Eating Disorders: Diagnosis and Management in the Primary Care Setting
Authors: Randy A. Sansone, MD, Associate Professor, Department of Psychiatry, Wright State University School of Medicine, Director of Psychiatry Education, Kettering Medical Center, Dayton, OH; Lori A. Sansone, MD, Family Physician, Kettering Medical Center Physicians, Inc., Dayton, OH; Michael W. Wiederman, PhD, Assistant Professor, Department of Psychological Science, Ball State University, Muncie, IN.Peer Reviewer: William M. Glazer, MD, Associate Clinical Professor of Psychiatry, Harvard Medical School, Massachusetts General Hospital.
Editor's Note-The eating disorders anorexia and bulimia nervosa continue to be clinical concerns for all primary care physicians. These disorders show no sign of abating in prevalence, perhaps because both are perpetuated by dieting behavior, body preoccupation, and a drive for thinness-all crucial elements for "success" in a culture plagued with overweight. In the United States, one-third of all adults1 as well as one-half of black and Hispanic women are overweight.2 The diet industry is flourishing, including avid interest in pharmaceutical agents that will control eating behavior. These are the sociocultural times that perpetuate body scrutiny and fears of fatness. These are the times of eating disorders.
Eating Disorder Diagnoses
In the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), there are three general categories of eating disorder diagnoses.3 Two represent relatively homogeneous disorders (i.e., anorexia nervosa, bulimia nervosa), and a third category (i.e., eating disorder, not otherwise specified) encompasses a variety of other eating disordered behaviors.Anorexia Nervosa. According to the criteria in DSM-IV, anorexia nervosa is characterized by: 1) a body weight that is below normal (i.e., < 85% of expected body weight); 2) intense fears of weight gain despite being underweight; 3) body image disturbance resulting in the misperception of one's weight or shape, undue self-evaluation based upon weight, or denial of the seriousness of the current low weight; and 4) in postmenarchal females, the absence of at least three consecutive menstrual cycles.3 For a DSM-IV diagnosis of anorexia nervosa, individuals must meet all four criteria.
There are two subtypes of anorexia nervosa. The first, restricting type, is characterized by restrictive eating patterns that do not entail binge-eating or purging behavior. The second, binge-eating/purging type, includes binge-eating episodes followed by purging behavior. Although the definition of a clinical binge is yet to be defined in terms of calories or food volume, a practical guide in the clinical setting is 2500 calories, or 2.5 times the normal amount of food. Binges are characterized by a lack of control over food intake during a discrete period of time (usually < 2 hours). Purging behaviors entail acute and active efforts to eradicate ingested calories and may include self-induced vomiting and/or the use of laxatives, diuretics, or enemas. In the primary care setting, a substantial number of patients may present with sub-syndromal eating disorders (i.e., eating disorder behaviors that are either very time-limited or do not meet full criteria for diagnosis).
Bulimia Nervosa. According to DSM-IV, bulimia nervosa is characterized by: 1) episodes of binge eating; 2) recurrent inappropriate behaviors that are intended to compensate for the ingested calories or prevent weight gain (e.g., self-induced vomiting; the use of laxatives, diuretics, or enemas; fasting; excessive exercise); 3) a frequency of bulimic episodes, on average, of at least twice per week for a period of three months; and 4) undue self-evaluation based on body weight or shape.3 For a DSM-IV diagnosis of bulimia nervosa, all criteria must be met.
Bulimia nervosa is further sub-divided into two groups: 1) purging type and 2) non-purging type. In the clinical setting, bulimia nervosa, purging type, is the most frequent eating disorder diagnosis. Purging type is characterized by compensatory purging behaviors such as self-induced vomiting or the use of laxatives, diuretics, or enemas. An unusual example is the avoidance of insulin use in diabetes, resulting in glycosuria, to control weight following binges.4 Non-purging type is characterized by compensatory behaviors that are non-invasive yet counter-regulatory; examples include fasting or excessive exercise. As in anorexia nervosa, individuals in the primary care setting may present with sub-syndromal bulimia nervosa (e.g., experimentation with purging behaviors following episodes of overeating).
Eating Disorder, Not Otherwise Specified. This DSM-IV diagnosis is reserved for those eating disorder patterns that fall outside the descriptions of anorexia or bulimia nervosa.3 Examples include low-weight patients who routinely purge small amounts of food (i.e., restricter purgers) or bulimic individuals in whom criteria are not met regarding frequency of episodes.
