Eating Disorders

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[edit] Eating Disorders

Jarol B. Knowles

The eating disorders—anorexia nervosa, bulimia nervosa, rumination syndrome, binge eating disorder, and anorexia athletica—are relatively common maladies. Once believed to be problems largely among young women, the disorders are being found increasingly among children, young athletes, men, and elderly women. Primary care physicians may be the first to suspect potential problems, including a patient's fixation on food, weight, dieting, physique, and exercise. Patients who have struggled in silence for years may turn to their trusted physician for support and understanding. Primary care physicians can encounter eating disorders when patients seek help with medical or psychiatric complications of malnutrition or illness-related behaviors or when family members bring them to the physician's attention (often against the patient's wishes). Eating disorders are complex and involve two sets of issues and behaviors: those directly relating to food and weight and those involving the relationships with self and others. The phrase “eating disorder” is somewhat misleading in that it implies that the essence of the problem is disordered eating and suggests that the solution is to learn to eat normally again. Often accompanied by depression, anxiety, and personality disorders, eating disorders may be difficult to diagnose.

[edit] ANOREXIA NERVOSA

[edit] Definition and Epidemiology

Anorexia nervosa is characterized by prominent behavioral, psychologic, and physiologic disturbances, including refusal to maintain a minimally healthy body weight (85% of that expected), dramatic weight loss, fear of gaining weight even though underweight, preoccupation with food, and abnormal food consumption patterns.^[1] Biologic indicators of anorexia nervosa include reductions in heart rate, blood pressure, and metabolic rate; increased cortisol production; and a profound decrease in the production of estrogen (or, in males, testosterone).^[2][3][4] Anorexia is not the result of a single biologic factor or psychologic aberration, but rather the product of a dynamic interaction of biologic, psychologic, and social influences.

Anorexia nervosa primarily affects women (about 95% of cases). In the United States, 27% of adolescent girls who view themselves as being at the “right weight” still attempt to lose weight, compared with less than 10% of adolescent boys.^[5] The prevalence of anorexia nervosa is an estimated 0.7% among randomly selected females, although it is higher among those in the uppermost socioeconomic strata (1% of a group of British private-school students). Both American and European studies imply that the incidence may be increasing, although these data may be skewed by increased media attention.

[edit] Pathogenesis and Pathophysiology

[edit] Sociocultural Factors.

In both anorexia nervosa and bulimia nervosa the modern cultural value for females to be thin plays a role in the pathogenesis. The increased prevalence of eating disorders among women who engage in certain activities and occupations (e.g., professional models, ballet dancers) is evidence of the strong influence of sociocultural phenomena in the genesis of anorexia nervosa. The higher prevalence of eating disorders among Western societies (and the development of these disorders among individuals of Eastern heritage transplanted to Western societies) is further evidence of a strong cultural influence on eating disorder pathogenesis. Social pressures from peers, particularly during adolescence, seem to influence young women and girls to engage in anorectic behaviors. Since anorexia nervosa has been described for more than 300 years, however, modern sociocultural ideals are not the sole cause of this disease but create the environment for the expression of an eating disorder in the predisposed individual.

[edit] Psychologic Factors.

Anorectic patients may have an incompletely developed personal identity and struggle to maintain a sense of control over their environment. These individuals often describe growing up with the sense that they are expected to excel, but they lack the sense that they are valued and loved for themselves. Low self-esteem has been cited as the most important predictor of future anorexia nervosa among several risk factors for the disease. In response to parental expectations, the preanorectic child learns to be hard working, eager to please, and attentive to family needs. In turn the parents may support and indulge their child's behaviors. These mutually reinforced actions produce interdependence among the family members (i.e., enmeshment). Rather than developing a sense of self-worth based on internal standards, the preanorectic girl becomes engaged in an obsessive quest for external approval; she has a difficult time separating her goals and desires from those of her environment. Furthermore, if the external environment values thinness, the preanorectic female is validated in her quest for thinness.

More than 80% of anorectic patients develop symptoms within 7 years of menarche. In a normal child, biologic and psychologic events (e.g., menarche, growth spurt, school, adolescent peer pressure) encourage individuation and separation from the family. The biologic and emotional changes associated with menarche lead to a feeling of being out of control. In the predisposed individual the conflicts and loss of control are resolved by the pursuit of thinness, which allows the person to control one aspect of life absolutely. The sensation of a loss of control is heightened by the major life changes (leaving home to start school, marriage, death of a parent) that may occur at this time of life. One of these events often precipitates the onset of symptoms.

Data indicate a high prevalence of sexual abuse among anorectic patients and, more frequently, among bulimic patients. In one study of 158 patients admitted to an eating disorder unit, 50% of the anorectic and bulimic patients reported sexual abuse, compared with 28% of the patients with other eating disorder diagnoses.^[6] The relation of this traumatic psychologic experience to the development of an eating disorder is uncertain. Abusive experiences may not be causative but may affect the clinical expression of the disorder.

