open-label trial.67 The first controlled trial by Alger et al68 found reductions in bingeing of 79% by naltrexone and 88% by imipramine; these reductions were not significantly greater than the 68% placebo response. However a significant reduction in bingeing compared to a control group was found in three small, short-term trials of antidepressant medication: desipramine,69 fluvoxamine,70 and sertraline,71 and in one trial of the appetite suppressant dexfenfluramine.30 Two of the studies reported weight loss70,71 and two did not.30,69 In two, therapeutic efficacy was shown by the prompt recurrence of bingeing when medication was discontinued.30,69 The studies described above ranged from 4–12 weeks in duration. Agras,72 in a review of pharmacotherapy for BED, reported high relapse rates of bingeing when antidepressants were discontinued after short-term trials. He suggested that initial trials last a minimum of six-months for more optimal results.
Weight reduction programs that ignore the issue of binge eating
A surprising development suggests that weight loss programs that ignore the issue of binge eating may perform as effectively as those designed solely to reduce binge eating. No fewer than 9 publications have reported this finding. Agras et al73 found that 36 weeks of treatment for weight loss that ignored binge eating reduced binge eating as effectively as cognitive behavior therapy and pharmacotherapy designed for this purpose. Marcus et al in 199561 reported a striking effect of a behavioral weight loss program which reduced the rate of bingeing from 21.7 to 2.7 binge days per 28 days. Nauta et al62 found the drop-out rates did not differ between binge eaters and non-binge eaters and that the two groups lost comparable amounts of weight. In no fewer than 4 reports on the use of behavioral treatment with very low calorie diets, the frequency of binge eating decreased. Furthermore, the presence of binge eating at the outset of treatment did not affect adherence to diet, attrition or the amount of weight lost.17,74,75,76
Clearly the presence of binge eating has not interfered with the effectiveness of traditional behavioral treatments for obesity. Two studies even suggest that binge eaters perform more adequately in these programs. Thus, Ho et al77 reported that binge eaters dropped out of a large treatment program for obesity only half as often as non-bingers. Gladis et al78 assessed a behavioral weight loss treatment that included no special provision for binge eating. They found that patients with BED lost significantly more weight than those without the disorder, and had comparable attrition rates and decreases in depression. They proposed that standard behavioral weight loss treatments are actually better able to address all of the treatment needs of binge eaters than are treatments directed toward binge eating.
These weight loss studies challenge the belief that had motivated the development of cognitive behavior therapy for BED and the concern that dietary restriction might exacerbate binge eating. Instead, dietary restriction appears to reduce binge eating. Furthermore, weight loss programs that ignore binge eating not only reduce binge eating but also reduce body weight. In striking contrast, cognitive behavior therapy programs designed to reduce binge eating have no effect on body weight.
What explains the control of bingeing by weight loss programs that pay no attention to the bingeing? Prominent among the reasons appears to be the high placebo responsiveness and spontaneous remission of BED (Table 2). Three studies of pharmacotherapy reported decreases in the rate of bingeing in the control group: from 41% to 68%.68,70,71 In the study by Alger et al68 the 68% placebo response did not differ statistically from that of the two active agents (79% and 88%), while in two other studies, statistical significance was achieved by differing the method of analysis. Thus, in the Hudson et al72 study, with a 41% placebo response, the difference from active medication and placebo was achieved only by a completer analysis whereas the difference in a last-observation-carried-forward (LOCF) analysis was not statistically significant. In the McElroy71 study, on the other hand, the 46% placebo response meant that only the LOCF analysis showed a significant effect whereas the completer analysis was not significant. A fourth study reported complete remission from bingeing in 15% of patients on placebo rather than reporting a percent in reduction in bingeing.69 In a fifth study binges decreased from 6.0 to 1.7 per week during a one-month placebo run-in29 (Figure 1).
Further evidence that helps to explain the favorable results of behavioral weight reduction programs is spontaneous remission of binge eating. Table 2 lists two community studies and one of waiting list controls in which rates of binge eating fell dramatically, 34% to 90% of diagnosable cases.64,79,80 A small increase in binge eating was found in only one, short, waiting list control study.62 Another explanation for the effectiveness of weight reduction programs that pay no attention to bingeing may be the provision of structured meal plans. Such plans may provide binge eaters with greater control of their food intake.
Weight control programs that pay no attention to bingeing not only control bingeing but also produce weight loss. Control of binge eating is not necessary for weight loss, raising the question of whether binge eating should be a specific object of therapeutic effort. We believe that it should not and make an unorthodox proposal.
We propose that BED be changed from an object of therapeutic endeavor to a marker for psychiatric comorbidity. We further propose that therapeutic attention be refocused on the psychopathology to which binge eating disorder calls attention.10,11,12,13,14,15,16,17,18,19 This psychopathology merits treatment. Alger et al81 found that depression was 59% more common among binge eaters than among non-binge eaters, and Specker et al15 reported that 47% of binge eaters vs 26% of non-binge eaters had a lifetime prevalence of major depressive disorder. Treatment directed towards specific psychopathology such as depression and anxiety will pay greater dividends than treatment directed towards an eating disorder that responds to non-specific treatment. We believe that the major value of the diagnosis of BED is as a marker for psychological problems that deserve consideration in their own right.
