20 - 15 Feeding and Eating Disorders

01 - 15.1 Anorexia Nervosa
15.1 Anorexia Nervosa
Feeding and Eating Disorders
15.1 Anorexia Nervosa
The term anorexia nervosa is derived from the Greek term for “loss of appetite” and a
Latin word implying nervous origin. Anorexia nervosa is a syndrome characterized by
three essential criteria. The first is a self-induced starvation to a significant degree—a
behavior. The second is a relentless drive for thinness or a morbid fear of fatness—a
psychopathology. The third criterion is the presence of medical signs and symptoms
resulting from starvation—a physiological symptomatology. Anorexia nervosa is often, but
not always, associated with disturbances of body image, the perception that one is
distressingly large despite obvious medical starvation. The distortion of body image is
disturbing when present, but not pathognomic, invariable, or required for diagnosis.
Two subtypes of anorexia nervosa exist: restricting and binge/purge. The theme in all
anorexia nervosa subtypes is the highly disproportionate emphasis placed on thinness as
a vital source, sometimes the only source, of self-esteem, with weight, and to a lesser
degree, shape, becoming the overriding and consuming daylong preoccupation of
thoughts, mood, and behaviors.
Approximately half of anorexic persons will lose weight by drastically reducing their
total food intake. The other half of these patients will not only diet but will also
regularly engage in binge eating followed by purging behaviors. Some patients
routinely purge after eating small amounts of food. Anorexia nervosa is much more
prevalent in females than in males and usually has its onset in adolescence. Hypotheses
of an underlying psychological disturbance in young women with the disorder include
conflicts surrounding the transition from girlhood to womanhood. Psychological issues
related to feelings of helplessness and difficulty establishing autonomy have also been
suggested as contributing to the development of the disorder. Bulimic symptoms can
occur as a separate disorder (bulimia nervosa, which is discussed in Section 15.2) or as
part of anorexia nervosa. Persons with either disorder are excessively preoccupied with
weight, food, and body shape. The outcome of anorexia nervosa varies from
spontaneous recovery to a waxing and waning course to death.
EPIDEMIOLOGY
Anorexia nervosa has been reported more frequently over the past several decades, with
increasing reports of the disorder in prepubertal girls and in boys. The most common
ages of onset of anorexia nervosa are the midteens, but up to 5 percent of anorectic
patients have the onset of the disorder in their early 20s. The most common age of onset
is between 14 and 18 years. Anorexia nervosa is estimated to occur in about 0.5 to 1
percent of adolescent girls. It occurs 10 to 20 times more often in females than in males.
The prevalence of young women with some symptoms of anorexia nervosa who do not
meet the diagnostic criteria is estimated to be close to 5 percent. Although the disorder
was initially reported most often among the upper classes, recent epidemiological
surveys do not show that distribution. It seems to be most frequent in developed
countries, and it may be seen with greatest frequency among young women in
professions that require thinness, such as modeling and ballet.
COMORBIDITY
Table 15.1-1 lists comorbid psychiatric conditions associated with anorexia nervosa.
Overall, anorexia nervosa is associated with depression in 65 percent of cases, social
phobia in 35 percent of cases, and obsessive-compulsive disorder in 25 percent of cases.
Table 15.1-1
Comorbid Psychiatric Conditions Associated with Anorexia Nervosa
ETIOLOGY
Biological, social, and psychological factors are implicated in the causes of anorexia
nervosa. Some evidence points to higher concordance rates in monozygotic twins than
in dizygotic twins. Sisters of patients with anorexia nervosa are likely to be afflicted, but
this association may reflect social influences more than genetic factors. Major mood
disorders are more common in family members than in the general population.
Neurochemically, diminished norepinephrine turnover and activity are suggested by
reduced 3-methoxy-4-hydroxyphenylglycol (MHPG) levels in the urine and the
cerebrospinal fluid (CSF) of some patients with anorexia nervosa. An inverse relation is
seen between MHPG and depression in these patients; an increase in MHPG is
associated with a decrease in depression.
Biological Factors
Endogenous opioids may contribute to the denial of hunger in patients with anorexia nervosa. Preliminary studies show
dramatic weight gains in some patients who are given opiate antagonists. Starvation results in many biochemical changes,
some of which are also present in depression, such as hypercortisolemia and nonsuppression by dexamethasone. Thyroid
function is suppressed as well. These abnormalities are corrected by realimentation. Starvation may produce amenorrhea,
which reflects lowered hormonal levels (luteinizing, follicle-stimulating, and gonadotropin-releasing hormones). Some
patients with anorexia nervosa, however, may become amenorrheic before significant weight loss. Several computed
tomographic (CT) studies reveal enlarged CSF spaces (enlarged sulci and ventricles) in anorectic patients during starvation,
a finding that is reversed by weight gain. In one positron emission tomographic (PET) scan study, caudate nucleus
metabolism was higher in the anorectic state than after realimentation.
Some authors have proposed a hypothalamic-pituitary axis (neuroendocrine) dysfunction. Some studies have shown
evidence for dysfunction in serotonin, dopamine, and norepinephrine, three neurotransmitters involved in regulating
eating behavior in the paraventricular nucleus of the hypothalamus. Other humoral factors that may be involved include
corticotropin-releasing factor (CRF), neuropeptide Y, gonadotropin-releasing hormone, and thyroid-stimulating hormone.
Table 15.1-2 lists the neuroendocrine changes associated with anorexia nervosa.
Table 15.1-2
Neuroendocrine Changes in Anorexia Nervosa and Experimental Starvation
Social Factors
Patients with anorexia nervosa find support for their practices in society’s emphasis on thinness and exercise. No family
constellations are specific to anorexia nervosa, but some evidence indicates that these patients have close, but troubled,
relationships with their parents. Families of children who present with eating disorders, especially binge eating or purging
subtypes, may exhibit high levels of hostility, chaos, and isolation and low levels of nurturance and empathy. An
adolescent with a severe eating disorder may tend to draw attention away from strained marital relationships.
Vocational and avocational interests interact with other vulnerability factors to increase the probability of developing
eating disorders. In young women, participation in strict ballet schools increases the probability of developing anorexia
nervosa at least sevenfold. In high school boys, wrestling is associated with a prevalence of full or partial eating-disorder
syndromes during wrestling season of approximately 17 percent, with a minority developing an eating disorder and not
improving spontaneously at the end of training. Although these athletic activities probably select for perfectionistic and
persevering youth in the first place, pressures regarding weight and shape generated in these social milieus reinforce the
likelihood that these predisposing factors will be channeled toward eating disorders.
A gay orientation in men is a proved predisposing factor, not because of sexual orientation or sexual behavior per se, but
because norms for slimness, albeit muscular slimness, are very strong in the gay community, only slightly lower than for
heterosexual women. In contrast, a lesbian orientation may be slightly protective, because lesbian communities may be
more tolerant of higher weights and a more normative natural distribution of body shapes than their heterosexual female
counterparts.
Psychological and Psychodynamic Factors
Anorexia nervosa appears to be a reaction to the demand that adolescents behave more independently and increase their
social and sexual functioning. Patients with the disorder substitute their preoccupations, which are similar to obsessions,
with eating and weight gain for other, normal adolescent pursuits. These patients typically lack a sense of autonomy and
selfhood. Many experience their bodies as somehow under the control of their parents, so that self-starvation may be an
effort to gain validation as a unique and special person. Only through acts of extraordinary self-discipline can an anorectic
patient develop a sense of autonomy and selfhood.
Psychoanalytic clinicians who treat patients with anorexia nervosa generally agree that these young patients have been
unable to separate psychologically from their mothers. The body may be perceived as though it were inhabited by the
introject of an intrusive and unempathic mother. Starvation may unconsciously mean arresting the growth of this
intrusive internal object and thereby destroying it. Often, a projective identification process is involved in the interactions
between the patient and the patient’s family. Many anorectic patients feel that oral desires are greedy and unacceptable;
therefore, these desires are projectively disavowed. Other theories have focused on fantasies of oral impregnation. Parents
respond to the refusal to eat by becoming frantic about whether the patient is actually eating. The patient can then view
the parents as the ones who have unacceptable desires and can projectively disavow them; that is, others may be voracious
and ruled by desire but not the patient.
DIAGNOSIS AND CLINICAL FEATURES
The onset of anorexia nervosa usually occurs between the ages of 10 and 30 years. It is
present when (1) an individual voluntarily reduces and maintains an unhealthy degree
of weight loss or fails to gain weight proportional to growth; (2) an individual
experiences an intense fear of becoming fat, has a relentless drive for thinness despite
obvious medical starvation, or both; (3) an individual experiences significant starvationrelated medical symptomatology, often, but not exclusively, abnormal reproductive
hormone functioning, but also hypothermia, bradycardia, orthostasis, and severely
reduced body fat stores; and (4) the behaviors and psychopathology are present for at
least 3 months. The fifth edition of the Diagnostic and Statistical Manual of Mental
Disorders (DSM-5) diagnostic criteria for anorexia nervosa are given in Table 15.1-3.
Table 15.1-3
DSM-5 Diagnostic Criteria for Anorexia Nervosa
An intense fear of gaining weight and becoming obese is present in all patients with
the disorder and undoubtedly contributes to their lack of interest in, and even resistance
to, therapy. Most aberrant behavior directed toward losing weight occurs in secret.
Patients with anorexia nervosa usually refuse to eat with their families or in public
places. They lose weight by drastically reducing their total food intake, with a
disproportionate decrease in high-carbohydrate and fatty foods.
As mentioned, the term anorexia is a misnomer, because loss of appetite is usually rare
until late in the disorder. Evidence that patients are constantly thinking about food is
their passion for collecting recipes and for preparing elaborate meals for others. Some
patients cannot continuously control their voluntary restriction of food intake and so
have eating binges. These binges usually occur secretly and often at night and are
frequently followed by self-induced vomiting. Patients abuse laxatives and even
diuretics to lose weight, and ritualistic exercising, extensive cycling, walking, jogging,
and running are common activities.
