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Case Report

Night Eating Syndrome Presenting as Anorexia in an Athlete

Case Report and Review

Trojian, Thomas H.; Jow, Veronica

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Current Sports Medicine Reports: July 2009 - Volume 8 - Issue 4 - p 182-185
doi: 10.1249/JSR.0b013e3181ae53bb
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INTRODUCTION

Night eating syndrome (NES) was first described by Stunkard in 1955 as "morning anorexia, evening or nocturnal hyperphagia in a fully conscious state, and insomnia" (21). Over time, the syndrome has been further characterized to distinguish it from other forms of nighttime eating. Although some debate still exists, NES encompasses a few key behaviors, including evening hyperphagia (or late night eating before initiating sleep) and eating after awakening from sleep (night eating) either in a fully or semi-conscious state (11). This is in contrast to binge eating disorder (BED), which describes episodes of consuming large quantities of food in discrete time periods without control (23), or sleep related eating disorder (SRED), which refers to involuntary nocturnal eating, often of bizarre foods or inedible items, that occurs after awakening (25). Late-night eating also can be found in other diagnoses, such as bulimia nervosa or dissociative disorders, but in these cases it is usually a part of a group of symptoms rather than the central problem.

The hallmark of NES is a delay of caloric intake until the evening and night hours. Birketvedt revealed that night eaters consume 56% of their daily caloric intake between the hours of 8 p.m. and 6 a.m., compared with 15% by control subjects (5). The foods consumed during episodes of evening hyperphagia and night eating tend to be carbohydrate-rich (7), with a high carbohydrate to protein ratio of 7:1. Nighttime awakenings are common among night eaters, and >50% of these episodes were associated with food intake, compared with 0% in control subjects (5).

CASE PRESENTATION

A 19-yr-old college softball player was referred to a sports medicine clinic by her team's strength staff and teammates for not eating during the daytime and a concern for possible anorexia nervosa. For most of the day, she reported a lack of appetite until approximately 3 p.m., when she ate her first meal. A teammate reported her to be seen pushing her food around the plate and not eating. She attempted to restrict calories during meals because of a bloated feeling in the morning. She denied binging or purging activities. She was seen 3 months earlier by another physician for a complaint of insomnia. She denied difficulty with initiating sleep, but experienced frequent nighttime awakenings, on average three to four times in one night. She had one roommate, and she denied excessive noise, poorly regulated temperature, or light disturbances. She did not discuss her nighttime eating with that physician. She also denied nightmares or night terrors. She had attempted over-the-counter sleep aids without improvement in her symptoms. She was started on zolpidem tartrate, which did not diminish the number of awakenings. Upon each awakening she would consume a snack, consisting of carbohydrate-rich foods, such as cookies or crackers, frequently more than 1000 calories over the night. Although she tried to refrain from eating, she felt unsatisfied and unable to reinitiate sleep until consuming food. Generally, she reported being conscious while eating. However, at times she only would become aware of the episodes by the food wrappers surrounding her bed the next morning. After eating she easily returned to sleep, but reawakened 1-2 h later. Her roommate reported having her personal food confiscated by the patient at night and engaging in conversations that the patient could not recall the following day. The following morning after an episode, she experienced a moderate amount of guilt related to her eating and modest weight gain of approximately 7 lb. She admitted to a mildly depressed mood and intermittent anhedonia. She reported anxiety related to increased life stressors over the past few months associated with softball, classes, and a new relationship. She denied having difficulty concentrating or a decline in academic work. However, she noticed decreased endurance and performance during softball practice and competitions, especially with morning activities during which she felt tired, bloated, and groggy. By not eating for most of the day, she often lacked enough energy to complete an entire afternoon practice. She denied suicidal or homicidal ideation. At the time of the visit about eating disorder concern, she was no longer taking any medication or supplements. She denied a personal or family history of eating disorders. A complete review of systems was otherwise negative. Upon examination, vital signs were normal; height was 5'6," and weight was 160 lb. The physical and psychiatric exams were unremarkable. Her Zung depression scale score was 24, and her night eating questionnaire score was 49.

EPIDEMIOLOGY

Although NES was described initially in the obesity literature, it is not limited to this demographic. The syndrome's prevalence among the general population is estimated at 1.5% (19). Up to 8.9% of obesity clinic patients meet the criteria for NES (16). However, the diagnostic patterns do not appear to be different for obese and non-obese individuals with NES (7). A recent study investigating familial aggregation showed that individuals with NES were more likely to have an affected first-degree relative than control subjects (OR = 4.9) (13).

Recently, the link between psychiatric illness and NES has become of interest because of its association with stress and depression. Lundgren et al. found that 12.3% of patients in an outpatient psychiatric clinic met the diagnostic criteria for NES and that these patients had a higher rate of substance abuse and atypical antipsychotic use than patients without NES (12).

