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Eating Disorders

Chapter 28

EATING DISORDERS

GAIL H. MANOS, MD*; JANIS CARLTON, MD, PhD†; and AILEEN KIM, MD‡

INTRODUCTION

OVERVIEW OF EATING DISORDERS

ETIOLOGY

CLINICAL FEATURES

DIFFERENTIAL DIAGNOSIS

COURSE AND PROGNOSIS

ABNORMAL EATING IN MILITARY POPULATIONS

MEDICAL AND PSYCHIATRIC TREATMENT OF EATING DISORDERS

TREATMENT OF EATING DISORDER ISSUES IN THE COMBAT ENVIRONMENT

AREAS FOR FURTHER RESEARCH

SUMMARY

*Captain, Medical Corps, US Navy; Navy Psychiatry Specialty Leader and Senior Medical Officer, Director of Mental Health, Naval Medical Center 

Portsmouth, 620 John Paul Jones Road, Portsmouth, Virginia 23708; formerly, Psychiatry Residency Training Director, Department of Psychiatry, 

Naval Medical Center Portsmouth, Portsmouth, Virginia

†

Commander, Medical Corps, US Navy; Department Head, Psychological Health and Traumatic Brain Injury, Building 7, Room 600, National Naval 

Medical Center, 8901 Wisconsin Avenue, Bethesda, Maryland 20889; formerly, Department Head, Mental Health, Naval Hospital, Camp Lejeune, 

North Carolina 

‡

Lieutenant Commander, Medical Corps, US Navy; Staff Psychiatrist, Department of Behavioral Health, Building 7, 3rd Floor, National Naval Medical 

Center, 8901 Wisconsin Avenue, Bethesda, Maryland 20889; formerly, Chief Resident, Department of Psychiatry, Naval Medical Center Portsmouth, 

Portsmouth, Virginia
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INTRODUCTION

Over the past decade, the growing obesity epidemic 

in the United States has received increased attention. 

Like the general population, the US military is experiencing an increase in those classified as overweight 

(54%) despite high physical activity levels.1 Although 

the majority of Americans are overweight or even 

obese by Centers for Disease Control and Prevention 

standards,2 the ideal body image as portrayed by 

television, movie, and fashion mediums appears to be 

underweight. This ideal may drive some individuals 

to abnormal eating behaviors, such as food restriction 

or bingeing with compensatory behaviors. Military 

service members may be particularly at risk because 

of the expectation that they conform to specific weight 

standards, with adverse career consequences for 

those who fail to live up to those standards. Under 

the stress of deployment to a combat zone, service 

members with an eating disorder may experience an 

exacerbation of their illness. Even those without a history of an eating disorder may develop poor eating 

habits as a reaction to stress, or, ironically, due to the 

ready availability of fast food in some locations. On 

the other hand, for some individuals, eating behaviors 

and overall fitness may improve in the military, with 

nutritional counseling and time for physical exercise 

more available.

The rates of eating disorders in the military parallel 

those reported in high-risk groups such as athletes and 

dancers, who place an emphasis on thinness.3,4 Abnormal eating and dieting behaviors are reported in 25% 

to 76% of female service members, with a significant 

increase around the time of personal fitness assessments (PFAs).5

 Because deployed service members 

are not subject to PFAs, they may feel less pressured to 

engage in the abnormal eating and dieting behaviors. 

Also, with meals eaten community style and public 

bathrooms, binge and purge behaviors may be more 

difficult to enact.

The diagnosis of an established eating disorder does 

not necessarily preclude deployment if the service 

member’s condition is in remission. For example, a 

physician deployed several years ago soon became 

overwhelmed with the stress of her duties and separation from family, leading to repetitive bingeing and 

intentional vomiting several times a day. She had 

previously avoided mental health treatment due to 

concerns about an adverse impact on her career. She 

was subsequently medically evacuated and treated 

for her bulimic behaviors and depression by one of 

the authors. Three years later, both her depressive 

symptoms and bulimia were in remission, allowing 

her to successfully deploy to a combat zone. Unlike 

the outcome in this case, other service members with 

eating disorders have experienced recurrence of their 

symptoms under the stress of deployment, resulting 

in early returns. 

This chapter presents information on the identification and recognition of eating disorders, medical 

complications, treatment, and prognoses. The authors 

also review available literature on eating disorder behaviors in military populations and potential risks of 

deploying individuals with an eating disorder.

OVERVIEW OF EATING DISORDERS

Eating disorders consist of a group of increasingly common psychiatric and medical conditions 

that have been studied extensively in women and 

in certain groups of men. The risks of both bulimia 

nervosa (BN) and binge eating disorder (BED) in 

the general population have increased with successive birth cohorts.6

 Anorexia nervosa (AN) was 

described in the scientific literature by Sir William 

Gull (in 1873) as a “mental state [that] destroys the 

appetite.”7 BN, marked by episodes of bingeing and 

purging, was first described in 1979.8 The lifetime 

prevalence for women in the general population is 

estimated as 0.5% to 1% for AN and 1% to 3% for BN. 

Rates for men were previously estimated to be about 

one tenth as high as those for women.9

 However, in 

2007, the National Comorbidity Survey Replication6

found that the estimated point prevalence of BN in 

men is significantly higher than previously thought, 

approximately one fifth that in women. Eating disorder not otherwise specified (EDNOS) is a residual 

category for conditions that do not meet the full 

criteria for AN or BN. It is difficult to determine 

the prevalence of EDNOS, but estimates range from 

1% to 30% in men and women.10 As many as 60% of 

treated eating disorder cases fall into the EDNOS 

category.11 It is estimated that only about one third 

of individuals with AN and 6% of those with BN 

receive mental healthcare,12 although the majority 

of persons with eating disorders receive treatment 

for another mental health complaint.6 Because physicians infrequently assess for eating disorders, and 

patients rarely spontaneously disclose them, these 

disorders may be underdiagnosed.6

 Healthcare providers should routinely ask patients about eating 

disorder symptoms even when these symptoms are 

not the presenting complaint.
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Eating Disorders

Anorexia Nervosa

AN is a psychiatric disorder characterized by extreme weight loss in the absence of a medical cause, 

refusal to regain weight, and intense determination to 

continue or maintain weight loss. Patients with AN 

may deny that they are underweight and take measures to conceal their emaciation with bulky clothes 

to avoid being “ordered” to gain weight by family 

members or doctors. Typically, onset is between the 

ages of 13 and 20, peaking at 17 to 18 years of age.10

AN is defined by the Diagnostic and Statistical Manual 

of Mental Disorders, 4th edition (DSM-IV),9 as including 

the following conditions: 

1. the refusal to maintain body weight at or 

above a minimally normal weight (approximately 85% of those with the AN are below 

ideal body weight);

2. an intense fear of gaining weight or becoming 

fat, even though underweight;

3. a disturbance in the way in which one’s 

body weight or shape is experienced, undue 

influence of body weight or shape on selfevaluation, or denial of the seriousness of 

current low body weight; and

4. in postmenarcheal females, amenorrhea (ie, 

the absence of at least three consecutive menstrual cycles).

AN can be divided into (a) the restricting type, in 

which the individual does not engage regularly in 

bingeing or purging behaviors, but severely restricts 

calories intake, and (b) the bingeing/purging type, 

in which the individual meets criteria for AN and 

engages regularly in binge/purge behaviors such as 

self-induced vomiting and laxative or diuretic misuse. 

Exhibit 28-1 lists the warning signs and symptoms of 

AN. 

Bulimia Nervosa

BN is defined according to the DSM-IV9

 as consisting of the following conditions:

1. recurrent episodes of binge eating, with the 

binge episode characterized by eating within 

a certain time period more food than most 

people would eat in the same time period 

and under the same circumstances, including 

a sense of lack of control over eating during 

the episode;

2. recurrent inappropriate compensatory behavior to prevent weight gain;

3. binge eating and inappropriate behaviors occurring at least twice weekly for 3 months;

4. self-evaluation unduly influenced by body 

shape and weight; and

5. episodes not occurring exclusively during 

episodes of AN.

BN can be divided into purging and nonpurging 

types; during the latter, individuals use inappropriate 

compensatory behaviors such as fasting or excessive 

exercise rather than engaging regularly in vomiting, 

laxative use, diuretics, or enemas. Purging-type BN 

differs from purging-type AN in that patients with 

the latter are significantly underweight. The onset 

of BN is usually late adolescence to early adulthood. 

EXHIBIT 28-1

WARNING SIGNS OF ANOREXIA 

NERVOSA

	 •	 Abnormal weight loss without a medical 

cause

	 •	 Severe restriction of food intake

	 •	 Denial of hunger and/or a problem with low

weight

	 •	 Strict food preferences, such as complete

avoidance of foods containing fat or strict 

vegetarianism

	 •	 Intense fear of gaining weight and determination to continue weight loss

	 •	 Abnormal reproductive functioning (loss of

interest in sex, amenorrhea in females, low 

testosterone in males)

	 •	 Excessive exercise despite fatigue and weakness

	 •	 Unusual behaviors or rituals with meal

preparation and eating

	 •	 Distorted perception of weight or body

shape

	 •	 Inability to stop losing weight or decrease

exercise

	 •	 Unrealistically high self-expectations; perfectionism with a sense of ineffectiveness

	 •	 Use of dangerous methods to lose weight

	 •	 Belief that body weight and shape are extremely important to self-esteem and selfdefinition

	 •	 Psychological symptoms of starvation (eg,

depression, difficulty concentrating, social 

withdrawal)

	 •	 Physical signs of starvation (eg, sensitivity to

cold, fine hair on the face or body, emaciation)
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Combat and Operational Behavioral Health

Warning signs and symptoms of BN are shown in 

Exhibit 28-2.

Eating Disorder Not Otherwise Specified

The EDNOS category is considered by some to be 

overly broad, whereas the criteria for BN or AN may be 

too rigid. Examples of EDNOS include meeting all the 

criteria of AN except for amenorrhea or being underweight, meeting criteria for BN except for frequency 

of episodes, or engaging in purging behaviors without 

binge episodes. BED, bingeing without compensatory 

behaviors, is a category proposed in the DSM-IV for 

further study. Although only 1% of the general population is felt to meet strict DSM-IV diagnostic criteria for 

BED,11 the prevalence of binge behaviors is thought to 

be significantly higher. Night-eating syndrome (NES) 

is characterized by continual eating during evening 

hours between dinner and breakfast, accompanied by 

negative feelings about the eating behavior, insomnia, 

and nocturnal awakenings followed by food intake. 

Prevalence for this condition is estimated at 1.5% of 

the general population.13 Like BED, the prevalence of 

NES is significantly higher in overweight and obese 

individuals. NES is also a category proposed in the 

DSM-IV for further study. 

Obesity

Increasing media attention has focused on overeating and obesity. According to the World Health 

Organization, a body mass index (BMI) of 18.5 to 24.9 

is normal, a BMI of 25 to 29.9 is overweight, and a 

BMI greater than 30 is obese. The Centers for Disease 

Control and Prevention report that 51% of American 

women are overweight and 34% are obese.2 Although 

obesity is not itself considered an eating disorder, up 

to 50% of obese individuals, particularly those seeking bariatric surgery, have BED or NES.11,13 A crosssectional analysis from the US Department of Defense 

Survey of Health-Related Behaviors found that 10% of 

active duty men and 4% of active duty women were 

obese.14 Based on data from the general population, it 

is likely that many of these individuals have an eating 

disorder contributing to their obesity; thus, recognition 

of eating disorders directly impacts fitness for duty 

and deployability. 