Patients with the disorder exhibit peculiar behavior about food. They hide food all
over the house and frequently carry large quantities of candies in their pockets and
purses. While eating meals, they try to dispose of food in their napkins or hide it in their
pockets. They cut their meat into very small pieces and spend a great deal of time
rearranging the pieces on their plates. If the patients are confronted with their peculiar
behavior, they often deny that their behavior is unusual or flatly refuse to discuss it.
Obsessive-compulsive behavior, depression, and anxiety are other psychiatric
symptoms of anorexia nervosa most frequently noted clinically. Patients tend to be rigid
and perfectionist, and somatic complaints, especially epigastric discomfort, are usual.
Compulsive stealing, usually of candies and laxatives but occasionally of clothes and
other items, may occur.
Poor sexual adjustment is frequently described in patients with the disorder. Many
adolescent patients with anorexia nervosa have delayed psychosocial sexual
development; in adults, a markedly decreased interest in sex often accompanies onset of
the disorder. A minority of anorexic patients has a premorbid history of promiscuity,
substance abuse, or both but during the disorder show a decreased interest in sex.
Patients usually come to medical attention when their weight loss becomes apparent.
As the weight loss grows profound, physical signs such as hypothermia (as low as 35°C),
dependent edema, bradycardia, hypotension, and lanugo (the appearance of neonatallike hair) appear, and patients show a variety of metabolic changes (Fig. 15.1-1). Some
female patients with anorexia nervosa come to medical attention because of
amenorrhea, which often appears before their weight loss is noticeable. Some patients
induce vomiting or abuse purgatives and diuretics; such behavior causes concern about
hypokalemic alkalosis. Impaired water diuresis may be noted.
FIGURE 15.1-1
A patient with anorexia nervosa. (Courtesy of Katherine Halmi, M.D.)
Electrocardiographic (ECG) changes, such as T wave flattening or inversion, ST
segment depression, and lengthening of the QT interval, have been noted in the
emaciated stage of anorexia nervosa. ECG changes may also result from potassium loss,
which can lead to death. Gastric dilation is a rare complication of anorexia nervosa. In
some patients, aortography has shown a superior mesenteric artery syndrome. Other
medical complications of eating disorders are listed in Table 15.1-4.
Table 15.1-4
Medical Complications of Eating Disorders
SUBTYPES
Anorexia nervosa has been divided into two clinical subtypes: the food-restricting
category and the purging category. In the food-restricting category, present in
approximately 50 percent of cases, food intake is highly restricted (usually with
attempts to consume fewer than 300 to 500 calories per day and no fat grams), and the
patient may be relentlessly and compulsively overactive, with overuse athletic injuries.
In the purging subtype, patients alternate attempts at rigorous dieting with intermittent
binge or purge episodes. Purging represents a secondary compensation for the
unwanted calories, most often accomplished by self-induced vomiting, frequently by
laxative abuse, less frequently by diuretics, and occasionally with emetics. Sometimes,
repetitive purging occurs without prior binge eating, after ingesting only relatively few
calories. Both types may be socially isolated and have depressive disorder symptoms and
diminished sexual interest. Overexercising and perfectionistic traits are also common in
both types.
A new diagnostic category in DSM-5 is binge eating disorder (see Section 15.3)
characterized by episodic bouts of the intake of excessive amounts of food but without
purging or similar compensatory behavior.
Those who practice binge eating and purging share many features with persons who
have bulimia nervosa without anorexia nervosa. Those who binge eat and purge tend to
have families in which some members are obese, and they themselves have histories of
heavier body weights before the disorder than do persons with the restricting type.
Binge eating–purging persons are likely to be associated with substance abuse, impulse
control disorders, and personality disorders. Persons with restricting anorexia nervosa
often have obsessive-compulsive traits with respect to food and other matters. Some
persons with anorexia nervosa may purge but not binge.
Persons with anorexia nervosa have high rates of comorbid major depressive
disorders; major depressive disorder or dysthymic disorder has been reported in up to 50
percent of patients with anorexia nervosa. The suicide rate is higher in persons with the
binge eating–purging type of anorexia nervosa than in those with the restricting type.
Patients with anorexia nervosa are often secretive, deny their symptoms, and resist
treatment. In almost all cases, relatives or intimate acquaintances must confirm a
patient’s history. The mental status examination usually shows a patient who is alert
and knowledgeable on the subject of nutrition and who is preoccupied with food and
weight.
A patient must have a thorough general physical and neurological examination. If the
patient is vomiting, a hypokalemic alkalosis may be present. Because most patients are
dehydrated, serum electrolyte levels must be determined initially and periodically.
Hospitalization may be necessary to deal with medical complications.
A young woman who weighed 10 percent above the average weight but was
otherwise healthy, functioning well, and working hard as a university student joined a
track team, started training for hours a day, more than her teammates, began to
perceive herself as fat and thought that her performance would be enhanced if she lost
weight. She started to diet and reduced her weight to 87 percent of the “ideal weight”
for her age according to standard tables. At her point of maximum weight loss, her
performance actually declined, and she pushed herself even harder in her training
regimen. She started to feel apathetic and morbidly afraid of becoming fat. Her food
intake became restricted and she stopped eating anything containing fat. Her
menstrual periods became skimpy and infrequent but did not cease. (Courtesy of
Arnold E. Andersen, M.D., and Joel Yager, M.D.)
PATHOLOGY AND LABORATORY EXAMINATION
A complete blood count often reveals leukopenia with a relative lymphocytosis in
emaciated patients with anorexia nervosa. If binge eating and purging are present,
serum electrolyte determination reveals hypokalemic alkalosis. Fasting serum glucose
concentrations are often low during the emaciated phase, and serum salivary amylase
concentrations are often elevated if the patient is vomiting. The ECG may show ST
segment and T-wave changes, which are usually secondary to electrolyte disturbances;
emaciated patients have hypotension and bradycardia. Young girls may have a high
serum cholesterol level. All these values revert to normal with nutritional rehabilitation
and cessation of purging behaviors. Endocrine changes that may occur, such as
amenorrhea, mild hypothyroidism, and hypersecretion of corticotrophin-releasing
hormone, are caused by the underweight condition and revert to normal with weight
gain.
DIFFERENTIAL DIAGNOSIS
The differential diagnosis of anorexia nervosa is complicated by patients’ denial of the
symptoms, the secrecy surrounding their bizarre eating rituals, and their resistance to
seeking treatment. Thus, it may be difficult to identify the mechanism of weight loss and
the patient’s associated ruminative thoughts about distortions of body image.
Clinicians must ascertain that a patient does not have a medical illness that can
account for the weight loss (e.g., a brain tumor or cancer). Weight loss, peculiar eating
behaviors, and vomiting can occur in several mental disorders. Depressive disorders and
anorexia nervosa have several features in common, such as depressed feelings, crying
spells, sleep disturbance, obsessive ruminations, and occasional suicidal thoughts. The
two disorders, however, have several distinguishing features. Generally, a patient with a
depressive disorder has decreased appetite, whereas a patient with anorexia nervosa
claims to have normal appetite and to feel hungry; only in the severe stages of anorexia
nervosa do patients actually have decreased appetite. In contrast to depressive
agitation, the hyperactivity seen in anorexia nervosa is planned and ritualistic. The
preoccupation with recipes, the caloric content of foods, and the preparation of gourmet
feasts is typical of patients with anorexia nervosa but is absent in patients with a
depressive disorder. In depressive disorders, patients have no intense fear of obesity or
disturbance of body image.
Weight fluctuations, vomiting, and peculiar food handling may occur in somatization
disorder. On rare occasions, a patient fulfills the diagnostic criteria for both
somatization disorder and anorexia nervosa; in such a case, both diagnoses should be
made. Generally, the weight loss in somatization disorder is not as severe as that in
anorexia nervosa, nor does a patient with somatization disorder express a morbid fear
of becoming overweight, as is common in those with anorexia nervosa. Amenorrhea for
3 months or longer is unusual in somatization disorder.
In patients with schizophrenia, delusions about food are seldom concerned with
caloric content. More likely, they believe the food to be poisoned. Patients with
schizophrenia are rarely preoccupied with a fear of becoming obese and do not have the
hyperactivity that is seen in patients with anorexia nervosa. Patients with schizophrenia
have bizarre eating habits but not the entire syndrome of anorexia nervosa.
Anorexia nervosa must be differentiated from bulimia nervosa, a disorder in which
episodic binge eating, followed by depressive moods, self-deprecating thoughts, and selfinduced vomiting occur while patients maintain their weight within a normal range.
Patients with bulimia nervosa seldom lose 15 percent of their weight, but the two
conditions frequently coexist.
Rare conditions of unknown etiology are seen in which hyperactivity of the vagus
nerve causes changes in eating patterns that are associated with weight loss, sometimes
of
severe
degree.
In
such
cases
bradycardia,
hypotension,
and
other
parasympathomimetic signs and symptoms are seen. Because the vagus nerve relates to
the enteric nervous system, eating may be associated with gastric distress such as nausea
or bloating. Patients do not generally lose their appetite. Treatment is symptomatic and
anticholinergic drugs can reverse hypotension and bradycardia, which may be lifethreatening.
COURSE AND PROGNOSIS
The course of anorexia nervosa varies greatly—spontaneous recovery without
treatment, recovery after a variety of treatments, a fluctuating course of weight gains
followed by relapses, and a gradually deteriorating course resulting in death caused by
complications of starvation. One study reviewing subtypes of anorectic patients found
that restricting-type anorectic patients seemed less likely to recover than those of the
binge eating–purging type. The short-term response of patients to almost all hospital
treatment programs is good. Those who have regained sufficient weight, however, often
continue their preoccupation with food and body weight, have poor social relationships,
and exhibit depression. In general, the prognosis is not good. Studies have shown a
range of mortality rates from 5 to 18 percent.
