The eating disorders, anorexia nervosa and bulimia nervosa, may be classified as true psychosomatic illnesses, inasmuch as an underlying biological vulnerability interacts with a particular cultural stress in order to produce behavioral and psychological symptoms. For example, anorexia and bulimia nervosa are more prevalent in industrialized societies, where there is an overabundance of food and where attractiveness in women is linked with being thin, than in agriculturally-based societies. Immigrants from cultures in which anorexia nervosa is rare are more likely to develop the illness as they assimilate the ideals of a thin body appearance.

Essentials of Diagnosis

DSM-IV-TR Diagnostic Criteria

1. 
   

   Refusal to maintain body weight at or above a minimally normal weight for age and height (e.g., weight loss leading to maintenance of body weight less than 85% of that expected; or failure to make expected weight gain during a period of growth, leading to body weight less than 85% of that expected).

   
   
2. 
   

   Intense fear of gaining weight or becoming fat, even though underweight.

   
   
3. 
   

   Disturbance in the way in which one’s body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or denial of the seriousness of the current low body weight.

   
   
4. 
   

   In postmenarcheal females, amenorrhea, i.e., the absence of at least three consecutive menstrual cycles. (A woman is considered to have amenorrhea if her periods occur only following hormone, e.g., estrogen, administration.)

Specify type:

• Restricting type: during the current episode of anorexia nervosa, the person has not regularly engaged in binge-eating or purging behavior (i.e., self-induced vomiting or the misuse of laxatives, diuretics, or enemas).
  
• Binge-eating/purging type: during the current episode of anorexia nervosa, the person has regularly engaged in binge-eating or purging behavior (i.e., self-induced vomiting or the misuse of laxatives, diuretics, or enemas).

(Reprinted, with permission, from Diagnostic and Statistical Manual of Mental Disorders, 4th edn, Text Revision. Copyright 2000 American Psychiatric Association.)

General Considerations

In some ways, the term anorexia nervosa is a misnomer, because the affected individual’s appetite and craving for food are usually preserved. Nevertheless, the individual will actively counter the feelings of hunger with disordered thinking, leading to self-imposed starvation. The threshold for defining the amount of weight loss considered to be serious enough to qualify for the diagnosis of anorexia nervosa is computed on the basis of the Metropolitan Life Insurance tables or pediatric growth charts. A body mass index less than or equal to 17.5 kg/m2 (calculated as weight in kilograms/height in meters2) represents an alternative guideline accepted by many researchers. Nevertheless, these standards are only suggested guidelines, and clinicians should also consider the individual’s body build and weight history.

Epidemiology

Lifetime prevalence rates for anorexia nervosa in females are approximately 0.5–1.0, or 1 in 100–200 individuals. Many more individuals exhibit symptoms that do not meet the criteria for the disorder (i.e., eating disorder not otherwise specified; see later in this chapter), but this is an area for continued research. More than 90% of affected individuals are female, and data concerning the prevalence of the illness in males are scant. Worldwide, the disorder appears to be most common in the United States, Canada, Europe, Australia, Japan, New Zealand, and South Africa; but few systematic studies of the illness have been conducted in other countries.

The onset of illness is bimodal: One peak occurs in early adolescence (age 12–15 years) and another in late adolescence and early adulthood (age 17–21 years); the mean age at onset is approximately 17 years. The illness rarely appears de novo before puberty or after age 40 years. Often an associated life event, such as moving away from home, precedes the first episode of anorexia nervosa. Although the prevalence of this disorder showed marked increases in the latter half of the twentieth century, more recently this rate of increase has slowed.

Etiology

The incidence and prevalence of eating disorders have increased greatly in the latter half of the 20th century. This increase is due in part to cultural pressures in industrialized societies (placed largely on women), including an overemphasis on a slim female figure with an almost prepubescent shape. This emphasis is depicted in magazines, the entertainment industry, and beauty contests. Nevertheless, anorexia nervosa cannot be completely culturally based, because it appears to have been described almost 300 years ago, when cultural pressures were different. Consequently, part of the etiology of eating disorders must be biological, with the degree of phenotypic expression determined by cultural factors. Disturbances in central nervous system monoamines, particularly norepinephrine and serotonin, and in certain neuropeptides have been reported in the acute phase of anorexia nervosa. Few of these abnormalities persist into the weight-restored phase of the illness, and those that do may be at least partially related to the state of malnutrition.