Programs for the study of eating disorders and sleep disorders have revealed conditions that combine both forms of disorder. A paper in 1955 proposed a ‘night eating syndrome’ comprising morning anorexia, evening hyperphagia, and insomnia.82 Although not a defining characteristic of the disorder, NES was reported to include depression, with an unusual circadian pattern: minimal in the morning and increasing during the evening and night. It is not included in the Diagnostic and Statistical Manual of the American Psychiatric Association.
The NES has been conceptualized as a disorder of biological rhythm, characterized by a phase onset delay. This view encompasses both the delay in onset of appetite in the morning and the continuation of overeating into the night. Strong evidence supporting this view of NES has recently been obtained from a treatment trial of NES with sertraline, a selective serotonin reuptake inhibitor (SSRI).83 Subjects who were significantly improved in terms of decreased night eating also showed improvement in the critical variable of morning anorexia; improvement was accompanied by the development of appetite for breakfast.
NES was originally described as ‘a special diurnal response to stress characteristic of some obese persons.’82 Current research supports this description as well as alleviation of the disorder with alleviation of the stress.
The night eating syndrome is uncommon in the general population (1.5%).84 It is present in non-obese persons, but is more common among obese persons. As in the case of BED, prevalence of the NES increases with increasing weight, from 8.9%,1 15%,85 and 43%86 in obesity clinics and from 10%85 to 27%84 and 42%33 among obese persons evaluated for surgical treatment. A value of only 7.9% in one report of bariatric surgery patients34 probably attests to different criteria for diagnosis.
Much of what we know about the NES was reported by Birketvedt et al in a study of 10 obese night eaters and 10 obese control subjects.4 This study confirmed the elements of the NES: morning anorexia, evening hyperphagia, and insomnia. Eating continued later at night among the NES subjects who consumed 2930 kcal during 24 h compared to 2334 kcal for the obese control subjects (P<0.055). Figure 2 shows that during the daylight hours the cumulative caloric intake of NES subjects lagged behind that of the control subjects, so that at 6:00 pm they had consumed only 37% of their daily intake, compared to 74% by the controls (P<0.001). The food intake of the controls then slowed while that of the NES subjects continued at a rapid pace until after midnight. During the period from 8:00 pm to 6:00 am, the NES subjects consumed 56% of their 24 h caloric intake, compared to 15% for the control subjects (P<0.001). Figure 2 also shows that the mood of the NES subjects was lower than that of the control subjects during the morning and that it fell significantly more than that of the controls during the evening and night.4
The NES subjects in this study suffered from both sleep-onset and sleep-maintenance insomnia, awakening 3.6 times per night, compared to 0.3 for the control subjects (P<0.001).4 Half of the 178 awakenings of the 10 NES subjects observed over a 5 day period were associated with food intake while none of the 10 controls ate while they were awake. The night time ingestions of the NES subjects were not binges but snacks of moderate size, averaging 271 kcal.4 Their carbohydrate content was very high (70% of kcal) compared to 47% for their food intake during the rest of the day (P<0.001). Furthermore, the carbohydrate to protein ratio of the night time snacks was also very high—7:1. This nutrient pattern, of a high carbohydrate to protein ratio, increases the availability of tryptophan for transport into the brain and conversion into serotonin, with its sleep promoting properties.88,89
The behavioral study of the night eating syndrome was complemented by the neuroendocrine study conducted in the Clinical Research Center of the University Hospital in Tromsø where subjects were admitted for 24 h periods.4 All subjects were women and consisted of both overweight and normal weight subjects with the NES and overweight and normal weight control subjects, matched for body mass index and age. Unlike their usual night time eating, NES subjects in the Clinical Research Center were restricted to four meals of 400 kcal at 8:00 am, 12:00 noon, 4:00 pm, and 8:00 pm.
Among NES subjects, both overweight and normal weight, there was a marked blunting of the plasma melatonin levels at night (P<0.001). As expected, plasma leptin levels of the overweight subjects were higher than those of the normal weight subjects, both for NES subjects and controls. The expected rise in leptin at night occurred among both the obese and normal weight control subjects. In striking contrast, there was no increase in leptin among NES subjects, either obese or non-obese. Confirming the earlier clinical impression that the NES was associated with stress, plasma cortisol levels of the NES subjects were higher than those of control subjects for most of the 24 h (see Figure 3).