Indicators of a favorable outcome are admission of hunger, lessening of denial and
immaturity, and improved self-esteem. Such factors as childhood neuroticism, parental
conflict, bulimia nervosa, vomiting, laxative abuse, and various behavioral
manifestations (e.g., obsessive-compulsive, hysterical, depressive, psychosomatic,
neurotic, and denial symptoms) have been related to poor outcome in some studies, but
not in others.
Ten-year outcome studies in the United States have shown that about one fourth of
patients recover completely and another one half are markedly improved and
functioning fairly well. The other one fourth includes an overall 7 percent mortality rate
and those who are functioning poorly with a chronic underweight condition. Swedish
and English studies over a 20- and 30-year period show a mortality rate of 18 percent.
About half of patients with anorexia nervosa eventually will have the symptoms of
bulimia, usually within the first year after the onset of anorexia nervosa.
TREATMENT
In view of the complicated psychological and medical implications of anorexia nervosa,
a comprehensive treatment plan, including hospitalization when necessary and both
individual and family therapy, is recommended. Behavioral, interpersonal, and
cognitive approaches are used and, in many cases, medication may be indicated.
Hospitalization
The first consideration in the treatment of anorexia nervosa is to restore patients’
nutritional state; dehydration, starvation, and electrolyte imbalances can seriously
compromise health and, in some cases, lead to death. The decision to hospitalize a
patient is based on the patient’s medical condition and the amount of structure needed
to ensure patient cooperation. In general, patients with anorexia nervosa who are 20
percent below the expected weight for their height are recommended for inpatient
programs, and patients who are 30 percent below their expected weight require
psychiatric hospitalization for 2 to 6 months.
Inpatient psychiatric programs for patients with anorexia nervosa generally use a
combination of a behavioral management approach, individual psychotherapy, family
education and therapy, and, in some cases, psychotropic medications. Successful
treatment is promoted by the ability of staff members to maintain a firm yet supportive
approach to patients, often through a combination of positive reinforcers (praise) and
negative reinforcers (restriction of exercise). The program must have some flexibility for
individualizing treatment to meet patients’ needs and cognitive abilities. Patients must
become willing participants for treatment to succeed in the long run.
Most patients are uninterested in psychiatric treatment and even resist it; they are
brought to a doctor’s office unwillingly by agonizing relatives or friends. The patients
rarely accept the recommendation of hospitalization without arguing and criticizing the
proposed program. Emphasizing the benefits, such as relief of insomnia and depressive
signs and symptoms, may help persuade the patients to admit themselves willingly to
the hospital. Relatives’ support and confidence in the physicians and treatment team are
essential when firm recommendations must be carried out. Patients’ families should be
warned that the patients will resist admission and, for the first several weeks of
treatment, will make many dramatic pleas for their families’ support to obtain release
from the hospital program. Compulsory admission or commitment should be obtained
only when the risk of death from the complications of malnutrition is likely. On rare
occasions, patients prove that the doctor’s statements about the probable failure of
outpatient treatment are wrong. They may gain a specified amount of weight by the
time of each outpatient visit, but such behavior is uncommon, and a period of inpatient
care is usually necessary.
Hospital Management.
The following considerations apply to the general
management of patients with anorexia nervosa during a hospitalized treatment
program. Patients should be weighed daily, early in the morning after emptying the
bladder. The daily fluid intake and urine output should be recorded. If vomiting is
occurring, hospital staff members must monitor serum electrolyte levels regularly and
watch for the development of hypokalemia. Because food is often regurgitated after
meals, the staff may be able to control vomiting by making the bathroom inaccessible
for at least 2 hours after meals or by having an attendant in the bathroom to prevent
the opportunity for vomiting. Constipation in these patients is relieved when they begin
to eat normally. Stool softeners may occasionally be given, but never laxatives. If
diarrhea occurs, it usually means that patients are surreptitiously taking laxatives.
Because of the rare complication of stomach dilation and the possibility of circulatory
overload when patients immediately start eating an enormous number of calories, the
hospital staff should give patients about 500 calories over the amount required to
maintain their present weight (usually 1,500 to 2,000 calories a day). It is wise to give
these calories in six equal feedings throughout the day, so that patients need not eat a
large amount of food at one sitting. Giving patients a liquid food supplement such as
Sustagen may be advisable, because they may be less apprehensive about gaining
weight slowly with the formula than by eating food. After patients are discharged from
the hospital, clinicians usually find it necessary to continue outpatient supervision of the
problems identified in the patients and their families.
Psychotherapy
Cognitive-Behavioral Therapy.
Cognitive and behavioral therapy principles can
be applied in both inpatient and outpatient settings and have been found effective for
inducing weight gain. Monitoring is an essential component of cognitive-behavioral
therapy. Patients are taught to monitor their food intake, their feelings and emotions,
their binging and purging behaviors, and their problems in interpersonal relationships.
Patients are taught cognitive restructuring to identify automatic thoughts and to
challenge their core beliefs. Problem solving is a specific method whereby patients learn
how to think through and devise strategies to cope with their food-related and
interpersonal problems. Patients’ vulnerability to rely on anorectic behavior as a means
of coping can be addressed if they can learn to use these techniques effectively.
Dynamic Psychotherapy.
Dynamic expressive-supportive psychotherapy is
sometimes used in the treatment of patients with anorexia nervosa, but their resistance
may make the process difficult and painstaking. Because patients view their symptoms
as constituting the core of their specialness, therapists must avoid excessive investment
in trying to change their eating behavior. The opening phase of the psychotherapy
process must be geared toward building a therapeutic alliance. Patients may experience
early interpretations as though someone else were telling them what they really feel and
thereby minimizing and invalidating their own experiences. Therapists who empathize
with patients’ points of view and take an active interest in what their patients think and
feel, however, convey to patients that their autonomy is respected. Above all,
psychotherapists must be flexible, persistent, and durable in the face of patients’
tendencies to defeat any efforts to help them.
Family Therapy.
A family analysis should be done for all patients with anorexia
nervosa who are living with their families, which is used as a basis for a clinical
judgment on what type of family therapy or counseling is advisable. In some cases,
family therapy is not possible; however, issues of family relationships can then be
addressed in individual therapy. Sometimes, brief counseling sessions with immediate
family members is the extent of family therapy required. In one controlled family
therapy study in London, anorectic patients under the age of 18 benefited from family
therapy, whereas patients over the age of 18 did worse in family therapy than with the
control therapy. No controlled studies have been reported on the combination of
individual and family therapy; however, in actual practice, most clinicians provide
individual therapy and some form of family counseling in managing patients with
anorexia nervosa.
Pharmacotherapy
Pharmacological studies have not yet identified any medication that yields definitive
improvement of the core symptoms of anorexia nervosa. Some reports support the use
of cyproheptadine (Periactin), a drug with antihistaminic and antiserotonergic
properties, for patients with the restricting type of anorexia nervosa. Amitriptyline
(Elavil) has also been reported to have some benefit. Other medications that have been
tried by patients with anorexia nervosa with variable results include clomipramine
(Anafranil), pimozide (Orap), and chlorpromazine (Thorazine). Trials of fluoxetine
(Prozac) have resulted in some reports of weight gain, and serotonergic agents may
yield positive responses in some cases. In patients with anorexia nervosa and coexisting
depressive disorders, the depressive condition should be treated. Concern exists about
the use of tricyclic drugs in low-weight, depressed patients with anorexia nervosa, who
may be vulnerable to hypotension, cardiac arrhythmia, and dehydration. Once an
adequate nutritional status has been attained, the risk of serious adverse effects from the
tricyclic drugs may decrease; in some patients, the depression improves with weight
gain and normalized nutritional status.
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15.2 Bulimia Nervosa
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differentiate bingeing-purging from restrictive anorexia nervosa. J Clin Endocrinol Metab. 2010;95:3057.
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nervosa? Results from a systematic review and meta-analysis. J Clin Psychiatry. 2012;73:e757.
Kumar KK, Tung S, Iqbal J. Bone loss in anorexia nervosa: Leptin, serotonin, and the sympathetic nervous system. Ann
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Lopez C, Davies H, Tchanturia K. Neuropsychological inefficiences in anorexia nervosa targeted in clinical practice: The
development of a module of cognitive remediation therapy. In: Fox J, Goss K, eds. Eating and Its Disorders. Hoboken, NJ:
Wiley; 2012:185.
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Zipfel S, et al. Focal psychodynamic therapy, cognitive behaviour therapy, and optimised treatment as usual in outpatients
with anorexia nervosa (ANTOP study): randomised controlled trial. Lancet. 2014;383(9912):127–137.
15.2 Bulimia Nervosa
Bulimia nervosa is characterized by episodes of binge eating combined with
inappropriate ways of stopping weight gain. Physical discomfort—for example,
abdominal pain or nausea—terminates the binge eating, which is often followed by
feelings of guilt, depression, or self-disgust. Unlike patients with anorexia nervosa, those
with bulimia nervosa typically maintain a normal body weight.
The term bulimia nervosa derives from the terms for “ox-hunger” in Greek and
“nervous involvement” in Latin. For some patients, bulimia nervosa may represent a
failed attempt at anorexia nervosa, sharing the goal of becoming very thin, but
occurring in an individual less able to sustain prolonged semistarvation or severe
hunger as consistently as classic restricting anorexia nervosa patients. For others, eating
binges represent “breakthrough eating” episodes of giving in to hunger pangs generated
by efforts to restrict eating so as to maintain a socially desirable level of thinness. Still
others use binge eating as a means to self-medicate during times of emotional distress.
Regardless of the reason, eating binges provoke panic as individuals feel that their
eating has been out of control. The unwanted binges lead to secondary attempts to
avoid the feared weight gain by a variety of compensatory behaviors, such as purging or
excessive exercise.
EPIDEMIOLOGY
Bulimia nervosa is more prevalent than anorexia nervosa. Estimates of bulimia nervosa
range from 1 to 4 percent of young women. As with anorexia nervosa, bulimia nervosa
is more common in women than in men, but its onset is often later in adolescence than
that of anorexia nervosa. The onset may also occur in early adulthood. Approximately
20 percent of college women experience transient bulimic symptoms at some point
during their college years. Although bulimia nervosa is often present in normal-weight
young women, they sometimes have a history of obesity. In industrialized countries the
prevalence is about 1 percent of the general population. In the United States, bulimia
nervosa may be more prevalent among Hispanics and blacks than non-Hispanic whites.