Binge-Eating Disorder. Within the appendix, DSM-IV also includes criteria for diagnostic proposals, primarily constructed by researchers, which are provided for further study.3 Included in this appendix is one final eating disorder diagnosis, binge-eating disorder. Like bulimia nervosa, binge- eating disorder is characterized by episodes of binge eating. The binge-eating episodes must meet at least three of the following criteria: 1) eating more rapidly than normal; 2) eating until uncomfortably full; 3) eating despite not feeling physically hungry; 4) eating alone due to embarrassment about the quantities of food being consumed; and 5) experiencing a negative effect after eating (e.g., disgust with oneself, depressed feelings, guilt). In addition, there must be marked distress with binge eating and a binge-eating frequency of at least two days a week for six months. Individuals with binge-eating disorder do not use any inappropriate compensatory methods such as purging behaviors, fasting, or excessive exercise. Many, if not most, of these individuals are overweight, and, among a significant minority, there may be a comorbid diagnosis of borderline personality disorder.5 Because this eating disorder remains a diagnostic proposal, the remainder of this article will focus primarily on anorexia and bulimia nervosas.
Epidemiology
Precise data regarding the epidemiology of eating disorders in the United States are scant, but it is clear that eating disorders are most prevalent among adolescent and young adult women. Within this group, the prevalence of anorexia nervosa appears to be 0.5-1% compared to the 1-3% prevalence for bulimia nervosa.6,7 The prevalence among males in the same age range is about one-tenth that of females.3 The onset of anorexia nervosa typically occurs during adolescence, whereas the onset of bulimia nervosa usually occurs later, during adolescence or early adulthood.There has been much speculation about the apparent increased incidence of eating disorders, but research suggests that the incidence has not increased as much as the public and medical recognition of these disorders.6,8 More importantly, from a clinical perspective, disordered eating exists along a continuum of severity, with subclinical or sub-syndromal cases being at least twice as prevalent as those meeting full diagnostic criteria.9
Etiology of Eating Disorders
Eating disorders are conceptualized as multi-factorial disorders (i.e., disorders due to a variety of causes) that culminate in a final common pathway. One etiological factor is cultural influences. As the affluent North American culture struggles with overweight and obesity, the body ideal becomes that which is most difficult to achieve-the physique of thinness. Both anorexia and bulimia nervosa are eating disorders that are preceded by dieting behavior.In examining genetic factors, studies suggest that, compared with controls, family members of individuals with eating disorders, especially bulimia nervosa, appear to have significantly higher rates of mood disorders,10 substance abuse,11 and other psychiatric disorders.12 In addition, serotonin appears intimately involved with satiety. These findings broach the possibility of a non-specific but contributory factor at a genetic (e.g., neurotransmitter) level.
Many individuals with eating disorders, particularly those with anorexia nervosa, have a personality style highlighted by perfectionism, strong needs to achieve, and obsessive-compulsive behaviors.13 This psychological style readily compliments the rigors inherent in dieting behavior (i.e., counting calories or fat grams, scheduling and timing exercise, categorizing foods as acceptable or not), and in turn, successful dieting and weight loss reinforce the illusion of self-control and mastery.
Some individuals exist in family environments that are excessively health- or weight-conscious. These families tend to overly emphasize body weight, eating behavior, food selection, and exercise. A more ominous family factor is sexual abuse, in which the eating disorder symptoms function as a means to avoid further abuse through the loss of sexual characteristics that are attractive to others.14 A variety of interpersonal factors may contribute to the development of an eating disorder.14 For example, the normal developmental demands of separation-individuation from the family can be suspended through the development of a debilitating eating disorder. The eating disorder may function as a form of non-verbal protest to parents, particularly in families where open protest is not normally tolerated. Achieving the fantasized ideal body may fulfill the limitless expectations of adolescence as well as result in a unique arena of competition with peers. Finally, in a world that appears devoid of caring, eating disorder symptoms may function to elicit validating emotional responses, such as concern, from family and peers.
In addition to the preceding contributory factors, among many cases, there is an acute situational event that precipitates the onset of eating disorder symptoms. Examples of these include parental divorce, loss of a significant relationship, or a family relocation. These situational stressors appear to mobilize the various underlying risk factors of an individual, resulting in the need for enhanced control or emotional homeostasis, which is actualized through the emergence of eating disorder symptoms.