Amenorrhea and loss of body fat may maintain the anorectic female in a prepubertal childlike state, thereby reducing the psychosocial pressures related to her developing sexuality.

[edit] Biologic Factors.

Biologic factors may increase susceptibility to developing anorexia nervosa. Anorexia nervosa has a 6% prevalence in siblings, and in one study of twin pairs, 9 of 12 monozygotic and 1 of 14 dizygotic pairs were concordant for the disorder.^[7] Also, anorexia nervosa and depressive disorder may coexist in first-degree relatives of anorectic patients.

Recent studies of serotonin and leptin in patients with anorexia nervosa suggest that physiologic abnormalities may play a role. Increases in brain serotonin function lead to reductions in food intake, and decreases in brain serotonin function are associated with depression. Cerebrospinal fluid (CSF) levels of the major serotonin metabolite, 5-hydroxyindoleacetic acid (5-HIAA), are low in underweight individuals with anorexia nervosa but then rise to above-normal levels in those with longstanding recovery.^[8] Low CSF levels of 5-HIAA are associated with impulsive behavior, such as suicide attempts. High levels of 5-HIAA in recovered patients may indicate perfectionism and rigidity, characteristics seen in many individuals with anorexia nervosa before the illness develops. Thus a premorbid disturbance in serotonergic function might be a risk factor for the development of this disorder.

Leptin is a hormone secreted by fat cells that plays a role in the regulation of body fat stores and appetite. Serum leptin levels correlate with fat mass and tend to be low in underweight anorexic patients. These levels increase with weight gain but appear to precede normalization of body weight. The negative feedback effect of serum leptin on the appetite center in the brain may explain patients' difficulties with attaining and maintaining normal weights.^[9]

[edit] Natural History.

Typically, patients with anorexia nervosa present in the teenage years. Some have described a bimodal incidence curve, with one peak at 13 to 14 years and another at 17 to 18 years. Many individuals who develop anorexia nervosa during adolescence eventually make full recoveries. For approximately 50% of patients the long-term outcome is variable, with a significant number reaching adulthood with irrational concerns about weight gain. The mortality, from complications of starvation or from suicide, is substantial, approximately 5% per decade of follow-up.^[10] The degree of social integration (with parents and friends) is a stronger predictor of a favorable outcome than either medical treatment or psychotherapy.

[edit] Patient History

Suspected anorexia nervosa demands a careful patient history with assessment of eating attitudes. Anorectic patients are often preoccupied with food and may exhibit bizarre food preferences or elaborately prepare food for others. Most lose weight through dietary restriction and exercise (i.e., restrictor subgroup), but up to 50% also self-induce vomiting or take purgatives (i.e., bulimic subgroup). Obtaining a history of these disorders requires sensitivity and recognition of the patient's reluctance to disclose “shameful” information. The primary care physician must establish a sense of trust and ask questions in a caring and nonjudgmental manner.

Patients are often brought to the physician's attention by friends or relatives. Recent media attention focusing on the dangers of anorexia nervosa has led to a generation of adolescents who deny their problem, creating a treatment challenge. Anorectic patients may also have constipation, crampy abdominal pain, abdominal bloating, or amenorrhea; a high index of suspicion is needed in such patients.

[edit] Physical Examination

A complete physical examination is important in patients with suspected anorexia nervosa and should include a nutritional assessment. Height and weight are usually sufficient screening parameters. Two methods can determine the degree of malnutrition: measurement of body mass index (BMI) or comparison to standardized weight tables for percentage of ideal body weight (% IBW). A BMI less than 18 is abnormal, but a % IBW less than 85% is more often used to diagnose anorexia nervosa.

Findings may include a thin body habitus, increased amounts of fine, downy body hair (lanugo), and acrocyanosis (Box 55-1). Subcutaneous fat may be greatly decreased. The skin of anorectic patients is often dry and scaly and may have a slightly yellow cast due to carotenemia. Mild peripheral edema, without associated hypoproteinemia, may be noted. Vital signs are frequently notable for decreased core body temperature, bradycardia, and mild hypotension. If symptoms develop before puberty, secondary sex characteristics may not have developed. Unlike patients with involuntary starvation, anorectic patients do not usually manifest signs and symptoms of vitamin deficiency, although scurvy and pellagra have been reported.

[edit] Psychologic and Behavioral Findings.

Anorectic patients frequently overestimate their body width and insist that they are overweight despite objective evidence to the contrary; however, their perception of others' body size is unimpaired. Abnormalities in perception of enteroceptive stimuli are also present; the sensation of satiety is altered, and patients often deny fatigue. Frequently they work or exercise to the point of exhaustion. Recognition of emotional states (e.g., anger, depression) is blunted. Disturbances in mood, primarily depression, are common, and on clinical presentation, major affective disorder is seen in approximately 50% of patients. Defects in conceptual thought and abstract reasoning are evidenced by the patient's sense of being controlled by the environment and resultant feelings of ineffectiveness. Anorectic patients tend to view situations in extremes; they have difficulty perceiving the “grays” in life and interpret the actions of others in a rigid and highly personalized form.