EXHIBIT 28-2

WARNING SIGNS OF BULIMIA NERVOSA

•	 Fluctuations in weight, usually within about

15 lb of normal weight

	 •	 Fear of gaining weight

	 •	 Uncontrollable, secretive episodes of binge

eating followed by attempts to purge by 

vomiting, laxatives, etc

	 •	 Excessive exercise for weight control

	 •	 Physical problems with the throat, stomach,

and colon; swelling of the parotid glands

	 •	 Dental problems, tooth decay

	 •	 Psychological problems such as depression,

mood swings, impulsivity

	 •	 Dissatisfaction with body shape and preoccupation with weight loss

	 •	 Belief that body weight and shape are extremely important to self-esteem and selfdefinition

•	 Unrealistically high self-expectations; perfectionism with a sense of ineffectiveness

ETIOLOGY

The etiology of eating disorders includes genetic, 

biological, sociocultural, psychological, familial, developmental, and comorbid factors.15 Although all eating 

disorders are characterized by an abnormal relationship with food, and usually a disturbance in body 

image, the underlying factors vary with the type of 

eating disorder. Although it is important to understand 

etiological factors commonly found in the different 

eating disorders, it is also necessary to remember that 

each person is an individual with a complex history 

and a unique set of characteristics.

Biological Factors

Brain serotonin, norepinephrine, dopamine, endogenous opioids, and a variety of neuropeptides 

(eg, leptin, neuropeptide Y) have been implicated in 

appetite, food intake, satiety, and the development of 

eating disorders.16 Traditionally, the catecholamines, 

particularly norepinephrine and dopamine, have been 

associated with appetite or onset of eating. Serotonin 

has been associated with satiety or cessation of an 

eating episode as well as specific carbohydrate cravings sometimes associated with binges. Disorders of 

appetite, satiety, or both, underlie abnormal eating 

behaviors. This may be relevant to the mechanism of 

action for medications, particularly antidepressants 

that modulate brain serotonin and catecholamine 

activity in the treatment of eating disorders.

Eating disorders co-occur more frequently in 
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Eating Disorders

monozygotic twins (50% concordance rate) than in 

dizygotic twins (10% concordance) and are more 

likely to occur in first-degree relatives of patients 

with eating disorders than in the general population. 

Genetic factors account for 58% to 76% of the variance 

in AN and for 54% to 83% of the variance in BN, with 

a 7- to 12-fold increase in prevalence among relatives.17 Some studies have found a link between the 

serotonin receptor 5-HT2A gene polymorphism in 

the promoter region and eating disorders.18 Enhanced 

5-HT2A receptor binding suggestive of serotonergic 

dysfunction has been found in AN and BN patients.19

Polymorphism of the 5-HT1B receptor gene has also 

been linked to minimum lifetime BMI in women with 

BN.20 These findings suggest that some individuals are 

more at risk genetically than others to developing an 

eating disorder. The increasing incidence of these disorders in society may be the result of the sociocultural 

importance placed on body image and thinness that 

has allowed more people with a genetic predisposition 

for AN or BN to develop an eating disorder.

Although all the complex peripheral and central 

mechanisms that regulate appetite, food intake, and 

body weight are not yet understood, most people 

maintain a body weight around a relatively stable 

“set point” or “settling point,” which changes across 

the age span in a predictable manner. In individuals 

with an eating disorder, regulation of appetite—and 

in many cases body weight—is thrown out of balance. People who engage in periods of excessive food 

restriction that may be followed by binges ignore the 

biological signals of hunger and satiation. Binge behaviors may be a natural holdover from a time when 

humans foraged or hunted for food and needed to eat 

as much as possible before food was lost to competitors or spoilage.

Sociocultural Factors

Social and cultural factors are important in the 

development of both AN and BN. Although the stereotype persists that these disorders, particularly AN, 

are more common in higher socioeconomic groups, 

most of this evidence is based on small, uncontrolled 

case series.7

 These eating disorders are most common 

in Western cultures, where tasty, high-calorie food is 

abundant. Evidence suggests that, as other cultures 

have become richer and more Westernized, body 

dissatisfaction has grown and eating disorders have 

increased.21

Obesity is considered a socioculturally driven eating 

disorder. Individuals and families dine more often in 

restaurants, where the food served is often high in fat 

and in large portions. The media present conflicting 

signals: on one hand, images show thin, happy families eating at fast food restaurants; on the other hand, 

magazines present not only the latest fad diet, but 

also recipes for beautiful, high-calorie dishes. Eating 

is a social or family event. From an early age, many 

people learn to see tasty foods as a reward for good 

behavior or accomplishment. As individuals struggle 

to lose or maintain weight by severely restricting intake 

or skipping meals, they may trigger the urge to binge 

or impulsively overeat, followed by guilt, and in the 

case of bulimics, purging or using other compensatory 

behaviors. In an effort to demonstrate control, patients 

with AN may simply refuse to indulge.

Psychological and Family Factors

Families or first-degree relatives of individuals 

with eating disorders have a higher rate of eating 

disorders (approximately 10% vs 1%–3% in the general population). Although these rates may indicate a 

genetic component, there is also evidence for learning 

and modeling within the family and from peers.22

Patients with eating disorders frequently report that 

their parents or siblings were overly concerned with 

body weight and external appearances. Often, their 

first diet was started in response to criticism from a 

family member or friend.

Families of patients with AN are often described as 

perfectionistic, with one or both parents described as 

authoritarian and having high expectations for their 

children. Psychological factors in the development of 

AN include a drive to perfection, unrealistic self-expectations, and perhaps a misdirected search for autonomy 

and self-control through control of food intake and 

weight. The primary comorbid psychiatric condition 

associated with AN is depression, although it is not clear 

if this is a preceding condition or a result of AN.

Families of patients with BN are more often described as chaotic, with a higher rate of mood disorders, substance abuse, and eating disorders. A history 

of sexual abuse during childhood has been reported in 

one third to nearly one half of women with BN.23,24 A 

review of 53 controlled studies that examined the link 

between sexual abuse and eating disorders found that 

childhood sexual abuse was a risk factor for eating disorders, particularly BN, with psychiatric comorbidity.25

Furthermore, women who had experienced both childhood sexual abuse and rape in adulthood had even 

higher rates of eating disorder behavior and marked 

impulsivity.25 Conditions associated comorbidly with 

BN—including borderline personality disorder, substance abuse, and mood instability—have also been 

found to be more prevalent in people with a history of 

childhood abuse.26 Childhood sexual abuse may lead 

to diminished self-esteem, development of maladaptive behaviors (including eating disorders), and place-
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ment of individuals at risk for further trauma.

A study of 1,887 female Navy recruits found that 

57% had a history of childhood physical or sexual 

abuse or both, and 35% had been sexually assaulted 

as adults.27 In addition, women who were raped as 

adults were 4.8-fold more likely to have experienced 

childhood sexual abuse. Trauma may also result in 

psychobiological changes that increase vulnerability 

to developing an eating disorder. These findings suggest that healthcare providers should ask about eating 

patterns, purging behaviors, and body image in female 

service members with a history of abuse.

CLINICAL FEATURES

Eating disorders are often hidden.28 The individual 

may consider these behaviors to be shameful or may 

lack insight into their pathological nature. Patients 

with restricting-type AN may move food around on 

their plates or otherwise disguise their lack of food 

consumption. Individuals with BN may eat normally 

but subsequently purge in secret. Those with AN may 

be easier to identify based on height and weight measurements and their emaciated appearance. A BMI of 

less than 17.5 in an individual from Western cultures, 

where food is abundant, should raise suspicion among 

healthcare workers and prompt further evaluation. It 

may be more difficult to spot BN or EDNOS among 

normal-weight individuals. 

In an operational environment, service members 

with BN may find it more difficult to binge and purge 

because of lack of privacy for these behaviors. One 

of the authors treated a female service member who 

carried a plastic bag into which she vomited in secret 

due to lack of privacy in the latrine area. She would 

then wait to dispose of the bag into a trash receptacle 

when no one was looking. On the other hand, excessive exercise as a compensatory behavior may easily be overlooked as adaptive rather than disguising 

pathological behavior.

Medical Findings

Anorexia Nervosa

In addition to an emaciated appearance with 

sunken cheeks, prominent bone structure, low body 

fat, and muscle wasting, patients with AN may have 

dry skin, hypercarotenemia (manifested by a yelloworange discoloration of the skin); lanugo (fine, downy 

hair covering the body to compensate for lower 

body temperature resulting from loss of body fat); 

acrocyanosis (digits of the hands and feet become 

blue and sweaty from decreased circulation); and 

atrophy of the breasts.28–30 Symptoms of concomitant 

hypothyroidism include hair loss, peripheral edema, 

and sensitivity to cold. Tachypnea and shortness of 

breath may result from metabolic alkalosis caused 

by vomiting. Conversely, metabolic acidosis may occur from laxative abuse.31 Gastrointestinal symptoms 

include pain, bloating, and severe constipation (from 

starvation, chronic laxative abuse, or both) that may 

result in obstruction and megacolon. Exercise-induced 

disorders (eg, hernias, shin splints, and other injuries) 

are also common.

Cardiac problems include mitral valve prolapse, 

prolongation of the corrected QT interval, sinus bradycardia, and arrhythmias from electrolyte imbalance 

(particularly hypokalemia).27 Pneumomediastinum 

induced by vomiting32 or cardiomyopathy (from ipecac poisoning)28 may be seen on a radiograph. The 

heart is often strophic due to chronic hypovolemia.33

The second leading cause of death in AN is cardiac 

arrhythmia. Central nervous system changes include 

nonspecific electroencephalogram changes and generalized reversible atrophy associated with starvation 

and dehydration.

Osteoporosis occurs in half of women with AN and 

can lead to compression fractures and kyphosis.34,35

Patients with AN have a 3-fold higher risk of fracture 

than those who do not. Bone loss may develop in as 

short a time as 6 months after onset of the illness and 

persist even after recovery, leading to a long-term risk 

of fractures. Fractures were found in 57% of women 

with AN in the ensuing 20-year period after onset.36

Although most studies of osteoporosis in AN have 

focused on women, one study37 found that 50% of men 

with eating disorders had lumbar spine and femoral 

neck bone densities more than two standard deviations below those of age-matched controls. Compared 

with women with eating disorders, this group of men 

had more severe bone loss. Andersen, Watson, and 

Schlechte37 suggested that the correlation between 

reduced body weight in men and lowered testosterone 

led to more bone loss. Given the increased physical 

demands in an operational environment, those with 

AN may be at even higher risk for fractures. 

Bulimia Nervosa

Patients with BN and other binge/purge conditions 

usually have normal weight without the concomitant 

features of starvation. Even patients with bingeing/

purging-type AN do not achieve as low a body weight 

as restrictive-type AN patients. External examination 
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Eating Disorders

may reveal damage to teeth and gums from acidic 

vomit. Russell sign is the calloused posterior surface 

of one or more fingers used to induce vomiting. Physical findings include gastrointestinal disorders (eg, 

sequelae of laxative abuse, esophageal tearing from 

excessive vomiting, and complications of electrolyte 

imbalance, including metabolic alkalosis and cardiac 

arrhythmias).28,31

Laboratory Studies

Serum chemistry may show electrolyte disturbances. Patients who purge may develop hypokalemia, 

hypochloremia, and elevated serum bicarbonate.38

Hypokalemia appears to be particularly common, occurring in up to one half of those who purge; however, 

the ratio of urinary sodium to urinary chloride may be 

a better predictor of purging behavior than serum hypokalemia.39 Metabolic acidosis with low serum bicarbonate may occur in laxative abusers.38 Hyponatremia 

may result from water intoxication or a syndrome of 

inappropriate antidiuretic hormone.28

Other laboratory abnormalities include anemia; 

leucopenia, neutropenia, and thrombocytopenia40; 

hypercholesterolemia41; and euthyroid sick syndrome 

with normal thyroid-stimulating hormone and low 

triiodothyronine and thyroxine.28,42 Hypercarotenemia has been proposed as a laboratory marker for 

restricting-type AN, with a sensitivity of 62% and a 

specificity of 83% when a cutoff marker of 200 μg/mL 

is used.30 In one study of patients with AN, high serum 

creatinine and uric acid levels were associated with a 

chronic disease course, whereas low serum albumin 

and low body weight predicted lethality.38

DIFFERENTIAL DIAGNOSIS

Medical conditions that must be considered in the 

differential diagnosis include inflammatory bowel 

disease, thyroid disease, abdominal malignancy, central nervous system disease or tumor, and new-onset 

diabetes mellitus. The psychiatric differential includes 

depression, substance abuse, psychosis, and obsessivecompulsive disorder. Comorbidity with psychiatric 

conditions (including depression, psychosis, anxiety, 

personality disorder, and substance abuse) must also 

be addressed.