The night eating syndrome appears to be a unique combination of an eating disorder, a sleep disorder and a mood disorder. The distinctive neuroendocrine findings are closely associated with the behavior of the NES subjects. Thus, the blunting of the night time rise in melatonin may contribute to the sleep maintenance insomnia, as has been suggested by Hajak et al,90 and to depression, as suggested by Kennedy et al.91 The failure of leptin to rise at night may limit its usual night time suppression of appetite and may permit the breakthrough of hunger impulses, further disrupting sleep. The elevated levels of cortisol reflect the clinical impression that night eating occurs during periods of life stress. Birketvedt et al92 recently reported that CRH-induced ACTH and cortisol responses were attenuated in NES patients compared to controls. These authors suggest that this finding represents an exhaustion of the HPA-axis and supports the idea that NES may be stress-induced. Others have also associated chronic activation of the HPA-axis with insomnia and depression, two of the core features of NES.93,94
Five studies have confirmed aspects of the NES. Gluck et al85 reported that NES subjects consumed more of their food intake than did controls during the latter part of the day, and that a test meal at this time was larger in night eaters than in controls. This study also found elevated levels of depression in NES subjects. Aronoff et al95 reported that 70% of the 24 h food intake of night eaters was consumed after 7:00 pm. Allison et al reported that NES subjects awakened 1.7 times per night, 73% of which were associated with food intake.96 Manni et al97 found NES in 7 of 120 sleep clinic patients, as confirmed by polysomnography. Patients ate ‘compulsively’ shortly after awakening, and ingestions were limited to small snacks. Spaggiari et al98 noted frequent awakenings, also confirmed by polysomnography, in 10 patients who ate during half of these occasions. More recent polysomnographic studies among obese women with NES and matched controls have revealed no significant levels of sleep apnea or other parasomnias among the NES patients (unpublished observations, Ringel, Allison, O'Reardon, Dinges & Stunkard).
Preliminary criteria for the night eating syndrome are noted in Table 3.4 The disorder is readily recognized by persons who suffer from it, and it is becoming more widely known in lay and medical circles.
The differential diagnosis of the NES is with BED, ‘nocturnal eating/drinking disorder’,99 and ‘nocturnal sleep-related eating disorder’.100 Diagnosis depends upon differences in the frequency and size of eating episodes and upon the state of consciousness during them.
Night eating syndrome vs binge eating disorder
The NES differs from BED in both the far greater frequency of night time awakenings and in the smaller size of the food ingested at these times: 270 kcal with each awakening4 compared to the 1300 kcal ingested during eating binges reported by Grilo and Schiffman.101 In a study of 231 obese persons, there was only minimal overlap between the two disorders, ranging from 21% in a sample seeking treatment for BED to 0% among persons seeking weight loss therapy.102 Furthermore, persons with NES do not appear to suffer to the same degree from the diet and body image disorders so common among those with BED.28 In contrast, the two disorders may share similarly high levels of co-morbidity with Axis I disorders (see Table 4). The relative stability of the two disorders was revealed by the results of biliopancreatic bypass of 63 severely obese persons (mean BMI=46.9).34 Twenty-seven were binge eaters, of whom 5 were also night eaters. By the third postoperative year, all patients who had been bingeing prior to surgery had stopped bingeing, while only one of the five night eaters had stopped night eating.
Night eating syndrome vs night eating/drinking syndrome and nocturnal sleep-related eating disorder
In the sleep disorders literature two additional types of night eating have been described: ‘night eating/drinking syndrome’ (NEDS) and ‘nocturnal sleep-related eating disorder’ (NSRED). NEDS involves ‘frequent and recurrent awakenings to eat and/or drink and normal sleep onset following the ingestion of the desired foods.’99 It too includes various psychological disorders.97,101 Any differences between NES and NEDS appear to be largely linguistic, dependent upon whether the author used ‘night’ or ‘nocturnal’ in describing the period of overeating. This view seems supported by the paper of Cerú-Björk, Andersson and Rössner103 who studied 194 obese persons, 14% of whom were characterized by having either evening hyperphagia (‘night eaters’) or by eating after going to bed (‘nocturnal eaters’). The authors concluded that, ‘there is more to unite the two syndromes than there are differences between them.’
NSRED, the subject of few reports from sleep research clinics, appears to differ from NEDS as well as NES. The key distinction lies in the extent of consciousness during the night eating. In the NSRED sleep disorder clinic patients reported by Schenck and Mahowald,100 84% of night eating occurred during total or partial unconsciousness and, for the majority, during stage 3/4 sleep. Winkelman104 noted that over 90% of these patients reported being either ‘half awake, half asleep’ or ‘asleep’ and that they experienced either consistent or occasional amnesia for these episodes. Both Schenck and Mahowald98 and Gupta105 reported that spontaneous ingestion of inedible objects occurred during some NSRED episodes. Gupta105 reported further that 10 of 32 patients being treated for bulimia nervosa experienced NSRED. These persons had only partial recollection of having eaten during the night. Witnesses reported that these patients typically engaged in eating behavior that appeared to be purposeful but not conscious. Another difference between NES and NSRED is in prevalence. Schenck and Mahowald reported only 0.5%, or 38 cases of NSRED out of approximately 8000 polysomnographic examinations.100
By contrast, NES patients do not complain of impaired consciousness while eating. Manni et al95 reported that of the seven NES patients (out of 120 insomniacs) in their sleep disorder clinic, all were fully conscious while eating at night. One polysomnographic study of a subject who ate while fully conscious found that he awoke to eat during stage II sleep.106 Spaggiari et al98 studied 10 night eaters polysomnographically; all were awake and fully aware of their eating episodes. Their awakenings occurred during NREM sleep, and they returned to sleep quickly after their ingestions.
