REVIEW Two forms of disordered eating in obesity: binge ... - Nature

International Journal of Obesity (2003) 27, 1–12 ß 2003 Nature Publishing Group All rights reserved 0307–0565/03 $25.00 www.nature.com/ijo

REVIEW Two forms of disordered eating in obesity: binge eating and night eating Albert J Stunkard* and Kelly Costello Allison Department of Psychiatry, University of Pennsylvania, Philadelphia, Pennsylvania, USA 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. International Journal of Obesity (2003) 27, 1 – 12. doi:10.1038/sj.ijo.0802186 Keywords: binge eating disorder; night eating syndrome; obesity; eating disorders; stress disorders; sleep disorders

Introduction

Binge eating disorder

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.

Diagnostic criteria 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.5 Table 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 – 19 Axis II disorders, particularly clusters B and C,11,13,15 occur frequently

*Correspondence: A Stunkard, 3535 Market Street, Suite 3024, Philadelphia, PA 19104-3309, USA. E-mail: [email protected] Received 6 March 2002; revised 16 July 2002; accepted 22 July 2002

Two eating disorders AJ Stunkard et al

2 Table 1 Proposed diagnostic criteria for binge eating disorder A. Recurrent episodes of binge eating. An episode of binge eating is characterized by the following: (1) eating, during a discrete period of time (eg within any 2 h period), an amount of food that is definitely larger than most people would eat during a similar period of time under similar circumstances (2) a sense of lack of control over eating during the episode (eg a feeling that one cannot stop eating or control what or how much one is eating) B. The binge eating episodes are associated with three or more of the following: (1) eating much more rapidly than normal (2) eating until feeling uncomfortably full (3) eating large amounts of food when not feeling physically hungry (4) eating alone because of being embarrassed by how much one is eating (5) feeling disgusted with oneself, depressed, or very guilty after overeating C. Marked distress regarding binge eating is present D. The binge eating occurs, on average, at least 2 days per week for 6 months E. The binge eating is not associated with the regular use of inappropriate compensatory behaviors (eg purging, fasting, excessive exercise) and does not occur exclusively during the course of Anorexia Nervosa or Bulimia Nervosa. Reprinted with permission from the Diagnostic and statistical manual of mental disorders, Fourth Edn, Text Revision. Copyright 2000, American Psychiatric Association.

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 – 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

Prevalence 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, International Journal of Obesity

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

Risk factors 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


3 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 – 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.

Psychological treatments. 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 – 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 – 62,64 Pharmacotherapy. 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 International Journal of Obesity


4 of binge eating at the outset of treatment did not affect adherence to diet, attrition or the amount of weight lost.17,74 – 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 lastobservation-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. A 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 – 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 psy-

Table 2 A. Responses among individuals with binge eating disorder to placebo-controlled trials and B. Binge eating in ‘no treatment’ groups Decrease in binges per week Author 65

Alger et al 1991 66 McCann and Agras 1990 67

Hudson et al 1998 McElroy et al 68 2000 Stunkard et al 29 1996

Author 61

Carter and Fairburn 1998 Cachelin et al 76 1999 Fairburn et al 77 2000 Peterson et al 62 2000

n

Duration

Drug

11 13

6 weeks 12 weeks

43 13 50

9 weeks 6 weeks 4 weeks

88% and 79% 63%, 60% remitted completely 57% 85% 73%

Type of observation

n

Duration

Waiting list control Community sample Community sample Waiting list control

24 21 40 11

12 weeks 6 months 5 years 8 weeks

*Information received from personal communication with the author.

International Journal of Obesity

Placebo 68% 16% increase, 15% remitted completely 41%* 46% 72%

Change in binge eating 34% reduction in frequency of binges 48% in partial remission 90% no longer met BED criteria 14% increase in bingeing


5

Figure 1 Decreases in binge eating. The figure on the left shows the 90% decline in persons diagnosed as binge eaters during a 5 y period when they received no treatment. The figure on the right shows the 73% decline in the frequency of binge eating during a 4 week placebo period.

chopathology 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.

Night eating 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 International Journal of Obesity


6 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 sleeponset 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.

Figure 2 24 h pattern of mean cumulative energy intake and mood for a 5 day period. The intake of the night eaters lags behind that of control subjects until 10 pm and then greatly exceeds it (P < 0.001). Daytime mood of the night eaters is lower than that of the controls (P < 0.001) and falls even lower during the evening and night (P < 0.001). Error bars represent s.e.m. in all figures. NES indicates night-eating syndrome.



7 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

Figure 3 24 h mean plasma cortisol levels in subjects with (n ¼ 12) and without (n ¼ 21) night eating syndrome (NES). The asterisk and bracket indicate a significant difference between the levels of the 2 groups (P < 0.001).



8

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). Differential diagnosis 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 ¼ 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)

Table 3 Provisional criteria for the night eating syndrome A. Morning anorexia, even if the subject eats breakfast B. Evening hyperphagia. At least 50% of the daily caloric intake is consumed in snacks after the last evening meal C. Awakenings at least once a night, at least three nights a week D. Consumption of high calorie snacks during the awakenings on frequent occasions E. The pattern occurs for a period of at least 3 months (Birketvedt et al, 1999)


4

Table 4

Comparison of BED and NES characteristics

Descriptors Size of ingestions Periodicity Familiality Prevalence Population Obesity clinics Morbid obesity Lifetime Comorbidity Major Depression Any substance abuse Any Axis I disorder Personality disorder Treatment Cognitive behavioral therapy Interpersonal Behavioral weight loss Pharmacotherapy Surgery

BED

NES

Large (over 1300 kcal) No 37 No

Modest (270 kcal) Yes Yes*

31

30

84

1.8 – 3.4% 29 27 8.9 – 18.8% 2732 – 47%35

1.5% 102 8.9 – 15% 7.934 – 42%33

3719 – 51%12 1212 – 72%15 2815 – 60%12 16 12 20 – 35%

44%* 25%* 77%* —

Reduces binge eating? Yes Yes Yes Yes Yes

Reduces night eating? — — — Yes No

*From Allison KC, and Stunkard AJ, unpublished data.

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 ¨ rk, Andersson and Ro ¨ ssner103 who studied paper of Ceru´ -Bjo 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


9 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 ¼ 0.28, P ¼ 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.

Acknowledgements Supported by NIDDK grant RO1 DK56735-0 and by a grant from Pfizer Pharmaceuticals.

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