Office Demeanor of the Patient
Anorexia Nervosa. When the individual suffering from anorexia nervosa presents to the primary care physician for evaluation of weight loss or a condition related to weight loss (e.g., amenorrhea), there is often an indifference to the eating disorder symptoms. Emaciated individuals with anorexia nervosa are often aloof, irritable, dysphoric, withdrawn, and hostile. These features are due to the biological stress of malnutrition and starvation as well as the patient's fear that treatment will entail weight gain. On occasion, some patients deny obvious signs and symptoms (e.g., hair loss, cold insensitivity, fatigue), dieting efforts, body preoccupation, or concern about weight loss. Others focus on specific symptoms such as amenorrhea or sleep disturbance, while avoiding disclosure of the underlying eating disorder.Bulimia Nervosa. Individuals with bulimia nervosa are typically engaging, expressive, and interactive. Although many suffer from mood disorders or mood lability, the professional encounter is far more social than those with individuals suffering from anorexia nervosa. Although some individuals with bulimia nervosa attempt to hide symptoms, many, if not most, respond candidly to compassionate inquiries about related signs and symptoms.
Assessment
Anorexia Nervosa. In the assessment of anorexia nervosa, the history is of utmost importance in confirming DSM-IV criteria, particularly the verification of dieting behavior. Indications of dieting behavior include preoccupation with body weight or specific body areas, attempts to restrict calories and fatty foods, frequent weighings, mirror gazing, conversation that is riddled with food and weight content, meal avoidance, preoccupation with clothes size, and attempts to hide weight loss with bulky clothing. An accurate history may need to be elicited from a parent or significant other.During the initial appointment, the physical examination should include blood pressure, height, and weight in underwear and gown. General physical findings include emaciation as well as evidence of slowed metabolic and physiological functions. (See Figure.) The patient may have lanugo, a fine, downy body hair that is particularly prominent on the arms, torso, and face, and may be an adaptive attempt to maintain body heat in the presence of depleted body fat.
Physical examination may disclose cardiovascular complications, which are fairly common and the most likely cause of death in anorexia nervosa.15 In addition to bradycardia and orthostatic hypotension, findings may include abnormalities in mitral valve motion, decreased left ventricular chamber dimension and mass, reduction in cardiac index due to low stroke index and heart rate, higher peripheral resistance, and systolic dysfunction.16 Across studies, the crude mortality rate in anorexia nervosa is approximately 6%, which is, in part, contributed to by sudden death.17
During psychological assessment, the patient may appear indifferent to the weight loss (denial). On mental status examination, affect is typically flat, and eye contact is poor. The patient's eyes may have a lackluster appearance due to the effects of starvation. Other observations may include impairment in concentration, lack of cooperation, limited verbalization, and dysphoric mood.
Affective disorders are difficult to assess in patients with poor nutritional intake or starvation. Many of the effects of the starvation state itself mimic depression (e.g., fatigue, dysphoria, irritability, poor concentration, sleep disturbance). Therefore, in low-weight patients, a diagnosis of underlying affective disorder should be tempered with an awareness of the contributory effects of starvation.
In addition to affective disorders, eating disorder patients may suffer from personality disorder.13 Personality disorders are grouped into three clusters (i.e., A, B, C) according to descriptive similarities. Among restricting individuals with anorexia nervosa, the most common personality disturbances are those in Cluster C (e.g., fearful or anxious personality styles such as avoidant, obsessive-compulsive, dependent personality disorders).13 Among those with binge-purge behaviors, Cluster B personality disturbances are most common (e.g., dramatic, erratic, or emotional personality styles such as borderline, histrionic, narcissistic personality disorders).13
A general laboratory screen is usually sufficient in the assessment of anorexia nervosa. Among individuals who purge, the determination of electrolyte status is the most imminent concern, particularly serum potassium status. Although individuals with anorexia nervosa may demonstrate a variety of laboratory abnormalities (see Table),18,19 these usually manifest only in extreme cases of starvation. An electrocardiogram is indicated in those individuals with cardiac symptoms, extremely low body weight (loss of > 25% of the original body weight), or histories of exposure to Syrup of Ipecac.
In general, starvation effects are most pronounced among individuals with acute and extreme weight loss and older individuals. Those individuals with previous histories of medical complications at specific low body weights (e.g., cardiac arrhythmias including conduction blocks) need to be carefully monitored during relapses to the same threshold weight.
Bulimia Nervosa. As in anorexia nervosa, the history is paramount to the DSM-IV diagnosis of bulimia nervosa. Binge eating patterns appear to develop in the aftermath of restrictive dieting efforts, and, therefore, a history of dieting behavior is usually present. It is important to screen for the presence of clearly defined binge-eating episodes as well as all possible compensatory behaviors (e.g., self-induced vomiting; the use of laxatives, diuretics, enemas, Syrup of Ipecac; food restriction; exercise).