In distinction to the limited evidence of a familial tendency in BED, NES shows a significant familial character. Eight of 29 subjects recruited for a study of NES reported at least one first-degree family member with the disorder and two of them described 3 first-degree family members (Allison and Stunkard, unpublished data).
Prognosis and treatment
Information about prognosis in the NES is limited to retrospective accounts which suggest that it follows a chronic course, exacerbated by stressful life situations. The number of those accounts, however, is limited.
In contrast to the plethora of treatments that have been proposed for BED, those of the NES are limited. The 1955 report on the disorder noted that long-term psychodynamic psychotherapy had been associated with improvement in some patients, attributed to a reduction in stress.82 One case study suggested that behavioral treatment of NES in a patient with bulimia nervosa was effective,107 while other attempts have not been so successful.108
A promising report on the pharmacotherapy of NES described 17 persons suffering from this disorder who were treated with sertraline.83 Of the 11 subjects who completed the 12-week trial, 8 met criteria for response and, of those, 5 achieved remission. The 5 subjects who achieved remission lost 3.9±3.0 kg compared to a gain of 0.6±4.9 kg for the other 12 subjects (P<0.05). The fact that an antidepressant (sertraline) improved the NES, which includes the presence of depression, raises the question of whether it did more than relieve the depression. The low correlation between improvement in depression and in NES (r=0.28, P=0.40) suggests that sertraline improved the NES independent of its effect on depression.
Before the sertraline trial prospective candidates were asked about any medication that had been helpful in the past.83 Of a total of 69 reports that mentioned medication, only 14 were described as at least ‘moderately effective’. Of these 14, improvement was attributed to fenfluramine in all 4 cases in which it had been used. This evidence of efficacy stands in sharp contrast to the general lack of reported efficacy of other agents, with melatonin being moderately effective in only 2 of 15 reports and hypnotics being ineffective in 16 of 16 reports. Notably, in view of the response to sertraline reported above, none of 9 reports of the use of sertraline in community treatment indicated efficacy.
Fenfluramine was reported by Spaggiari98 to relieve the NES in 6 of 7 patients in whom it was tried; Manni et al97 also reported a good response in 1 of 4 NES patients. The efficacy of this powerful serotonin agonist suggests the importance of inadequate serotonin levels in the genesis of the NES. It also may help to explain the effectiveness of sertraline, a selective serotonin reuptake inhibitor (SSRI), when administered at doses found effective for treating eating disorders.
Summary and conclusions
The identification of two different eating disorders helps to define two subsets of obese persons who may benefit from special attention. Studies of binge eating disorder show that, in many cases, traditional weight reduction programs reduce both binge eating and body weight and may be the treatment of choice. The diagnosis of binge eating disorder may be most useful as a marker for the psychological problems that often affect binge eaters and that deserve treatment in their own right.
Delineation of the night eating syndrome has several benefits. It focuses attention on the processes that may underlie disorders of sleeping, eating and mood. It suggests the role played by stress in the disorder, as manifested by both clinical appraisals and elevated levels of cortisol. It draws attention to the roles of melatonin and leptin in preserving sleep and night time anorexia and the problems presented when these functions become disordered. Finally, the therapeutic response to an SSRI suggests the critical role played by depressed serotonergic function in NES at the same time that it gives promise of effective treatment. More research on both pharmacological and psychotherapeutic/behavioral treatments, including attention to established eating and sleep disorder treatments, is warranted.
Stunkard AJ . Eating patterns and obesity. Psychiatr Q 1959; 33: 284–294.
Spitzer RL, Devlin M, Walsh BT, Hasin D, Wing R, Marcus M, Stunkard AJ, Wadden T, Yanovski S, Agras S, Mitchell J & Nonas C . Binge eating disorder: a multisite field trial of the diagnostic criteria. Int J Eat Disord 1992; 11: 191–203.
Spitzer RL, Yanovski S, Wadden TA, Wing R, Marcus MD, Stunkard AJ, Devlin M, Mitchell J, Hasin D & Horne RL . Binge-eating disorder: its further validation in a multisite study. Int J Eat Disord 1993; 13: 137–150.
Birketvedt G, Florholmen J, Sundsfjord J, Osterud B, Dinges D, Bilker W & Stunkard AJ . Behavioral and neuroendocrine characteristics of the night-eating syndrome. JAMA 1999; 282: 657–663.
American Psychiatric Association. Diagnostic and statistical manual of mental disorders, Fourth Edition, Text Revision, American Psychiatric Association: Washington, DC; 2000; 787
Telch CF, Agras WS & Rossiter FM . Binge eating increases with increasing adiposity. Int J Eat Disord 1988; 7: 115–119.
Marcus MD, Wing RR & Lamporski DM . Binge eating and dietary restraint in obese patients. Addict Behav 1985; 10: 163–168.
