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Keywords:

  • binge eating disorder;
  • night eating syndrome;
  • non-normative eating patterns

Abstract

  1. Top of page
  2. Abstract
  3. Acknowledgment
  4. References

Binge eating disorder (BED) and night eating syndrome (NES) are putative eating disorders frequently seen in obese individuals. Data suggest that BED fulfills criteria for a mental disorder. Criteria for NES are evolving but at present do not require distress or functional impairment. It remains unclear whether BED and NES, as they are currently defined, are optimally useful for characterizing distinct patient subgroups. We propose that a distinction be made between “eating disorders” and “non-normative” eating patterns without associated distress or impairment. Although non-normative eating patterns may not be considered mental disorders, they may be very important in terms of their impact on body weight and health. More precise behavioral and metabolic characterization of subgroups with eating disorders and non-normative eating behaviors has important implications for understanding the etiology, pathophysiology, and treatment of obesity. Ultimately, better understanding of the many pathways to increased energy intake may lead to targeted strategies for prevention of overweight and obesity in at-risk individuals and populations.

Eating disorders and disturbed eating patterns are often associated with obesity. Aberrant eating behaviors that result in an imbalance between energy intake and energy expenditure not only contribute to excess weight gain but may also be associated with psychological distress. Although research has been inconsistent regarding whether obesity leads to disturbances in eating (1, 2, 3) or disordered eating is a risk factor for the development of obesity (4, 5), many obese individuals presenting for weight loss treatment report non-normative eating patterns. Atypical eating patterns may result in poor treatment outcome (6, 7, 8). Thus, understanding the characteristics of eating behaviors that may contribute to the development of obesity or complicate weight loss efforts is imperative for developing effective prevention and treatment strategies.

Binge eating disorder (BED)1 and night eating syndrome (NES) are putative eating disorders frequently associated with obesity. The criteria for BED are included in the Appendix to the DSM (DSM-IV-TR) (9) as a category for further research and involve a pattern of recurrent binge eating and distress temporally associated with the behavior (Table 1). NES, first described by Stunkard in 1955 (10), has been characterized as a syndrome that includes morning anorexia, evening hyperphagia, and insomnia (11). The initial description of NES noted that the syndrome was most prominent during periods of life stress (10), although more recently proposed criteria do not include a stress requirement. Sleep researchers also describe a “nocturnal sleep-related eating disorder,” with only partial consciousness during the eating episodes (12). In contrast, individuals with NES are sufficiently awake and cognizant of their nighttime eating episodes. The diagnostic criteria for NES are evolving, and no accepted criteria have been proposed in the DSM-IV-TR. As a result, studies have often used differing definitions of night eating, making comparison among studies difficult. Table 1 shows one proposal for diagnostic criteria (11, 13).

Table 1.  Research criteria for BED and NES
BED (9, 13)
 A. Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following:
  (1) Eating, in a discrete period of time (e.g., within any 2-hour period), an amount of food that is definitely larger than most people would eat in a similar period of time under similar circumstances
  (2) A sense of lack of control over eating during the episode (e.g., 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 a week for 6 months.
 E. The binge eating is not associated with the regular use of inappropriate compensatory behaviors (e.g., purging, fasting, excessive exercise) and does not occur exclusively during the course of anorexia nervosa or bulimia nervosa.
NES (5) includes all of the following:
 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 3 nights a week
 D. Frequent consumption of snacks during the awakenings
 E. The pattern occurs for a period of at least 3 months

Despite a wealth of data on BED and a developing literature on NES, whether these syndromes will be elevated to the status of full psychiatric disorders has yet to be determined. Many individuals with eating disorders are categorized as having eating disorder not otherwise specified (EDNOS), which encompasses patients with a broad scope of eating disordered symptoms. Individuals with EDNOS range from those who engage in chewing and spitting food to those who present with more typical eating disorder symptoms but fail to meet full criteria for anorexia nervosa, bulimia nervosa, or BED (e.g., frequency of binges is too low or binge size is too small). At present, BED is classified as an example of EDNOS.