On physical examination, findings are closely related to the method of purging or compensatory behavior.20,21 Self-induced vomiting, the most common form of purging in a clinical population, has varying frequencies from occasional to multiple times per day. Whereas some patients are able to spontaneously vomit, most induce a gag reflex. Food types seem to vary in their ease of purgation, and binge foods may be selected, in part, for this characteristic. In addition, self-induced vomiting may be facilitated by volume loading, fluid loading, or manual abdominal pressure.
Self-induced vomiting tends to precipitate upper gastrointestinal complications. Dental erosion, or perimylolysis, may result in discoloration of tooth enamel, temperature sensitivity of the teeth, spaces or gaps between teeth, loose fillings or amalgams due to the erosion of the supporting tooth, and a receding distal surface of the upper front teeth (note that the tongue protects the lower front teeth during vomiting). In extreme cases, the deterioration in dentition may result in extensive crown work (particularly the six upper front teeth) or dentures.
Salivary gland enlargement (parotid and/or submandibular) occurs in some individuals who induce vomiting. The enlargement is nearly always bilateral, and the glands may be tender to palpation. Among those individuals who are susceptible to this complication, enlargement recedes in 4-6 weeks with the cessation of vomiting. We are aware of no long-term medical complications related to salivary gland enlargement.
When vomiting is induced by a gag reflex using the hand or fingers, there may be small cuts, excoriations, or calluses on the hand, particularly in the area of the knuckles. These findings are usually unilateral and involve the dominant hand.
The exposure of the upper gastrointestinal tract to gastric acid may result in frequent sore throats as well as esophageal irritation (i.e., heartburn). Vomiting due to any cause may result in aspiration and a resulting chemical pneumonitis. In addition, the internal forces generated with the act of vomiting may precipitate small mucosal tears along the gastroesophageal juncture (Mallory-Weiss tears), resulting in hematemesis. On very rare occasion, the muscular layer of the esophagus or stomach may rupture during self-induced vomiting (Borhaave's syndrome, which has a reported mortality rate of 25%22).
Finally, some individuals with eating disorders use Syrup of Ipecac to induce vomiting. The active emetic agent, emetine, has a long half-life, accumulates with frequent dosing, and induces cardiac arrhythmias.23 Emetine is also known to cause myopathies resulting in muscle weakness of the neck and proximal muscles of the extremities.23
Like self-induced vomiting, laxative abuse varies in frequency and amount. While some individuals use laxatives only episodically, others ingest 10-20 or more per day. In our practice, we have had three individuals who ingested 150 laxative units per day and one patient who sporadically ingested 500 units per day. Laxative abuse can cause acute as well as chronic lower gastrointestinal complications.
The acute effects of laxative loads may include abdominal distention, discomfort, pain, and bloating; nausea; vomiting; and constipation. Chronic laxative abuse may lead to laxative dependence (i.e., reliance on laxatives, no significant physiological damage) or cathartic colon (i.e., physiological damage to the colon characterized by thinning of the muscular and mucosal layers, loss of propulsion, areas of spasm called pseudostrictures, and low-grade inflammation).
The abuse of senna or cascara-containing laxatives may produce a discoloration of the lower colon and rectum (melanosis coli), which causes no physiological impairment and disappears 4-12 months after discontinuing laxatives. In addition, laxatives that contain phenolphthalein can result in fixed drug eruptions in sensitive individuals. Fixed drug eruptions are inflammatory reactions on the skin surface that resolve leaving residual pigmentation. Re-exposure to the offending agent results in an inflammatory response in the same location (i.e., "fixed"), and the subsequent resolution is characterized by a deepening of the pigmentation.
In our experience, diuretic abuse is the least frequent form of purgation among eating disorder patients, particularly those in younger age groups. Some individuals who abuse diuretics appear to have unusual forms of body image disturbance (i.e., dysmorphophobic features) that impede treatment efforts to discontinue these drugs. Diuretic abuse, like self-induced vomiting and laxative abuse, can lower serum potassium levels. When potassium levels are chronically low, it is possible to develop hypokalemic nephropathy. Therefore, in addition to acute potassium depletion and its medical complications (e.g., paresthesias, fatigue, cardiac arrhythmias, tetany, seizures), chronic potassium depletion takes its toll. Diuretic abuse should always be suspected in patients with unexpectedly low serum potassium levels without other co-existing medical problems or associated prescribed medications.