ETIOLOGY
Biological Factors
Some investigators have attempted to associate cycles of binging and purging with various neurotransmitters. Because
antidepressants often benefit patients with bulimia nervosa and because serotonin has been linked to satiety, serotonin and
norepinephrine have been implicated. Because plasma endorphin levels are raised in some bulimia nervosa patients who
vomit, the feeling of well-being after vomiting that some of these patients experience may be mediated by raised
endorphin levels. Increased frequency of bulimia nervosa is found in first-degree relatives of persons with the disorder.
Recent research using functional magnetic resonance imaging (MRI) suggests that overeating in bulimia nervosa may
result from an exaggerated perception of hunger signals related to sweet taste mediated by the right anterior insula area of
the brain.
Social Factors
Patients with bulimia nervosa, as with those with anorexia nervosa, tend to be high achievers and to respond to societal
pressures to be slender. As with anorexia nervosa patients, many patients with bulimia nervosa are depressed and have
increased familial depression, but the families of patients with bulimia nervosa are generally less close and more
conflictual than the families of those with anorexia nervosa. Patients with bulimia nervosa describe their parents as
neglectful and rejecting.
Psychological Factors
Patients with bulimia nervosa, as with those with anorexia nervosa, have difficulties with adolescent demands, but
patients with bulimia nervosa are more outgoing, angry, and impulsive than those with anorexia nervosa. Alcohol
dependence, shoplifting, and emotional lability (including suicide attempts) are associated with bulimia nervosa. These
patients generally experience their uncontrolled eating as more ego-dystonic than do patients with anorexia nervosa and so
seek help more readily.
Patients with bulimia nervosa lack superego control and the ego strength of their counterparts with anorexia nervosa.
Their difficulties in controlling their impulses are often manifested by substance dependence and self-destructive sexual
relationships in addition to the binge eating and purging that characterize the disorder. Many patients with bulimia
nervosa have histories of difficulties separating from caretakers, as manifested by the absence of transitional objects during
their early childhood years. Some clinicians have observed that patients with bulimia nervosa use their own bodies as
transitional objects. The struggle for separation from a maternal figure is played out in the ambivalence toward food; eating
may represent a wish to fuse with the caretaker, and regurgitating may unconsciously express a wish for separation.
DIAGNOSIS AND CLINICAL FEATURES
Bulimia nervosa is present when (1) episodes of binge eating occurs relatively
frequently (once a week or more) for at least 3 months; (2) compensatory behaviors are
practiced after binge eating to prevent weight gain, primarily self-induced vomiting,
laxative abuse, diuretics, enemas, abuse of emetics (80 percent of cases), and, less
commonly, severe dieting and strenuous exercise (20 percent of cases); (3) weight is not
severely lowered as in anorexia nervosa; and (4) the patient has a morbid fear of
fatness, a relentless drive for thinness, or both and a disproportionate amount of selfevaluation that depends on body weight and shape. When making a diagnosis of
bulimia nervosa, clinicians should explore the possibility that the patient has
experienced a brief or prolonged prior bout of anorexia nervosa, which is present in
approximately half of those with bulimia nervosa. Binging usually precedes vomiting by
about 1 year. The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) diagnostic criteria for bulimia nervosa are listed in Table 15.2-1.
Table 15.2-1
DSM-5 Diagnostic Criteria for Bulimia Nervosa
Vomiting is common and is usually induced by sticking a finger down the throat,
although some patients are able to vomit at will. Vomiting decreases the abdominal
pain and the feeling of being bloated and allows patients to continue eating without
fear of gaining weight. The acid content of vomitus can damage tooth enamel, a not
uncommon finding in patients with the disorder. Depression, sometimes called postbinge
anguish, often follows the episode. During binges, patients eat food that is sweet, high in
calories, and generally soft or smooth textured, such as cakes and pastry. Some patients
prefer bulky foods without regard to taste. The food is eaten secretly and rapidly and is
sometimes not even chewed.
Annie is a 26-year-old Dutch woman. She works as a nurse in a city hospital and
lives alone. Annie would wake up at night, go to her kitchen, and start eating
whatever food she could lay her hands on. She stopped only after an hour or two
when she could find no more food. The bouts of overeating went on for 5 years until
she consulted her general practitioner, who referred her to outpatient psychiatric
treatment for a depression related to the eating spells. Annie’s spells of uncontrollable
overeating were preceded by a feeling of severe tension and were followed by
relaxation, although this was coupled with shame and despair. During the year before
her referral, the frequency of the overeating spells had increased to two or three times
a week. They usually appeared at night after just a few hours of sleep. After eating
her way through whatever she could find, she would feel bloated but would not vomit.
She tried to get rid of the food by taking large quantities of laxatives. Her weight was
unstable, but she managed to keep it within normal limits simply by fasting between
the overeating spells. Annie despised obesity but had never really been slim. Her
bouts of overeating made her feel increasingly low-spirited and despairing. She had
even considered committing suicide by taking an overdose of the sleeping tablets that
her general practitioner had prescribed because of her interrupted sleep. Annie
managed to do her job adequately and had taken only a few days of sick leave.
Annie was brought up in a village, where her father was a schoolteacher. After
secondary school she trained as a nurse and had various jobs on geriatric wards.
Annie had always been very sensitive and fearful of criticism and had low self-esteem.
She tried hard to live up to expectations and felt frustrated by minor criticisms. She
had been in love more than once, but never dared to become engaged because she
feared rejection and possibly also because she feared a sexual relationship. She had
only a few close friends because she had difficulty engaging in close relationships. She
often felt tense and diffident in company. She avoided going to meetings or parties
because she feared being criticized or rejected.
On examination Annie appeared quiet and reticent. Her mood was mildly
depressed, and she cried silently as she described her difficulties. No psychotic features
were suspected. She was otherwise healthy and of average weight. She perceived her
own weight to be slightly higher than the weight she would prefer. She said she was
afraid of becoming obese. (Courtesy of International Statistical Classification of Diseases
and Related Health Problems, 10th ed. Casebook)
Most patients with bulimia nervosa are within their normal weight range, but some
may be underweight or overweight. These patients are concerned about their body
image and their appearance, worried about how others see them, and concerned about
their sexual attractiveness. Most are sexually active, compared with anorexia nervosa
patients, who are not interested in sex. Pica and struggles during meals are sometimes
revealed in the histories of patients with bulimia nervosa.
Bulimia nervosa occurs in persons with high rates of mood disorders and impulse
control disorders. Bulimia nervosa is also reported to occur in those at risk for substancerelated disorders and a variety of personality disorders. Patients with bulimia nervosa
also have increased rates of anxiety disorders, bipolar I disorder, dissociative disorders,
and histories of sexual abuse.
Subtypes
Evidence indicates that bulimic persons who purge differ from binge eaters who do not purge in that the latter tend to
have less body-image disturbance and less anxiety concerning eating. Those with bulimia nervosa who do not purge tend to
be obese. Distinct physiological differences also exist between patients with bulimia who purge and those who do not.
Because of all these differences, the diagnosis of bulimia nervous is sometimes subtyped into a purging type, for those who
regularly engage in self-induced vomiting or the use of laxatives or diuretics, and a nonpurging type, for those who use
strict dieting, fasting, or vigorous exercise but do not regularly engage in purging. Patients who purge may have a different
course from that of patients who binge and then diet or exercise.
Patients with purging type may be at risk for certain medical complications such as hypokalemia from vomiting or
laxative abuse and hypochloremic alkalosis. Those who vomit repeatedly are at risk for gastric and esophageal tears,
although these complications are rare.
PATHOLOGY AND LABORATORY EXAMINATIONS
Bulimia nervosa can result in electrolyte abnormalities and various degrees of
starvation, although it may not be as obvious as in low-weight patients with anorexia
nervosa. Thus, even normal-weight patients with bulimia nervosa should have
laboratory studies of electrolytes and metabolism. In general, thyroid function remains
intact in bulimia nervosa, but patients may show nonsuppression on a dexamethasonesuppression test. Dehydration and electrolyte disturbances are likely to occur in patients
with bulimia nervosa who purge regularly. These patients commonly exhibit
hypomagnesemia and hyperamylasemia. Although not a core diagnostic feature, many
patients with bulimia nervosa have menstrual disturbances. Hypotension and
bradycardia occur in some patients.
DIFFERENTIAL DIAGNOSIS
The diagnosis of bulimia nervosa cannot be made if the binge-eating and purging
behaviors occur exclusively during episodes of anorexia nervosa. In such cases, the
diagnosis is anorexia nervosa, binge eating-purging type.
Clinicians must ascertain that patients have no neurological disease, such as epilepticequivalent seizures, central nervous system tumors, Klüver-Bucy syndrome, or KleineLevin syndrome. The pathological features manifested by Klüver-Bucy syndrome are
visual agnosia, compulsive licking and biting, examination of objects by the mouth,
inability to ignore any stimulus, placidity, altered sexual behavior (hypersexuality), and
altered dietary habits, especially hyperphagia. The syndrome is exceedingly rare and is
unlikely to cause a problem in differential diagnosis. Kleine-Levin syndrome consists of
periodic hypersomnia lasting for 2 to 3 weeks and hyperphagia. As in bulimia nervosa,
the onset is usually during adolescence, but the syndrome is more common in men than
in women.
Patients with bulimia nervosa who have concurrent seasonal affective disorder and
patterns of atypical depression (with overeating and oversleeping in low-light months)
may manifest seasonal worsening of both bulimia nervosa and depressive features. In
these cases, binges are typically much more severe during winter months. Bright light
therapy (10,000 lux for 30 minutes, in early morning, at 18 to 22 inches from the eyes)
may be a useful component of comprehensive treatment of an eating disorder with
seasonal affective disorder.
