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
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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,
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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
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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
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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
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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
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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.
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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).
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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)
International Journal of Obesity
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
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
Two eating disorders
AJ Stunkard et al
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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