[edit] Medical Findings.

The medical findings of anorexia nervosa are primarily the result of starvation (see Box 55-1). The progression of complications correlates with the severity of malnutrition.

Endocrine abnormalities are among the most consistent medical findings among anorectic patients. Amenorrhea is part of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) diagnostic criteria; its onset may precede weight loss (Box 55-2). Amenorrhea in anorexia nervosa is caused by hypothalamic-pituitary dysfunction. Serum estradiol levels in anorectic patients are uniformly lower than in normal controls, as are serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels. The patterns of LH secretion in anorectic patients are similar to those seen in pubescent or prepubescent females. Patients who recover normal weight often have resumption of menses; amenorrhea may persist in up to 38% of these patients. Studies have shown that a body fat content of 17% is required for the initiation of gonadotropin cycling. Weight loss below this level before menarche results in primary amenorrhea; weight loss below this level after menarche results in secondary amenorrhea. Resumption of menses after a weight loss cessation usually requires a higher body fat content (about 22%). Psychogenic amenorrhea (amenorrhea in times of severe psychologic stress in the absence of weight loss) is a well-recognized phenomenon and may account for some of the menstrual irregularities observed in anorectic patients. Hypoestrogenemia, along with nutritional deficiencies, contributes to the osteoporosis sometimes seen in anorexia nervosa.

Neuroimaging in anorexic patients has revealed morphologic and functional alterations in the brain, most of which are currently interpreted as consequences of the anorectic state that are reversible, at least partially, after weight gain. Enlargement of CSF spaces, mainly of cortical sulci, is evident on computed tomography (CT) and magnetic resonance imaging (MRI). This reversible shrinkage of brain tissue (pseudoatrophy) also affects the pituitary gland. Positron emission tomography (PET) has revealed caudate hyperactivity during the anorectic state; several mild right-left asymmetries, possibly related to alterations of mental state (e.g., vigilance, depression), have also been reported in bulimia nervosa.

Starvation-induced alterations of neuropeptide activity probably contribute to neuroendocrine dysfunction in anorexia nervosa. For example, corticotropin-releasing hormone (CRH) alterations contribute to hypercortisolemia, and neuropeptide Y alterations may contribute to amenorrhea. Alterations of these peptides and in opioid, vasopressin, and oxytocin activity could contribute to other characteristic psychophysiologic disturbances (e.g., reduced feeding) in acutely ill patients. Such neuropeptide disturbances may contribute to the vicious cycle hypothesized to occur in anorexia nervosa; that is, the consequences of malnutrition perpetuate pathologic behavior.

Findings consistent with hypothyroidism (dry skin, brittle nails, coarse hair, cold intolerance, bradycardia, delayed deep tendon reflex relaxation, and constipation) are often seen; however, clinically significant hypothyroidism does not occur in anorexia nervosa, and thyroid supplementation is not indicated. Thyroid-stimulating hormone (TSH) and free thyroxine levels are usually normal. Reverse triiodothyronine (rT₃) is elevated in response to starvation and is responsible for a decreased metabolic rate as an adaptive response to starvation. Increasing weight results in a reversal of the relative hypothyroid state.

Adrenal hormone abnormalities include normal or slightly increased plasma cortisol and decreased levels of urinary 17-hydroxycorticosteroids. These changes probably result from decreased clearance of cortisol from the plasma and an increase in cortisol-binding capacity, since 24-hour cortisol production rate and basal adrenocorticotropic hormone (ACTH) secretion are normal. Plasma norepinephrine levels are diminished, a finding also seen in starvation; these values return to normal with weight increase.

Cardiovascular findings include left ventricular wall thinning, decreased left ventricular chamber size, and consequent decreased cardiac output. These are adaptive changes to decreases in circulating catecholamine levels and can lead to decreased blood pressure and peripheral edema. Electrocardiographic (ECG) abnormalities (e.g., decreased QRS amplitude, prolongation of QT interval, nonspecific ST segment changes, U waves) may be related to electrolyte abnormalities. Arrhythmias (dysrhythmias) may occur, especially in patients with electrolyte abnormalities, and sudden death has occurred in severely malnourished patients. Refeeding may precipitate acute congestive heart failure.

Changes in gastrointestinal function are common in anorectic patients, who typically complain of early satiety, bloating, belching, vomiting, and constipation. Evidence indicates gastric electrical dysrhythmias, impaired antral contraction, and delayed emptying of a solid meal. Improvement in gastric emptying with domperidone suggests dysfunction of dopaminergic peptides or their receptors in the central and enteric nervous systems. Chronic constipation results from decreased oral intake, decreased intestinal transit, laxative or diuretic abuse, or any combination. Fecal impaction should be considered if constipation suddenly develops. With or without laxative abuse, barium enema studies may show a dilated, atonic, and ahaustral colon. Rapid refeeding in anorectic patients can result in acute gastric dilation, acute pancreatitis, and malabsorptive diarrhea (which may be caused by deficiencies in pancreatic and intestinal brush border digestive enzymes). Elevations in serum transaminases and alkaline phosphatase are caused by starvation-induced hepatic steatosis. Most of the gastrointestinal manifestations resolve with careful refeeding.