Some patients with bulimia nervosa—perhaps 15 percent—have multiple comorbid
impulsive behaviors, including substance abuse, and lack of ability to control themselves
in such diverse areas as money management (resulting in impulse buying and
compulsive shopping) and sexual relationships (often resulting in brief, passionate
attachments and promiscuity). They exhibit self-mutilation, chaotic emotions, and
chaotic sleeping patterns. They often meet criteria for borderline personality disorder
and other mixed personality disorders and, not infrequently, bipolar II disorder.
COURSE AND PROGNOSIS
Bulimia nervosa is characterized by higher rates of partial and full recovery compared
with anorexia nervosa. As noted in the treatment section, those treated fare much better
than those who are untreated. Patients who are untreated tend to remain chronic or
may show small, but generally unimpressive, degrees of improvement with time. In a
10-year follow-up study of patients who had previously participated in treatment
programs, the number of women who continued to meet the full criteria for bulimia
nervosa declined as the duration of follow-up increased. Approximately 30 percent
continued to engage in recurrent binge-eating or purging behaviors. A history of
substance use problems and a longer duration of the disorder at presentation predicted
worse outcome. Approximately 40 percent of women were fully recovered at follow-up.
The mortality rate for bulimia nervosa has been estimated at 2 percent per decade
according to DSM-5.
TREATMENT
Most patients with uncomplicated bulimia nervosa do not require hospitalization. In
general, patients with bulimia nervosa are not as secretive about their symptoms as
patients with anorexia nervosa. Therefore, outpatient treatment is usually not difficult,
but psychotherapy is frequently stormy and may be prolonged. Some obese patients
with bulimia nervosa who have had prolonged psychotherapy do surprisingly well. In
some cases—when eating binges are out of control, outpatient treatment does not work,
or a patient exhibits such additional psychiatric symptoms as suicidality and substance
abuse—hospitalization may become necessary. In addition, electrolyte and metabolic
disturbances resulting from severe purging may necessitate hospitalization.
Psychotherapy
Cognitive-Behavioral Therapy.
Cognitive-behavioral therapy (CBT) should be
considered the benchmark, first-line treatment for bulimia nervosa. The data supporting
the efficacy of CBT are based on strict adherence to rigorously implemented, highly
detailed, manual-guided treatments that include about 18 to 20 sessions over 5 to 6
months. CBT implements a number of cognitive and behavioral procedures to (1)
interrupt the self-maintaining behavioral cycle of binging and dieting and (2) alter the
individual’s dysfunctional cognitions; beliefs about food, weight, body image; and
overall self-concept.
Dynamic Psychotherapy.
Psychodynamic treatment of patients with bulimia
nervosa has been of limited success. Psychodynamic formulations revealed a tendency to
concretize introjective and projective defense mechanisms. In a manner analogous to
splitting, patients divide food into two categories: items that are nutritious and those
that are unhealthy. Food that is designated nutritious may be ingested and retained
because it unconsciously symbolizes good introjects. But junk food is unconsciously
associated with bad introjects and, therefore, is expelled by vomiting, with the
unconscious fantasy that all destructiveness, hate, and badness are being evacuated.
Patients can temporarily feel good after vomiting because of the fantasized evacuation,
but the associated feeling of “being all good” is short-lived because it is based on an
unstable combination of splitting and projection.
Other Modalities.
Controlled trials have shown that a variety of novel ways of
administering and facilitating cognitive-behavioral therapy are effective for bulimia
nervosa. Some have been incorporated in “stepped-care” programs and including
Internet-based platforms, computer facilitated programs, email enhanced programs, and
administration of cognitive-behavioral therapy via telemedicine to remote areas.
Pharmacotherapy
Antidepressant medications have been shown to be helpful in treating bulimia. This
includes the selective serotonin reuptake inhibitors (SSRIs), such as fluoxetine (Prozac).
This may be based on elevating central 5-hydroxytryptamine levels. Antidepressant
medications can reduce binge eating and purging independent of the presence of a
mood disorder. Thus, antidepressants have been used successfully for particularly
difficult binge-purge cycles that do not respond to psychotherapy alone. Imipramine
(Tofranil), desipramine (Norpramin), trazodone (Desyrel), and monoamine oxidase
inhibitors (MAOIs) have been helpful. In general, most of the antidepressants have been
effective at dosages usually given in the treatment of depressive disorders. Dosages of
fluoxetine that are effective in decreasing binge eating, however, may be higher (60 to
80 mg a day) than those used for depressive disorders. Medication is helpful in patients
with comorbid depressive disorders and bulimia nervosa. Carbamazepine (Tegretol) and
lithium (Eskalith) have not shown impressive results as treatments for binge eating, but
they have been used in the treatment of patients with bulimia nervosa with comorbid
mood disorders, such as bipolar I disorder. Evidence indicates that the use of
antidepressants alone results in a 22 percent rate of abstinence from binging and
purging; other studies show that CBT and medications are the most effective
combination.
REFERENCES
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of Psychiatry. 9th ed. Philadelphia: Lippincott Williams & Wilkins; 2009:2128.
Glasner-Edwards S, Mooney LJ, Marinelli-Casey P, Ang A, Rawson R. Bulimia nervosa among methamphetamine dependent
adults: Association with outcomes 3 years after treatment. Eat Disord. 2011;19:259.
Hildebrandt T, Alfano L, Tricamo M, Pfaff DW. Conceptualizing the role of estrogens and serotonin in the development and
maintenance of bulimia nervosa. Clin Psychol Rev. 2010;30:655.

03 - 15.3 Binge Eating Disorder and Other Eating D
15.3 Binge Eating Disorder and Other Eating Disorders
Levitan RD, Kaplan AS, Davis C, Lam RW, Kennedy JL. A season-of-birth/DRD4 interaction predicts maximal body mass
index in women with bulimia nervosa. Neuropsychopharmacology. 2010;35:1729.
Lowe MR, Witt AA, Grossman SL. Dieting in bulimia nervosa is associated with increased food restriction and
psychopathology but decreased binge eating. Eat Behav. 2013;14(3):342–347.
Oberndorfer TA, Frank GKW. Altered insula response to sweet taste processing after recovery from anorexia and bulimia
nervosa. Am J Psychiatry. 2013;170(10):1143–1151.
Poulsen, S., Lunn, S., Daniel, SI, Folke, S., Mathiesen, BB, Katznelson, H., Fairburn, CG. A randomized controlled trial of
psychoanalytic psychotherapy or cognitive-behavioral therapy for bulimia nervosa. Am J Psychiatry. 2014;171(1):109–
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Sandberg K, Erford BT. Choosing assessment instruments for bulimia practice and outcome research. J Counsel Dev.
2013;91(3):359–366.
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Zimmerli EJ, Devlin MJ, Kissileff HR, Walsh BT. The development of satiation in bulimia nervosa. Physiol Behav.
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Zunker C, Peterson CB, Crosby RD, Cao L, Engel SG, Mitchell JE, Wonderlich SA. Ecological momentary assessment of
bulimia nervosa: Does dietary restriction predict binge eating? Behav Res Ther. 2011;49(10):714.
15.3 Binge Eating Disorder and Other Eating Disorders
BINGE EATING DISORDER
Individuals with binge eating disorder engage in recurrent binge eating during which
they eat an abnormally large amount of food over a short time. Unlike bulimia nervosa,
patients with binge eating disorder do not compensate in any way after a binge episode
(e.g., laxative use). Binge episodes often occur in private, generally include foods of
dense caloric content, and, during the binge, the person feels he or she cannot control
his or her eating.
Epidemiology
Binge eating disorder is the most common eating disorder. It appears in approximately
25 percent of patients who seek medical care for obesity and in 50 to 75 percent of
those with severe obesity (body mass index [BMI] greater than 40). It is more common
in females (4 percent) than in males (2 percent).
Etiology
The cause of binge eating disorder is unknown. Impulsive and extroverted personality
styles are linked to the disorder as are persons who place themselves on a very low
calorie diet. Binge eating may also occur during periods of stress. It may be used to
reduce anxiety or alleviate depressive moods.
Diagnosis and Clinical Features
To be diagnosed with binge eating disorder the binges must be characterized by four
features: (1) eating more rapidly than normal and to the point of being uncomfortably
full, (2) eating large amounts of food even when not hungry, (3) eating alone, and (4)
feeling guilty or otherwise upset about the episode. Binges must occur at least once a
week for at least 3 months. The guidelines from the fifth edition of the Diagnostic and
Statistical Manual of Mental Disorders are presented in Table 15.3-1.
Table 15.3-1
DSM-5 Diagnostic Criteria for Binge Eating Disorder
Approximately half of individuals with binge eating disorder are obese. Additionally,
obese individuals with binge eating disorder have an earlier onset of obesity than those
without the disorder. Patients with binge eating disorder are also more likely to have an
unstable weight history with frequent episodes of weight cycling (the gaining or losing
of more than 10 kg). The disorder may be associated with insomnia, early menarche,
neck or shoulder and lower back pain, chronic muscle pain, and metabolic disorders.
Differential Diagnosis
Binge eating disorder and bulimia nervosa share the same core feature of recurrent
binge eating. Binge eating disorder is distinct from bulimia nervosa, however, in that
binge eating disorder patients do not report recurrent compensatory behavior such as
vomiting, laxative abuse, or excessive dieting. Binge eating disorder is distinct from
anorexia nervosa in that patients do not exhibit an excessive drive for thinness and are
of normal weight or are obese.
The prevalence of binge eating disorder is higher in overweight populations (3
percent) than in the general population (approximately 2 percent). However there are
some distinctions. Obese patients with binge eating disorder have a greater caloric
intake during binging and nonbinging episodes, greater eating disorder pathology (i.e.,
more emotional eating, chaotic eating habits), and higher rates of comorbid psychiatric
disorders. Binge eating disorder is also more prevalent in families than obesity.
Course and Prognosis
Little is known about the course of binge eating disorder. Severe obesity is a long-term
effect in over 3 percent of patients with the disorder. One prospective study of women
in the community with binge eating disorder suggested that by 5 years of follow-up
fewer than one fifth of the sample still had clinically significant eating disorder
symptoms.
