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CHAPTER 25
The Night Eating Syndrome
Abstract
T
Introduction
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he typical behavioral characteristics of the night eating
syndrome have been described as morning anorexia,
evening hyperphagia and insomnia. The neuroendocrine
characteristics have been described as changes in the circadian
rhythm by an attenuation in the nocturnal rise of the plasma
concentrations of melatonin and leptin and an increased circadian secretion of cortisol. The night eaters also have an
overexpressed hypothalamic-pituitary-adrenal axis with an attenuated response to stress. The night eating syndrome appears to
represent a new eating disorder, different from the established
disorders of anorexia nervosa, bulimia nervosa, and binge eating
disorders. It differs in the frequency and size of ingestions at
night, and the elevated plasma levels of cortisol reflect increased
activity of CRH, as expressed by an attenuated ACTH and cortisol response. In conclusion the mechanisms behind the increased
CRH stimulation may involve alterations in the neurotransmitter systems, causing increased nocturnal appetite and disruption
in the sleep pattern. This may, to some extent, explain the disturbances in the circadian secretions of melatonin and leptin and
the behavioral characteristics of the night eating syndrome.
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Grethe Støa Birketvedt and Jon R. Florholmen
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The night eating syndrome (NES) is characterized by morning anorexia, evening hyperphagia and insomnia and was first
described in 1955 by Dr. Albert Stunkard and his colleagues at
the University of Pennsylvania.1 The night eating was found to
occur during periods of stress and was associated with a poor
outcome of efforts at weight reduction. Depression in the evening
and at night was also another characteristic included in the definition used. In the 1955 publication, clinicians observed that the
syndrome only appeared among obese persons. Since 1955, NES
has not been subjected to careful clinical study, but its prevalence
has been estimated at 1.5% in the general population.2 Twelve
percent of the obese patients in a nutrition clinic was found to
suffer from the Night Eating Syndrome3 and 27% and 28%, respectively, in 2 samples of severely obese persons.2,4 The Night
Eating Syndrome has so far not been included in any of the Diagnostic and Statistical Manuals of the American Psychiatric Association.
Figure 1. Twenty-four hour 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 p.m. and then greatly exceeds it (p <
.001). Daytime mood of the night eaters is lower than that of the
controls (p < .001) and falls even lower during the evening and night (p
< .001). Error bars represent SEM in all figures. NES indicates
night-eating syndrome.
Although night eating occurs among nonobese persons as well,
the prevalence seems to increase with increasing weight, from 7.9%
in a surgical sample5 to 8.9%3 and 15%6 in obesity clinics.
Between 1955 and 1995 little attention was given the Night
Eating syndrome. In 1995 Dr. Grethe Støa Birketvedt at the
University of Pennsylvania started to characterize the syndrome
in more detail.7 The study reported in the American Journal og
Medical Association in 1999 confirmed the elements of the night
eating syndrome previously reported, including morning anorexia, evening hyperphagia, and insomnia. It quantified the evening
hyperphagia, showing that food intake, which continued later
Sleep and Sleep Disorders: A Neuropsychopharmacological Approach, edited by Malcolm Lader, Daniel P. Cardinali
and S.R. Pandi-Perumal. ©2004 Landes Bioscience/Eurekah.com.
Sleep and Sleep Disorders: A Neurophychopharmacological Approach
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Figure 2. Daytime mood of the night eaters is lower than that of the
controls (p<.001) and falls even lower during the evening and night
(p<.001). Error bars represent SEs in all figures.
weight and normal weight night eaters and overweight and normal weight control subjects, matched for body mass index and
age. Unlike their usual nighttime eating, night eaters in the Clinical
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than that of obese controls subjects, was 2930 kcal compared to
2334 kcal for the control subjects (p < .055). In Figure 1 we have
shown that the cumulative caloric intake of the night eaters lagged
behind that of the obese control subjects, so that at 4:00 p.m.
they had consumed only 37% of their daily intake, compared to
74% by the controls (p < .001). The food intake of the controls
then slowed while that of the night eaters continued until after
midnight. During the period of 6:00 p.m. to 6:00 a.m., the night
eaters consumed 56% of their caloric intake, compared to 15%
for the control subjects (p < .001).
As also reported in the 1999 paper (Fig. 2), the mood of the
night eaters was lower than that of the control subjects during
the morning hours and fell significantly during the evening and
night. Furthermore, after 4:00 p.m. the mood of the night eaters
fell at a rate of 0.25 units per hour while that of the controls
remained unchanged.
The night eaters suffered from both sleep onset and sleep
maintenance insomnia, and the number of nighttime awakenings was 3.6 for the night eaters and 0.3 for the control subjects
(p < .001). Half of the 178 awakenings of the night eaters were
associated with food intake while none of the controls ate while
they were awake (Fig. 3).