COURSE AND PROGNOSIS

Anorexia Nervosa

AN is associated with significant morbidity and 

mortality. It is usually a chronic, sometimes life-long 

disease with low full recovery rates. In a review of 

studies43 conducted with patients at least 4 years after 

onset of illness, approximately 24% had what was 

considered a poor outcome (eg, never reached target 

weight gain within 15% of normal, had not established 

regular menses). Another 44% were considered to have 

a good outcome (eg, achieved and maintained weight 

within 15% of normal, had regular menses). About 28% 

had outcomes that fell between poor and good. The 

mortality rate was 5%. Even among those judged to 

be recovered based on body weight and menses, two 

thirds continued to struggle with body image, obsessive preoccupation with weight and appearance, and 

disordered eating habits.

Crude 10-year mortality rates for patients receiving 

treatment for AN has been cited at 3.3% to 5.6%.44,45

Twenty-year mortality rates are 15% to 20%, with suicide and cardiac arrest the leading causes of death.46–49

The annual mortality rate associated with AN is 12-

fold higher than the annual death rate as a result of all 

causes of death for women in the general population 

15 to 24 years of age.46 AN is associated with social and 

functional impairments,41 as well as with medical and 

psychiatric morbidities.47 

Bulimia Nervosa

There is limited evidence that some untreated 

patients with BN have modest rates of improvement 

or recovery. For patients treated with either psychotherapy or medication, the short-term improvement 

rates are 50% to 70%; however, relapse rates are high 

(30%–50% in 6 months to 6 years follow-up).50,51 Longer-term prognosis may be somewhat better. Patients 

with milder symptoms and fewer medical and psychiatric comorbidities who do not require hospitalization 

have a better course and prognosis. The mortality rate 

for BN has been cited at 0.3% per year.52 A metaanalysis of standardized mortality rates in BN 5 to 11 years 

after diagnosis found a 7-fold greater mortality rate 

than expected.51 

Eating Disorder Not Otherwise Specified

The only study to date that reported mortality information on EDNOS found that 4 of 28 subjects had 

died in an 11-year follow-up.53 The risk of dying may 

be greater in the first few years after diagnosis of an 
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Combat and Operational Behavioral Health

eating disorder. A review of 10 eating disorder populations found a 2% risk of dying for women in the first year after presentation and a 5% risk of dying for men 

in the first and second years.53

ABNORMAL EATING IN MILITARY POPULATIONS

Research on eating disorders in military populations 

primarily consists of case reports54–56 and surveys of 

military populations within gender or service. These 

surveys generally rely on self-reporting, which in civilian populations has been shown to underestimate 

pathological weight-control behaviors.57 A summary of 

the published literature assessing eating disorders in 

military populations is provided in Table 28-1. There 

are no studies of eating disorders in military populations in combat operational environments.

McNulty5 surveyed prevalence and contributing 

factors of abnormal eating behaviors in 3,000 active 

duty women in the US Army, Navy, Air Force, and 

Marine Corps. The rate of AN was highest in the 

Marine Corps, at 4.9%. Rates across the other services 

were Army, 1.3%; Navy, 1.1%; and Air Force, 0.8%. 

The rate of BN was again highest among marines at 

15.9%. Rates in other services were Army, 4.3%; Navy, 

5.2%; and Air Force, 9.3%. Rates of EDNOS were far 

higher: 62.8% of the total population met the criteria 

for this diagnosis. Again, the Marine Corps reported 

a significantly higher rate: 76.7%. The rates for the 

other services were Army, 57.4%; Navy, 61.2%; and Air 

Force, 58.6%. Notably, more than 60% of respondents 

had some type of eating disorder, and nearly every 

Marine Corps respondent (97.5%) met criteria for an 

eating disorder. Of those with an eating disorder at the 

time of the survey, the overwhelming majority had no 

history of previous eating disorder and negative family histories. Fasting or purging increased during PFA 

periods, suggesting that the military environment may 

put women at risk for eating disorders and increased 

use of unhealthy strategies of weight reduction to 

meet standards.

In a survey of 423 active duty Army women (officers and enlisted personnel) from medical and field 

commands, Lauder and colleagues58 found that 142 

women (33.6%) were at risk for abnormal eating behaviors. These at-risk women admitted to abnormal 

eating or purging behaviors more than once a month 

for 3 months, or had high scores of body dissatisfaction and a drive for thinness associated with a BMI 

of less than 21. Of the 142 women deemed at risk 

by the survey, 108 completed a structured interview 

with a board-certified psychiatrist. Of this number, 

33 were diagnosed with an eating disorder. The other 

women had specific stressors, such as PFA periods, that 

prompted their abnormal eating behaviors. Therefore, 

8% of the total sample was diagnosed with an eating 

disorder, and 3.1% met criteria for an eating disorder 

situational to the military environment. In a follow-up 

study of this same population, Lauder et al59 evaluated 

their subjects for the prevalence of the female athlete 

triad, defined by the presence of an eating disorder, 

amenorrhea, and osteoporosis. They found no subjects who met the full triad, although, as they pointed 

out, the military physical activities that the subjects 

participated in may have had a protective effect on 

bone mass density.

McNulty60 surveyed 1,425 Navy men from medical and line communities. She reported prevalence 

for AN (2.5%), BN (6.8%), and EDNOS (40.8%) in this 

population. Purging behaviors increased dramatically 

(up to 15%) during PFA periods. Fasting during these 

times occurred in nearly one third of respondents. 

Stressors of military life significant for AN, BN, or 

EDNOS included failing to be selected for advanced 

training schools, fear of being involuntarily separated, 

mandatory physical fitness, nonsupport of a supervisor, height/weight requirements, and rotating shifts. 

McNulty further reported that some sailors spoke of 

anger and discouragement over the PFA and their personal struggles with weight. One soldier even reported 

past suicidal ideation associated with the issue.

In a similar survey of 1,323 female Navy nurses, 

McNulty61 reported the prevalence of AN (1.1%), BN 

(12.5%), and EDNOS (36%). To lose weight rapidly, 

these respondents reported skipping meals (44.4%), 

binge eating (19.2%), exercising excessively (16.9%), 

using diet pills (8.5%), using laxatives (7.1%), and 

vomiting (3%). Poor body image and satisfaction 

were predictors of eating disorders, as were height 

(in AN) and weight (in BN). Work-related stressors 

that adversely impacted eating disorder behaviors 

included working in an undesired area or in the intensive care unit, rotating shifts, and being a staff nurse. 

It is unclear if the high rates of BN and EDNOS in the 

survey personnel, compared with the general population, were related to their status as military officers 

or their occupation as nurses. Other studies of eating 

behaviors in nursing students have found conflicting results. A study of female medical students and 

nursing students found abnormal eating behaviors 

in one fifth of the respondents, with a higher rate in 

the nursing students.62 Another study found a similar 

rate of overall abnormal eating behaviors in nursing, 

medical, and art students (~20%), but no difference 

among the three groups.63
457

Eating Disorders

TABLE 28-1 

SUMMARY OF ABNORMAL EATING BEHAVIOR STUDIES IN MILITARY POPULATIONS

Subjects N Findings Study

Army ROTC 310 20% subjects with increased bulimic 

behaviors, body dissatisfaction, drive for 

thinness

Lauder TD. Abnormal eating behaviors in 

female Reserve Officer Training Corps cadets. 

Mil Med. 2001;166:264–268.

Women in the 

Army, Navy, 

Air Force, and 

Marines

3,000 AN (%) BN (%) EDNOS (%)

Marines 4.9 15.9 76.7

Navy 1.1 5.2 61.2

Air Force 0.8 9.3 58.6

Army 1.3 4.3 57.4

McNulty P. Prevalence and contributing factors 

of eating disorder behaviors in active duty 

service women in the Army, Navy, Air Force, 

and Marines. Mil Med. 2001;166:53–58.

Army women 423 33.6% abnormal eating or purging behaviors and increased body dissatisfaction; 

8% diagnosed with eating disorder; 3.1% 

situational eating disorder

Lauder T, Williams MV, Campbell CS, Davis 

GD, Sherman RA. Abnormal eating behaviors in military women. Med Sci Sports Exerc.

1999;31:1265–1271.

Army women 

with “at- risk” 

eating behaviors

108 None with female athlete triad (osteoporosis, amenorrhea, eating disorder)Lauder T, Williams M, Campbell C, Davis 

G, Sherman R. The female athlete triad: 

prevalence in military women. Mil Med. 

1999;164:630–635.

Navy men

Navy women 

(nurses)

1,425

1,323

AN (%) BN (%) EDNOS (%)

Men 2.5 6.8 40.8

Women 1.1 12.5 36.0

McNulty P. Prevalence and contributing factors 

of eating disorder behaviors in active duty 

Navy men. Mil Med. 1997;162:753–758.

McNulty P. Prevalence and contributing 

factors of eating disorder behaviors in a 

population of female Navy nurses. Mil Med. 

1997;162:703–706.

Air Force weightmanagement 

patients 

+

Civilian weightmanagement 

patients

+

Military control 

population

155 Air Force group: 4 times more purging 

behaviors than civilian group, 2–5 times 

more purging behaviors than military 

control group; great fluctuations in weight

Peterson AL, Talcott GW. Bulimic weightloss behaviors in military versus civilian 

weight-management programs. Mil Med. 

1995;160:616–620.

Israeli Army 

women diagnosed with 

anorexia

16 6/1,000 had AN; 16 treated with CBT and 

clomipramine; 12 returned to full duty; 3 

returned to limited duty; 1 discharged

Mark M, Rabinowitz J, Rabinowitz S, Gaoni B, 

Babur I, Danon Y. Brief treatment of anorexia 

nervosa in military personnel. Hosp Community Psychiatry. 1993;44:69–71.

Male Hungarian 

military college 

students

Male Hungarian 

general college 

students

480

752

No anorexic or bulimic subjects but general 

college students more likely to have behavioral and psychological characteristics 

of eating disorders. Body builders in both 

groups more likely to be perfectionistic

Lukacs L, Muranyi I, Tury F. Eating and 

body attitudes related to noncompetitive 

bodybuilding in military and general Hungarian male student populations. Mil Med. 

2007;172:152–156.

Army women 

and men in 

advanced individual training

1,090 40% overweight; 10.8% with prior psychiatric history; 25.4% with history of verbal 

abuse; 9.8% reported disordered eating. 

Females, overweight, and those with previous psychiatric treatment and history of 

verbal abuse most at risk

Warner C, Warner C, Matuszak T, Rachal J, 

Flynn J, Grieger TA. Disordered eating in 

entry-level military personnel. Mil Med. 

2007;172:147–151.