Marcus MD, Smith D, Santelli R & Kaye W . Characterization of eating disordered behavior in obese binge eaters. Int J Eat Disord 1992; 12: 249–255.
Yanovski SZ . Binge eating disorder: current knowledge. Obes Res 1993; 1: 306–324.
Marcus MD, Wing RR & Hopkin J . Obese binge eaters: affect, cognitions and response to behavioral weight control. J Consult Clin Psychol 1988; 56: 433–439.
Marcus MD, Wing RR, Ewing L, Kern E, Gooding W & McDermott, M . Psychiatric disorders among obese binge eaters. Int J Eat Disord 1996; 9: 69–77.
Yanovski SZ, Nelson JE, Dubbert BK & Spitzer RL . Association of binge eating disorder and psychiatric comorbidity in obese subjects. Am J Psychiatry 1993; 150: 1472–1479.
Mitchell JE & Mussell MP . Comorbidity and binge eating disorder. Addict Behav 1995; 20: 725–732.
Antony MM, Johnson WG, Carr-Nangle RE & Abel JL . Psychopathology correlates of binge eating and binge eating disorder. Compr Psychiatry 1994; 35: 386–392.
Specker S, De Zwaan M, Raymond N & Mitchell J . Psychopathology in subgroups of obese women with and without binge eating disorder. Compr Psychiatry 1994; 35: 185–190.
Telch C & Stice E . Psychiatric comorbidity in a non-clinical sample of women with binge eating disorder. J Consult Clin Psychol 1998; 66: 768–776.
Wadden TA, Foster GD & Letizia KA . One-year behavioral treatment of obesity: comparison of moderate and severe caloric restriction and the effects of weight maintenance therapy. J Consult Clin Psychol 1994; 62: 165–171.
Kuehnel RH & Wadden, TA . Binge eating disorder, weight cycling, and psychopathology. Int J Eat Disord 1994; 15: 321–329.
Mussell MP, Mitchell JE, de Zwaan M, Crosby RD, Seim HC & Crow SJ . Clinical characteristics associated with binge eating in obese females: a descriptive study. Int J Obes Relat Metab Disord 1996; 20: 324–331.
Wilson GT, Nonas CA & Rosenblum GD . Assessment of binge eating in obese patients. Int J Eat Disord 1993; 150: 1472–1479.
Wilfley DE, Schwartz MH, Spurrell EB & Fairburn CG . Using the eating disorder examination to identify specific psychopathology of binge eating disorder. Int J Eat Disord 2000; 27: 259–269.
Tanofsky MB, Wilfley DE, Spurrell EB, Welch R & Brownell KD . Comparison of men and women with binge eating disorder. Int J Eat Disord 1997; 21: 49–54.
Fairburn CG & Cooper Z . The eating disorders examination. In: Fairburn CG, Wilson GT (eds). Binge eating: nature, assessment and treatment, Guilford Press: New York; 1993; 317–360.
Wilfley DE, Agras WS, Telch CF, Rossiter EM, Schneider JA, Cole, AG, Sifford L & Raeburn SD . Group cognitive-behavioral therapy and group interpersonal psychotherapy for the nonpurging bulimic individual: a controlled comparison. J Consult Clin Psychol 1993; 61: 296–305.
Basdevant A, Puillon M & Lahlon W . Prevalence of binge eating disorder in different populations of French women. Int J Eat Disord 1995; 18: 309–315.
Rossiter EM, Agras WS, Telch CF & Brusch D . The eating patterns of non-purging bulimic subjects. Int J Eat Disord 1992; 11: 111–120.
Brody ML, Walsh BT & Devlin MJ . Binge eating disorder: reliability and validity of a new diagnostic category. J Consult Clin Psychol 1994; 62: 381–386.
Yanovski SZ & Stunkard AJ . Obesity and eating disorders. In: Bray GA, Bouchard C (eds). Handbook of obesity, 2nd edn. Marcel Dekker: New York. In press
Stunkard AJ, Berkowitz R, Wadden T, Tanrikut C, Reiss E & Young, L . Binge eating disorder and the night eating syndrome. Int J Obes Relat Metab Disord 1996; 20: 1–6.
Stunkard AJ, Berkowitz R, Tanrikut C, Reiss E & Young L . d-fenfluramine treatment of binge eating disorder. Am J Psychiatry 1996; 153: 1455–1459.
Bruce B & Agras WS . Binge eating in females: a population-based investigation. Int J Eat Disord 1992; 12: 365–373.
Wadden TA, Sarwer DB, Womble LG, Foster GD, McGuckin BG & Schimmel A . Psychosocial aspects of obesity and obesity surgery. Sur Clin North Amer 2001; 81: 1001–1024.
Hsu LKG, Betancourt S & Sullivan SP . Eating disturbances before and after vertical banded gastroplasty: a pilot study. Int J Eat Disord 1996; 19: 23–34.
Adami GF, Meneghelli A & Scopinaro N . Night eating and binge eating disorder in obese patients. Int J Eat Disord 1999; 25: 335–338.
Adami GF, Bandolfo P, Bauer B & Scopinaro N . Binge eating in massively obese patients undergoing bariatric surgery. Int J Eat Disord 1995; 17: 45–50.
