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Revista de Psiquiatria do Rio Grande do Sul

Print version ISSN 0101-8108

Rev. psiquiatr. Rio Gd. Sul vol.31 no.3 Porto Alegre Sept./Dec. 2009 



Eating disorders and circadian eating pattern: a review



Fabiana BernardiI; Ana Beatriz Cauduro HarbII; Rosa Maria LevandovskiIII; Maria Paz Loayza HidalgoIV

ISpecialist, Member, Group of Human Chronobiology, Hospital de Clínicas de Porto Alegre (HCPA), Universidade Federal do Rio Grande do Sul (UFRGS), Master's degree student, Medical Sciences Program, School of Medicine, UFRGS, Porto Alegre, RS, Brazil
IIMaster's Degree, Member, Group of Human Chronobiology, HCPA, UFRGS, Professor, Universidade do Vale do Rio dos Sinos (UNISINOS), PhD student, Medical Sciences Program, School of Medicine, UFRGS, Porto Alegre, RS, Brazil
IIIMaster's Degree, Pharmacist and biochemist, Hospital Nossa Senhora da Conceição (HNSC), Porto Alegre, RS, PhD student, Medical Sciences Program, School of Medicine, UFRGS, Porto Alegre, RS, Brazil

IVPhD, Psychiatrist, Associate professor, Department of Psychiatry, School of Medicine, UFRGS, Department of Psychiatry, HCPA, UFRGS, Porto Alegre, RS, Brazil

Study conducted at Hospital de Clínicas de Porto Alegre (HCPA), Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brazil





This review aims at reviewing aspects related to eating disorders arising from changes in circadian rhythm. There was a systematic search in PubMed databases, using the following descriptors: eating disorders, circadian rhythm, night eating syndrome, binge eating disorder, and sleep patterns. Eating disorders, such as night eating syndrome and binge eating disorder, have been considered and related to a delay in circadian rhythm in food intake and impaired satiety. Circadian rhythms are those that show a period of 24 h, for example, sleep-wake cycle, body temperature, activity and eating behavior. Disorders related to changes in sleep-wake schedules influence the appetite, satiety and consequently food intake, which seems to increase such disorders. Circadian rhythm can influence eating behavior. However, more studies and knowledge about food rhythmicity might contribute to better understanding the current eating behavior, acting in prevention and/or treatment of eating disorders.

Keywords: Eating disorders, circadian rhythm, night eating syndrome, binge eating disorder, sleep patterns.




The etiopathogenesis of eating disorders is complex. The biological, psychological, and environmental factors that can affect the circadian rhythms have been considered to play a role in the development of disorders such as the night eating syndrome (NES) and binge eating disorder (BED).1 The hormone circadian rhythm alteration and the disorders caused by changes in sleep-wake cycle have an influence on appetite, satiety, and, as a consequence, on the eating intake,2 which seems to promote the development of these disorders.

Circadian rhythms, similarly to the sleep-wake cycle and the eating behavior, are managed by an internal clock, which is synchronized according to the 24-hour period. The circadian system is responsible for guaranteeing the synchronization between behaviors and physiological and molecular systems, controlling expressions of adipokines, enzyme activities, and the hormones responsible for controlling the eating process. Desynchronization of the circadian rhythms has been studied in eating disorders such as NES and BED, considered as clinical examples of dissociation in the circadian eating pattern and in satiety.3

NES has been related to a delay in the circadian rhythm of food intake, combined with depressed mood.4,5 It was first described by Stunkard in a group of obese patients who had similar characteristics such as morning anorexia, evening hyperphagia, and insomnia6 Current estimates indicate that 0.5 to 1.5% of the U.S. population has NES. In outpatient clinics for obesity care, these rates range from 6 to 14%, reaching 42% in patients who seeking surgery for obesity in h the USA.7 Psychiatric patients have a prevalence of 12%, regardless of their weight.8 NES has also been reported in 15% of the individuals seeking treatment for BED.9