The focus of psychological assessment is the determination of possible comorbid psychiatric conditions. In bulimia nervosa, acute mood disturbances may be 1) intermittent (e.g., episodic lability and irritability) and directly related to eating disorder behaviors or 2) sustained (i.e., a bonafide affective disorder). Therefore, the clinical task is to determine if acute affective symptoms among patients with bulimia nervosa are sustained to a degree that they meet criteria for major depression (e.g., at least 2 weeks in duration). Bulimic symptoms, themselves, may have a seasonal pattern24 or undergo premenstrual exacerbation,25 both observations suggesting a mood component among some individuals.
Table. Possible Laboratory Abnormalities in Anorexia Nervosa18,19
| HEMATOLOGIC |
| Anemia |
| Leukopenia |
| Thrombocytopenia |
| Reduced erythocyte sedimentation rate |
| Impaired cell-mediated immunity |
| METABOLIC |
| Hypercholesterolemia |
| Hypocalcemia |
| Hypomagnesemia |
| Hypophosphatemia |
| Hypokalemia (vomiting, laxatives, diuretics) |
| ENDOCRINOLOGIC |
| Hypercortisolemia |
| Hypoglycemia |
| Elevated growth hormone levels |
| Reduced estrogen levels |
| Reduced basal levels of luteinizing and follicle-stimulating hormones |
| GASTROINTESTINAL |
| Elevated liver function tests |
| Elevated amylase (vomiting) |
Borderline personality disorder may be a comorbid psychiatric condition, especially in the presence of impulsive behaviors such as binge eating and purging. Borderline personality is a longstanding disorder characterized by chronic impulsivity (i.e., self-regulation difficulties, self-destructive behavior), unstable interpersonal relationships, and dysphoric affect which is coupled with an intact social facade. It is highlighted by chronic self-destructive behavior. Among individuals with eating disorder symptoms and self-destructive behaviors that are unrelated to food and weight issues (e.g., suicide attempts, promiscuity, substance abuse), this personality disorder is likely. Studies indicate that the co-existence of eating disorder symptoms and substance abuse is highly associated with a diagnosis of borderline personality disorder.26 The presence of comorbid borderline personality disorder in an eating disorder patient indicates that treatment will be more complicated and long-term, and behavioral improvement will evolve slowly, as illustrated in those with substance abuse.27 For further information about borderline personality disorder in the primary care setting, the reader is referred to other sources.28,29
Other psychiatric comorbidity may include dysthymia (chronic depression) or panic disorder (the latter sometimes associated with the weight loss, itself). Patients with trauma histories may have symptoms of post-traumatic stress disorder including dissociative symptoms.
Laboratory examination among individuals with bulimia nervosa is usually unremarkable, with the exception of an occasionally low serum potassium level. Therefore, in most instances, a general laboratory screen is sufficient. In the absence of a low serum potassium level, cardiac symptoms, or a pre-existing cardiac history, an electrocardiogram is not routinely indicated. Electrocardiograms are indicated in those individuals using Syrup of Ipecac.
Less frequent findings may include hyperamylasemia (which may correlate to the frequency of binging and purging);30 and hypocalcemia, hyperchloremia, and steatorrhea (which may be associated with laxative abuse).
Management in the Primary Care Setting
Anorexia Nervosa. An ongoing task in the management of anorexia nervosa is to weigh the patient with each visit. Weighings should be standardized. For individuals not previously overweight, weight loss of more than 25% of the previous body weight will require referral to a structured refeeding program in a specialized inpatient or day treatment program for eating disorder patients. In patients with lesser degrees of weight loss, outpatient psychological management by a mental health professional with experience in eating disorders is indicated.The primary care physician should review and address laboratory abnormalities, including hypokalemia and abnormal cardiac findings. Avoid the treatment of starvation-induced hypothyroidism, as thyroid replacement may accelerate weight loss. A DEXA scan should be considered for patients with low body weight of more than six months duration.31 To protect the patient's bone mass, preventive hormonal replacement therapy may be initiated,31 although low-weight patients may not evidence significant benefit.32
Triage comorbid psychiatric conditions, when present. For example, quickly address imminent problems (e.g., suicidal ideation will require psychiatric hospitalization) and assess pre-existing depression, which will require antidepressant treatment. In low-weight patients, avoid antidepressants with marked cardiovascular effects (e.g., tricyclic antidepressants), and elect antidepressants with anti-obsessional features (i.e., selective serotonin reuptake inhibitors). Note, however, that responses to antidepressant medications are tempered by the starvation state, which may be the cause of, or a contributory factor to, the current psychiatric symptoms. To date, no psychotropic medication has been shown to consistently induce weight gain or change the core features of anorexia nervosa.33 Consider psychiatric consultation for patients with extensive psychiatric comorbidity, with atypical presentations, or who are unresponsive to routine intervention.