Renal complications include prerenal azotemia, which is caused by increased protein catabolism and intravascular volume depletion, resulting in decreased glomerular filtration rate (GFR). Decreased GFR may result in an increased tendency toward nephrolithiasis. Refeeding may cause volume overload secondary to aldosterone-induced sodium retention; such changes may take months to reverse completely.

Other miscellaneous findings include increases in serum carotene, cholesterol, and vitamin A levels, in contrast to most patients with starvation where these are decreased. The reason for these differences in the anorectic population is unknown, although the increased intake of vegetables high in β-carotene and thus vitamin A value may account for their elevated levels, and shifts in adrenocortical or thyroid metabolism may cause the elevated cholesterol. Mild decreases in serum albumin and other serum proteins may be seen in anorexia nervosa; these findings are less pronounced relative to similar abnormalities seen in other starved patients. Finally, anorectic patients may manifest hematologic abnormalities, including leukopenia, mild anemia, and thrombocytopenia. Hypocomplementemia has been reported. However, these patients do not have a substantially increased risk of infectious complications.

[edit] Differential Diagnosis

The diagnosis of anorexia nervosa is made using the DSM-IV diagnostic criteria (see Box 55-2). Although definitive diagnosis must exclude specific diseases that produce malnutrition, such considerations should include only those with a reasonable index of suspicion because of historic or physical examination data. The differential diagnosis includes Addison's disease, diabetes mellitus, panhypopituitarism, hyperparathyroidism, hypothyroidism or hyperthyroidism, celiac disease, Crohn's disease, intestinal parasitosis, tuberculosis, acquired immunodeficiency syndrome (AIDS), lymphoma (or other neoplastic processes), hypothalamic tumor, schizophrenia, and primary major depression. Laboratory tests should be individualized and obtained only if the diagnosis is in question or to assess metabolic derangements (Box 55-3). Some patients require minimal tests, whereas others, particularly extremely malnourished patients, require more diagnostic testing.

[edit] Management

The treatment of anorexia nervosa must address the nutritional and medical consequences of the disorder and the psychologic and environmental factors that maintain the anorectic behavior. A multidisciplinary approach, with medical, psychologic, and nutritional support, is therefore crucial.

The primary care physician is usually responsible for medical and nutritional care as well as psychologic support. Factors in the effectiveness of this ongoing care include fostering a sense of autonomy in the patient by encouraging her to take responsibility in the treatment, remaining objective and honest to maintain the patient's sense of trust, working with the family, and serving as the liaison (and patient's advocate) with consultants and counselors. The physician must help the patient to acknowledge and relate thoughts and feelings and should strive to encourage behaviors that reinforce the patient's status as a fully differentiated individual. It is essential to inform the patient that she may see treatments as undesirable, that she may feel that her control is threatened by them, and that a return to better health is in her best interest. The methods and goals of treatment and any later changes should be explained, with ample time for the patient to express thoughts and feelings. Any lack of consistency, evasiveness, or judgmental behavior will undermine the patient's sense of trust; such a loss of trust substantially impedes the treatment process. Family involvement is encouraged. Initially, therapy should be directed toward modifying the dysfunctional pattern within the family that helps maintain the patient's anorectic behavior. Later, family members can be used to aid the patient in weight gain through positive reinforcement. The primary care physician, with the input of appropriate consultants, should make all long-term treatment decisions.

[edit] Correction of Nutritional Deficits.

Nutritional repletion is usually accomplished on an outpatient basis, unless a life-threatening condition (e.g., cardiac dysrhythmias, severe electrolyte and mineral deficiencies) requires hospital admission. Adaptation to a lower energy intake over time usually results in normal serum chemistries. Hospitalization should be considered for abnormal serum chemistries (low serum albumin, potassium, phosphorus, or magnesium). Postural hypotension is an indication for intravenous fluid replacement. Fluid and electrolyte replacement can be accomplished in the emergency room, with careful measurement of electrolyte abnormalities; electrolyte and mineral deficiencies are often seen after fluid replacement. Careful monitoring for electrolyte imbalance, especially potassium, phosphorus, and magnesium, is important during fluid replacement. Refeeding syndrome is a common complication of rapid repletion of energy deficits and is avoided by a judicious rate of replacement. Care should be taken during refeeding to observe for congestive heart failure, acute gastric dilation, and pancreatitis. A follow-up plan should be provided to the patient before discharge from the hospital.