Genetics

Concordance rates for monozygotic twins with anorexia nervosa are higher than those for dizygotic twins. Among first-degree biological relatives, there is an increased risk for anorexia nervosa and for mood disorder, the latter found particularly among the relatives of individuals with the binge-eating/purging type. More recent studies have identified a susceptibility locus on chromosome 1. There is at least preliminary evidence for certain candidate genes which confer susceptibility, including the norepinephrine transporter (NET) gene, the monoamine oxidase A (MAO-A) gene, and the serotonin transporter (SERT) gene.

Clinical Findings

Signs & Symptoms

Weight loss is frequently accomplished by reduction in total food intake and also involves the exclusion of highly caloric foods, leading to an extremely restricted diet. Patients may lose weight by purging (via either self-induced vomiting or misuse of laxatives and diuretics) or by exercising excessively. As weight continues to decline, the patient’s fear of becoming fat may increase, as do feelings of being overweight. The body image distortion that these individuals experience has a wide range, from the fervently held belief that one is globally overweight, to a realization that one is thin but that certain body parts such as the abdomen, buttocks, or thighs are too big. Such disturbed self-perceptions may be modified by cultural factors and may not present prominently. Instead, the patient may complain of a distaste for food or epigastric discomfort as the expressed motivation for food restriction.

Self-esteem in patients with anorexia nervosa is overly dependent on body shape and weight, and these patients seem obsessed with employing a wide variety of techniques to estimate body size, including frequent weighing, measuring of body parts, and looking in the mirror for perceived fat. Losing weight is judged to be an admirable achievement of unusual self-discipline, whereas weight gain is regarded as an unacceptable failure of self-control. Meanwhile, patients typically deny the serious medical implications of malnutrition.

Most patients with anorexia nervosa have food-related obsessions. They frequently hoard food or collect recipes and may be involved in food preparation for the family or in food-related professions (e.g., waitress, cook, dietitian, nutritionist). They may also have fears of eating in public. Such obsessions have also been observed in other forms of starvation, including experimental starvation.

Signs of starvation account for most of the physical findings in anorexia nervosa. These signs include emaciation; significant hypotension, especially orthostatic; bradycardia; hypothermia; skin dryness and flakiness; Lanugo, or the presence of downy body hair on trunks or extremities; peripheral edema, especially ankle edema; petechiae on extremities; sallow complexion; salivary gland hypertrophy, particularly of the parotid gland; dental enamel erosion; osteoporosis (which results from reduced estrogen secretion, increased cortisol secretion, and inadequate calcium intake); and Russell’s sign, or scars and calluses on the back of the hand. Amenorrhea may precede the onset of appreciable diminished weight, because it may be related to the loss of body fat stores rather than decrease of body mass. Menarche may be delayed in prepubertal females.

Among patients who frequently engage in purging behaviors, many do not binge eat. Instead, they regularly vomit after consuming small meals.

It is not clear which of the many psychological manifestations seen in anorexia nervosa are a cause or consequence of malnutrition, as studies of forced starvation in volunteers have reported symptoms of food preoccupations, food hoarding, binge eating, unusual taste preferences, as well as other personality changes, such as depression, obsessionality, apathy, and irritability. Such symptoms remit with nutritional rehabilitation.

Psychological Testing

Although extensive psychological testing is not used in the diagnosis of anorexia nervosa, screening tests can be extremely valuable in identifying eating psychopathology in community samples. Two such tests are the Eating Disorders Inventory and the Eating Attitudes Test. These tests are also useful in documenting improvement during treatment. It is also important to assess coexisting Axis I and Axis II psychiatric illness with relevant instruments such as the Structured Clinical Interview for the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) or the Beck Depression Inventory. It is felt that deficits on neuropsychological tests that persist after refeeding are associated with poorer outcomes.

Laboratory Findings & Imaging

Most organ systems are affected by malnutrition, and a variety of physical disturbances can be noted (Table 26–1). Coexisting dehydration may be indicated by an elevated blood urea nitrogen. If induced vomiting is part of the clinical picture, then metabolic alkalosis may ensue, with elevated serum bicarbonate, hypochloremia, and hypokalemia. Laxative abuse may cause metabolic acidosis and a positive stool for occult blood. Neuroendocrine abnormalities are also common.

Amenorrhea is the result of abnormally low levels of estrogen secretion, which is due to a diminution of pituitary release of follicle-stimulating hormone and luteinizing hormone. For patients who have been amenorrheic for 6 months or more, a bone density examination is recommended.