The primary care physician should engage a mental health professional who is experienced in the treatment of eating disorders to begin psychological treatment with the patient. Anorexia nervosa is a psychiatric disorder, and the earlier the psychological intervention, the better the prognosis. Psychological intervention may include a structured outpatient refeeding program, cognitive-behavioral therapy, individual psychotherapy, and/or group or family therapy. Support groups may also be helpful. For a given individual, the various contributory etiologies generally dictate which treatments are selected.
During the ongoing psychological treatment, continue to provide medical support, including periodic assessment of electrolytes for patients who purge, monitoring of body weight, and education and support to family members and the patient with regard to the disorder and the treatment. Among some patients, acute medical intervention will be indicated for emergent medical complications such as cardiac arrhythmias. Among others, education will be important (e.g., a body weight within approximately 90% of standard body weight for height is usually necessary for a return of menses).34
When treating the patient with an eating disorder, address purging behaviors with the following recommendations. For patients who induce vomiting, encourage the use of fluoride-containing toothpastes, fluoride treatments through the dentist, and sodium bicarbonate rinses after vomiting. For patients who are laxative-dependent, encourage gradual weaning of laxatives, gradual increase in dietary fiber, adequate hydration, and the use of non-stimulant laxatives should constipation develop in the future. Patients who undergo laxative weaning will also need reassurance and support regarding the fluid retention that may develop shortly after the cessation of laxatives. Barium studies may be indicated in the rare patient who has symptoms or a history suggestive of cathartic colon. For patients who abuse diuretics, discontinue prescribed diuretics, actively discourage over-the-counter diuretic use, monitor serum potassium levels, and observe the patient for rebound edema. An electrocardiogram should be obtained in those patients who are abusing Syrup of Ipecac.
Bulimia Nervosa. The recommendations for bulimia nervosa are similar to those for anorexia nervosa, with the following modifications. First, because most individuals with bulimia nervosa are within a normal weight range, an initial weighing is probably sufficient unless the patient begins to lose weight. Second, electrolyte status is most important in the assessment of the majority of patients with bulimia nervosa, particularly serum potassium levels. Third, psychiatric comorbidity may include personality disorder (particularly borderline personality), substance abuse, and/or mood disorder. Comorbidity may indicate the need for psychiatric consultation. Fourth, it is essential to consult a mental health professional with experience in the treatment of eating disorders. Psychological treatment may entail cognitive-behavioral therapy, individual psychotherapy, group therapy with other bulimic individuals, and nutritional counseling. Most individuals can be treated in an outpatient setting. Fifth, continuing medical support most frequently entails: 1) periodic evaluation and treatment of electrolyte status; 2) review of interventions for specific purging behaviors, as noted previously; 3) encouraging routine contact with a dentist; and 4) prescription of antidepressants.
In our experience, the use of antidepressants is a low-risk, potentially high-yield intervention. We recommend beginning with fluoxetine, sertraline, or paroxetine (i.e., selective serotonin reuptake inhibitors). Antidepressants appear to reduce binge/purge behavior, even in the absence of a mood disorder.33 In addition, selective serotonin reuptake inhibitors alleviate the ruminative, obsessive psychological style that characterizes many of these patients.
The collaborative efforts of the primary care physician and the mental health professional are of paramount importance in treating patients with eating disorders. In many cases, there may be a team of professionals including a primary care physician, psychiatrist, non-physician mental health professional, dietitian, and support group leader. Eating disorders exist along a behavioral continuum, and those patients with more severe and frequent eating disordered behaviors will require more professional support.