Treatment
Psychotherapy.
Cognitive-behavioral therapy (CBT) is the most effective
psychological treatment for binge eating disorder. CBT has been shown to lead to
decreases in binge eating and associated problems (e.g., depression); however, studies
have not shown marked weight loss as a result of CBT, and CBT combined with
psychopharmacological treatments such as selective serotonin reuptake inhibitors
(SSRIs) show better results than CBT alone. Exercise has also shown a reduction in binge
eating when combined with CBT. Interpersonal psychotherapy (IPT) has also shown to
be effective in the treatment of binge eating disorder; however, therapy focuses more on
the interpersonal problems that contribute to the disorder rather than disturbances in
eating behavior.
Self-Help Groups.
Self-help groups such as Overeaters Anonymous (OA) have
proven to be helpful in patients with binge eating disorder. For the treatment of
moderate obesity, organizations such as Weight Watchers can be extremely helpful and
do not involve common fads or quick fixes.
Psychopharmacotherapy.
Symptoms of binge eating may benefit from
medication treatment with several SSRIs, desipramine (Norpramin), imipramine
(Tofranil), topiramate (Topamax), and sibutramine (Meridia). SSRI medications that
have demonstrated improvement in mood as well as binge eating include fluvoxamine
(Luvox), citalopram (Celexa), and sertraline (Zoloft). Some studies showed that highdose SSRI treatment (e.g., fluoxetine [Paxil] at 60 to 100 mg) often initially resulted in
weight loss. However, the weight loss was ordinarily short lived, even when medication
was continued, and weight always returned when medication was discontinued.
Amphetamine and amphetamine-like drugs may help but are of little use over the long
term.
Most, but not all, studies show that medication added to CBT is more effective than
medication alone. For example, studies indicate that CBT did better than fluvoxamine or
desipramine as a monotherapy for binge eating disorder; however, when CBT was used
in combination with these agents, more improvement was seen in terms of weight loss
compared with CBT alone.
OTHER SPECIFIED FEEDING OR EATING DISORDER
The diagnostic category of “other specified feeding or eating disorder” can be used for
eating conditions that may cause significant distress but do not meet the full criteria for
a classified eating disorder. Conditions included in this category include night eating
syndrome, purging disorder, and subthreshold forms of anorexia nervosa, bulimia
nervosa, and binge eating disorder.
Night Eating Syndrome
Night eating syndrome is characterized by the consumption of large amounts of food
after the evening meal. Individuals generally have little appetite during the day and
suffer from insomnia.
Epidemiology.
Night eating syndrome occurs in approximately 2 percent of the
general population; however, it has a higher prevalence among patients with insomnia,
obesity (10 to 15 percent), eating disorders, and other psychiatric disorders. The
disorder usually begins in early adulthood.
Etiology.
Little is known about the cause of night eating disorder; however, the
hormones melatonin, leptin, ghrelin, and cortisol have been studied in relation to the
disorder. Night eating syndrome also appears to run in families; patients with night
eating syndrome are five times more likely to have a first-degree relative with night
eating syndrome.
Diagnosis and Clinical Features
The diagnosis of night eating disorder includes recurrent episodes of hyperphagia or
night eating; the lack of desire for food in the morning; and insomnia. Symptoms must
persist for at least 3 months and cannot be secondary to another medical or mental
condition.
Patients with night eating syndrome usually consume a large portion of their daily
calorie intake after the evening meal. They are also more likely to wake up during the
night and to eat upon awakening. Nocturnal eating tends to occur during non-rapid eye
movement (REM) sleep and is usually short in duration. Patients are also prone to low
sleep efficiency. Patients believe that they can only sleep if they eat. Depressed mood is
common among these patients, especially during the evening and night hours.
Differential Diagnosis.
Night eating disorder is common among patients with
other eating disorders, particularly bulimia nervosa and binge eating disorder. Although
night eating can be found in bulimia nervosa and binge eating disorder, it is the
characteristic sign of night eating disorder. Also, the amount of food consumed during
eating episodes is usually lower in night eating disorder than in bulimia nervosa and
binge eating disorder. Unlike other eating disorders, patients with night eating
syndrome are not overly concerned about body image and weight. Patients with night
eating disorder are also at higher risk for obesity and metabolic syndrome.
Sleep-related eating disorder is characterized by recurrent episodes of involuntary
eating during the night. These episodes can lead to serious consequences such as the
ingesting of nonedible foods or substances, dangerous behaviors while searching for or
preparing food, and sleep-related injury. The eating episodes usually occur after the
patient has gone to sleep and may occur while the patient is unconscious or asleep.
Sleep-related eating disorder also has a high comorbidity with sleepwalking, restless leg
syndrome, and obstructive sleep apnea, conditions that are rarely found among night
eating syndrome patients. Episodes of sleep-related eating disorder have been reported
after the use certain medications, including zolpidem (Ambien), triazolam (Halcion),
olanzapine (Zyprexa), and risperidone (Risperdal).
Course and Prognosis.
The age of onset for night eating syndrome ranges from
the late teens to late 20s and has a long-lasting course with periods of remission with
treatment. Patients who experience poor sleep quality are more likely to develop
diabetes, obesity, hypertension, and cardiovascular disease.
Treatment.
Various studies have shown positive results in patients treated with
SSRIs who showed improvement in nighttime awakenings, nocturnal eating, and
postevening caloric intake. Weight loss and a reduction in nocturnal eating have been
associated with an addition of topiramate to medication regimens.
In patients with comorbid major depression and night eating syndrome, bright light
therapy has shown to decrease depressed mood. CBT has also been helpful.
Purging Disorder

04 - 15.4 Obesity and the Metabolic Syndrome
15.4 Obesity and the Metabolic Syndrome
Purging disorder is characterized by recurrent purging behavior after consuming a small
amount of food in persons of normal weight who have a distorted view of their weight
or body image. Purging behavior includes self-induced vomiting, laxative abuse,
enemas, and diuretics. To make the diagnosis, the behavior must not be associated with
anorexia nervosa. Purging disorder is differentiated from bulimia nervosa because
purging behavior occurs after eating small quantities of food or drink and does not
occur as a result of a binge episode. Purging episodes should occur at least once a week
over a 3-month period before the diagnosis is made.
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binge eating disorder. Eat Behav. 2013;14(3):309–313.
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symptomatology in normal-weight vs. obese individuals with binge eating disorder. Obesity. 2011;19:1515.
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prospective, observational study. Obes Res. 2011;19:1220.
15.4 Obesity and the Metabolic Syndrome
Obesity is a chronic illness manifested by an excess of body fat. It is generally measured
by the body mass index (BMI), but a more accurate method is to use body composition
analysis also known as biometric impedance analysis (BIA). Excess body fat generally
results from a greater amount of calories consumed than are burnt off. In healthy
individuals, body fat—which is different from the BMI—varies by gender. It ranges from
10 to 13 percent of essential fat to 25 to 31 percent on average of body weight in
healthy women. In men, it ranges from 2 to 5 percent of essential fat to 18 to 24
percent on average. The global epidemic of obesity has resulted in an alarming increase
in associated morbidity and mortality. Although manifestation of obesity and its
comorbid states are largely physical, it has overwhelming psychological ramifications.
The diagnosis of obesity using the BMI is discussed below.
COMORBIDITY
Evidence shows a correlation between obesity and psychiatric disorders. In fact, among
treatment-seeking obese patients, there is a higher prevalence of morbid psychiatric
illness by 40 to 60 percent. Disorders associated with obesity include eating disorders
(particularly binge eating disorder), substance use disorders, psychotic disorders
(schizophrenia), mood disorders, anxiety disorders, personality disorders, attentiondeficit/hyperactivity disorder (ADHD), and posttraumatic stress disorder (PTSD).
There are two eating disorders that can be associated with obesity: bulimia nervosa
and binge eating disorder. Both of these disorders are distinct in their clinical
characteristics and have some similarities. They both are associated with significant
psychopathology and need to be addressed multimodally to ensure success. It is
important to note that not all patients with bulimia nervosa are obese; they may be
overweight or of normal weight. See Sections 15.2 and 15.3 for further discussions on
bulimia nervosa and binge eating disorder, respectively.
EPIDEMIOLOGY
Obesity rates continue to grow at epidemic proportions in the United States and other
industrialized nations, representing a serious public health threat to millions of people.
In the United States, approximately 36 percent of adults are obese. The prevalence of
obesity is highest in minority populations, particularly among non-Hispanic black
women. More than one half of these individuals, 40 years of age or older, are obese and
more than 80 percent are overweight. The prevalence of obesity in adolescents in the
United States has also increased from about 15 percent in 2000 to about 35 percent in
2012, while the prevalence rates for overweight children ages 6 to 11 range from 14 to
25 percent; however, there has been a slight decrease in recent years.
Obesity also has economic effects. On an individual level, medical spending is
approximately 42 percent higher for an obese person compared with that for a person
of normal weight. On a national level, costs attributed to both overweight (BMI 25 to
29.9) and obesity (BMI greater than 30) account for 9.1 percent of US health care costs,
and if the current trend continues, obesity will account for 16 percent of US health care
costs by 2030.
ETIOLOGY
Persons with no medical etiology accumulate fat by eating more calories than are
expended as energy; thus intake of energy exceeds its dissipation. To reduce body fat,
fewer calories must be consumed or more calories must be burnt. An error of no more
than 10 percent in either intake or output would lead to a 30-pound change in body
weight in 1 year.
Satiety
Satiety is the feeling that results when hunger is satisfied. Persons stop eating at the end of a meal because they have
replenished nutrients that had been depleted. Persons become hungry again when nutrients restored by earlier meals are
once again depleted. It seems reasonable that a metabolic signal, derived from food that has been absorbed, is carried by the
blood to the brain, where the signal activates receptor cells, probably in the hypothalamus, to produce satiety. Some
studies have shown evidence for dysfunction in serotonin, dopamine, and norepinephrine involvement in regulating eating
behavior through the hypothalamus. Other hormonal factors that may be involved include corticotrophin-releasing factor
(CRF), neuropeptide Y, gonadotropin-releasing hormone, and thyroid-stimulating hormone. A newly found substance,
obestatin, which is made in the stomach, is a hormone that in animal experiments produces satiety and may have
potential use as a weight-loss agent in humans. Hunger results from a decrease in the strength of metabolic signals,
secondary to the depletion of critical nutrients.