Encouraging oral intake can be extremely difficult. The anorectic patient often survives on 250 kcal per day and has adapted to this low energy intake. Oral nutritional supplements can be helpful because real food is often shunned. The patient should be told that the supplements are like prescription medicine that needs to be taken three or four times daily. Addition of a prokinetic agent (domperidone, metoclopramide) may help with gastric emptying. An initial goal of 750 to 1000 kcal per day (three or four cans of a nutritional supplement) is reasonable. This level of feeding provides the recommended nutrition intake (RNI) for vitamins. A multivitamin may be added and is rarely refused. Forced feedings may worsen the patient's sense of a loss of control; focusing on the medical consequences of continued weight loss helps to involve the patient in the therapy without forced feedings. The oral intake should be maintained above starvation levels.

If the patient refuses to comply with this approach, the physician should consider initiation of tube feedings, which most anorectic patients try to avoid. Rarely, parenteral nutrition is necessary, especially with a noncompliant patient or multiple complications of malnutrition. When parenteral supplements are used, caloric delivery should start at half the daily requirement on day 1 to three fourths on day 2, with full repletion on day 3 and thereafter. This is to minimize the possible complications from rapid infusion of hyperosmolar solutions. Refeeding peripheral edema is common. Elevated transaminases associated with tender hepatomegaly may result from fatty infiltration of the liver during refeeding; this responds to decreasing the infusion rate.

When considering involuntary feeding measures in anorectic patients, a balance must be struck between the patient's willingness to undergo such feedings and their medical necessity. Forced feedings may exacerbate psychologic symptoms of the illness, but if the patient understands the medical need for such feedings and actively participates in the decision to initiate them, these effects may be minimized. Nutrition intervention strategies designed to correct specific medical concerns are effective if the patient can see a direct relationship between food intake and health.

Some patients with anorexia nervosa are refractory to outpatient treatment and may require referral to a residential treatment center. A hospital or residential setting provides a safe, controlled environment for initiating or reestablishing medical, psychologic, and nutritional rehabilitation. A defined nutrition care plan establishes the daily caloric intake, rate of weight gain, weight range goal for discharge, limitations in food choices, and need for supervision during and immediately after meals. In addition, limits on activity may be useful in ensuring weight gain in patients with low body weight. Unfortunately, most residential treatment centers operate on a for-profit basis and are financially inaccessible for some families.

The goals of supplemental nutrition in anorexia nervosa are (1) to achieve a weight that removes the patient from acute medical danger and (2) to correct overt metabolic derangements. Supplemental feedings should be discontinued when the medical and nutritional goals are achieved. This period often allows for mobilization of a multidisciplinary team or referral to a specialized facility. Since each patient's recovery process is unique, treatment plans need to be highly individualized. The key to success in nutrition intervention for outpatients is a very gradual change in food intake patterns and related behaviors.

[edit] Psychotherapy.

It is essential to separate food-related and weight-related behaviors from feelings and psychologic issues. This process involves helping patients separate their identity, feelings, and unresolved issues from the focus on food, hunger, and weight so that the two problems can be addressed separately. The drive to be thin can be put in the context of societal expectations about weight and body issues.

Psychotherapy has met with variable success. Behavioral therapy uses operant conditioning to promote weight gain and may include cognitive methods and social skills training. Coming to terms with the need for control, the need for perfection, and external factors that influence behavior can be useful in some patients. Family therapy has also been used and appears to have some success in the long term, especially in younger patients with a shorter duration of illness. Combined behavioral modification and family therapy approaches have demonstrated impressive long-term positive results. No current consensus exists on a uniform method of psychotherapy in anorexia nervosa.

[edit] Pharmacotherapy.

Drugs have no proven benefit in anorexic patients, although the selective serotonin reuptake inhibitors (SSRIs) may be helpful in certain patients. Patients with anorexia nervosa often exhibit symptoms of other psychiatric disorders. Many are depressed, and many are obsessed with thoughts about weight and eating and engage in compulsive rituals suggestive of obsessive-compulsive disorder (OCD). The SSRIs are useful in the treatment of depression and OCD but have limited value during the weight gain phase of treatment.^[11][12] One study reported that patients receiving fluoxetine after weight restoration in a hospital had a lower rate of relapse during the succeeding year than did patients receiving placebo.^[13]

[edit] BULIMIA NERVOSA

[edit] Definition and Epidemiology

Bulimia (from the Greek terms for “ox hunger”) is a compulsive behavior defined by episodic bouts of overeating (binge eating) usually followed by acts designed to avert weight gain (self-induced vomiting, cathartic or diuretic use). This behavior can be seen in anorexia nervosa, but patients with bulimia nervosa are distinguished by their normal body size. Bulimia nervosa also typically affects young (under 30 years) white women (90% to 95%). Although the point prevalence using the DSM-IV criteria is about 1% of the general population, studies of female high-school and college students report that 4.5% to 18% have had bulimia and that 19.6% of college women had binge-purge behaviors consistent with bulimia. The prevalence of bulimic behaviors among men is less than among women, although the estimated prevalence of such behaviors among college-age men is 10%. Most patients exercise their bulimic behaviors in secret; one British survey revealed that only a third of a group of about 500 women who met diagnostic criteria for bulimia had ever discussed their eating problems with a physician.^[14] As with anorexia nervosa, bulimia nervosa is believed to have a multifaceted origin; biologic predisposition combines with psychologic and sociobehavioral determinants to yield the integrated syndrome.