The nighttime snacks of the night eaters were not binges, but
of only moderate size, averaging 271 kcal. The carbohydrate content of these nighttime snacks was 70% of the total caloric intake
compared to 47% for their food intake during the rest of the day
(p < .001). Furthermore, the carbohydrate to protein ratio of the
nighttime snacks was 7:1. This nutrient pattern, of a carbohydrate to protein ratio, increases the availability of tryptophan for
transport into the brain and conversion into serotonin with its
sleep promoting properties.8,9
The behavioral study was complemented by a neuroendocrine
study conducted in the Clinical Research Center of the University Hospital in Tromsø where subjects were admitted for 24-hour
periods.7 All subjects were women and consisted of both over-
Figure 3. Nighttime snacks of the night eaters and controls
Figure 4. Twenty-four-hour mean plasma melatonin levels in overweight
and normal weight night eaters and overweight and normal weight
controls. The single asterisk and bracket indicate a significant difference
(p<.001) in levels between the normal-weight night eaters and
normal-weight control group, and between the overweight night eaters
and the overweight control group. The 2 asterisks and bracket indicate
significant difference (p<.001) in levels between the normal-weight and
overweight control groups. NES indicates night eating syndrome.
The Night Eating Syndrome
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Figure 6. Twenty-four-hour mean plasma cortisol levels in subjects with
and without night-eating syndrome. The asterisk and bracket indicate
a significant difference between the levels of the 2 groups (p=.001).
Figure 5. Twenty-four-hour mean plasma leptin levels in overweight
and normal weight night eaters and overweight and normal weight
controls. Asterisks and brackets indicate significant differences in levels
of nocturnal concentrations (when compared with the baseline concentrations at 8 AM) between the night eaters and control subjects, both
overweight and normal-weight (p<.001).
Research Center received four meals of 300 kcal at 8:00 a.m.,
12:00 noon, 4:00 p.m. and 8:00 p.m.
Among night eaters, both overweight and normal weight, there
was a marked blunting of the plasma melatonin levels at night (p
< .001) (Fig. 4).
Plasma leptin levels were higher among the overweight subjects than among the normal-weight subjects (both night-eaters
and controls) (p<.001) (see Fig. 5). When compared with their
respective control groups, the rise in the nocturnal (12AM to 6
AM) plasma leptin levels was lower in both normal-weight and
overweight night eaters (p<.001). The time of the highest plasma
leptin concentration did not differ between the normal-weight
groups (p=.28) or between the overweight groups (P=.63).
Confirming the earlier clinical impression that the night eating syndrome was associated with stress, plasma cortisol levels of
the night eaters were higher than those of control subjects for
most of the 24 hours (Fig. 6).
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 in
a pattern that helps to link these findings with the behavior of the
night eaters. Thus, the blunting of the nighttime rise in melatonin may contribute to the sleep maintenance insomnia10 and to
depression.11
The failure of leptin to rise at night must limit its usual nighttime 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.
A later study6 has confirmed circadian aspects of the Birketvedt
et al study from 1999.7 Not only did night eaters consume a
greater part of their food intake during the latter part of the day
than controls, but their predisposition to eat later in the day was
confirmed by the greater consumption of a test meal. This study
also found elevated levels of depression in night eaters as assessed
by the Zung Depression Inventory.
In 2002 Birketvedt et al tested the hypothesis that night eaters
have an overexpressed hypothalamic-pituitary-adrenal axis with
an attenuated response to stress. They performed a 120-min
corticotropin-releasing hormone (CRH) test (100 ug i.v.) in female subjects suffering from the night eating syndrome, and
measured the plasma concentration of ACTH and cortisol. The
results showed that, in night eaters compared with controls, the
CRH-induced ACTH and cortisol response to CRH was significantly decreased (Fig. 7).
Sleep and Sleep Disorders: A Neurophychopharmacological Approach
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tions of an overexpressed HPA axis with a subsequent attenuation of the pituitary neuroendocrine response.
It is well known that night eaters experience wide variability
in frequency of symptoms. They can have periods when they
experience many awakenings and eating episodes, but also periods when these events are minimal.
The night eating syndrome appears to represent a new eating
disorder, different from the established disorders of anorexia
nervosa, bulimia nervosa, and binge eating disorders. It differs
from the latter two disorders in the frequency and size of ingestions
at night. The elevated plasma levels of cortisol reflect increased
activity of CRH, as expressed by an attenuated ACTH and cortisol response that may well explain the disrupted sleep and appetite pattern observed in night eaters. Several other disorders, such
as obesity, fatigue syndrome, anorexia nervosa, bulimia nervosa,
insomnia and depression, have been linked to disturbances in the
HPA axis. All of these disorders share some phenotypes with the
night eaters, such as mood disruptions, eating disorders, and sleeping disorders. Whether these clinical features are the result of
common pathophysiological mechanisms in the HPA axis remains
to be clarified and awaits further studies.