Smith DE, Marcus MD, Lewis CE, Fitzgibbon M & Schreiner P . Prevalence of binge eating disorder, obesity, and depression in a biracial cohort of young adults. Annals Behav Med 1998; 20: 227–232.
le Grange D, Telch CF & Agras WS . Eating and general psychopathology in a sample of Caucasian and ethnic minority subjects. Int J Eat Disord 1997; 21: 285–293.
Pike KM, Dohm FA, Striegel-Moore RH, Wilfley DE & Fairburn CG . A comparison of black and white women with binge eating disorder. Am J Psychiatry 2001; 158: 1455–1460.
Fairburn CG, Doll HA, Welch SL, Hay PJ, Davies BA & O'Connor ME . Risk factors for binge eating disorder—a community based, case-control study. Arch Gen Psychiatry 1998; 55: 425–432.
Lee YH, Abbott DW, Seim H, Crosby RD, Monson N, Burgard M & Mitchell JE . Eating disorders and psychiatric disorders in the first degree relatives of obese probands with binge eating disorder and obese non-binge eating disorder controls. Int J Eat Disord 1999; 26: 322–332.
Herman CP & Polivy J . Restrained eating. In: Stunkard AJ (ed). Obesity, W.B. Saunders: Philadelphia; 1980; 208–225.
Herman CP & Polivy J . From dietary restraint to binge eating: attaching causes to effects. Appetite 1990; 14: 123–125.
Polivy J & Herman CP . Dieting and bingeing: a causal analysis. Am Psychol 1985; 40: 193–201.
Polivy J, Herman C, Olmsted M & Jazwinski C . Restraint and binge eating. In: Hawkins RC, Frenow WJ, Clement PP (eds). The binge-purge syndrome: diagnosis, treatment and research, Springer: New York; 1984; 104–122.
National Task Force on the Prevention and Treatment of Obesity. Dieting and the development of eating disorders in overweight and obese adults. Arch Int Med 2000; 160: 2581–2589.
Berkowitz R, Stunkard AJ & Stallings VA . Binge eating disorder in obese adolescent girls. Ann N Y Acad Med 1993; 699: 200–296.
Spurrell EM, Wilfley DE, Tanofsky MB & Brownell KD . Age of onset for binge eating disorder: are there different pathways to binge eating? Int J Eat Disord 1997; 21: 55–65.
Grilo CM & Masheb RM . Onset of dieting vs binge eating in outpatients with binge eating disorder. Int J Obes Relat Metab Disord 2000; 24: 404–409.
Abbott DW, de Zwaan M, Mussell MP, Raymond NC, Seim HC, Crow SJ, Crosby RD & Mitchell JE . Onset of binge eating and dieting in overweight women: implications for etiology, associated features and treatment. J Psychosom Res 1998; 44: 367–374.
Mussell MP, Mitchell JE, Fenna CJ, Crosby RD, Miller JP & Hoberman HM . A comparison of onset of binge eating vs dieting in the development of bulimia nervosa. Int J Eat Disord 1997; 12: 353–360.
Brewerton TD, Dansky BS, Kilpatrick DG & O'Neil PM . Which comes first in the pathogenesis of bulimia nervosa: dieting or bingeing? Int J Eat Disord 2000; 28: 259–264.
Stunkard AJ & Messick S . The Three-Factor Eating Questionnaire to measure dietary restraint, disinhibition and hunger. J Psychosom Res 1985; 29: 71–83.
Yanovski SZ & Sebring NG . Recorded food intake of obese women with binge eating disorder before and after weight loss. Int J Eat Disord 1994; 15: 135–150.
Charnock DJK . A comment on the role of dietary restraint in the development of bulimia nervosa. Br J Clin Psychol 1989; 28: 329–340.
Gorman BS & Allison DB . Measures of restrained eating. In: Allison DB (ed).. History of assessment methods for eating behavior and weight related problems, Sage: Thousand Oaks, CA; 1995.
Telch CF, Agras WS, Rossiter FM, Wilfley DE & Kenardy J . Group cognitive behavioral treatment for non-purging bulimics: an initial evaluation. J Consult Clin Psychol 1990; 58: 629–635.
Kalarchian MA, Wilson GT, Brolin RE & Bradely L . Binge eating in bariatric surgery patients. Int J Eat Disord 1998; 23: 89–92.
Wilfley DE & Cohen LR . Psychological treatment of bulimia nervosa and binge eating disorder. Psychopharmacol Bull 1997; 33: 437–454.
Smith DE, Marcus MD & Kaye W . Cognitive-behavioral treatment of obese binge eaters. Int J Eat Disord 1992; 12: 57–262.
Agras WS, Telch CF, Arnow B, Eldredge K & Marnell M . One-year follow-up of cognitive behavioral therapy for obese individuals with binge eating disorder. J Consult Clin Psychol 1997; 65: 343–347.