The DSM-IV-TR states that a mental disorder “is conceptualized as a clinically significant behavioral or psychological syndrome or pattern that occurs in an individual and that is associated with present distress (e.g., a painful symptom) or disability (i.e., impairment in one or more important areas of functioning) or with a significantly increased risk of suffering death, pain, disability, or an important loss of freedom (p. xxxi).” To date, research on BED supports many of these requirements. Individuals with BED suffer from more impaired social functioning, higher levels of disabilities, lower quality of life, and poorer physical health than those without an eating disorder (14, 15), in addition to eating and weight-related psychopathology at levels similar to those with bulimia nervosa (16, 17, 18, 19). Moreover, although recurrent binge eating in obese persons has been consistently associated with Axis I (psychiatric disorders such as depression and anxiety disorders) and Axis II (personality disorders) diagnoses (20, 21, 22, 23), individuals with BED may have higher rates of distress and impairment than controls even after controlling for co-occurring psychiatric disorders (14).

Despite an abundance of data indicating that the proposed BED diagnosis meets the DSM-IV-TR criteria of a clinically significant syndrome with associated distress, impairment, or disability, studies regarding its course and treatment cast doubt on the validity of the current definition of BED. One community study found that BED and subthreshold BED may remit on their own in a substantial percentage of cases (24). However, preliminary results from a longitudinal study examining only persons meeting full criteria for BED found that the disorder tends to persist until treated (25). A potential explanation for these discrepant findings may be that participants in the former study were younger and less obese, whereas those in the latter study were more characteristic of individuals presenting for BED treatment (26). Thus, the current definition of BED may be unsuited to capturing a consistent syndrome. Furthermore, BED appears to be responsive, at least in the short term, to a broad range of treatments (27), as well as placebo (28), further suggesting that its definition is in need of greater specificity. However, there is some additional evidence for differential response between binge and nonbinge eaters to weight loss treatments, which may be mediated by affective state (26). Thus, the question at hand should be not whether binge eating in obese persons describes a clinically significant syndrome that meets the requirements of the DSM-IV-TR, but rather how the criteria for BED as currently defined should be modified to better describe individuals with a persistent maladaptive behavioral pattern associated with functional impairment, distress, and potential disability.

Research on NES is still in its infancy. Limited data suggest that overweight individuals with NES suffer from lower mood and neuroendocrine disruption, including attenuation of the nocturnal rise plasma melatonin and leptin and higher circadian levels of plasma cortisol compared with overweight controls without NES (11). Another study of persons seeking weight loss treatment found that those diagnosed with NES had lower self-esteem, higher depression scores, and poorer response to weight loss treatment compared with those without NES based on data collected by self-report questionnaires (6). Although the literature on NES focuses primarily on obese individuals, one study comparing NES in obese and nonobese samples found few qualitative differences between groups (29). However, compared with obese participants, the nonobese group was significantly younger in age, suggesting that NES may contribute to the development of excess weight gain.

Because NES and BED often share an association with obesity, some studies have examined both disorders within the same samples. Although Stunkard and colleagues found little overlap between participants with NES and BED (30), other studies have found that ∼16% of weight loss treatment-seeking adults meet criteria for both disorders (31, 32). Grilo and Masheb found that among individuals with BED, 28% reported nighttime eating (NE), broadly defined as “waking up at night and eating,” and that more men than women reported NE (33). Moreover, those with NE and BED had higher BMIs than those with BED alone. In comparing individuals with NES [defined by Stunkard's 1996 criteria (13)], BED, and both disorders, Napolitano et al. found that those with both NES and BED had higher state anxiety than those with NES alone and that BED patients had greater disinhibition than those with NES (31). These findings are not surprising given that the criteria proposed for NES have no requirement that loss of control be present during episodes of nighttime eating. Moreover, the construct of loss of control, as opposed to the amount of food eaten, has been suggested as the more salient component for identifying those with BED's associated psychopathology and adiposity in adult and child samples (34, 35, 36, 37). For example, in a study of overweight and normal-weight children, we found that those endorsing loss of control eating, regardless of whether the amount of food eaten was contextually large, experienced greater eating disordered cognitions and more adiposity compared with children overeating without experiencing loss of control (37). Future studies of NES would benefit from an assessment of loss of control during night eating episodes because the presence of loss of control may distinguish individuals with clinically meaningful NES from those whose culture (38) or peer groups (e.g., college students) render the NES pattern of eating normative. Table 2 shows a comparison of the key criteria proposed for BED and NES.