AN: anorexia nervosa

BN: bulimia nervosa

CBT: cognitive-behavioral therapy

EDNOS: eating disorder not otherwise specified

ROTC: Reserve Officer Training Corps
458

Combat and Operational Behavioral Health

Peterson and colleagues64 compared the prevalence 

of bulimic weight-loss behaviors in patients enrolled 

in an Air Force weight-management program with 

civilians enrolled in a weight-management program 

and with normal military controls. The Air Force members in the weight-management program vomited, 

engaged in strenuous exercise, or used the sauna/

steam room four times more often than the civilian 

group. They were 2- to 5-fold more likely than the 

military comparison group to engage in bulimic 

weight-loss behaviors. They also lost more weight than 

the other two groups: 53% of the Air Force members 

in the weight-management program, but only 10% of 

the other two groups, reported a weight loss of more 

than 10 pounds in 1 month. The Air Force members 

in the weight-management group also showed more 

variability, with 41% gaining more than 5 pounds in 

1 week, compared with 27% in the civilian group and 

14% in the military control group. Fixed-interval reinforcement operant conditioning may have affected 

the fluctuations in weight and heightened weight-loss 

behaviors seen in the Air Force weight-management 

group, because participants were required to weigh 

in every month on a specified date. Thus, they may 

have continued with their routine eating habits until 

just a few days before the weigh-in and made drastic, 

last-minute attempts to drop weight, similar to the 

behaviors seen in the 6-month PFA cycles.

Warner et al65 assessed prevalence and risks factors 

for disordered eating in a cross-sectional survey of over 

1,000 advanced individual training soldiers. Even in 

this entry-level population, 40% were overweight and 

9.8% endorsed disordered eating (7.0% of the men, 

29.6 % of the women). Risk factors for abnormal eating 

behaviors included being a woman, being overweight, 

having a history of previous psychiatric treatment, and 

having a history of verbal abuse.

Carlton et al66 surveyed eating disorders in a mixed 

military population at a large Navy medical center. A 

relatively high percentage of respondents were men, 

officers, or both, which reflected the general makeup 

of the population studied. The average BMI reported 

by the respondents—both men and women—would 

put them in the overweight category. More than 50% 

of respondents reported a BMI of 25 or greater. 

Overall, the findings were consistent with those of 

other studies on eating and dieting behavior in the 

military, with high rates of body image dissatisfaction, abnormal patterns of eating and dieting, and a 

high correlation between these behaviors and the PFA 

cycle. Nearly 40% of respondents reported bingeing 

or binge-like behaviors, 18% or more reported some 

type of purging behavior, and 25% reported fasting. 

These behaviors were associated with worrying about 

the PFA and were more likely to occur in those with 

higher BMI, poor body image, or both. A high percentage of the study population reported dissatisfaction 

with body appearance and self-esteem dependent on 

body image. Women scored higher; however, data 

indicated that a significant proportion of men in the 

Navy are also dissatisfied with their bodies and engage in abnormal eating behaviors. These unhealthy 

attitudes and behaviors were common even though the 

sample was from a medical command; however, other 

studies in Navy personnel have found lower rates of 

abnormal eating behaviors in healthcare workers (30%) 

and medical doctors (6%), compared with the rate in 

shipboard service members (65%).60

Although the data indicate that one third or more 

of the population sample exhibited abnormal eating 

and weight-loss behaviors, only 2% had actually been 

clinically diagnosed.66 This finding is consistent with 

other indications that eating disorders are underreported in the military, even at a medical command. It 

is not surprising that service members are reluctant 

to come forward. In addition to the stigma, the diagnosis may be grounds for disqualification from many 

assignments, mandatory enrollment in weight-loss 

programs, denial of promotion, and involuntary 

separation from service. McNulty5 reported that in 

fiscal year 1995 approximately 5,000 people were 

discharged from military service for failure to meet 

weight standards. Military providers may be reluctant 

to diagnose eating disorders because they are traditionally considered difficult to treat and may end a service 

member’s career.

MEDICAL AND PSYCHIATRIC TREATMENT OF EATING DISORDERS

Anorexia Nervosa

Medical Assessment and Treatment

Patients with AN have poor insight into their conditions. They may perceive their low body weight as 

an accomplishment and have limited motivation to 

change their behaviors.67 The American Psychiatric Association guidelines recommend that patients weighing less than 75% of ideal body weight be treated on an 

inpatient basis.68 Other indications for hospitalization 

are shown in Exhibit 28-3. The hospital utilization 

rate for individuals with AN is higher than that for 

any other psychiatric disorder except schizophrenia 

and organic mental disorders.69 The cost of treatment 

is substantial and is estimated to be even higher than 
459

Eating Disorders

that for schizophrenia.70 Some patients may refuse 

treatment out of dread of weight gain and limited insight. In these cases, involuntary hospitalization may 

be necessary. Patients involuntarily committed for AN 

may show short-term benefit as manifested by weight 

gain, but have a higher mortality rate than those who 

undergo treatment voluntarily.71 With changes in managed care, treatment for AN is increasingly moving 

toward partial-day programs or outpatient treatment. 

Hospitalization is often reserved for patients with serious life-threatening medical complications or those 

who can afford to pay privately.

Once diagnosed with AN, an individual’s general 

medical condition should be assessed. Medical comorbidities, if they exist, must be addressed, although 

many (such as electrolyte imbalance) may resolve or 

improve once malnutrition and purging behaviors are 

rectified. Patients who require hospitalization need 

careful management because rapid refeeding can lead 

to gastric bloating, edema, arrhythmia, tachycardia, 

congestive heart failure, and sudden cardiac death.33,72

Vitamin supplementation, with calcium at doses of 

1,000 to 1,500 mg in addition to a multivitamin, is recommended.73 Alendronate74 and etidronate75 have been 

found helpful in promoting bone formation in patients 

with anorexia; however, bone restoration appears to 

be most determined by weight restoration. 

Psychotherapy

There are fewer controlled trials in the psychotherapeutic management of AN compared to BN.76 Family 

therapy for adolescent patients may be one of the 

more effective treatments77,78; however, this approach 

is impractical in the military setting. Although better 

studied in BN, cognitive-behaviorial therapy (CBT)—

in which cognitive distortions of body image and feelings of self-worth are addressed—has been applied 

with some success to patients with AN.79

Mark et al80 reported on a treatment protocol 

implemented by the Israeli Defence Forces to treat 

AN in their armed forces. They surveyed, weighed, 

and measured all female soldiers over a 6-month 

period. In this sample, 6 of every 1,000 (0.6%) female 

soldiers were anorexic. Requirements for enrollment 

in the treatment program were an identifiable trigger for the disorder, motivation for treatment and 

military service, a social support system, and selfacknowledgment of the eating disorder. As part of 

the treatment program, the soldiers were educated 

on the serious medical nature of AN and instructed 

that they could be discharged if they failed or refused 

treatment. Service members were hospitalized for 4 

to 6 weeks. During this time, each underwent a thorough medical workup, was placed on a high-calorie 

diet, and set goals for weekly weight gain. Therapy 

was based on a CBT model. All patients were initially 

given clomipramine to decrease obsessional ruminations; this drug was tapered off over several months.

Of the 16 patients followed in the study for 1 year 

after discharge from the program, 12 were returned 

to full duty, three were returned to limited duty, and 

one was discharged.

In one study,81 interpersonal therapy (IPT), CBT, 

and “nonspecific supportive clinical management”—

defined as supportive therapy techniques, education, 

and nutritional advice—were compared in a randomized trial. Surprisingly, nonspecific supportive clinical 

management was found superior to both CBT and IPT, 

with CBT yielding superior results to IPT. Therapists 

administering the treatments investigated in the study 

were not eating-disorder specialists. Results of this 

study have yet to be replicated, but may have implications for the feasibility of treating AN in the military 

healthcare setting.

In general, the treatment plan for AN patients 

should involve a multidisciplinary team, including experts in mental health, nutrition, and internal medicine 

or primary care. The therapeutic approach should be to 

treat the whole patient. It is often better to focus away 

from food and toward resolving underlying issues of 

self-esteem and perfectionism.

EXHIBIT 28-3

INDICATIONS FOR HOSPITALIZATION IN 

ANOREXIA NERVOSA*

•	 Limited motivation to change abnormal eating behaviors

	 •	 Intractable (or rapid) weight loss despite

treatment

	 •	 Refusal to eat

	 •	 Prolonged QT interval

	 •	 Bradycardia < 40 beats per minute

	 •	 Arrhythmia

	 •	 Hypothermia

	 •	 Symptomatic hypotension

	 •	 Less than 75% ideal body weight

	 •	 Persistent suicidal ideation

	 •	 Need for withdrawal/detoxification from

laxatives, diet pills, or diuretics

*This list is not all-inclusive, and a decision to admit a 

patient to a hospital should always be based on a clinical 

assessment of the patient’s psychiatric and general medical 

conditions.
460

Combat and Operational Behavioral Health

Medications

Controlled trials of medications in the treatment of 

AN are summarized in Exhibit 28-4. Restoring weight 

and subsequent metabolic stabilization are treatment 

priorities for patients with AN. Cyproheptadine 

(32 mg/day) was found to improve weight gain in 

patients with restricting-type AN but not those with 

bingeing/purging-type AN.78 Because zinc deficiency 

has been linked to AN through inhibition of release of 

neuropeptide Y,82 supplementation with this mineral 

may be beneficial in promoting recovery from AN and 

improving these patients’ levels of anxiety and depression.83 In a controlled trial of 35 female inpatients with 

AN, supplementation with zinc promoted a rate of 

increase of BMI twice that of placebo.84 Birmingham 

and Gritzner85 recommend oral administration of 14 

mg daily of elemental zinc for 2 months. A doubleblind trial86 of cisapride (10 mg tid) found reduction 

EXHIBIT 28-4

MEDICATIONS EFFECTIVE* AS MONOTHERAPY IN PLACEBO-CONTROLLED 

TRIALS FOR ANOREXIA NERVOSA

	 •	 Zinc1

	 •	 Cyproheptadine2

	 •	 Fluoxetine (after weight restoration, bingeing/purging subtype) 3,4

	 •	 Naltrexone (bulimic subtype)5

	 •	 Olanzapine6

*Defined as fewer days to reach healthy BMI or reduction 

in binge/purge behavior for bulimia nervosa subtype of 

anorexia nervosa.

BMI: body mass index

(1) Birmingham CL, Goldner FM, Bakan R. Controlled trial 

of zinc supplementation in anorexia nervosa. Int J Eat Disord. 

1994;15:251–255. (2) Halmi KA, Eckert E, LaDu TJ, Cohen 

J. Anorexia nervosa. Treatment efficacy of cyproheptadine 

and amitriptyline. Arch Gen Psychiatry. 1986;43:177–181. (3) 

Kaye WH, Nagata T, Weltzin TE, et al. Double-blind placebocontrolled administration of fluoxetine in restricting- and 

restricting-purging-type anorexia nervosa. Biol Psychiatry. 

2001;49:644–652. (4) Walsh BT, Kaplan AS, Attia E, et al. 

Fluoxetine after weight restoration in anorexia nervosa: a 

randomized controlled trial. JAMA. 2006;295:2605–2612. (5) 

Marrazzi MA, Bacon JP, Kinzie J, Luby ED. Naltrexone use 

in the treatment of anorexia nervosa and bulimia nervosa. Int 

Clin Psychopharmacol. 1995;10:163–172. (6) Bissada H, Tasca 

GA, Barber AM, Bradwejn J. Olanzapine in the treatment 

of low body weight and obsessive thinking in women with 

anorexia nervosa: a randomized, double-blind, placebocontrolled trial. Am J Psychiatry. 2008;165:1281–1288.

in subjective distress during meals in a small group 

of AN patients, but did not find a difference in gastric 

emptying or weight gain. 