Marcus MD, Wing RR & Fairburn CG . Cognitive behavioral treatment of binge eating vs behavioral weight control on the treatment of binge eating disorder. Ann Behav Med 1995; 17: S090
Nauta H, Hospers H, Kok G & Jansen A . A comparison between a cognitive and a behavioral treatment for obese binge eaters and obese non-binge-eaters. Behavior Therapy 2000; 31: 441–461.
Fairburn CG . Overcoming binge eating, Guilford Press: New York; 1995.
Carter JC & Fairburn CG . Cognitive behavioral self-help for binge eating disorder: a controlled effectiveness study. J Consult Clin Psychol 1998; 66: 616–623.
Peterson CB, Mitchell JE, Engbloom S, Nugent S, Mussell MP & Miller JP . Group cognitive-behavioral treatment of binge eating disorder: a comparison of therapist-led vs self-help formats. Int J Eat Disord 1998; 24: 125–136.
Devlin MJ, Goldfein JA, Carino JS & Wolk SL . Open treatment of overweight binge eaters with phentermine and fluoxetine as an adjunct to cognitive behavioral therapy. Int J Eat Disord 2000; 28: 325–332.
Ricca V, Mannucci E, Mezzani B, Moretti S, DiBernardo M, Bertelli M, Rotella CM & Faravelli C . Fluoxetine and Fluvoxamine combined with individual cognitive-behavioral therapy in binge eating disorder: a one-year follow-up study. Psychother Psychosom 2001; 70: 298–306.
Alger SA, Schwalberg MD, Bigaoutte JM, Michalek AV & Howard IJ . Effect of a tricyclic antidepressant and opiate antagonist on binge-eating behavior: a double-blind, placebo-controlled study. Am J Clin Nutr 1991; 53: 865–871.
McCann UD & Agras WS . Successful treatment of nonpurging bulimia nervosa with desipramine: a double-blind, placebo-controlled study. Am J Psychiatry 1990; 147: 1509–1513.
Hudson JI, McElroy SL, Raymond NC, Crow S, Keck PE, Carter WP, Mitchell JE, Strakowski SM, Pope HG, Coleman BS & Jeffrey, JM . Fluvoxamine in the treatment of binge eating disorder: a multicenter placebo-controlled, double-blind trial. Am J Psychiatry 1998; 155: 1756–1762.
McElroy SL, Casuto L, Nelson E, Lake KA, Soutullo C, Keck P & Hudson JI . Placebo-controlled trial of sertraline in the treatment of binge eating disorder. A randomized trial. Am J Psychiatry 2000; 157: 1004–1006.
Agras WS . Pharmacotherapy of bulimia nervosa and binge eating disorder: longer term outcomes. Psychopharmac Bull 1997; 33: 433–436.
Agras WS, Telch CF, Arnow B, Eldredge K, Wilfley DE, Raeburn, ED, Henderson J & Marnell, M . Weight loss, cognitive, behavioral and desipramine treatments in binge eating disorder: an additive design. Behavior Therapy 1994; 25: 225–238.
Telch CF & Agras WS . The effects of a very low calorie diet on binge eating. Behavior Therapy 1993; 24: 177–193.
LaPorte DJ . Treatment response in obese binge eaters: preliminary results using a very low calorie diet (VLCD) and behavior therapy. Addict Behav 1992; 17: 247–257.
Wadden TA, Foster GD & Letizia KA . Response of obese binge eaters to treatment by behavior therapy combined with very low calorie diet. J Consult Clin Psychol 1992; 60: 808–811.
Ho KSI, Nichaman MZ, Taylor WC, Lec ES & Foreyt JP . Binge eating disorder, retention and drop-out rate in an adult obesity program. Int J Eat Disord 1995; 18: 291–294.
Gladis MM, Wadden TA, Vogt R, Foster G, Kuehnel RH & Bartlett SJ . Behavioral treatment of obese binge eaters: do they need different care? J Psychocom Res 1998; 44: 375–384.
Cachelin FM, Striegel-Moore RH, Elder KA, Pike KM, Wilfley DE & Fairburn CG . Natural course of a community sample of women with binge eating disorder. Int J Eat Disord 1997; 25: 45–54.
Fairburn CG, Cooper, Z, Doll HA, Norman PA & O'Connor ME . The natural course of bulimia nervosa and binge eating disorder in young women. Arch Gen Psychiatry 2000; 57: 659–665.
Alger SA, Malone M, Cerulli J, Fein S & Howard L . Beneficial effects of pharmacotherapy on weight loss, depressive symptoms, and eating patterns in obese binge eaters and non-binge eaters. Obes Res 1999; 7: 469–476.
Stunkard AJ, Grace WJ & Wolff HG . The night-eating syndrome: a pattern of food intake among certain obese patients. Am J Med 1955; 19: 78–86.
O'Reardon JP, Stunkard AJ, Allison KC & Ringel B . A clinical trial of the selective serotonin reuptake inhibitor sertraline in the treatment of the night eating syndrome. Int J Eat Disord 2002; submitted.
Rand CSW, Macgregor MD & Stunkard AJ . The night eating syndrome in the general population and among post-operative obesity surgery patients. Int J Eat Disord 1997; 22: 65–69.