BED was also described for the first time in the 1950s in a group of obese patients with difficulty to lose weight and that had an eating behavior similar to attacks of bulimia of patients with bulimia nervosa.10 In 1994, its diagnostic criteria were included in the Appendix B of the DSM-IV,11, characterizing the disorder by the intake of large amounts of food, followed by feelings of loss of control, sadness, and guilt after eating and lack of compensatory behaviors. The prevalence of BED is 2% in the general population. In clinical obesity, the rates range from 9 to 19% among obese patients and between 9 to 47% among patients for bariatric surgery.12

NES and BED occur more often in obese individuals, but also in individuals with normal weight and, therefore they may contribute to the development and maintenance of obesity. These disorders have been associated with delay in the circadian rhythm, impaired satiety, depressed mood, stress, low self-esteem, and psychiatric comorbidities.13,14

Taking into consideration the influence of circadian rhythm on eating behavior and development of eating disorders, the objective of this review was to describe concepts and findings related to the rhythm of eating patterns, as well as eating disorders resulting from changes in the circadian rhythm.



In order to achieve such objective, we carried out a systematic search of information in the MEDLINE (PubMed) database (1955-2009). To present the main topic of the present study, we based our search on experimental, observational and review studies, using the following keywords: eating disorders, sleep patterns, circadian rhythm, night eating syndrome, and binge eating disorder. The keywords were combined as follows: circadian rhythm and night eating syndrome, circadian rhythm and binge eating disorder, night eating syndrome and sleep patterns. The list of references of the selected studies was also used to find those articles deemed relevant. We selected the articles whose factors studied and outcomes were related to the scope of this review, only including those studies conducted in adults, written in English or Spanish.



Review of the literature

Night eating syndrome

NES is a clinical example of dissociation between eating and sleep patterns.3 It has been related to a delay in the circadian rhythm of food intake, which is combined with depressed mood.4,5 NES was first described in 1955 in a group of obese female patients. Stunkard reported that 64% of these patients showed evidence of morning anorexia, evening hyperphagia, and insomnia.6 Different criteria have been used over the years (Harb AB, Levandovski RM, Oliveira C, Hidalgo MP, Night eating syndrome:) a correlation study with body mass index and sleep and eating behavior, unpublished manuscript, 2008). However, the current criterion was established during the International Night Eating Symposium, held in April 2008,15 which defined the concept for the new diagnostic criteria of NES.

NES has been associated with changes in the eating pattern and neuroendocrine factors that are related to the circadian rhythms of endocrine secretions such as cortisol, melatonin, adipokines (leptin and ghrelin), and sleep disorders. Some studies have shown a decrease in melatonin during the night in patients with NES and have recorded reports of patients with difficulties to sleep or to fall asleep and stay asleep. Such responses lead us to consider that the reduction of melatonin may help to keep the individual with insomnia and a depressed mood.16 A study assessing night eaters and a control group showed that patients with NES have a reduction in the effectiveness and quality of their sleep and are more depressed than the control group.17

A study conducted with individuals with NES (obese and nonobese) and a control group showed a disruption in the circadian rhythm of melatonin, leptin, and cortisol. The levels of melatonin and leptin were lower at night in the night eater group than in the control group, and cortisol levels tend to be higher during the day in patients with NES.16 Low leptin levels at night may contribute to a lower inhibition of the night hunger urges that disrupt sleep, while the increased levels of cortisol may be related to these individuals' stress.18

NES was initially described as a response to the daytime stress typical of some obese individuals. Its symptoms were believed to decrease with stress relief.18 Glucose and insulin levels appear to be affected, increasing the risk for developing diabetes melito.16 A study conducted with night eaters and a control group showed that glucose and insulin levels increased more at night in night eaters; however, these are lower in the morning19 as a response to the consumption of large amounts of carbohydrates, since night eaters tend to eat mainly this nutrient in their night awakenings.16,20