Differential Diagnosis

General medical conditions such as chronic inflammatory bowel disease, hyperthyroidism, malignancies, and AIDS can cause serious weight loss; however, it is rare for patients with these disorders to have a distorted body image, a fear of becoming obese, or a desire for further weight loss. Such medical conditions are also usually not associated with increased exercise and activity, except for hyperthyroidism. Superior mesenteric artery syndrome, a disorder characterized by postprandial vomiting secondary to intermittent gastric outlet obstruction, may precede or occur concurrently with anorexia nervosa when significant emaciation is present.

Coexisting major depressive disorder may present a difficult differential diagnosis. Most individuals with uncomplicated major depression do not have an excessive fear of gaining weight; however, even after weight restoration, anorexic patients may experience episodes of depression that require intervention. Individuals with schizophrenia may present with fluctuating weight patterns and bizarre beliefs related to food, but rarely demonstrate the body image disturbance and fear of fat associated with anorexia nervosa.

Because the diagnostic criteria for social phobia, obsessive–compulsive disorder, and body dysmorphic disorder overlap with those of anorexia nervosa, additional diagnoses of these disorders should be made only if individuals with anorexia nervosa have fears, obsessions, or body distortions unrelated to eating, food, or body shape and size.

Treatment

Anorexic individuals seldom seek professional assistance on their own, but instead are persuaded or coerced by family members to be evaluated for treatment. These individuals rarely complain about the weight loss per se but rather will describe the somatic or psychological distress related to the consequences of starvation, such as cold intolerance, muscle weakness or loss of stamina, constipation, abdominal pain, and mental depression. Frequently patients deny the core problem, and the history obtained from such patients is unreliable. Consequently it is advisable for the clinician to obtain information from family members or other outside sources to accurately evaluate features of the illness, such as the degree of weight loss.

A multidisciplinary approach utilizing multiple modalities is essential in treating anorexia nervosa. This is because no controlled treatment studies exist to determine the comparative efficacy of any particular management model for any eating disorder, nor have any potential adverse effects of psychosocial stratagems been systematically assessed. The Psychiatrist may coordinate a treatment team that includes other disciplines, such as psychologists, social workers, registered dietitians, and other physicians and dentists. Educational materials, including self-help workbooks; information on community-based and Internet resources; and direct advice should be provided to patients and their families by trained professionals. Such materials also help to counter other misinformation disseminated over the Internet by ‘pro-ana’ websites that promulgate a permissive attitude towards eating disorder lifestyles.

Patients may require acute intensive medical intervention to correct fluid and electrolyte imbalances, cardiac problems, and organ failure. It may be beneficial to the patient to institute such intensive treatment earlier rather than later in the course of the illness, when the consequences of malnutrition, such as cortical gray matter loss, osteoporosis, or delayed physical growth and development, have become evident. Hospitalization should most certainly occur prior to the development of medical instability, such as orthostatic hypotension, heart rhythm abnormalities, or hypothermia.

The advent of behavior therapies has reduced markedly the morbidity and mortality of the illness; these therapies are now the centerpiece of most inpatient therapeutic programs. There is general agreement that weight restoration should be a central goal for seriously underweight adult patients, and for children and adolescents who are well below their expected height and weight, and most of these patients will require inpatient management, during which controlled conditions can be achieved. In such an environment, patients are encouraged to consume increased numbers of calories in order to earn specific privileges, such as increased activity, decreased need for staff supervision, visits from relatives, and therapeutic sessions. During this phase, it is felt by clinicians that patients must be engaged in individual and family therapy in order to secure their cooperation and alliance with the treatment program. In some cases, forced nasogastric or parenteral feeding is necessary, but such invasive medical procedures have considerable risk of inducing refeeding syndrome, or infection. Although family therapy is felt to be essential in children and adolescents, adults who have had the illness for more than 5 years rarely demonstrate much response to this modality, or any other form of psychotherapeutic intervention. Group psychotherapy is frequently utilized as a therapeutic modality, but its efficacy has not been adequately assessed in any scientific study to date.