[edit] Pathogenesis and Pathophysiology

[edit] Biologic Factors.

Evidence of an underlying biologic defect in bulimia nervosa is circumstantial but compelling. As noted in patients with anorexia nervosa, bulimic patients have a higher familial incidence of affective disorders than the general population. Alcoholism and major depression have the strongest correlations. Bulimic patients, even those of normal weight, frequently have menstrual abnormalities; a significant proportion have amenorrhea. The strongest evidence of a biologic aberration may be the neurotransmitter abnormalities noted with bulimia nervosa. Evidence exists for a defect in serotonin-mediated satiety regulation; serotonin metabolism in bulimic patients is abnormal. Norepinephrine metabolism is persistently altered in bulimic patients as well. Cholecystokinin (CCK), a gut peptide secreted in response to food intake, is also a neurotransmitter in the central nervous system (CNS) involved in the regulation of the satiety response. One study found that postprandial serum CCK levels in bulimic patients were blunted compared with normal controls.^[15] Satiety sensation was also blunted in the bulimic group. A subgroup of bulimic patients treated with antidepressants had a significant increase in both CCK response to eating and satiety sensation. These data imply that bulimic behaviors are related to CNS neurotransmitter and receptor dysregulation, supporting the use of psychopharmacologic agents in treatment.

[edit] Psychologic Factors.

The psychologic underpinnings of bulimia nervosa are similar to those of anorexia nervosa. Bulimic patients also tend to come from families with conflict resolution problems and express similar feelings of a loss of control, low self-esteem, and use of external sources (e.g., parents) for validation of self-worth. Childhood sexual abuse, as mentioned earlier, is emerging as a risk factor for the development of bulimia nervosa.

[edit] Sociocultural Factors.

The same social pressures to be thin noted in the discussion of anorexia nervosa apply to the genesis of bulimia nervosa. Purging behavior becomes a prominent manner in which the bulimic patient attempts to control weight to attain a perceived ideal body habitus in the face of a periodic uncontrollable urge to have an eating binge.

[edit] Natural History.

Bulimia nervosa classically begins later in life than anorexia nervosa (usually ages 17 to 25) and may occur in an individual with a history of anorexia. The prebulimic patient is typically mildly overweight and has attempted to lose weight by dieting without success. She may be introduced to purging as a means of weight control by a friend or relative; often, purging behaviors precede binge eating. At some point the hallmark of the disorder appears: the uncontrollable urge to eat and the inability to stop. Subsequently, repeated cycles of binge-purge behavior ensue; the patient's sense of a lack of control intensifies after each binge episode, with reduced self-esteem. Because of the secretive nature of their behaviors and their usually normal weight, patients often do not present for treatment until their 30s or 40s. Bulimic patients may be diagnosed because of a medical complication or major psychologic distress. By this time most bulimic patients are clinically depressed, and 5% have attempted suicide. They are more likely to exhibit impulsive behaviors (e.g., kleptomania, substance abuse, sexual promiscuity) than anorectic patients. The risk of drug and alcohol use among bulimic patients is three to five times greater than in nonbulimic women in the general population. Bulimia is often characterized as having an irregular course, with frequent relapses and remissions. In general, bulimic outpatients with at least 1-year follow-up demonstrate recovery rates of 30% to 70% (average 50%). Most recoveries have been noted within 1 year of presentation; those who fail to recover by that point are unlikely to do so. Relapse rates are high (40% to 63%). Factors predictive of a poor outcome include a history of ethanol abuse, suicide attempts, and increased depressive symptoms. Mortality is not increased over the rate in the general female population.

[edit] Patient History

Although bulimic patients are more distressed by their behaviors than anorectic patients (and therefore are more likely to seek medical attention), they also are often embarrassed by their binge-purge activities and may not be willing to reveal these activities to their primary care physician. Again, a careful history with assessment of eating attitudes is essential (Box 55-4). As with anorectics, bulimics may have constipation, crampy abdominal pain, and amenorrhea; they may also have complications from their binge-purge activity.

[edit] Physical Examination

As with anorexia nervosa patients, a complete physical examination is important in bulimia nervosa patients and may provide clues to the diagnosis in patients with suspected bulimia. Physical findings associated with bulimia include painless parotid or salivary gland swelling, bruised or abraded knuckles secondary to self-induced vomiting (Russell sign), and facial ecchymoses, conjunctival hemorrhages, pharyngitis, and dental enamel erosions caused by repeated emesis (Box 55-5).