Cannabinoid receptors are related to appetite and are stimulated with cannabis (marijuana) use. A cannabinoid inverse
antagonist has been developed that blocks appetite.
Satiety occurs soon after the beginning of a meal and before the total caloric content of the meal has been absorbed;
therefore, satiety is only one regulatory mechanism controlling food intake. Appetite, defined as the desire for food, is also
involved. A hungry person may eat to full satisfaction when food is available, but appetite can also induce a person to
overeat past the point of satiety. Appetite may be increased by psychological factors such as thoughts or feelings, and an
abnormal appetite may result in an abnormal increase in food intake. Eating is also affected by cannabinoid receptors,
which, when stimulated, increase appetite. Marijuana acts on that receptor that accounts for the “munchies” associated
with marijuana use. A drug called rimonabant (Acomplia) is an inverse agonist to the cannabidiol receptor, meaning that it
blocks appetite. It was withdrawn from the market because of adverse effects; however, in theory, inverse cannabinoid
receptor agonists may have clinical use.
The olfactory system may play a role in satiety. Experiments have shown that strong stimulation of the olfactory bulbs
in the nose with food odors by use of an inhaler saturated with a particular smell produces satiety for that food. This may
have implications for therapy of obesity.
Genetic Factors
The existence of numerous forms of inherited obesity in animals and the ease with which adiposity can be produced by
selective breeding make it clear that genetic factors can play a role in obesity. These factors must also be presumed to be
important in human obesity.
About 80 percent of patients who are obese have a family history of obesity. This fact
can be accounted for not only by genetic factors but also in part by identification with
fat parents and by learned oral methods for coping with anxiety. Nonetheless, studies
show that identical twins raised apart can both be obese, an observation that suggests a
hereditary role. To date, no specific genetic marker of obesity has been found. Table
15.4-1 lists the genetic factors affecting body weight.
Table 15.4-1
Genetic Factors Affecting Body Weight
Developmental Factors
Early in life, adipose tissue grows by increases in both cell number and cell size. Once the number of adipocytes has been
established, it does not seem to be susceptible to change. Obesity that begins early in life is characterized by adipose tissue
with an increased number of adipocytes of increased size. Obesity that begins in adult life, on the other hand, results solely
from an increase in the size of the adipocytes. In both instances, weight reduction produces a decrease in cell size. The
greater number and size of adipocytes in patients with juvenile-onset diabetes may be a factor in their widely recognized
difficulties with weight reduction and the persistence of their obesity.
The distribution and amount of fat vary in individuals, and fat in different body areas
has different characteristics. Fat cells around the waist, flanks, and abdomen (the socalled potbelly) are more active metabolically than those in the thighs and buttocks. The
former pattern is more common in men and has a higher correlation with cardiovascular
disease than does the latter pattern. Women, whose fat distribution is in the thighs and
buttocks, may become obsessed with nostrums that are advertised to reduce fat in these
areas (so-called cellulite, which is not a medical term), but no externally applied
preparation to reduce this fat pattern exists. Men with abdominal fat may attempt to
reduce their girth with machines that exercise the abdominal muscles, but exercise has
no effect on loss of this type of fat. A hormone called leptin, which is made by fat cells,
acts as a fat thermostat. When the blood level of leptin is low, more fat is consumed;
when high, less fat is consumed. Further research is needed to determine whether this
might lead to new ways of managing obesity.
Physical Activity Factors
The marked decrease in physical activity in affluent societies seems to be the major factor in the rise of obesity as a public
health problem. Physical inactivity restricts energy expenditure and may contribute to increased food intake. Although
food intake increases with increasing energy expenditure over a wide range of energy demands, intake does not decrease
proportionately when physical activity falls below a certain minimum level.
Brain-Damage Factors
Destruction of the ventromedial hypothalamus can produce obesity in animals, but this is probably a very rare cause of
obesity in humans. There is evidence that the central nervous system, particularly in the lateral and ventromedial
hypothalamic areas, adjusts to food intake in response to changing energy requirements so as to maintain fat stores at a
baseline determined by a specific set point. This set point varies from one person to another and depends on height and
body build.
Health Factors
In only a small number of cases is obesity the consequence of identifiable illness. Such cases include a variety of rare
genetic disorders, such as Prader-Willi syndrome, as well as neuroendocrine abnormalities (Table 15.4-2). Hypothalamic
obesity results from damage to the ventromedial region of the hypothalamus (VMH), which has been studied extensively
in laboratory animals and is a known center of appetite and weight regulation. In humans, damage to the VMH may result
from trauma, surgery, malignancy, or inflammatory disease.
Table 15.4-2
Illnesses that Can Explain Some Cases of Obesity
Some forms of depression, particularly seasonal affective disorder, are associated with weight gain. Most persons who
live in seasonal climates report increases in appetite and weight during the fall and winter months, with decreases in the
spring and summer. Depressed patients usually lose weight, but some will gain weight.
Other Clinical Factors
A variety of clinical disorders are associated with obesity. Cushing’s disease is associated with a characteristic fat
distribution and moon-like face (Fig. 15.4-1). Myxedema is associated with weight gain, although not invariably. Other
neuroendocrine disorders include adiposogenital dystrophy (Fröhlich’s syndrome), which is characterized by obesity and
sexual and skeletal abnormalities.
FIGURE 15.4-1
Cushing’s syndrome. Plethoric, “moon-faced” with “sun-fish” mouth. (From Douthwait
AH, ed. French’s Index of Differential Diagnosis. 7th ed. Baltimore: Williams & Wilkins;
1954:513, with permission.)
Psychotropic Drugs
Long-term use of steroid medications is associated with significant weight gain, as is the
use of several psychotropic agents. Patients treated for major depression, psychotic
disturbances, and bipolar disorder typically gain 3 to 10 kg, with even larger gains with
chronic use. This can produce the so-called metabolic syndrome discussed below.
Psychological Factors
Although psychological factors are evidently crucial to the development of obesity, how
such psychological factors result in obesity is not known. The food-regulating
mechanism is susceptible to environmental influence, and cultural, family, and
psychodynamic factors have all been shown to contribute to the development of obesity.
Although many investigators have proposed that specific family histories, precipitating
factors, personality structures, or unconscious conflicts cause obesity, overweight
persons may suffer from every conceivable psychiatric disorder and come from a variety
of disturbed backgrounds. Many obese patients are emotionally disturbed persons who,
because of the availability of the overeating mechanism in their environments, have
learned to use hyperphagia as a means of coping with psychological problems. Some
patients may show signs of serious mental disorder when they attain normal weight
because they no longer have that coping mechanism.
DIAGNOSIS AND CLINICAL FEATURES
The diagnosis of obesity, if done in a sophisticated way, involves the assessment of body
fat. As this is rarely practical, the use of height and weight to calculate BMI is
recommended. Figure 15.4-2 presents a chart for determining BMI from height and
weight.
FIGURE 15.4-2
Body mass index (BMI) chart. To determine BMI, find the patient’s weight on the left of
the graph and their height on the top of the graph. Follow the two categories toward the
middle of the graph until they intersect. This point represents the patient’s BMI.
In most cases of obesity, it is not possible to identify the precise etiology, given the
multitude of possible causes and their interactions. Instances of secondary obesity
(described in Table 15.4-3) are rare but should not be overlooked.
Table 15.4-3
Psychiatric Medications and Changes in Body Weight
The habitual eating patterns of many obese persons often seem similar to patterns
found in experimental obesity. Impaired satiety is a particularly important problem.
Obese persons seem inordinately susceptible to food cues in their environment, to the
palatability of foods, and to the inability to stop eating if food is available. Obese
persons are usually susceptible to all kinds of external stimuli to eating, but they remain
relatively unresponsive to the usual internal signals of hunger. Some are unable to
distinguish between hunger and other kinds of dysphoria.
DIFFERENTIAL DIAGNOSIS
Other Syndromes
The night eating syndrome, in which persons eat excessively after they have had their
evening meal, seems to be precipitated by stressful life circumstances and, once present,
tends to recur daily until the stress is alleviated. Night eating may also occur as a result
of using sedatives to sleep, which may produce sleepwalking and eating. This has been
reported with the use of zolpidem (Ambien) in patients. (See Section 15.3 for further
discussion on night eating syndrome.)
Binge eating disorder is characterized by sudden, compulsive ingestion of very large
amounts of food in a short time, usually with great subsequent agitation and selfcondemnation. Binge eating also appears to represent a reaction to stress. In contrast to
night eating syndrome, however, these bouts of overeating are not periodic, and they
are far more often linked to specific precipitating circumstances. Pickwickian syndrome
is said to exist when a person is 100 percent over desirable weight and has associated
respiratory and cardiovascular pathology.
Body Dysmorphic Disorder (Dysmorphophobia)
Some obese persons feel that their bodies are grotesque and loathsome and that others
view them with hostility and contempt. This feeling is closely associated with selfconsciousness and impaired social functioning. Emotionally healthy obese persons have
no body image disturbances, and only a minority of neurotic obese persons have such
disturbances. The disorder is confined mainly to persons who have been obese since
childhood; even among them, less than half suffer from it. (See Section 10.2 for a
complete discussion of body dysmorphic disorder.)
COURSE AND PROGNOSIS
Effects on Health
Obesity has adverse effects on health and is associated with a broad range of illnesses
(Table 15.4-4). There is a strong correlation between obesity and cardiovascular
disorders. Hypertension (blood pressure higher than 140/90 mm Hg) is three times
higher for persons who are overweight, and hypercholesterolemia (blood cholesterol
over 240 mg/dL) is twice as common. Studies show that blood pressure and cholesterol
levels can be reduced by weight reduction. Diabetes, which has clear genetic
determinations, can often be reversed with weight reduction, especially type 2 diabetes
(mature-onset or noninsulin-dependent diabetes mellitus).