To date, no antidepressant or antipsychotic has been 

demonstrated to improve the long-term recovery rate 

from anorexia.87,88 Tricyclic antidepressants (TCAs) 

have not only been shown ineffective, but also given 

their potential lethality, may be risky in this patient 

population.89,90 Selective serotonin reuptake inhibitors (SSRIs) have not been found useful in low-weight 

patients.91 This may be because of the general state of 

malnutrition of low-weight patients with AN, resulting 

in deficiency of tryptophan, the amino acid required 

for serotonin synthesis.92 One SSRI, fluoxetine, was 

shown to be useful at higher doses in preventing relapse in those who have regained weight93; however, 

a larger study reported negative results.94

Antipsychotic drugs may have an augmenting role, 

particularly in patients with AN who have poor insight 

into their conditions.95–98 However, not all studies 

have demonstrated the efficacy of antipsychotics,99,100

and their use may have serious adverse effects in this 

population.73 In a small, randomized trial, olanzapine was superior in reducing ego-syntonic anorexic 

ruminations compared to chlorpromazine, although 

there was no difference in weight gain.101 Theoretically 

opiate antagonists may be helpful for subgroups of 

eating-disorder patients who fit an addiction model. 

Marrazzi et al102 reported reduction in binge/purge 

EXHIBIT 28-5

INDICATIONS FOR HOSPITALIZATION IN 

BULIMIA NERVOSA*

	 •	 Changes in vital signs (pulse, blood pressure)

	 •	 Syncope

	 •	 Hypothermia

	 •	 Suicide risk

	 •	 Alcohol or drug abuse

	 •	 Uncontrolled vomiting

	 •	 Hematemesis (vomiting of blood)

	 •	 Arrhythmia

	 •	 Electrolyte imbalance

	 •	 Need for withdrawal from laxatives, diet

pills, and diuretics

*This list is not all-inclusive, and a decision to admit a patient to the hospital should always be based on a clinical 

assessment of the patient’s psychiatric and general medical 

conditions.
461

Eating Disorders

behaviors in a mixed population of BN and AN (bulimic subtype) patients treated with naltrexone in a 

randomized trial of 37 patients.

Bulimia Nervosa

Literature to guide treatment of BN is fairly extensive; hospitalization is seldom necessary unless there 

are medical complications (Exhibit 28-5). Compared 

to AN, evidence shows that BN can be treated more 

effectively with medication, although psychotherapy 

remains the cornerstone of treatment. The most established treatment for BN is CBT; in one study,103

however, fewer than 10% of patients with bulimia who 

received psychotherapy were treated with this type 

of therapy. Guided self-help manuals that use CBT 

principles have also been found effective.92,104 Even 

with CBT, it is estimated that only 50% of patients 

with BN recover.105

Patients with BN who fail to respond to psychotherapeutic techniques may benefit from pharmacotherapy. Medications that have been shown effective in 

randomized, placebo-controlled trials in the treatment 

of BN are listed in Exhibit 28-6. Controlled trial data 

have shown efficacy for TCAs106–110 and monoamine 

oxidase inhibitors,111,112 with the latter demonstrating some superiority.113 Both TCAs and monoamine 

oxidase inhibitors may have lethal adverse effects in 

EXHIBIT 28-6

MEDICATIONS EFFECTIVE IN PLACEBO-CONTROLLED TRIALS FOR BULIMIA NERVOSA

*Contraindicated in treatment of bulimia because of increased risk of seizure.

(1) Pope HG Jr, Hudson JI, Jonas JM, Yurgelun-Todd D. Bulimia treated with imipramine: a placebo-controlled, double-blind study. 

Am J Psychiatry. 1983;140:554–558. (2) Agras WS, Dorian B, Kirkley BG, Arnow B, Bachman J. Imipramine in the treatment of bulimia: 

a double-blind controlled study. Int J Eat Disord. 1987;6:29–38. (3) Barlow J, Blouin J, Blouin A, Perez E. Treatment of bulimia with 

desipramine: a double-blind crossover study. Can J Psychiatry. 1988;33:129–133. (4) Hughes PL, Wells LA, Cunningham CJ, Ilstrup 

DM. Treating bulimia with desipramine. A double-blind, placebo-controlled study. Arch Gen Psychiatry. 1986;43:182–186. (5) Walsh 

BT, Gladis M, Roose SP, Stewart JW, Stetner F, Glassman AH. Phenelzine vs placebo in 50 patients with bulimia. Arch Gen Psychiatry.

1988;45:471–475. (6) Kennedy SH, Piran N, Warsh JJ, et al. A trial of isocarboxazid in the treatment of bulimia nervosa. J Clin Psychopharmacol. 1988;8:391–396. (7) Blouin AG, Blouin JH, Perez EL, Bushnik T, Zuro C, Mulder E. Treatment of bulimia with fenfluramine

and desipramine. J Clin Psychopharmacol. 1988;8:261–269. (8) Walsh BT, Agras WS, Devlin MJ, et al. Fluoxetine for bulimia nervosa 

following poor response to psychotherapy. Am J Psychiatry. 2000;157:1332–1334. (9) Fluoxetine Bulimia Nervosa Collaborative Study 

Group. Fluoxetine in the treatment of bulimia nervosa: a multicenter, placebo-controlled, double-blind trial. Arch Gen Psychiatry.

1992;49:139–147. (10) Goldstein DJ, Wilson MG, Thompson VL, Potvin JH, Rampey AH Jr. Fluoxetine Bulimia Nervosa Research 

Group. Long-term fluoxetine treatment of bulimia nervosa. Br J Psychiatry. 1995;166:660–666. (11) Romano SJ, Halmi KA, Sarkar 

NP, Koke SC, Lee JS. A placebo-controlled study of fluoxetine in continued treatment of bulimia nervosa after successful acute 

fluoxetine treatment. Am J Psychiatry. 2002;159:96–102. (12) Horne RL, Ferguson JM, Pope HG Jr, et al. Treatment of bulimia with 

bupropion: a multicenter controlled trial. J Clin Psychiatry. 1988;49:262–266. (13) Pope HG Jr, Keck PE Jr, McElroy SL, Hudson JI. A 

placebo-contolled study of trazodone in bulimia nervosa. J Clin Psychopharmacol. 1989;9:254–259. (14) Marrazzi MA, Bacon JP, Kinzie 

J, Luby ED. Naltrexone use in the treatment of anorexia nervosa and bulimia nervosa. Int Clin Psychopharmacol. 1995;10:163–172. (15) 

Faris PL, Kim SW, Meller WH, et al. Effect of decreasing afferent vagal activity with ondansetron on symptoms of bulimia nervosa: 

a randomised, double-blind trial. Lancet. 2000;355:792–797. (16) Hoopes SP, Reimherr FW, Hedges DW, et al. Treatment of bulimia 

nervosa with topiramate in a randomized, double-blind, placebo-controlled trial, part 1: improvement in binge and purge measures. 

J Clin Psychiatry. 2003;64:1335–1341. (17) Nickel C, Tritt K, Muehlbacher M, et al. Topiramate treatment in bulimia nervosa patients: a 

randomized, double-blind, placebo-controlled trial. Int J Eat Disord. 2005;38:295–300. (18) Sundblad C, Landén M, Eriksson T, Bergman L, Eriksson E. Effects of the androgen antagonist flutamide and the serotonin reuptake inhibitor citalopram in bulimia nervosa: 

a placebo-controlled pilot study. J Clin Psychopharmacol. 2005;25:85–88. (19) Leombruni P, Amianto F, Delsedime N, Gramaglia C, 

Abbate-Daga G, Fassino S. Citalopram versus fluoxetine for the treatment of patients with bulimia nervosa: a single-blind randomized controlled trial. Adv Ther. 2006;23:481–494. (20) Milano W, Petrella C, Sabatino C, Capasso A. Treatment of bulimia nervosa with 

sertraline: a randomized controlled trial. Adv Ther. 2004;21:232–237.

	 •	 Tricyclic antidepressants (desipramine, imipramine)1–4

	 •	 Monoamine oxidase inhibitors (phenelzine,

isocarboxazid)5,6

	 •	 Fenfluramine7

	 •	 Fluoxetine8–11

	 •	 Buproprion*,12

	 •	 Trazodone13

	 •	 Naltrexone (high dose)14

	 •	 Ondansetron15

	 •	 Topiramate16,17

	 •	 Flutamide18

	 •	 Citalopram19

	 •	 Sertraline2o

	 •	 Fluvoxamine11
462

Combat and Operational Behavioral Health

this patient population (potentially made worse by 

underlying electrolyte imbalance) and are not currently 

recommended as first-line treatment. Fenfluramine, 

a serotonergic agonist withdrawn from the market, 

was shown to be superior to both placebo and desipramine (a TCA).110 The SSRI antidepressants are, 

similarly, serotonergic agonists and theoretically may 

work through a similar mechanism. Fluoxetine at high 

doses (60 mg/day) was superior to placebo in two 

8-week trials114,115 and one 16-week trial.116 Fluoxetine’s 

efficacy in BN, as with the TCAs,117 is not a secondary 

effect of its antidepressant properties.118 As many as 

one third of initial responders may relapse by the end 

of 1 year despite continued treatment,119 suggesting 

that, whereas continued treatment may afford some 

protective effect, additional treatments may be needed 

for sustained effectiveness.

Although fluoxetine is the only antidepressant 

currently approved for BN, other SSRIs may also be 

effective. In a randomized, placebo-controlled trial, 

sertraline 100 (mg/d for 12 weeks) was found to be 

significantly more effective than placebo in reducing 

binge/purge behaviors in 20 female outpatients.120

Fluvoxamine has been found effective in preventing 

relapse in patients with BN who had responded to 

inpatient behavioral psychotherapy.121 In a singleblind trial comparing citalopram to fluoxetine, both 

agents resulted in significant improvement in eating 

psychopathology. Patients on fluoxetine displayed 

greater reduction in introjected anger, whereas those 

on citalopram demonstrated greater improvement in 

depressive feelings.122 In comparison, another study 

found that use of the androgen receptor antagonist 

flutamide reduced craving and binge behaviors but 

not purging, whereas citalopram did not separate 

from placebo on these measures.123 Among the newer, 

non-SSRI antidepressants, only bupropion has been 

studied in a controlled trial. Although bupropion was 

highly effective in reducing bingeing, there was a 5.8% 

incidence of seizure among study participants.124 As a 

result, this agent is contraindicated in BN. As a class, 

antidepressants reduce binge eating by 61.4% (remission rate: 22%) and reduce purging by 58.9% (remission 

rate: 34%).125 Unfortunately, up to 45% of patients who 

respond to pharmacotherapy may relapse in the first 

6 months.126

Topiramate is becoming increasingly popular for 

treating BN after two randomized, double-blind, 

placebo-controlled trials established efficacy.127,128

Other agents that have been found effective in at least 

one double-blind trial include the 5-HT3 antagonist 

ondansetron,129 the opioid antagonist naltrexone,102

and trazodone.130

Several studies have compared psychotherapy to 

pharmacotherapy and failed to find any advantage 

of combining medication with therapy versus therapy 

alone.131–133 Results from two metaanalyses found 

that combination approaches were associated with 

higher remission rates, although adding medication to 

therapy increased the dropout rate.134,135 In summary, 

the preference is to treat BN with psychotherapy, primarily CBT, or a combination of psychotherapy and 

medication.