DIAGNOSIS

As NES is not included in the Diagnostic and Statistical Manual of Mental Disorder (DSM-IV), variance in diagnostic criteria is widely seen in both past and present studies. In a recent evaluation of diagnostic criteria, Allison et al. report that the definition of night eating has ranged from 7 p.m. to 11 p.m. to the more general "after the evening meal," while the proportion of total calories consumed has varied from 25% to 50% (2). These inconsistencies create some difficulty in generalizing investigational results to the general population, as well as clearly identifying whether a patient meets criteria for the actual syndrome or is a variant of normal. In reality, many people have episodes of late-night eating, and in households that often spend evenings watching television, after-dinner snacking may be the norm. In addition, there is variation in the average dinnertime among cultures, with the average person in the United States eating between 5 p.m. and 7 p.m., while the average person in Europe has dinner between 8 p.m. and 10 p.m.

The question of whether to include NES in the DSM-V has prompted further investigation into the diagnostic tools and criteria currently used. In an attempt to assess two screening instruments, Vander Wal et al. found that use of a single simple screening question had adequate sensitivity but poor specificity to identify patients correctly with NES (24). Additionally, while the NEQ was correlated positively with increasing diagnostic detail, there was an inability to achieve both high sensitivity and specificity with varying cut points. Vander Wal concluded that the difference between eating late at night versus waking from sleep to eat might be the key to distinguishing NES as a true pathologic state. By evaluating several items from the Night Eating Questionnaire (NEQ), Allison et al. found that three items appear to be core aspects of the disorder: 1) evening hyperphagia and/or nocturnal eating, 2) initial insomnia, and 3) awakenings from sleep (4).

Their analysis suggests that the presence of morning anorexia and a delayed morning meal added little additional information.

The NEQ has evolved alongside research to characterize NES. Developed as a standardized screening tool for diagnosing NES, the current version is a 14-item questionnaire that addresses both behavioral and psychological aspects of the syndrome. The questions investigate the following aspects of NES: morning hunger and timing of first food consumption, cravings, control over eating before bedtime and during nighttime awakenings, percentage of post-dinner food consumption, initial insomnia, frequency of awakenings, associated food consumption during awakenings and awareness during these episodes, and mood disturbance (4). By varying the cut score, Allison et al. calculated that a positive predictive value of up to 77% can be attained (2). While the NEQ has been shown to be an efficient and valid measure of the severity of NES, its primary use is as a screening tool and it should not replace clinical interview for diagnosis.

PATHOPHYSIOLOGY

In general, it has been recognized that the pattern of intake rather than the total calories ingested is different in NES subjects compared with controls (17). NES has been linked to changes in the circadian rhythm and disturbances in the hypothalamic-pituitary axis (HPA). Therefore, NES has been described as delayed circadian eating patterns superimposed upon normal sleep-wake cycles (17). An inpatient study by Allison et al. showed a decrease in overnight ghrelin levels, a stomach-derived appetite stimulant, compared with control subjects, whereas insulin and glucose increased at night (1). No difference was found in secretion of thyroid stimulating hormone (TSH), melatonin, leptin, cortisol, or prolactin. In comparison, Birketvedt et al. found attenuated secretions of nocturnal leptin (an adipocyte-derived appetite suppressant) and melatonin, whereas cortisol was increased (5).

In a small study comparing the response to corticotropin-releasing hormone among people with NES and control subjects, an attenuated response of adrenocorticotropic hormone (ACTH) and cortisol release was observed, suggesting an overexpressed HPA (10). The authors interpret this finding to be a result of the constant stressful stimuli to which people with NES are exposed, but they note that, alternately, it may be a direct result of a fasting state. They hypothesize that the behaviors of disordered sleep and increased nighttime appetite may be related directly to the neurotransmitter alterations that are caused by an increase in corticotropin-releasing hormone (CRH) stimulation.

Based upon the observed caloric intake and neuroendocrine assays in a study of 15 women with NES and 14 control subjects, Goel et al. theorized that NES might represent dissociation between a central timing mechanism in the suprachiasmatic nucleus and other presumed regulator systems in the central nervous system, stomach, or liver (9). Again, the question of causality arises in interpreting whether the observed differences in ghrelin, leptin, melatonin, insulin, and glucose amplitudes and timing are altered independently compared with control subjects or are results of the abnormal behaviors of nocturnal waking and eating.