A study showed that, in subjects with daytime habits, insulin tends to increase as a response to meals, whereas, in subjects with nighttime habits, insulin tends to be high for a longer period of time. In daytime subjects, peak glucose concentration was found after meal times (9 a.m., 3 p.m., and 9 p.m.), and peak insulin concentrations were similar to peak glucose concentrations, showing a rhythmic pattern of release, while in subjects with nighttime habits, peaks occurred at 12 a.m. and 9 p.m., and lasted up to 6 a.m. That is, the concentration of plasma glucose was significantly higher in the group with nocturnal lifestyle.21 Glucose and insulin have complementary circadian rhythms, but in night eaters its phases are late, demonstrating metabolic difficulties due to drinking at night, especially meals/snacks rich in carbohydrates.22

Ghrelin tends to be reduced at night in patients with NES. Decreased levels of ghrelin suggest that food intake decrease its levels, i.e., its concentration tends to be reduced after meals, and lower levels at night are a consequence of the increase in night eating.19 A recent study with night eaters and a control group, who were assessed in a laboratory for three nights, presented an advanced stage for the circadian rhythm of ghrelin, thereby promoting increases appetite. The study suggests that the influence of sleep deprivation, changes in eating behavior or changes in the pattern of insulin and/or glucose may interfere with the pace of disruption in the circadian rhythm of ghrelin.22

Among the behavioral factors involved in the NES, the main one are: time of energy consumption, mood levels during the time when they are awake, and the frequency of nocturnal awakening.23-25

Recent circadian analysis of food intake of individuals with NES have shown a significant delay of about 1.5 h during the phase of total calorie intake and consumption of nutrients such as carbohydrates and fats. These studies demonstrate that such individuals keep eating for a longer period of time during the night than the control group, experiencing a phenomenon that chronobiologists call phase delay.22,26 An observational study conducted in obese individuals with NES and a control group showed that the night eaters consume more daily calories, and 56% of their calorie intake occurs between 10 p.m. and 6 a.m.16 However, some studies have shown that the total daily calorie intake is similar to that of the control group and that the food intake at night is still higher among night eaters, demonstrating that they consume more calories during the period from 8 p.m. to 8 a.m. and a tendency to eat fewer calories from 8 a.m. to 8 p.m.3,19,26

It has also been found that night eaters wake up significantly more often during the night than the control group, and half of the awakenings includes food intake. In addition, this study showed that the average mood of the patients investigated was lower than the control group, with the significant finding that, in 24 hours, there was a decline in mood beginning late in the afternoon.16 Numerous studies have shown that obese night eaters have higher levels of depression and low self-esteem.5,7,13,27

The association between night eaters and obesity has been widely reported (Harb AB, Levandovski RM, Oliveira C, Hidalgo MP, Night eating syndrome: a correlation study with body mass index and sleep and eating behavior, unpublished manuscript, 2008).28 A recent study including 100 participants showed a correlation between night eaters and high body mass index (BMI). This study found that the NES may be a risk factor for obesity and, among obese people, there is a positive relationship between NES and weight gain (Harb AB, Levandovski RM, Oliveira C, Hidalgo MP, Night eating syndrome: a correlation study with body mass index and sleep and eating behavior, unpublished manuscript, 2008).

Prevalence estimates suggest that the NES is more common among obese individuals, but not all individuals with NES are overweight.20,29,30 Lundgren et al.,30 in a descriptive study with night eaters and a nonobese control group, showed that nonobese night eaters also have negative implications on their health, being associated with eating behaviors, mood, stress, and sleep disorders. There is no difference between obese and nonobese night eaters with regard to morning appetite, evening hyperphagia, sleep difficulties, and mood. The only difference is that nonobese night eaters are significantly younger and reported more difficulty to keep asleep, that is, they wake up more often and eat more at night. The authors also suggest the need of longitudinal studies with a larger number of participants to establish if night eating causes weight gain during long periods of time.

Binge eating disorder

Irregular patterns of eating behavior have also been observed in individuals with BED. In some studies, it has been related to overweight and obesity, which has an important role in health and body weight.