Eating Disorder Not Otherwise Specified

Because EDNOS is a nonspecific diagnostic category, treatment approaches depend on symptoms. The 

one category of EDNOS for which there appears to be a 

growing body of literature is BED. In general, the treatment resembles that for BN, with outcome measures 

defined by reduction in bingeing. The best-studied 

psychotropic agents used to treat BED and obesity are 

antidepressants and anticonvulsants. SSRIs have been 

found effective in double-blind trials for treatment of 

BED.136–138 The anticonvulsant topiramate has also been 

found effective in double-blind trials for BED associated with obesity,139 and a similar agent, zonisamide, 

was also associated with significant weight loss in 

a double-blind trial of obese adults.140 Alternatively, 

agents specifically marketed for weight loss (including phentermine, sibutramine, and orlistat)141,142 have 

been used to treat weight gain in overweight or obese 

patients with BED. Although several agents have been 

found effective for short-term weight loss, there are 

relatively few data on long-term efficacy with these 

agents. A review of the Cochrane database system 

found that, compared with placebo, the number of 

patients achieving 10% or more weight loss was 12% 

higher with orlistat and 15% higher with sibutramine 

in double-blind trials that lasted more than 1 year.143

However, there was significant attrition in these studies, with an average of 33% of those on orlistat and 43% 

of those on sibutramine dropping out.

TREATMENT OF EATING DISORDER ISSUES IN THE COMBAT ENVIRONMENT

No formal studies have been conducted of disorders of eating behavior among military personnel in 

a combat environment. Operation Enduring Freedom 

and Operation Iraqi Freedom are the first US military 

actions in which women play a major part in combat; 

given their higher incidence in this group, eating disorders may become an increasingly important issue. 

Although significant evidence shows that abnormal 
463

Eating Disorders

eating and weight-loss behaviors are more prevalent 

in the military than in the general population, the actual rates of eating-disorder diagnoses in the military 

are at or below the civilian rates. This discrepancy 

may be due to a variety of reasons, including the 

pronounced situational component in the military 

(such as the PFA) producing abnormal eating and 

dieting patterns, the fear of adverse career actions 

probably leading to underreporting, and the fact 

that those with severe eating disorders are screened 

out prior to enlistment or are discharged when their 

eating disorders become evident. Additionally, service members with an eating disorder may try to 

conceal it in order to deploy, because operational 

and combat experience can be an important step 

toward promotion. 

It is likely that few service members with a recognized eating disorder will be deployed to a combat 

zone. Individuals who meet criteria for AN clearly 

should not deploy, and probably should not be on active duty, due to the high rates of morbidity and mortality in AN as well as specialized treatment requirements. Those with a history of BN or EDNOS whose 

symptoms are well controlled should be considered 

on a case-by-case basis. 

A careful history and evaluation should be conducted prior to the decision allowing affected service 

members to deploy. Given the chronicity of eating, only 

those who display good insight, treatment compliance, 

adequate symptom control, and a general high function should be considered for deployment. Potential 

side effects and availability of the prescribed medication should be considered. If multiple psychotropic 

agents, antipsychotics, or anticonvulsants are required 

for symptom stabilization, the service member should 

not be deployed. In particular, it should be noted that 

topiramate is becoming increasingly popular for bulimia but carries a warning for anhidrosis and hyperthermia,144 which would be particularly problematic 

in a desert environment. Additional factors to consider 

include assessment of strengths and weaknesses, support systems, past aggravating factors, comorbidity 

with substance abuse or depression, motivation for 

deployment, anticipated job while deployed, the 

deployment site, and anticipated access to mental 

healthcare. 

It is more likely that a service member with a previously concealed or controlled eating disorder will 

present in theater when symptoms become obvious 

to coworkers or impact the individual’s ability to 

perform. Once again a careful assessment is needed to 

determine if the service member can remain in theater 

or should be returned. Factors to consider are similar 

to those above and include the severity of current 

symptoms, prior history, comorbidity, the individual’s 

job, the location, access to care, and impact on the mission. Metabolic abnormalities and dehydration are of 

particular concern in strenuous or hot climates; thus, 

bulimic patients with such abnormalities should be 

medically evacuated.

Both positive and negative situational factors are 

associated with deployment, and their effects may 

vary on an individual basis. During deployment PFAs 

are suspended, so the pressure of the weigh-in and 

measurements are removed. In most deployment situations personnel have more time to exercise. Also, a hot 

climate affects appetite and food intake. Most dining 

facilities offer a variety of foods so that an individual 

can make healthy choices; however, some may find 

that the buffet style (usually including a dessert and 

ice cream bar) leads to overeating. The communal 

eating and living environment may make bingeing 

and purging less likely (although not impossible). 

Laxatives and diuretics are more difficult to obtain 

in the combat environment, thus further reducing 

purging options. Structured meal times can also either 

decrease the likelihood of overeating or increase the 

urge to binge. There are clearly fewer environmental 

cues such as food commercials and restaurants, although many areas have fast food restaurants that are 

open for extended hours. The separation from home 

environment and family may have either a positive or 

negative impact and should be individually assessed 

for each patient. 

AREAS FOR FURTHER RESEARCH

Further research is necessary to improve the understanding of eating disorders in several areas. It is 

likely that the global war on terror will continue for 

some time, either as continued combat or with a US operational presence at widespread locations around the 

world. Given the known high incidence of abnormal 

eating behaviors in military personnel across services, 

military medical providers must understand how or 

if these conditions impact operational readiness and 

performance. Anecdotally, it appears that most service 

members who deploy lose weight during the deployment, most likely in healthy ways from increased 

exercise and decreased food intake. Deployment may 

somehow be protective for eating disorders due to 

decreases in certain types of stress. Additionally, a primary symptom in eating disorders is an overconcern 

about physical appearance and self-esteem tied to appearance. It may be that in a combat zone these issues 
464

Combat and Operational Behavioral Health

are less important, and that personal satisfaction and 

feelings of reward derive from sources other than food 

or physical appearance. Other valuable research would 

be measuring the actual amount of weight loss during 

deployment, identifying any difference in weight loss 

among those who are and are not overweight prior to 

deployment, and determining whether the incidence 

of eating disorder behaviors is increased or decreased 

with deployment. 

Another area of research interest is the potential 

for comorbid development of posttraumatic stress 

disorder (PTSD) in patients with eating disorders. 

Both eating disorders23–27 and adult PTSD145,146 have 

been linked independently to a history of childhood 

trauma and sexual abuse. It is not known if there is 

an independent link between eating disorders and 

the development of PTSD. An additional area for 

further research is the effect, currently unknown, of 

combat trauma on the risk of developing an eating 

disorder.

SUMMARY

Eating disorders are common among service members, and the military environment includes stressors 

that may contribute to unhealthy behaviors. Healthcare providers must be aware of the signs and symptoms of each disorder, capable of accurate diagnoses, 

and proactive in offering the available treatments, 

both medial and psychiatric. Vigilance is especially 

important with troops preparing for deployment, for 

these disorders may be exacerbated in theater, with 

negative consequences for individuals, their units, and 

their missions. Despite significant long-term morbidity and mortality associated with these conditions, 

eating disorders are treatable. The military may be 

an advantageous environment to provide deterrents 

to unhealthy behaviors, structured support and treatment for affected individuals, and opportunities for 

further research to increase the understanding of these 

disorders. 

REFERENCES

1. Lindquist CH, Bray RM. Trends in overweight and physical activity among US military personnel, 1995–1998. Prev 

Med. 2001;32:57–65.

2. Centers for Disease Control and Prevention. Overweight and Obesity: Selected US National Research Findings. Available 

at: http://www.cdc.gov/women/natstat/overwght.htm. Accessed March 2, 2010.

3. Byrne S, McLean N. Eating disorders in athletes: a review of the literature. J Sci Med Sport. 2001;4:145–159.

4. Marshall JD, Harber VJ. Body dissatisfaction and drive for thinness in high performance field hockey athletes. Int J 

Sports Med. 1996;17:541–544.

5. McNulty PA. Prevalence and contributing factors of eating disorder behaviors in active duty service women in the 

Army, Navy, Air Force, and Marines. Mil Med. 2001;166:53–58.

6. Hudson JI, Hiripi E, Pope HG Jr, Kessler RC. The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Biol Psychiatry. 2007;61:348–358.

7. Silverman JA. Sir William Gull (1819–1890). Limner of anorexia nervosa and myxoedema. An historical essay and 

encomium. Eat Weight Disord. 1997;2:111–116.

8. Gard MCE, Freeman CP. The dismantling of a myth: a review of eating disorders and socioeconomic status. Int J Eat 

Disord. 1996;20:1–12.

9. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: APA; 

1994.

10. Dorian BJ, Garfinkel PE. The contributions of epidemiologic studies to the etiology and treatment of the eating disorders. Psychiatric Ann. 1999;29:187–196.

11. Andersen AE, Bowers WA, Watson T. A slimming program for eating disorders not otherwise specified. Reconceptualizing a confusing, residual diagnostic category. Psychiatr Clin North Am. 2001;24:271–280.
465

Eating Disorders

12. Hoek HW, van Hoeken D. Review of the prevalence and incidence of eating disorders. Int J Eat Disord. 2003;34:383–

396.

13. O’Reardon JP, Peshek A, Allison KC. Night eating syndrome: diagnosis, epidemiology and management. CNS Drugs.

2005;19:997–1008.

14. Kress AM, Peterson MR, Hartzell MD. Association between obesity and depressive symptoms among US military 

active duty service personnel, 2002. J Psychosom Res. 2006;60(3):263–271.

15. Rodin G. The etiology of eating disorders: lessons from high-risk groups. Psychiatr Ann. 1999;29:181–182.

16. Bailer UF, Kaye WH. A review of neuropeptide and neuroendocrine dysregulation in anorexia and bulimia nervosa. 

Curr Drug Targets CNS Neurol Disord. 2003;2:53–59.

17. Klump KL, Kaye WH, Strober M. The evolving genetic foundations of eating disorders. Psychiatr Clin North Am.

2001;24:215–225.

18. Nacmias B, Ricca V, Tedde A, Mezzani B, Rotella CM, Sorbi S. 5-HTA receptor gene polymorphisms in anorexia nervosa 

and bulimia nervosa. Neurosci Lett. 1999;277:134–136. 

19. Spigset O, Andersen T, Hägg S, Mjöndal T. Enhanced platelet serotonin 5-HT2A receptor binding in anorexia nervosa 

and bulimia nervosa. Eur Neuropsychopharmacol. 1999;9:469–473.

20. Levitan RD, Kaplan AS, Masellis M, et al. Polymorphism of the serotonin 5-HT1B receptor gene (HTR1B) associated 

with minimum lifetime body mass index in women with bulimia nervosa. Biol Psychiatry. 2001;50:640–643.

21. King M. The epidemiology of eating disorders. Epidemiol Psichiatr Soc. 1998;7:32–41.

22. Levine MP, Smolak L, Moodey AF, Shuman MD, Hessen LD. Normative developmental challenges and dieting and 

eating disturbances in middle school girls. Int J Eat Disord. 1994;15:11–20.

23. Connors ME, Morse W. Sexual abuse and eating disorders: a review. Int J Eat Disord. 1993;13:1–11. 

24. Léonard S, Steiger H, Kao A. Childhood and adulthood abuse in bulimic and nonbulimic women: prevalences and 

psychological correlates. Int J Eat Disord. 2003;33:397–405.

	 25.	 Wonderlich SA, Brewerton TD, Jocic Z, Dansky BS, Abbott DW. Relationship of childhood sexual abuse and eating

disorders. J Am Acad Child Adolesc Psychiatry. 1997;36:1107–1115.

26. Wonderlich SA, Crosby RD, Mitchell JE, et al. Eating disturbance and sexual trauma in childhood and adulthood. Int 

J Eat Disord. 2001;30:401–412.

27. Merrill LL, Newell CE, Thomsen CJ, et al. Childhood abuse and sexual revictimization in a female Navy recruit sample. 