In conclusion, subjects suffering from night-eating episodes
have signs of disturbances in the HPA axis with an attenuated
ACTH and cortisol response to CRH. The mechanisms behind
the increased CRH stimulation may involve alterations in the
neurotransmitter system, causing increased nocturnal appetite and
disruption in the sleep pattern. This may, to some extent, explain
the disturbances in the circadian secretion of melatonin and leptin
and the behavioral characteristics of the night eating syndrome.
Differential Diagnosis
Figure 7. Effect of intravenous injection of corticotropin-releasing hormone (CRH) on plasma concentrations of ACTH in subjects with night
eating syndrome and healthy controls. Effect of intravenous injection of
CRH on plasma concentrations of cortisol in subjects with NES. Asterisks show difference from the control group.
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They concluded that disturbances in the
hypothalamic-pituitary-adrenal axis with an attenuated ACTH
and cortisol response to CRH were found in subjects with the
night eating syndrome.10
In night eaters, there are complex neuroendocrine characteristic changes, with attenuation in nocturnal secretions of melatonin and leptin and increased secretion of cortisol. An attenuated
response of ACTH and cortisol in plasma after injection of CRH
has also been described. Studies performed so far may indicate
that the night-eating syndrome is associated with an attenuated
pituitary-adrenal response to CRH.
A healthy response to acute stress is of great importance in our
daily physical and psychological challenges. This response is mediated from the hypothalamus to the pituitary gland, which in
turn mediates various neuroendocrine signals. When the stressor
is gone, the neuroendocrine responses are normally terminated.
Failure to terminate this response is observed in various condi-
The first step in defining a disease or disorder has been taken
in the case of the night eating syndrome: it is readily recognized
by persons manifesting the disorder and physicians are becoming
familiar with it. The differential diagnosis is with binge eating
disorder and “nocturnal sleep-related eating disorders”. It depends upon differences in the frequency and size of eating episodes and in the state of consciousness during them.
The night eating syndrome differs from binge eating disorder
in both the far greater frequency of nighttime awakenings and in
the modest size of the ingested food: 270 kcal during night-time
ingestions,7 compared to the 1300 kcal ingested during eating
binges reported by others.12 Furthermore, night eaters do not
appear to suffer to the same degree from the intense food, diet,
and body image disorders that characterize binge eaters.5
The night eating syndrome appears to differ also from the
“nocturnal sleep-related eating disorders” reported from sleep research clinics, often in association with sleep walking and
parasomnia states. A key distinction between the two disorders
lies in the extent of consciousness during the night eating. In the
sleep disorder clinic patients reported by Schenck and
Mahowald,13 84% of night eating occurred during total or partial unconsciousness and, for the majority, during stage 3/4 sleep.
By contrast, in their sleep disorders clinic,14 Manni, Ratti, and
Tartara reported that 5.8% of 120 persons referred for insomnia
manifested night eating during full consciousness. Finally Aronoff
et all reported in 1994 the only polysomnographic studies of a
subject who ate while fully conscious found that he awoke to eat
during stage II sleep. The prevalence of “nocturnal sleep- related
eating disorders” appears to be far lower than that of the night
eating syndrome noted above: 0.5%, or 38 cases out of approximately 8,000 polysomnographic examinations13 as reported by
The Night Eating Syndrome
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Prognosis and Treatment
Summary and Conclusions
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Information about prognosis in the night eating syndrome is
limited, confined to retrospective accounts. Researchers suggest
that it follows a chronic course, exacerbated by stressful life situations.
In contrast to the plethora of treatments that have been proposed for binge eating disorder, there have been no formal studies of the treatment of the night eating syndrome. 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 stress1. The blunted rise in
nighttime melatonin, suggests that provision of this agent at bedtime might be a reasonable option. Several night eaters have tried
to take melatonin at night with both successful and not successful results, and different food containing tryptophan has been
suggested. But neither one of the treatments proposed have a successful ending.
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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 traditional
behavioral weight reduction programs reduce binge eating and
body weight and are the treatment of choice. The diagnosis of
binge eating disorder may be most useful as a marker for the
psychological problems that frequently affect binge eaters and
that deserve treatment in their own right.
The relative ease with which the night eating syndrome can
be identified suggests that, when treatments are developed, they
may find ready acceptance. Anecdotal reports to the author from
night eaters who have explored treatment options suggest that
selective serotonin reuptake inhibitors have been helpful, as might
be expected from their effects on disturbances in mood and sleep.
In view of the lack of rise in nighttime melatonin, provision of
this agent at bedtime would seem a rational option.
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