BED is characterized by the consumption of large amounts of food within up to 2 hours, followed by feelings of loss of control, sadness, and guilt after eating and lack of compensatory behaviors.31,32 In 1994, BED was included in the Appendix B of the DSM-IV11, as a disorder that needs further studies to be better characterized. It includes physiological abnormalities in the action of hormones that have an influence on food intake, such as insulin, leptin, ghrelin, among others.31,33

In the clinical practice, it has been observed that obese patients report stress as a factor for the onset of binge eating and other eating disorders. However, the mechanism for this relationship has not been clarified yet.31,35 A study assessing obese women with and without BED showed that baseline cortisol was significantly higher in individuals with BED.19 In a review of the literature, Gluck31 concluded that many studies link stress, cortisol, food intake, and abdominal fat. More recently, another study assessing levels of cortisol at night in obese women with and without BED showed that the presence of BED was not associated with increased levels of cortisol secretion. The limitation of this study may be the choice of the sample, classification of individuals, and sample size, limiting the power of the study to demonstrate the difference (beta error).32

Stress and negative emotions have been associated with alterations in the food intake of human beings. Peptides, such as leptin and ghrelin among others, may have an influence on food intake and regulation of stress response. The interaction between ghrelin and cortisol has been studied in human beings. A study assessing obese and nonobese patients with and without BED showed that stress can induce an increase in plasma ghrelin levels associated with serum cortisol.23 However, most studies show significantly lower fasting ghrelin levels and a slight decrease after meals in patients with BED.24,35-37

Some studies have reported increased leptin levels in obese patients with BED, suggesting that leptin may be a sensitive marker of metabolic changes in binge eating and that increased levels of this adipokine may be involved in the development and/or maintenance of the compulsive behavior.24,25 A study involving 30 obese women (BED and non-BED), with the purpose of assessing leptin levels and correlate data and eating attitudes, showed a positive relationship between increased levels of body fat and eating patterns, influencing the frequency of binge eating, increase in energy intake, and adipose tissue.25

The levels of glucose and insulin in BED are the same as in obese individuals,24 and high when compared to individuals with normal weight.33,38

BED occurs in normal-weight individuals, but it affects overweight or obese individuals and may contribute to the development and/or maintenance of obesity.39 Studies have also shown that night eaters may be compulsive. A literature review showed that night eaters with a subtype for BED and dual diagnosis have been associated with high BMI.5 Another study comparing individuals with BED, night eaters and a control group showed that those with BED and NES report more inappropriate behaviors and attitudes regarding the eating pattern and are more depressed than the control group.12

There are few controlled studies assessing BED and NES. A study has found higher levels of dietary restraint and eating problems in patients with BED and NES when compared to a control group. BED has been related to high levels of restriction of food intake, followed by moments of binge eating, showing an irregular eating pattern.12,13,31,40 Napolitano et al.13 compared the psychological and behavioral characteristics of individuals with BED, night eaters, individuals diagnosed with BED and NES and individuals without eating disorders, demonstrating that night eaters have less inhibitions than individuals with BED and that patients with both disorders reported higher anxiety. This study suggests that the two disorders may be associated with psychiatric comorbidity and reinforces the need for future studies.

It has been observed that changes in the food intake may induce delayed metabolic regulation22 and that circadian rhythms of sleep-wake cycle, hormones, appetite, and stress can be related to eating disorders and alter the levels and release pattern of components responsible for controlling the eating process throughout the day and, thus, promote changes in the eating pattern.