[edit] Psychologic and Behavioral Findings.

The characteristic behavioral manifestation of bulimia nervosa is the binge-purge cycle. This is typified by episodes of compulsive eating with a failure to respond to or achieve normal satiety. Patients typically binge on high-calorie foods rich in carbohydrates that require little chewing. Binge episodes, during which the bulimic individual consumes between 1000 and 55,000 kcal during a relatively brief interval, usually occur in secret after extensive planning. The binge is usually terminated by feelings of guilt or physical discomfort (nausea, abdominal pain). At this point most patients self-induce vomiting or take laxatives. Although patients report feelings of excitement and anticipation while planning a binge, most feel shame afterward. Bulimic patients are typically embarrassed by their symptoms and are reluctant to reveal details of their illness to family members and health care providers. Their obsession with food-related and binge-related activities can interfere with social interactions. Unlike anorectics, however, bulimics are usually outgoing and engage in heterosexual relationships.

Bulimic patients view their behavior as an uncontrollable compulsion and thus are more willing to try and stop. By contrast, anorectic patients hide their behavior from friends and co-workers because they are unwilling to change.

Affective disorders are common; estimates of depression in bulimic patients range from 20% to 80%. They also have a higher incidence of anxiety disorders (45%) than either anorectic patients or the general population. The presence of bulimia has been correlated with personality disorders, particularly borderline personality disorder. Obese bulimic patients are less likely to use purgatives than normal-weight patients and are more prone to have affective disorders (91% vs. 70%), especially major depression.

[edit] Medical Findings.

Endocrine abnormalities may include menstrual irregularities (40% to 50%), and 20% of bulimic women without a history of anorexia have amenorrhea for at least 3 months at some point during their illness. Approximately 50% have abnormal dexamethasone suppression tests. Serum cortisol levels and secretion patterns are normal.

Gastrointestinal effects of bulimia primarily related to repeated emesis may include oropharyngeal complications (dental erosions, pharyngitis, parotid enlargement), esophagitis, esophageal erosions and ulcerations, Mallory-Weiss tears, and esophageal rupture (see Box 55-5). Peptic acid esophageal injury has a higher incidence in bulimic patients than in the general population. Delayed gastric emptying and prolonged whole-gut transit times in bulimic patients may explain the symptoms of bloating and crampy abdominal pain. Acute gastric dilation has been described, usually in relation to the ingestion of large meals, as has gastric rupture. Constipation is a common complaint. Degeneration of Auerbach's plexus results from chronic stimulant laxative use (cathartic colon). With asymptomatic elevations in serum amylase, the salivary isoenzyme fraction is predominant in most cases. Acute pancreatitis may be caused by alcohol abuse or abrupt pancreatic stimulation during binge eating.

Cardiovascular effects of bulimia may include ipecac cardiotoxicity from alkaloid poisoning and dysrhythmias from hypokalemia, a common electrolyte abnormality in bulimic patients. Pulmonary findings may include pneumomediastinum, resulting from pulmonary rupture caused by vigorous emesis, and aspiration pneumonia, often from vomiting while under the influence of alcohol. Metabolic complications may include metabolic alkalosis from repeated emesis (the most common finding), metabolic acidosis from laxative abuse, hypochloremia, hypokalemia, hypomagnesemia, hypocalcemia, hyponatremia, and hypophosphatemia. Dehydration may also occur, leading to secondary hyperaldosteronism and to reflex peripheral edema, which may be pronounced with cessation of the abused diuretics or laxatives.

[edit] Differential Diagnosis

The DSM-IV diagnosis of bulimia nervosa is based on the presence of the binge eating pattern, the persistent overconcern about body shape and size, and the exclusion of other medical conditions (Box 55-6). The differential diagnosis is limited and includes schizophrenia, seizure disorders, and rare neurologic disorders (e.g., Kleine-Levin syndrome, Klüver-Bucy syndrome). Diagnostic testing is usually not necessary, except as indicated by historic and physical examination data and as needed to monitor complications.

[edit] Management

Because bulimic patients are cognizant of the maladaptive nature of their behaviors, they are often willing to work with their physician in therapy. The patient can usually interpret symptoms in terms of current and past emotional issues, so psychologic concerns and establishment of better coping methods should be discussed. The family may need to be involved. Generally, inpatient therapy is not recommended.

[edit] Psychotherapy.

The psychotherapeutic approach to bulimia usually emphasizes controlling the abnormal behaviors. Cognitive behavioral therapy is often used; the patient recognizes the specific abnormal behaviors and uses behavior modification techniques to control them. This technique uses a three-stage approach, beginning with a self-monitoring period, during which the patient is taught to become more aware of her eating behavior and to establish a regular pattern of eating, with conscious avoidance of binge behavior by decreasing available food. This is followed by a recognition period (patient recognizes association between binges and stress, achieving greater control over eating pattern) and a maintenance period (patient records tactics used to avert bingeing and purging during stress to reinforce learned behavioral adaptations). Both individual and group approaches have been used successfully.^[16]

[edit] Pharmacotherapy.