TREATMENT

Researchers have explored several pharmacologic and nonpharmacologic therapeutic options for NES, including serotonin reuptake inhibitors, topiramate, cognitive behavioral therapy, relaxation training, and light therapy. Lundgren et al. demonstrated elevated binding of midbrain serotonin transporters, which may amplify the reuptake of serotonin and impair postsynaptic serotonin transmission (14). This theory can explain why selective serotonin reuptake inhibitors (SSRI) are useful in treating individuals with NES. Early studies and case reports related reduction in night eating episodes and decrease in overall caloric intake to both short-term (2 wk) (15) and long-term (6-15 months) (20) SSRI use.

In an 8-wk randomized, placebo-controlled study of sertraline for NES, 12/17 in the sertraline group responded to therapy compared with 3/17 in the control group (16). Seven of the 12 responders in the sertraline group had a remission or complete resolution of symptoms, compared with one of the three responders in the control group. This study was different than previous SSRI trials because it included a small number of normal weight subjects. Of these, two of the three in the sertraline group responded, compared with zero of three in the control group. Participants in the study group had a 30% chance of responding at 2 wk and a 50% chance of responding between weeks 4 and 8. Overall, the sertraline group had a significant reduction in the symptoms of NES, including a reduction in nocturnal ingestions (80%), lower caloric intake after the evening meal (32.5%), and weight loss (approximately 1 lb·wk−1). The changes in night eating did not correlate with changes in depressive symptoms, which were modest at baseline.

Because individuals with NES report greater levels of depression and anxiety in addition to displaying evidence of elevated stress (increased cortisol and CRH), Pawlow et al. designed a study to evaluate effects of relaxation training (18). The study focused upon the short-term effects on a group (N = 10) randomized to abbreviated progressive muscle relaxation technique (APRT) compared with control subjects (N = 10). Participants in the APRT group reported lower levels of anxiety and stress and higher levels of relaxation immediately after a session, which correlated to lower levels of salivary cortisol. After 7 d of home practice, the significant decrease in levels of anxiety and stress persisted in the APRT group compared with control subjects. The relaxation group also had a significant increase in morning appetite and decrease in evening appetite rating, but had a nonsignificant decrease in days with post-bedtime eating.

Bright-light therapy has been suggested as a therapy for weight loss in obese subjects (6). A case report of an obese woman with NES demonstrated resolution of night eating symptoms when exposed to light therapy, in addition to decreased depression scores (8). NES symptoms recurred when light therapy was discontinued. Light therapy's ability to alter the circadian pattern changes seen in NES may explain this therapeutic observation.

DISCUSSION

We used the following provisional criteria outlined by Birketvedt (1999) (5) to diagnose our athlete with NES: 1) morning anorexia, even if breakfast is eaten; 2) evening hyperphagia, in which >50% of daily energy intake is consumed after the evening meal; 3) awakenings at least once per night; 4) consumption of snacks during awakenings; 5) repetition of provisional criteria longer than 3 months; and 6) does not meet the criteria for bulimia nervosa or binge eating disorder.

To our knowledge, there have been no studies or case reports focusing upon NES in the athletic population. However, there is a well-accepted association between sports participation and eating disorders. While determining the true prevalence in athletes has been difficult, one Norwegian study estimated that 13.5% of elite athletes have eating disorders, defined as anorexia nervosa, bulimia nervosa, and eating disorder not otherwise specified, compared with 4.6% in the control population (22). Our patient was diagnosed before the Allison et al. (2009) proposed diagnostic criteria for night eating syndrome (3). Our patient fulfilled these criteria as well as the older Birketvedt criteria.

With regard to NES, there are specific issues to consider in the athletic population. First, although morning anorexia may exist, athletes may force themselves to eat breakfast to meet the energy demands of early morning practice or competition. Similarly, athletes may appear to have a normal percentage of preevening meal calories, but their calorie requirements may far exceed their intake. As in our athlete, symptoms of underperformance as a result of a negative energy balance and inadequate sleep may be the driving factor to seek medical attention. Finally, although some athletes may notice weight gain, overall they are less likely to be clinically overweight or obese given the intense training required to perform at a high level.

Our athlete's initial complaint was of insomnia, and she was instructed initially in basic sleep-hygiene practices. Her nighttime eating was not mentioned on the first visit, and the prescription of a sleep aid may have exacerbated her problem. Once NES was diagnosed, she was started on sertraline (50 mg daily). She was titrated gradually up to a dose of 200 mg daily over the next 6 wk. She was simultaneously sent to the college mental health center for cognitive-behavioral therapy. She went for four visits and reported a significant reduction in symptoms with the treatments. Although she awoke on average once per night, down from the previous three to four times each night, she was usually able to return to sleep almost immediately without eating. She developed regular eating patterns, consuming three regular meals per day with one to two snacks. Her mood improved and anhedonia also resolved. She continued softball participation throughout her treatment, with noticeable improvements and increased consistency in performance once her night eating resolved.

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© 2009 American College of Sports Medicine