Table 2.  Comparison of key diagnostic criteria for BED and NES
Domain assessedBEDNES
Eating Behaviors (e.g., amount of food, duration of eating, time of eating)YesYes
Distress or impairmentYesNo
Loss of controlYesNo
Hunger/anorexiaYes (nonessential criterion)Yes
Frequency of eating episodesYesYes (number not specified)
Duration of symptomsYesYes

It remains unclear whether BED and NES, as they are currently defined, are optimally useful for understanding etiology, pathophysiology, or prognosis, including response to weight loss treatments or psychotherapy. Researchers have addressed this issue with regard to BED. In a recent paper, Devlin et al. (39) considered four different models to describe BED: BED as a distinct eating disorder, BED as a variant of bulimia nervosa, binge eating as a behavioral subtype of obesity, and binge eating as an associated feature of an eating disorder. They noted that a core psychological feature of all eating disorders across the weight spectrum is body image distress and over-evaluation of weight and shape, which has been found consistently to be greater in obese persons with BED than in those without BED. In their literature review, the authors found that BED does differ from purging bulimia nervosa but that it is not a useful behavioral subtype of obesity due to lack of evidence for a differential response to obesity treatment outcome. In another paper, Vandereycken proposed criteria for “overeating overweight disorder” that like anorexia nervosa, but unlike bulimia nervosa, is diagnosed based on body weight status (BMI ≥ 25) and a preoccupation with shape and weight and recurrent overeating (40). Cooper and Fairburn recommend refining the current BED criteria by placing BED in a similar time frame (3 months) as anorexia nervosa and bulimia nervosa, emphasizing that a “definite sense of loss of control at the time of eating, rather than retrospectively inferred lack of control” be present, and by setting limits on the number of compensatory behaviors in response to the binge episodes to clearly distinguish BED from nonpurging bulimia nervosa (41). Additionally, there may be subgroups of patients with BED characterized by low or high negative affect, with high levels of weight and shape concerns and other comorbid mental disorders in the latter group (26, 42, 43, 44). This “dieting/negative affect” subgroup may have poorer response to eating disorder or weight loss treatment and could potentially benefit from psychotherapy targeted to the negative affect (26). However, whether binge eating is really a marker for associated psychopathology in obese individuals, rather than a central feature of an eating disorder requiring specific treatment, remains controversial (39).

Further research is required to refine the diagnostic criteria for eating disorders in obese individuals. To assess the clinical significance of these mental disorders adequately, criteria should ideally be based on variables that relate to distress and functional impairment associated with the non-normative eating. Variables such as the time of eating, size or length of the eating episode (e.g., “large amount of food in a discrete period of time”), or macronutrient composition of the episodes may be useful constructs only as they relate to better characterizing a distinct affected population. For example, proposed diagnostic criteria for NES require frequent awakenings with snack consumption during the awakenings, consumption of at least 50% of daily caloric intake in snacks after the last evening meal, and morning anorexia, but not distress or impairment (13). Furthermore, even within the population meeting criteria for an eating disorder based on behavioral variables, there may be differences in outcome based on factors not previously considered, such as genetic variation. For example, polymorphisms of the melanocortin 4 (MC4) receptor have been identified in one study as being associated with binge eating (45). In that same population, a preliminary analysis found that patients with BED who had an MC4 receptor polymorphism had less robust weight loss in response to bariatric surgery than patients with BED who did not have an MC4 receptor variant (46). Another preliminary study found decreased dopamine D2 receptor availability, as measured by positron emission tomography scanning, in obese individuals relative to normal-weight controls (47), suggesting a potential role for alterations in dopaminergic circuits as either a cause or a consequence of obesity. Thus, our emerging understanding of the complex biology of body weight regulation will need to be integrated into clinical research on human behavior to better define and characterize obese persons.