Outcome of Eating Disorders
Anorexia Nervosa. Outcome studies in the field of eating disorders are fraught with methodological concerns (e.g., inpatient vs outpatient populations, prevalence of comorbid personality disorders, determination of outcome measures). In one recent study, one-fourth of patients fully recovered, while two-thirds subsequently developed bulimic behavior.35 A general clinical maxim is that one- third of patients fully recover, one-third improve, and one-third remain meaningfully impaired. This latter third is characterized by psychiatric comorbidity, particularly personality disorder. In addition, lower weight at treatment entry appears to be a predictor for lower weight at long-term follow-up.36 Other long-term concerns in individuals with anorexia nervosa include osteoporosis secondary to reduced bone mass,32,37 decreased fertility38 as well as a higher risk of prematurity and perinatal mortality,39 persistent gray matter volume deficits after weight recovery,40 and mortality (around 6%).17,35 Abnormally low serum albumin levels (< 36 g/L) and low body weight (< 60% of average), at initial examination, may be predictors of a lethal course.41Bulimia Nervosa. The long-term outcome for women with bulimia nervosa remains unclear.42 Greater impulsivity may be a predictor variable for poor outcome.43 In our clinical experience, relapse rates are fairly high and parallel increases in psychosocial stressors. In one study, one-third of patients relapsed within two years of treatment; relapse was associated with younger age and higher frequency of self-induced vomiting before treatment.44
Other long-term concerns in bulimia nervosa include dental erosion and hypokalemic nephropathy. In addition, up to 50% of normal-weight women with bulimia nervosa have disturbed menstrual function that may be associated with an abnormal 24-hour luteinizing hormone secretion, particularly if current weight is less than 85% of past high weight.45
Summary
The treatment and outcome of patients with eating disorders is clearly a concern for all professionals in primary care settings. Studies indicate that patients who endorse eating disorder symptoms on questionnaire, as well as obese individuals (a significant number who probably have binge-eating disorder), have greater healthcare utilization in the primary care setting.46,47 The primary care physician is in a unique role-one that may facilitate early diagnosis of these patients. Early diagnosis is a fundamental element in the successful treatment of individuals with eating disorders.48References
1. Kuczmarski RJ, Flegal KM, Campbell SM, et al. Increasing prevalence of overweight among US adults: The national health and nutrition examination surveys, 1960-1991. JAMA 1994; 272:205-211.
2. Rand CS, Kuldau JM. The epidemiology of obesity and self-defined weight problem in the general population: Gender, race, age, and social class. Int J Eat Disord 1990;9:329-343.
3. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. Washington, DC: American Psychiatric Association; 1994.
4. Hudson JI, Hudson MS, Wentworth SM. Self-induced glycosuria. A novel method of purging in bulimia. JAMA 1983;249:2501.
5. Specker S, de Zwaan M, Raymond N, et al. Psychopathology in subgroups of obese women with and without binge eating disorder. Compr Psychiatry 1994;35:185-190.
6. Fombonne E. Anorexia nervosa: no evidence of an increase. Br J Psychiatry 1995;166:462- 471.
7. Hsu LKG. Epidemiology of the eating disorders. Psychiatr Clin North Am 1996;19:681-700.
8. Fombonne E. Is bulimia nervosa increasing in frequency? Int J Eat Disord 1996;19:287-296.
9. Shisslak CM, Crago M, Estes LS. The spectrum of eating disturbances. Int J Eat Disord 1995;18:209-219.
10. Kuntz B, Groze V, Yates WR. Bulimia: A systemic family history perspective. Fam Soc J Contemp H 1992;73:604-612.
11. Kasset JA, Gershon ES, Maxwell ME, et al. Psychiatric disorders in the first-degree relatives of probands with bulimia nervosa. Am J Psychiatry 1989;146:1468-1471.
12. Boumann CE, Yates WR. Risk factors for bulimia nervosa: A controlled study of parental psychiatric illness and divorce. Addict Beh 1994;19:667-675.
13. Dennis AB, Sansone RA. Treatment of patients with personality disorders. In: Garner DM, Garfinkel PE, eds. Handbook of Treatment for Eating Disorders. New York: Guilford; 1997:437-449.
14. Johnson CL, Sansone RA, Chewning M. Good reasons why young women would develop anorexia nervosa: The adaptive context. Pediatr Ann 1992;21:731-737.
15. Sharp CW, Freeman CP. The medical complications of anorexia nervosa. Br J Psychiatry 1993;162:452-462.
16. de Simone G, Scalfi L, Galderisi M, et al. Cardiac abnormalities in young women with anorexia nervosa. Br Heart J 1994; 71:287-292.
17. Neumarker KJ. Mortality and sudden death in anorexia nervosa. Int J Eat Disord 1997;21:205-212.
18. Mehler PS. Eating disorder 1. Anorexia nervosa. Hosp Pract 1996;31:109-113.
19. Haller E. Eating disorders: A review and update. West J Med 1992;157:658-662.
20. Sansone RA. Complications of hazardous weight-loss methods. Am Fam Physician 1984;30:141-146.
21. Sansone RA, Sansone LA. Medical complications in bulimia nervosa. In: Alexander Mott L, Lumsden DB, eds. Understanding Eating Disorders: Anorexia Nervosa, Bulimia Nervosa and Obesity. New York: Taylor & Francis; 1994:181-201.