Antidepressants can successfully treat bulimia, with striking reductions (average 50%) in binge frequency compared with placebo in both depressed and nondepressed bulimic patients. Most studies have been short term (6 to 8 weeks' duration), however, and some reports indicate that long-term efficacy is not as high for all medications tested. Notably, patients taking fluoxetine seem to maintain their response as long as they take the medication, although higher doses (e.g., 60 mg/day) may be needed in some patients. The usual tricyclic antidepressant dose (e.g., 100 to 250 mg/day of desipramine) seems to be effective. The best candidates for pharmacotherapy are those who have failed cognitive behavioral therapy, severely depressed patients, and responsible patients capable of communicating potential beneficial and adverse drug effects to the physician. Patients with a partial response to cognitive behavioral therapy or pharmacotherapy may benefit from combined therapy.^[17]

[edit] RUMINATION SYNDROME

Rumination syndrome (merycism), considered a medical curiosity for more than 300 years, is infrequently diagnosed because physician recognition is lacking. The patient with this eating disorder repetitively regurgitates small amounts of food from the stomach, rechews the food, and reswallows it. The three subgroups with rumination disorder are (1) emotionally deprived or mentally impaired children and adults; (2) persons in whom the behavior develops as a maladaptive habit, worsening in times of stress; and (3) persons in whom rumination is associated with bulimia.

The prevalence of rumination in adults is unknown. Patients who seek treatment report symptoms of weight loss, regurgitation, or vomiting and may express concern of an underlying medical disorder. The diagnosis is made by manometric or radiographic studies, which reveal that episodes are initiated by a belch or a swallow. The lower esophageal sphincter pressure is lowered to allow creation of a common channel between the stomach and esophagus.^[18] At the same time, diaphragmatic and rectus muscle contractions raise intraabdominal pressure, leading to regurgitation. Diagnosis is based on identifying the typical clinical features and excluding other medical or psychiatric disease. Extensive diagnostic testing is usually not needed. Since the disorder appears to be a learned maladaptive habit, behavioral modification and biofeedback techniques are recommended as treatment approaches.

[edit] EATING DISORDER NOT OTHERWISE SPECIFIED

The DSM-IV classification of eating disorder not otherwise specified is reserved for disorders of eating that do not meet the criteria for anorexia nervosa or bulimia nervosa. If the primary symptom is recurrent episodes of binge eating without the regular use of inappropriate compensatory behaviors (e.g., self-induced vomiting, fasting), the diagnosis of binge eating disorder can be applied. The typical patient is overweight and consults the primary care physician for help with weight loss. In weight loss clinics about one quarter to one third of patients meet criteria for binge eating disorder. The arbitrary choice of two episodes of bingeing per week suggests the diagnosis.

Binge eating also appears to be associated, independent of weight, with a greater frequency of psychiatric problems, such as depression, larger and more frequent weight fluctuations, and more severe weight-related distress. These findings suggest a meaningful distinction between obese binge eaters and nonbinge eaters. Some of these individuals may initially resist psychotherapy because they do not understand the relationship between underlying emotional or psychologic issues and the inability to cease binge eating.

Starvation and self-imposed dieting may result in eating binges (once food is available) and psychologic manifestations (preoccupation with food and eating, increased emotional responsiveness, dysphoria, distractibility). Caution is thus advisable in counseling patients to restrict their eating to lose weight, since the negative sequelae may outweigh the benefits of restrained eating. Instead, healthful, balanced eating without specific food restrictions should be recommended as a long-term strategy to avoid the perils of restrictive dieting.

[edit] ANOREXIA ATHLETICA

Evidence suggests an increasing prevalence of eating disorders and body weight obsessions in certain subpopulations of female athletes. The pressure on female athletes to improve their performances and physiques, coupled with the general sociocultural demand placed on all women to be thin, often results in attempts to achieve unrealistic body size and body weight goals. For some female athletes the pressure to achieve and maintain a low body weight leads to potentially harmful patterns of restrictive eating or chronic dieting. The interrelationships among menstrual dysfunction, athletic training, and disordered eating are not fully understood. The high incidence of menstrual abnormalities in female athletes has critical health consequences, however, because amenorrheic athletes are at greater risk of developing osteopenia and bone injury compared with normally menstruating athletes or nonathletic, normally cycling females.

Body weight should be monitored frequently to check calorie intake. Athletes with low caloric intakes who train for more than 90 minutes a day should consume 45 to 50 kcal/kg body weight/day, as well as foods with high contents of iron, calcium, magnesium, zinc, and vitamin B₁₂. Fluid, electrolyte, and energy supplementation supports circulatory, metabolic, and thermoregulatory functions. No special food will help elite athletes perform better; the most important aspect of athletes' diet is that it follows the basic guidelines for healthy eating.

[edit] REFERENCES