We believe that it may be useful to differentiate eating disorders from disordered, or non-normative, eating. Non-normative eating behaviors, such as objective overeating episodes without loss of control, eating in the absence of hunger, irregular meal patterns, or continual grazing have been understudied for their role in energy balance. Although non-normative eating that does not cause distress or impairment should probably not be considered a mental disorder, such eating patterns may be a contributing factor to inappropriate weight gain and the development of obesity or, alternatively, may protect against obesity development. For example, constant grazing may be associated with weight gain in some individuals. By contrast, persons who eat small, frequent meals as opposed to three large meals may protect themselves from inappropriate weight gain.

Emerging knowledge regarding the impact of brain, gut, adipocyte, and other biological factors, acting peripherally or centrally, provides an exciting opportunity for those engaged in clinical behavioral research to form partnerships with those studying more basic aspects of weight regulation. Studies should investigate not only the biological basis for behavior but also the potential impact of behavior on biology. For example, recurrent binge eating may increase stomach capacity (48), which might alter gastrointestinal responsiveness to intrinsic signals for satiation or satiety. Cohort, intervention, and laboratory studies designed to assess more precisely the relationships among mood, cognitions, appetite, types and patterns of food intake, and biological factors may lead to useful clinical criteria that meaningfully identify subgroups with consistent behavioral and physiological phenotypes. Table 3 proposes some variables that may be useful in characterizing eating patterns in these types of studies.

Table 3.  Research variables characterizing eating disorders and non-normative eating among obese persons
Behavioral variables
 1. Amount of food eaten during meals and snacks
 2. Context (e.g., alone, at an occasion, restaurant, time of day)
 3. Hunger
 4. Satiety
 5. Satiation
 6. Fullness
 7. Rate of eating
 8. Physical state (e.g., tired, alert)
 9. Energy intake
 10. Macronutrient composition
 11. Emotional experience surrounding eating by assessing
  a. Cognitive stimuli
  b. Affective stimuli
  c. Experience or lack of experience of loss of control
  d. Feelings before (e.g., anger, loneliness), during (e.g., “numbing out,” shame), and after (e.g., disgust, calmness)
 12. Eating in the absence of hunger
 13. Eating following dietary restriction
 14. Eating after ingesting a food prohibited on diet
Assessment of biological variables
 1. Neuroendocrine, hormonal, or metabolic (e.g., ghrelin, Peptide YY, leptin, insulin, cholecystokinin)
 2. Functional neuroimaging (e.g., positron emission tomography scanning, functional magnetic resonance imaging)
 3. Genetic (e.g., polymorphisms in genes involved in melanocortin signaling)
 4. Gastrointestinal physiology (e.g., stomach capacity; impact of malabsorptive vs. restrictive surgical procedures on appetite)

More precise behavioral and metabolic characterization of subgroups with both eating disorders and non-normative eating has important implications for understanding the etiology, pathophysiology, and treatment of inappropriate weight gain and obesity. Ultimately, better understanding of the many pathways to increased energy intake may lead to targeted strategies for prevention of overweight and obesity in at-risk individuals and populations.

Acknowledgment

  1. Top of page
  2. Abstract
  3. Acknowledgment
  4. References

We thank Michael J. Devlin, Carlos M. Grilo, and Jack A. Yanovski for their thoughtful review and helpful comments. This work was supported by Grant ZO1 HD-00641 from the National Institute of Child Health and Human Development, NIH, Department of Health and Human Services.

Footnotes
  • 1

    Nonstandard abbreviations: BED, binge eating disorder; NES, night eating syndrome; EDNOS, eating disorder not otherwise specified; NE, nighttime eating; MC4, melanocortin 4.

References

  1. Top of page
  2. Abstract
  3. Acknowledgment
  4. References