22. Larsen K, Skov Jensen B, Axelsen F. Perforation and rupture of the esophagus. Scand J Thorac Cardiovasc Surg 1983;17:311-316.
23. Board of Directors of the American Society of Hospital Pharmacists. AHFS Drug Information. Bethesda, MD: Author; 1997.
24. Blouin A, Blouin J, Aubin P, et al. Seasonal patterns of bulimia nervosa. Am J Psychiatry 1992;149:73-81.
25. Gladis MM, Walsh BT. Premenstrual exacerbation of binge eating in bulimia. Am J Psychiatry 1987;144:1592-1595.
26. Sansone RA, Fine MA, Nunn JL. A comparison of borderline personality symptomatology and self-destructive behavior in women with eating, substance abuse, and both eating and substance abuse disorders. J Pers Disord 1994;8:219-228.
27. Sansone RA, Dennis AB. The treatment of eating disorder patients with substance abuse and borderline personality disorder. Eat Disord 1996;4:180-186.
28. Sansone RA, Sansone L. Borderline personality disorder: _Office diagnosis and management. Am Fam Physician 1991; 44:194-198.
29. Sansone RA, Sansone LA. Borderline personality disorder: Interpersonal and behavioral problems that sabotage treatment success. Postgrad Med 1995;97:169-179.
30. Gwirtsman HE, Kaye WH, George DT, et al. Hyperamylasemia and its relationship to binge-purge episodes: Development of a clinical relevant laboratory test. J Clin Psychiatry 1989;50:196-204.
31. Hergenroeder AC. Bone mineralization, hypothalamic amenorrhea, and sex steroid therapy in female adolescents and young adults. J Pediatr 1995;126:683-689.
32. Klibanski A, Biller BM, Schoenfeld DA, et al. The effects of estrogen administration on trabecular bone loss in young women with anorexia nervosa. J Clin Endocrinol Metab 1995;80:898-904.
33. Johnson WG, Tsoh JY, Varnado PJ. Eating disorders: Efficacy of pharmacological and psychological interventions. Clin Psychol Rev 1996;16:457-478.
34. Golden NH, Jacobson MS, Schebendach J, et al. Resumption of menses in anorexia nervosa. Arch Pediatr Adolesc Med 1997; 151:16-21.
35. Eckert ED, Halmi KA, Marchi P, et al. Ten-year follow-up of anorexia nervosa: Clinical course and outcome. Psychol Med 1995;25:143-156.
36. Hebebrand J, Himmelmann GW, Herzog W, et al. Prediction of low body weight at long-term follow-up in acute anorexia nervosa by low body weight at referral. Am J Psychiatry 1997;154:566-569.
37. Rigotti NA, Neer RM, Skates SJ, et al. The clinical course of osteoporosis in anorexia nervosa. A longitudinal study of cortical bone mass. JAMA 1991;265:1133-1138.
38. Andersen AE. Sexuality and fertility: Women with anorexia nervosa and bulimia. Med Aspects Hum Sex 1986;20:138-143.
39. Brinch M, Isager T, Tolstrup K. Anorexia nervosa and motherhood: Reproduction pattern and mothering behavior of 50 women. Acta Psychiatr Scand 1988;77:611-617.
40. Lambe EK, Katzman DK, Mikulis DJ, et al. Cerebral gray matter volume deficits after weight recovery from anorexia nervosa. Arch Gen Psychiatry 1997;54:537-542.
41. 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.
42. Keel PK, Mitchell JE. Outcome in bulimia nervosa. Am J Psychiatry 1997;154:313-321.
43. Sohlberg S, Norring C, Holmgren S, Rosmark B. Impulsivity and long-term prognosis of psychiatric patients with anorexia nervosa/bulimia nervosa. J Nerv Ment Dis 1989;177:249-258.
44. Olmsted MP, Kaplan AS, Rockert W. Rate and prediction of relapse in bulimia nervosa. Am J Psychiatry 1994;151:738-743.
45. Weltzin TE, Cameron J, Berga S, Kaye WH. Prediction of reproductive status in women with bulimia nervosa by past high weight. Am J Psychiatry 1994;151:136-138.
46. Sansone RA, Wiederman MW, Sansone LA. Healthcare utilization among women with eating disordered behavior. Am J Man Care 1997;3:1721-1723.
47. Sansone RA, Sansone LA, Wiederman MW. The relationship between obesity and medical utilization among women in a primary care setting. Int J Eat Disord (in press).
48. Woodside DB. A review of anorexia nervosa and bulimia nervosa. Curr Probl Pediatr 1995;25:67-89.
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