Circadian rhythm of food intake

The circadian rhythm of food intake is inherited and species-specific, since human beings are basically day-oriented. It is synchronized according to the light/dark cycle2, 41,42 and the levels of cortisol, serotonin, leptin, cytokines, among others.2,41 In addition, the social rhythm has a significant effect on the regulation of diet, since contemporary society works during 24 hours and its impact on the quantity and quality of food and eating times has been huge. As an example, we can mention the delayed meals in order to adapt to work hours.41

Circadian rhythms are those involving a 24-hour period such as, for instance, the sleep-wake cycle and the body temperature. The synchronization of these rhythms is carried out by the suprachiasmatic nucleus, located in the hypothalamus (central nervous system), which is responsible for the coordination of behavioral and physiologic rhythms.3 There are some situations in which there is a desynchronization of the rhythm, since food quantity and quality and meal hours seem to be determined by conditioned reflexes, routine, and a sensation that "it's time to eat". Meals would act as a Zeitgeber, German neologism that means "time giver", indicating that the meals would be determined by a social organization or synchronization of the biological rhythm. For most organisms, the most important Zeitgeber of the circadian rhythms is the light/dark cycle. However, other cyclical factors also act as synchronizers, such as, for instance, the social, temperature, and eating cycles. The Zeitgebers interfere with digestive and absorption functions, as well as with variations of the concentration of carbohydrates, amino acids, and lipids in the bloodstream during the day.2

Circadian and diurnal rhythms affect food intake. Many behaviors, including energy intake, vary in terms of level and intensity throughout the day in these processes. Recent studies have shown that the amount of calories of each meal, the post-meal intervals, and the satiety levels decrease during the day. Meal hours may be related to the total intake during the day. The results of these studies suggest that eating a higher amount of calories in the morning (or early in the day) may result in a decrease in the total intake during the day, while eating a great amount of energy at night can result in an increase in the total intake.43

The alteration in adipokine levels is considered an important mechanism that may change the pattern of food intake and lead to nutritional imbalances. The rhythm and synchronization of the secretion of these adipokines are important for the daily meal pattern. Studies indicate that a reciprocal rhythmic pattern between leptin and ghrelin establishes rhythm in the neuropeptide Y (NPY) system, which is the final common pathway for the expression of appetite in the hypothalamus. Thus, leptin inhibits both the secretion of ghrelin and the stimulation of the appetite by ghrelin, indicating that leptin is responsible for feedback communication between the periphery and the hypothalamus for the homeostasis of the body mass.44

Leptin is secreted by the adipose tissue. The central nervous system promotes the reduction of food intake and the increase of energy expenditure, in addition to regulating the neuroendocrine function and the metabolism of glucose and fats. The expression of leptin is controlled by several substances such as insulin, glucocorticoids, and proinflammatory cytokines. Thus, an increase in the leptin levels reduces food intake, while low leptin levels induce food intake.16,18 Leptin levels are increased at night in patients with diurnal habits and healthy weight.21

Insulin level, a hormone secreted by the pancreas, is stimulated by plasma glucose after meals. A study with individuals with diurnal habits demonstrated that peaks in glucose concentrations occurred at 9 a.m., 15 p.m., and 9 p.m., following the normal rhythm of meals (breakfasts, lunch, and dinner), while in individuals with nocturnal habits, glucose concentrations increased at night from 9 p.m. to 6 a.m.21

Ghrelin is first synthesized by the stomach and it is responsible for the increased secretion of the growth hormone (GH). It also acts in the control of energy expenditure, control of acid secretion and gastric motility, having an influence on the pancreatic endocrine function and glucose metabolism. It is involved in signaling the hypothalamic centers that regulate food intake and energy balance. Circulating levels of ghrelin are increased during long-lasting fasting and in a state of hypoglycemia, and their concentration decreases after meals.

The nutrients present in the meal, instead of their quantity, are responsible for the postprandial increase or decrease. Ghrelin levels decrease in the presence of carbohydrates and increase after the intake of proteins and lipids. These levels are influenced by changes in energy balance and has been shown that insulin may play an important role in the decrease of ghrelin after meals.45,46

Cortisol is a corticosteroid hormone produced by the adrenal gland. It is involved in the stress response and may have an important role in the eating behavior; in addition, it is associated with increased energy intake in healthy subjects.47 The production of cortisol has a circadian rhythm that depends on the stimulation of the adrenocorticotropic hormone (ACTH). Its level is high close to the beginning of daily activities, decreasing throughout the 24-hour period.