J Trauma Stress. 1999;12:211–225.

28. Becker AE, Grinspoon SK, Klibanski A, Herzog DB. Eating disorders. N Engl J Med. 1999;340:1092–1098.

29. Birmingham CL. Hypercarotenemia [letter]. N Engl J Med. 2002;347:222–223.

	 30.	 Boland B, Beguin C, Zech F, Desager JP, Lambert M. Serum beta-carotene in anorexia nervosa patients: a case-control

study. Int J Eat Disord. 2001;30:299–305.

31. Mitchell JE, Seim HC, Colon E, Pomeroy C. Medical complications and medical management of bulimia. Ann Intern 

Med. 1987;107:71–77.

32. Karim A, Ahmed S, Rossoff L. Pneumomediastinum simulating a panic attack in a patient with anorexia nervosa. Int 

J Eat Disord. 2003;33:104–107.
466

Combat and Operational Behavioral Health

33. Casiero D, Frishman WH. Cardiovascular complications of eating disorders. Cardio Rev. 2006;14:227–231.

34. Mehler PS. Osteoporosis in anorexia nervosa: prevention and treatment. Int J Eat Disord. 2003;33:113–126.

35. Powers PS. Osteoporosis and eating disorders. J Pediatr Adolesc Gynecol. 1999;12:51–57.

36. Lucas AR, Melton LJ 3rd, Crowson CS, O’Fallon WM. Long-term fracture risk among women with anorexia nervosa: 

a population-based cohort study. Mayo Clin Proc. 1999;74:972–977.

37. Andersen AE, Watson T, Schlechte J. Osteoporosis and osteopenia in men with eating disorders. Lancet. 2000;355:1967–

1968.

38. Wolfe BE, Metzger ED, Levine JM, Jimerson DC. Laboratory screening for electrolyte abnormalities and anemia in 

bulimia nervosa: a controlled study. Int J Eat Disord. 2001;30:288–293.

39. Crow SJ, Rosenberg ME, Mitchell JE, Thuras P. Urine electrolytes as markers of bulimia nervosa. Int J Eat Disord.

2001;30:279–287.

40. Devuyst O, Lambert M, Rodhain J, Lefebvre C, Coche E. Haematological changes and infectious complications in 

anorexia nervosa: a case-control study. Q J Med. 1993;86:791–799.

41. Pauporte J, Walsh BT. Serum cholesterol in bulimia nervosa. Int J Eat Disord. 2001;30:294–298.

42. Pritts SD, Susman J. Diagnosis of eating disorders in primary care. Am Fam Physician. 2003;67:297–304.

43. American Psychiatric Association. Practice Guideline for the Treatment of Patients With Eating Disorders. 2nd ed. Washington, DC: APA; 2000.

44. Patton GC. Mortality in eating disorders. Psychol Med. 1988;18:947–951.

45. Sullivan PF. Mortality in anorexia nervosa. Am J Psychiatry. 1995;152:1073–1074.

46. Eckert ED, Halmi KA, Marchi P, Grove W, Crosby R. Ten-year follow-up of anorexia nervosa: clinical course and 

outcome. Psychol Med. 1995;25:143–156.

47. Herzog W, Deter HC, Fiehn W, Petzold E. Medical findings and predictors of long-term physical outcome in anorexia 

nervosa: a prospective 12-year follow-up study. Psychol Med. 1997;27:269–279.

48. Ratnasuriya RH, Eisler I, Szmukler GI, Russell GF. Anorexia nervosa: outcome and prognostic factors after 20 years. 

Br J Psychiatry. 1991;158:495–502.

	 49.	 Zipfel S, Löwe B, Reas DL, Deter HC, Herzog W. Long-term prognosis in anorexia nervosa: lessons from a 21-year

follow-up study. Lancet. 2000;355:721–722.

50. Herzog DB, Nussbaum KM, Marmor AK. Comorbidity and outcome in eating disorders. Psychiatr Clin North Am.

1996;19:843–859.

51. Keel PK, Mitchell JE. Outcome in bulimia nervosa. Am J Psychiatry. 1997;154:313–321.

52. Nielsen S. Epidemiology and mortality of eating disorders. Psychiatr Clin North Am. 2001;24:201–214, vii–viii.

53. Nielsen S, Moller-Madsen S, Isager T, Jorgensen J, Pagsberg K, Theander S. Standardized mortality in eating disorders—

a quantitative summary of previously published and new evidence. J Psychosom Res. 1998;44:413–434.

54. Davidson DM. Anorexia nervosa in a serviceman: case report. Mil Med. 1976;141:617–619.

55. Voge VM, Yacavone D. Bulimia: an uncommon problem in aircrewmen—a case report. Aviat Space Environ Med.

1987;58:347–349.
467

Eating Disorders

56. Berg JS, Moore JL. A case of “eating disorder NOS”: aeromedical implications of DSM-IV diagnostic criteria. Aviat 

Space Environ Med. 1996;67:157–160.

57. Sundgot-Borgen J. Risk and trigger factors for the development of eating disorders in female elite athletes. Med Sci 

Sports Exerc. 1994;26:414–419.

58. Lauder TD, Williams MV, Campbell CS, Davis GD, Sherman RA. Abnormal eating behaviors in military women. Med 

Sci Sports Exerc. 1999;31:1265–1271.

59. Lauder TD, Williams MV, Campbell CS, Davis G, Sherman R, Pulos E. The female athlete triad: prevalence in military 

women. Mil Med. 1999;164:630–635.

60. McNulty PA. Prevalence and contributing factors of eating disorder behaviors in active duty Navy men. Mil Med.

1997;162:753–758.

61. McNulty PA. Prevalence and contributing factors of eating disorder behaviors in a population of female Navy nurses. 

Mil Med. 1997;162:703–706.

62. Babar N, Alam M, Ali SS, et al. Anorexic behaviour and attitudes among female medical and nursing students at a 

private university hospital. J Pak Med Assoc. 2002;52:272–276.

63. Szweda S, Thorne P. The prevalence of eating disorders in female health care students. Occup Med (Lond). 2002;52:113–

119.

64. Peterson AL, Talcott GW, Kelleher WJ, Smith SD. Bulimic weight-loss behaviors in military versus civilian weightmanagement programs. Mil Med. 1995;160:616–620.

65. Warner C, Warner C, Matuszak T, Rachal J, Flynn J, Grieger TA. Disordered eating in entry-level military personnel. 

Mil Med. 2007;172:147–151.

66. Carlton JR, Manos GH, Van Slyke JA. Anxiety and abnormal eating behaviors associated with cyclical readiness testing 

in a naval hospital active duty population. Mil Med. 2005;170:663–667.

67. Vitousek K, Watson S, Wilson GT. Enhancing motivation for change in treatment-resistant eating disorders. Clin Psychol 

Rev. 1998;18:391–420.

68. American Psychiatric Association. Practice Guidelines for the Treatment of Patients with Eating Disorders [revised]. 

Am J Psychiatry. 2000;157(suppl):1.

69. McKenzie JM, Joyce PR. Hospitalization for anorexia nervosa. Int J Eat Disord. 1992;11:235–241.

70. Agras WS. The consequences and costs of the eating disorders. Psychiatr Clin North Am. 2001;24:371–379.

71. Russell GF. Involuntary treatment in anorexia nervosa. Psychiatr Clin North Am. 2001;24:337–349.

72. Rigotti NA. Eating disorders. In: Carlson KJ, Eisenstat SA, eds. Primary Care of Women. St Louis, Mo: Mosby-Year Book; 

1995: 443–449.

73. Becker AE, Hamburg P, Herzog DB. The role of psychopharmacologic management in the treatment of eating disorders. 

Psychiatr Clin North Am. 1998;5:17–51.

74. Golden NM, Iglesias EA, Jacobson MS, et al. Alendronate for the treatment of osteopenia in anorexia nervosa: a randomized, double-blind, placebo-controlled trial. J Clin Endocrinol Metab. 2005;90:3179–3185.

75. Nakahara T, Nagai N, Tanaka M, et al. The effects of bone therapy on tibial bone loss in young women with anorexia 

nervosa. Int J Eat Disord. 2006;39:20–26.

76. Mitchell JE, Peterson CB, Myers T, Wonderlich S. Combining pharmacotherapy and psychotherapy in treatment of 

patients with eating disorders. Psychiatr Clin North Am. 2001;24:315–323.
468

Combat and Operational Behavioral Health

77. Russell GF, Szmukler GI, Dare C, Eisler I. An evaluation of family therapy in anorexia nervosa and bulimia nervosa. 

Arch Gen Psychiatry. 1987;44:1047–1056.

78. Lock J, le Grange D, Agras WS, Dare C. Treatment Manual for Anorexia Nervosa: A Family Based Approach. New York, 

NY: Guilford Press; 2001.

79. Bowers WA. Basic principles for applying cognitive-behavioral therapy to anorexia nervosa. Psychiatr Clin North Am.

2001;24:293–303, x.

80. Mark M, Rabinowitz J, Rabinowitz S, Gaoni B, Babur I, Danon Y. Brief treatment of anorexia nervosa in military personnel. Hosp Community Psychiatry. 1993;44:69–71.

81. McIntosh VV, Jordan J, Carter FA, et al. Three psychotherapies for anorexia nervosa: a randomized, controlled trial. 

Am J Pscyhiatry. 2005;162:741–747.

	 82.	 Levenson CW. Zinc regulation of food intake: new insights on the role of neuropeptide Y. Nutr Rev. 2003;61:247–

249.

	 83.	 Su JC, Birmingham CL. Zinc supplementation in the treatment of anorexia nervosa. Eat Weight Disord. 2002;7:20–22.

84. Birmingham CL, Goldner FM, Bakan R. Controlled trial of zinc supplementation in anorexia nervosa. Int J Eat Disord.

1994;15:251–255.

85. Birmingham CL, Gritzner S. How does zinc supplementation benefit anorexia nervosa? Eat Weight Disord. 2006;11:e109–

e111.

86. Szmukler GI, Young GP, Miller G, Lichenstein M, Binns DS. A controlled trial of cisapride in anorexia nervosa. Int J 

Eat Disord. 1995;17:347–357.

87. Attia E, Schroeder L. Pharmacologic treatment of anorexia nervosa: where do we go from here? Int J Eat Disord. 

2005;37(suppl):s60–s63.

88. Bulik CM, Berkman ND, Brownley KA, Sedway JA, Lohr KN. Anorexia nervosa treatment: a systematic review of 

randomized controlled trials. Int J Eat Disord. 2007;40:310–320. 

89. Halmi KA, Eckert E, LaDu TJ, Cohen J. Anorexia nervosa. Treatment efficacy of cyproheptadine and amitriptyline. 

Arch Gen Psychiatry. 1986;43:177–181.

90. Lacey JH, Crisp AH. Hunger, food intake and weight: the impact of clomipramine on a refeeding anorexia nervosa 

population. Postgrad Med J. 1980;56(suppl 1):79–85.

91. Ruggiero GM, Laini V, Mauri MC, et al. A single blind comparison of amisulpride, fluoxetine and clomipramine in 

the treatment of restricting anorectics. Prog Neuropsychopharmacol Biol Psychiatry. 2001;25:1049–1059.

92. Mitchell JE, Fletcher L, Hanson K, et al. The relative efficacy of fluoxetine and manual-based self-help in the treatment 

of outpatients with bulimia nervosa. J Clin Psychopharmacol. 2001;21:298–304.

93. Kaye WH, Nagata T, Weltzin TE, et al. Double-blind placebo-controlled administration of fluoxetine in restricting- and 

restricting-purging-type anorexia nervosa. Biol Psychiatry. 2001;49:644–652.