Gluck ME, Geliebter A & Satov T . Night eating syndrome is associated with depression, low self-esteem, reduced daytime hunger, and less weight loss in obese outpatients. Obes Res 2001; 9: 264–267.
Napolitano MA, Head S, Babyak MA & Blumenthal JA . Binge eating disorder and night eating syndrome: psychological and behavioral characteristics. Int J Eat Disord 2001; 30: 193–203.
Powers PS, Perez A, Boyd F & Rosemurgy A . Eating pathology before and after bariatric surgery: a prospective study. Int J Eat Disord 1999; 25: 293–300.
Berry EM, Growdon, JH, Wurtman, JJ, Caballero B & Wurtman RJ . A balanced carbohydrate: protein diet in the management of Parkinson's disease. Neurology 1991; 41: 1295–1297.
Yokogoshi H & Wurtman RJ . Meal composition and plasma amino acid ratios: effects of various proteins or carbohydrates, and of various protein concentrations. Metab Clin Exp 1986; 35: 637–642.
Hajak G, Rodenbeck A, Staedt J, Bandelow B, Huether G & Ruther, E . Nocturnal plasma melatonin levels in patients suffering from chronic primary insomnia. J Pineal Res 1995; 19: 116–122.
Kennedy SH, Garfinkel PE, Parienti V, Costa D & Braun GM . Changes in melatonin levels but not cortisol levels are associated with depression in patients with depression and eating disorders. Arch Gen Psychiatry 1989; 46: 73–78.
Birketvedt G, Sundsfjord J & Florholmen JR . Hypothalamic-pituitary-adrenal axis in the night eating syndrome. Am J Physiol Endocrinol Metab 2002; 282: E366–E369.
Vgontzas AN, Bixler EO, Lin HM, Prolo P, Mastorakos G, Vela-Bueno A, Kales A & Chrousos GP . Chronic insomnia is associated with nyctohemeral activation of the hypothalamic-pituitary-adrenal axis: clinical implications. J Clin Endocrinol Metab 2001; 86: 3787–3794.
Chrousos GP & Gold PW . The concepts of stress and stress system disorders: Overview of physical and behavioral homeostatsis. JAMA 1992; 267: 1244–1252.
Aronoff NJ, Geliebter A & Zammit G . Gender and body mass index as related to the night eating syndrome in obese outpatients. J Am Dietet Assn 2001; 101: 102–104.
Allison KC, O'Reardon J, Stunkard AJ & Dinges D . Characterizing the night eating syndrome. Obes Res 2001; 9 (Suppl 3): 93S
Manni R, Ratti MT & Tartara A . Nocturnal eating: prevalence and features in 120 insomniac referrals. Sleep 1997; 20: 734–738.
Spaggiari MC, Granella F, Parrino L, Marchesi C, Melli I & Terzano, MG . Nocturnal eating syndrome in adults. Sleep 1994; 17: 339–344.
Thorpy MJ . The International Classification of Sleep Disorders: diagnostic and coding manual, American Sleep Disorders Association, Diagnostic Classification Steering Committee. Allen Press: Lawrence, KS; 1990.
Schenk CH & Mahowald MW . Review of nocturnal sleep-related eating disorders. Int J Eat Disord 1994; 16: 343–356.
Grilo CM & Shiffman S . Longitudinal investigation of the abstinence violation effect in binge eaters. J Consult Clin Psychol 1994; 62: 611–619.
Stunkard A, Berkowitz R, Wadden T, Tanrikut C, Reiss E & Young L . Binge eating disorder and the night eating syndrome. Int J Obes Relat Metab Disord 1996; 20: 1–6.
Cerú-Björk C, Andersson I & Rössner S . Night eating and nocturnal eating—two different or similar syndromes among obese patients? Int J Obes Relat Metab Disord 2001; 25: 365–372.
Winkelman JW . Clinical and polysomnographic features of sleep-related eating disorder. J Clin Psychiatry 1998; 59: 14–19.
Gupta MA . Sleep-related eating in bulimia nervosa: an underreported parasomnia disorder. Sleep Research 1991; 20: 182
Aronoff NJ, Geliebter A, Hashim SA & Zammit GK . The relationship between daytime and nighttime food intake in an obese night-eater. Obes Res 1994; 2: 145–151.
Williamson DA, Lawson OD, Bennett SM & Hinz L . Behavioral treatment of night bingeing and rumination in an adult case of bulimia nervosa. J Behav Ther & Exp Psychiat 1989; 20: 73–77.
Oswald I & Adam K . Rhythmic raiding of refrigerator related to rapid eye movement sleep. Br Med J 1986; 292: 589
Supported by NIDDK grant RO1 DK56735-0 and by a grant from Pfizer Pharmaceuticals.
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Stunkard, A., Costello Allison, K. Two forms of disordered eating in obesity: binge eating and night eating. Int J Obes 27, 1–12 (2003). https://doi.org/10.1038/sj.ijo.0802186
- binge eating disorder
- night eating syndrome
- eating disorders
- stress disorders
- sleep disorders
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