Sleep-wake cycle and eating behavior

The sleep-wake cycle is one of the most often studied rhythms; the regulation of most of the behaviors and physiological activities depends on falling asleep or waking up.47 The main hormone involved in sleep-wake cycle is melatonin, and to fall asleep is a sign of secretion, that is, it starts to increase in the evening and to decrease at dawn. Sleeping conditions can have an influence on melatonin secretion. A study conducted in subjects with nocturnal showed a decrease in the production of melatonin.21 The decreased levels of melatonin have been associated with impaired sleep, depression, and NES.16

A partial sleep deprivation appears to influence the levels of several hormones. Studies have shown that sleep restriction for a few days is enough to cause an increase in glucose levels and decreased insulin action, showing that long periods of sleep disturbance may be a risk factor for the development of diabetes mellitus. Sleep deprivation also resulted in lower levels of leptin, increased levels of ghrelin, cortisol and apetite.47 Under normal sleeping conditions, leptin and ghrelin levels are increased while the individual is asleep,44, while cortisol levels tend to be lower at night, getting higher early in the morning.

The increase in appetite and the preference for more caloric foods seem to be present in sleep deprivation. A nocturnal eating pattern rich in carbohydrates increases the transport of tryptophan to the brain, converting it into serotonin and resulting in less difficulty to fall asleep.16 A study showed that the appetite for nutrients containing high amount of carbohydrates, including sweets, salty biscuits, and tubercles increased from 33 to 45%, but the appetite for fruits, vegetables, and foods with high amounts of protein was slightly affected.44 Lennernas et al.48 observed a strong preference for the consumption of fast food and caloric meals during working hours in night-shift workers.



Our review of the literature evidences the influence of circadian rhythms and the importance of several regulatory hormones for the feeding behavior and development of eating disorders. Neuroendocrine and behavioral changes are present in eating disorders, and a delay in the circadian rhythm of food intake and impaired satiety can lead to the development of eating disorders, such as NES and BED, being associated in many studies with high BMI, depressed mood, stress and anxiety.

Rhythm and timing in the secretion of regulatory hormone levels are important for the daily meal pattern, changing the pattern of food intake and resulting in nutritional imbalances. Studies indicate that a reciprocal rhythmic pattern between leptin and ghrelin establish a rhythm for the expression of appetite. Thus, leptin plays a role in the feedback communication between the periphery and the hypothalamus to the homeostasis of body mass. Since sleep alterations also resulted in lower levels of leptin, increased ghrelin levels, cortisol and increased appetite and the preference for more caloric foods. Decrease in the production of melatonin, associated with sleep restriction and increased levels of glucose and decreased insulin action, was also observed in the studies, resulting in desynchronization of the eating rhythm. Changes in the food intake may induce delay in metabolic regulation of circadian rhythms and they were related to eating disorders such as NES and BED, which may contribute to the development and maintenance of obesity.

However, current studies do not define whether factors such as BMI, stress, and mood are cause or consequence of the eating disorder. Prospective studies with larger number of participants, control of confounding factors, use of validated instruments, consensus on diagnostic criteria, inclusion of the NES on DSM,49 and use of appropriate questionnaires, such as the Night Eating Questionnaire (NEQ) 50 and the Binge Eating Scale ( BES), 51 translated and validated for the Brazilian population are still needed to elucidate this relationship. Thus, there is need of further research to elucidate the study of circadian rhythms in the eating behavior and to increase knowledge in this area, contributing to a better understanding of the current feeding behavior, acting in the prevention and/or treatment of eating disorders.



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Maria Paz Loayza Hidalgo
Castro Alves, 167/204
CEP 90430-131, Porto Alegre, RS, Brazil

Received Jul 1, 2009.
Aceito em 16/09/2009.



There are no conflicts of interest associated with the publication of this manuscript.

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