Careful attention must be paid to caloric intake, so that these patients are not fed too quickly, but they must receive enough food to overcome their metabolic resistance (occasionally reaching 70–100 kcal/kg per day, especially in male patients), both during and immediately after the weight-gaining phase. This curious phenomenon of resistance to weight gain has been linked to energy wasting and relatively higher resting energy expenditure (REE) in malnourished patients. Most clinicians attempt to achieve weight goals of 2–3 lbs/week for hospitalized patients, and 0.5–1 lb/week in partial or outpatient programs. For seriously underweight patients, exercise should be be carefully monitored and supervised, and in some cases restricted, as there is considerable risk of pathological fracture with high-impact activities, such as running or jumping. Care should be taken to avoid refeeding syndrome, consisting of hypophosphatemia, hypomagnesemia, hypocalcemia, and fluid retention. This is especially true in patients who have abruptly been withdrawn from diuretics or laxatives, as they have elevated aldosterone levels due to chronic dehydration, a consequence of abusing such substances. Hypothyroidism in underweight patients is a physiological reaction to malnutrition, and should not be treated with exogenous hormone replacement, as it will reverse with weight restoration. Nutritional status may be monitored with serum complement 3 and 4, and serum transferr in levels.

Healthy target weights for female patients should be determined by the weight at which normal menstrual function returns, which may be higher than the weight at which such patients first experienced amenorrhea. Usually, this weight is at least 90% of average body mass index (i.e., 20–25). For male patients, a target weight should be determined by the restoration of normal testicular function. In prepubertal children and adolescents, growth curves should be followed. It has been reported that anorexic patients who achieve their target weights prior to discharge from the hospital have lower rehospitalization rates than those patients who are discharged before achieving their target weight.

Pharmacologic agents, such as antidepressants, second generation antipsychotics, cyproheptadine, and lithium, may be helpful adjuncts, especially for patients who have coexisting depressive or psychotic features. Some patients may show some response to pro-motility agents, such as metoclopramide, during the refeeding phase of their treatment. Antianxiety agents have also been given before mealtimes by clinicians to mitigate anticipatory anxiety. No specific psychopharmacologic agent has been discovered that can induce an anorexic patient to eat and gain weight outside of a structured behaviorally oriented program. Medications should be utilized with caution in malnourished patients, as they are much more susceptible to their potential side effects.

However, there is some evidence that certain medications, such as olanzapine may aid in weight gain in adult and adolescent underweight anorexics, and that fluoxetine in dosages of up to 60 mg/day, may have some utility in preventing relapse in patients whose weight has been restored. Some patients have also benefited from zinc-containing supplements. Although hormone replacement therapy is frequently prescribed, there is no evidence that estrogen replacement, biphosphonates (e.g. alendronate), or calcium or vitamin D supplementation can reverse the reduced bone mineral density caused by malnutrition in anorexic patients.

Controlled trials and clinical consensus suggest that cognitive–behavioral therapies (CBT) and interpersonal psychotherapies (IPT) may be helpful to patients with anorexia nervosa in maintaining weight and healthy eating behaviors. It is felt that ongoing psychotherapeutic treatment is indicated for one or more years following weight restoration.

Complications/Adverse Outcomes of Treatment

Medical complications of anorexia nervosa are common, especially if the disease has been present for 5 years or more. Complications include anemia, which is usually normochromic and normocytic (i.e., with normal erythrocyte indices); impaired renal function, which is associated with chronic dehydration and hypokalemia, or the direct toxicity of laxatives; cardiovascular complications such as arrhythmias and hypotension; osteoporosis, resulting from diminished dietary calcium, increased cortisol, and decreased estrogen secretion; and dental decay.

Many patients with anorexia nervosa exhibit symptoms of depressed mood, social withdrawal, obsessional symptoms, irritability, insomnia, and diminished interest in sex. Almost 50% meet criteria for major depressive disorder, but these features may be complications of starvation rather than a truly comorbid condition. Such depressive symptoms should be reassessed after weight restoration, because they persist in a subset of patients. Patients with the bulimic type of anorexia nervosa are more likely to abuse alcohol or other drugs, exhibit labile mood, be sexually active, and have other impulse-control problems. If anorexia nervosa develops prior to puberty, it may be associated with more severe comorbid mental disturbances.

Obsessive–compulsive symptoms unrelated to food, body shape, or weight may be present and may warrant a diagnosis of obsessive–compulsive disorder in up to one-quarter of anorexic patients. Other psychological symptoms, such as feelings of ineffectiveness, a need to control one’s environment, inflexible thinking, limited social spontaneity, and overly restrained initiative and emotional expression, may also be observed during the course of the illness (Table 26–2).