94. Anderson IM, Parry-Billings M, Newsholme EA, Fairburn CG, Cowen PJ. Dieting reduces plasma tryptophan and 

alters brain 5-HT function in women. Psychol Med. 1990;20:785–791.

95. Walsh BT, Kaplan AS, Attia E, et al. Fluoxetine after weight restoration in anorexia nervosa: a randomized controlled 

trial. JAMA. 2006;295:2605–2612.

96. Cassano GB, Miniati M, Pini S, et al. Six-month open trial of haloperidol as an adjunctive treatment for anorexia nervosa: a preliminary report. Int J Eat Disord. 2003;33:172–177.
469

Eating Disorders

97. La Via MC, Gray N, Kaye WH. Case reports of olanzapine treatment of anorexia nervosa. Int J Eat Disord. 2000;27:363–

366.

98. Hansen L. Olanzapine in the treatment of anorexia nervosa. Br J Psychiatry. 1999;175:592.

99. Vandereycken W. Neuroleptics in the short-term treatment of anorexia nervosa. A double-blind placebo-controlled 

study with sulpiride. Br J Psychiatry. 1984;144:288–292.

100. Vandereycken W, Pierloot R. Pimozide combined with behavior therapy in the short-term treatment of anorexia nervosa. A double-blind pacebo-controlled cross-over study. Acta Psychiatr Scand. 1982;66:445–450.

101. Mondraty N, Birmingham CL, Touyz S, Sundakov V, Chapman L, Beumont P. Randomized controlled trial of olanzapine in the treatment of cognitions in anorexia nervosa. Australas Psychiatry. 2005;13:72–75.

102. Marrazzi MA, Bacon JP, Kinzie J, Luby ED. Naltrexone use in the treatment of anorexia nervosa and bulimia nervosa. 

Int Clin Psychopharmacol. 1995;10:163–172.

103. Crow S, Mussell MP, Peterson C, Knopke A, Mitchell J. Prior treatment received by patients with bulimia nervosa. Int 

J Eat Disord. 1999;25:39–44.

104. Thiels C, Schmidt U, Treasure J, Garthe R, Troop N. Guided self-change for bulimia nervosa incorporating use of a 

self-care manual. Am J Psychiatry. 1998;155:947–953.

105. Agras WS, Crow SJ, Halmi KA, Mitchell JE, Wilson GT, Kraemer HC. Outcome predictors for the cognitive behavior 

treatment of bulimia nervosa: data from a multisite study. Am J Psychiatry. 2000;157:1302–1308.

106. Pope HG Jr, Hudson JI, Jonas JM, Yurgelun-Todd D. Bulimia treated with imipramine: a placebo-controlled, doubleblind study. Am J Psychiatry. 1983;140:554–558.

107. Agras WS, Dorian B, Kirkley BG, Arnow B, Bachman J. Imipramine in the treatment of bulimia: a double-blind controlled study. Int J Eat Disord. 1987;6:29–38.

108. Barlow J, Blouin J, Blouin A, Perez E. Treatment of bulimia with desipramine: a double-blind crossover study. Can J 

Psychiatry. 1988;33:129–133.

109. Hughes PL, Wells LA, Cunningham CJ, Ilstrup DM. Treating bulimia with desipramine. A double-blind, placebocontrolled study. Arch Gen Psychiatry. 1986;43:182–186.

	110.	 Blouin AG, Blouin JH, Perez EL, Bushnik T, Zuro C, Mulder E. Treatment of bulimia with fenfluramine and desipramine. J Clin Psychopharmacol. 1988;8:261–269.

111. Walsh BT, Gladis M, Roose SP, Stewart JW, Stetner F, Glassman AH. Phenelzine vs placebo in 50 patients with bulimia. 

Arch Gen Psychiatry. 1988;45:471–475.

112. Kennedy SH, Piran N, Warsh JJ, et al. A trial of isocarboxazid in the treatment of bulimia nervosa. J Clin Psychopharmacol. 1988;8:391–396.

113. Rothschild R, Quitkin HM, Quitkin FM, et al. A double-blind placebo-controlled comparison of phenelzine and imipramine in the treatment of bulimia in atypical depressives. Int J Eat Disord. 1994;15:1–9.

114. Walsh BT, Agras WS, Devlin MJ, et al. Fluoxetine for bulimia nervosa following poor response to psychotherapy. Am 

J Psychiatry. 2000;157:1332–1334.

115. Fluoxetine Bulimia Nervosa Collaborative Study Group. Fluoxetine in the treatment of bulimia nervosa: a multicenter, 

placebo-controlled, double-blind trial. Arch Gen Psychiatry. 1992;49:139–147.

116. Goldstein DJ, Wilson MG, Thompson VL, Potvin JH, Rampey AH Jr. Fluoxetine Bulimia Nervosa Research Group. 

Long-term fluoxetine treatment of bulimia nervosa. Br J Psychiatry. 1995;166:660–666.
470

Combat and Operational Behavioral Health

117. Blouin J, Blouin A, Perez E, Barlow J. Bulimia: independence of antibulimic and antidepressant properties of desipramine. Can J Psychiatry. 1989;34:24–29.

118. Goldstein DJ, Wilson MG, Ascroft RC, al-Banna M. Effectiveness of fluoxetine therapy in bulimia nervosa regardless 

of comorbid depression. Int J Eat Disord. 1999;25:19–27.

119. Romano SJ, Halmi KA, Sarkar NP, Koke SC, Lee JS. A placebo-controlled study of fluoxetine in continued treatment 

of bulimia nervosa after successful acute fluoxetine treatment. Am J Psychiatry. 2002;159:96–102.

120. Milano W, Petrella C, Sabatino C, Capasso A. Treatment of bulimia nervosa with sertraline: a randomized controlled 

trial. Adv Ther. 2004;21:232–237.

121. Fichter MM, Krüger R, Rief W, Holland R, Döhne J. Fluvoxamine in prevention of relapse in bulimia nervosa: effects 

on eating-specific psychopathology. J Clin Psychopharmacol. 1996;16:9–18.

122. Leombruni P, Amianto F, Delsedime N, Gramaglia C, Abbate-Daga G, Fassino S. Citalopram versus fluoxetine for the 

treatment of patients with bulimia nervosa: a single-blind randomized controlled trial. Adv Ther. 2006;23:481–494.

123. Sundblad C, Landén M, Eriksson T, Bergman L, Eriksson E. Effects of the androgen antagonist flutamide and the 

serotonin reuptake inhibitor citalopram in bulimia nervosa: a placebo-controlled pilot study. J Clin Psychopharmacol.

2005;25:85–88.

124. Horne RL, Ferguson JM, Pope HG Jr, et al. Treatment of bulimia with bupropion: a multicenter controlled trial. J Clin 

Psychiatry. 1988;49:262–266.

125. Nathan PE, Gorman JM. Treatments That Work. 2nd ed. New York, NY: Oxford University Press; 2002: 560.

126. Walsh BT, Hadigan CM, Devlin MJ, Gladis M, Roose SP. Long-term outcome of antidepressant treatment for bulimia 

nervosa. Am J Psychiatry. 1991;148:1206–1212.

127. Hoopes SP, Reimherr FW, Hedges DW, et al. Treatment of bulimia nervosa with topiramate in a randomized, doubleblind, placebo-controlled trial, part 1: improvement in binge and purge measures. J Clin Psychiatry. 2003;64:1335–

1341.

128. Nickel C, Tritt K, Muehlbacher M, et al. Topiramate treatment in bulimia nervosa patients: a randomized, double-blind, 

placebo-controlled trial. Int J Eat Disord. 2005;38:295–300.

129. Faris PL, Kim SW, Meller WH, et al. Effect of decreasing afferent vagal activity with ondansetron on symptoms of 

bulimia nervosa: a randomised, double-blind trial. Lancet. 2000;355:792–797.

130. Pope HG Jr, Keck PE Jr, McElroy SL, Hudson JI. A placebo-contolled study of trazodone in bulimia nervosa. J Clin 

Psychopharmacol. 1989;9:254–259.

131. Goldbloom DS, Olmsted M, Davis R, et al. A randomized controlled trial of fluoxetine and cognitive behavioral therapy 

for bulimia nervosa: short-term outcome. Behav Res Ther. 1997;35:803–811.

132. Fichter MM, Leibl K, Rief W, Brunner E, Schmidt-Auberger S, Engel RR. Fluoxetine versus placebo: a double-blind 

study with bulimic inpatients undergoing intensive psychotherapy. Pharmacopsychiatry. 1991;24:1–7.

	133.	 Mitchell JE, Pyle RL, Eckert ED, Hatsukami D, Pomeroy C, Zimmerman R. A comparison study of antidepressants

and structured intensive group psychotherapy in the treatment of bulimia nervosa. Arch Gen Psychiatry. 1990;47:149–

157.

134. Bacaltchuk J, Trefiglio RP, de Oliveira IR, Lima MS, Mari JJ. Antidepressants versus psychotherapy for bulimia nervosa: 

a systematic review. J Clin Pharm Ther. 1999;24:23–31.

135. Bacaltchuk J, Trefiglio RP, Oliveira IR, Hay P, Lima MS, Mari JJ. Combination of antidepressants and psychological 

treatments for bulimia nervosa: a systematic review. Acta Psychiatr Scand. 2000;101:256–264.
471

Eating Disorders

136. Arnold LM, McElroy SL, Hudson JI, Welge JA, Bennett AJ, Keck PE. A placebo-controlled, randomized trial of fluoxetine in the treatment of binge-eating disorder. J Clin Psychiatry. 2002;63:1028–1033.

137. Ricca V, Mannucci E, Mezzani S, et al. Fluoxetine and fluvoxamine combined with individual cognitive-behaviour 

therapy in binge eating disorder: a one-year follow-up study. Psychother Psychosom. 2001;70:298–306.

138. Guerdjikova AI, McElroy SL, Kotwal R, et al. High-dose escitalopram in the treatment of binge-eating disorder with 

obesity: a placebo-controlled monotherapy trial. Hum Psychopharmacol. 2008;23:1–11.

139. McElroy SL, Arnold LM, Shapira NA, et al. Topiramate in the treatment of binge eating disorder associated with 

obesity: a randomized, placebo-controlled trial. Am J Psychiatry. 2003;160:255–261.

	140.	 Gadde KM, Franciscy DM, Wagner HR II, Krishnan KR. Zonisamide for weight loss in obese adults: a randomized

controlled trial. JAMA. 2003;289:1820–1825.

141. Wilfley DE, Crow SJ, Hudson JI, et al. Efficacy of sibutramine for the treatment of binge eating disorder: a randomized 

multicenter placebo-controlled double-blind study. Am J Psychiatry. 2008;165:51–58. Epub December 3, 2007.

142. Bays H, Dujovne C. Pharmacotherapy of obesity: currently marketed and upcoming agents. Am J Cardiovasc Drugs. 

2002;2:245–253.

143. Padwal R, Li SK, Lau DC. Long-term pharmacotherapy for obesity and overweight. Cochrane Database Syst Rev. 

2004;3:CD004094.

144. Hulihan J, Ortho-McNeil Pharmacutical. Important drug warning letter to healthcare professionals, December 18, 2003. 

http://www.fda.gov/downloads/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/

UCM169494.pdf. Accessed March 2, 2010.

145. Clancy CP, Graybeal A, Tompson WP, et al. Lifetime trauma exposure in veterans with military-related posttraumatic 

stress disorder: association with current symptomatology. J Clin Psychiatry. 2006;67:1346–1353.

146. Lapp KG, Bosworth HB, Strauss JL, et al. Lifetime sexual and physical victimization among male veterans with combatrelated post-traumatic stress disorder. Mil Med. 2005;170:787–790.
472

Combat and Operational Behavioral Health