Table 15.4-4
Health Disorders Thought to Be Caused or Exacerbated by Obesity
According to the National Institutes of Health data, obese men, regardless of smoking
habits, have a higher mortality from colon, rectal, and prostate cancer than men of
normal weight. Obese women have a higher mortality from cancer of the gallbladder,
biliary passages, breast (postmenopause), uterus (including cervix and endometrium),
and ovaries than women of normal weight.
Longevity
Reliable studies indicate that the more overweight a person is, the higher is that person’s
risk for death. A person who reduces weight to acceptable levels has a mortality decline
to normal rates. Weight reduction may be lifesaving for patients with extreme obesity,
defined as weight that is twice the desirable weight. Such patients may have
cardiorespiratory failure, especially when asleep (sleep apnea).
A number of studies have demonstrated that decreasing caloric intake by 30 percent or more in young or middle-aged
laboratory animals prevents or retards age-related chronic diseases and significantly prolongs the maximal lifespan. The
mechanisms through which this effect is mediated are not known, but they may include reductions in metabolic rate,
oxidative stress, and inflammation; improved insulin sensitivity; and changes in neuroendocrine and sympathetic nervous
system function. Whether long-term calorie restriction with adequate nutrition slows aging in humans is not yet known.
Prognosis
The prognosis for weight reduction is poor, and the course of obesity tends toward
inexorable progression. Of patients who lose significant amounts of weight, 90 percent
regain it eventually. The prognosis is particularly poor for those who become obese in
childhood. Juvenile-onset obesity tends to be more severe, more resistant to treatment,
and more likely to be associated with emotional disturbance than is adult obesity.
Discrimination Toward the Obese.
Overweight and obese individuals are
subject to significant prejudice and discrimination in the United States and other
industrialized nations. In a culture in which beauty ideals are thin and highly
unrealistic, overweight people are blamed for their condition and are the subject of
teasing, bias, and discrimination (sometimes called “fatism”). Income and earning
power are suppressed in overweight people, and untoward social conditions, such as
absence of romantic relationships, are more common. Furthermore, obese individuals
face limited access to health care and may receive biased diagnoses and treatment from
medical and mental health providers.
TREATMENT
As mentioned above, many patients routinely treated for obesity may develop anxiety
or depression. A high incidence of emotional disturbances has been reported among
obese persons undergoing long-term, in-hospital treatment by fasting or severe calorie
restriction. Obese persons with extensive psychopathology, those with a history of
emotional disturbance during dieting, and those in the midst of a life crisis should
attempt weight reduction cautiously and under careful supervision.
Diet
The basis of weight reduction is simple—establish a caloric deficit by bringing intake
below output. The simplest way to reduce caloric intake is by means of a low-calorie
diet. This strategy requires an adequate amount of protein intake with balanced
carbohydrate and fat intake and should be done under medical supervision. The best
long-term effects are achieved with a balanced diet that contains readily available
foods. For most persons, the most satisfactory reducing diet consists of their usual foods
in amounts determined with the aid of tables of food values, which are available in
standard books on dieting. Such a diet gives the best chance of long-term maintenance
of weight loss. Total unmodified fasts are used for short-term weight loss, but they have
associated morbidity including orthostatic hypotension, sodium diuresis, and impaired
nitrogen balance.
Ketogenic diets are high-protein, high-fat diets used to promote weight loss. They have high cholesterol content and
produce ketosis, which is associated with nausea, hypotension, and lethargy. Many obese persons find it tempting to use a
novel or even bizarre diet. Table 15.4-5 contains details and comparisons of various types of diets. Whatever effectiveness
these diets may have in large part results from their monotony. When a dieter stops the diet and returns to the usual fare,
the incentives to overeat are multiplied.
In general, the best method of weight loss is a balanced diet of 1,100 to 1,200 calories.
Such a diet can be followed for long periods but should be supplemented with vitamins,
particularly iron, folic acid, zinc, and vitamin B6.
Table 15.4-5
Types of Diets
Exercise
Increased physical activity is an important part of a weight-reduction regimen. Because
caloric expenditure in most forms of physical activity is directly proportional to body
weight, obese persons expend more calories than persons of normal weight with the
same amount of activity. Furthermore, increased physical activity may actually decrease
food intake by formerly sedentary persons. This combination of increased caloric
expenditure and decreased food intake makes an increase in physical activity a highly
desirable feature of any weight-reduction program. Exercise also helps maintain weight
loss. It is essential in the treatment of the metabolic syndrome.
Lifestyle Change
A lifestyle change empowers the patient to set goals of weight management. Simple
lifestyle modification strategies that patients should be encouraged to follow include:
Personal behavior during a meal:
Eat slowly and savor each mouthful
Chew each bite 30 times before swallowing
Put the fork down between bites
Delay eating for 2 to 3 minutes and converse
Postpone a snack for 10 minutes
Serve food on a smaller plate
Divide portions in half so another portion may be permitted
Reduce eating cues:
Eat only at one designated place
Leave the table as soon as eating is done
Do not combine eating with other activities (e.g., reading or watching television)
Do not put bowls of food on the table
Stock home with healthier food choices
Shop for groceries from a list after a full meal
Plan meals
Keep a food diary to link eating with hunger and nonhunger episodes
Substitute other activities for snacking
Pharmacotherapy
Various drugs, some more effective than others, are used to treat obesity. Table 15.4-6
lists the drugs currently available for this use. Drug treatment is effective because it
suppresses appetite, but tolerance to this effect may develop after several weeks of use.
An initial trial period of 4 weeks with a specific drug can be used; then, if the patient
responds with weight loss, the drug can be continued to see whether tolerance develops.
If a drug remains effective, it can be dispensed for a longer time until the desired weight
is achieved.
Table 15.4-6
Common Drugs for the Treatment of Obesity
Orlistat.
One weight-loss medication approved by the Food and Drug
Administration (FDA) for long-term use is orlistat (Xenical), which is a selective gastric
and pancreatic lipase inhibitor that reduces the absorption of dietary fat (which is then
excreted in stool). In clinical trials, orlistat (120 mg, three times a day), in combination
with a low-calorie diet, induced losses of approximately 10 percent of initial weight in
the first 6 months, which were generally well maintained for periods up to 24 months.
Because of its peripheral mechanism of action, orlistat is generally free of the central
nervous system effects (i.e., increased pulse, dry mouth, insomnia) that are associated
with most weight-loss medications. The principal adverse effects of orlistat are
gastrointestinal; patients must consume 30 percent or fewer calories from fat to prevent
adverse events that include oily stool, flatulence with discharge, and fecal urgency. A
lower dosed over-the-counter formulation of orlistat (Alli) was approved by the FDA in
2007.
Sibutramine.
Sibutramine (Meridia) is a β-phenylethylamine that inhibits the
reuptake of serotonin and norepinephrine (and dopamine to a limited extent). It was
approved by the FDA in 1997 for weight loss and the maintenance of weight loss (i.e.,
long-term use).
Lorcaserin.
Lorcaserin (Belviq) has been approved by the FDA for the treatment of
obesity in adults. Lorcaserin is a selective serotonin agonist that suppresses appetite and
reduces food intake. One double-blind, placebo-controlled trial showed that obese
patients lost about 4 percent more of their body weight in 1 year while on lorcaserin
compared with controls. Additionally, weight loss was maintained in 70 percent of
patients who took lorcaserin for 2 years. Another trial showed that obese patients who
took lorcaserin 10 mg 1 to 2 times per day in conjunction with nutritional and exercise
programs lost 6 percent of their body weight after 1 year. The recommended dosage is
10 mg twice a day. If the patient does not see a 5 percent reduction of their body weight
within 12 weeks of treatment, lorcaserin treatment should be discontinued. Side effects
of lorcaserin include headaches, dizziness, fatigue, nausea, dry mouth, and constipation.
Rare but serious side effects include a chemical imbalance (serotonin syndrome), suicidal
thoughts, psychiatric problems, and problems with memory or comprehension. Pregnant
women should not take lorcaserin.
Phentermine-topiramate.
Phentermine-topiramate (Qsymia) has been approved
by the FDA for weight management treatment in conjunction with diet and exercise. It
combines lower doses of immediate-release phentermine, a weight-loss drug prescribed
for short-term use, and controlled-release topiramate, an anticonvulsant. Patients should
start at the lowest dose (3.75 mg phentermine/23 mg topiramate extended release),
then increase to the recommended dose (7.5 mg/46 mg). In some circumstances,
patients may have their dose increased to the highest dose (15 mg/92 mg). In clinical
trials, patients have shown an average weight loss ranging from 7 percent (lowest dose)
to 9 percent (recommended dose) over those taking a placebo. Side effects include
paraesthesia, dry mouth, altered taste, increased heart rate, possible birth defects, and
psychiatric problems (depression, suicidal thoughts, impaired memory, and
concentration). If the patients do not see a 3 percent reduction in their body weight
after 12 weeks on the recommended dose, the dosage may be increased to the highest
dose. If patients do not see a 5 percent reduction in their body weight after 12 weeks on
the highest dose, treatment with Qsymia should be discontinued.
Surgery
Gastroplasty.
Vertical banded gastroplasty (VBG) is a restrictive-only operation
that involves creating a small gastric reservoir or pouch measuring 15 to 20 mL in
volume, which then empties into the residual stomach through a calibrated or banded
outlet. On average, patients lose 40 to 50 pounds of excess body weight over the first 1
to 2 years postoperatively. Vomiting, electrolyte imbalance, and obstruction may occur.
A syndrome called dumping, which consists of palpitations, weakness, and sweating,
may follow surgical procedures in some patients if they ingest large amounts of
carbohydrates in a single meal. Due to such complications, VBG is now only performed
in a few centers in the United States.
Gastric Bypass.
Since the early 1990s, gastric bypass (Fig. 15.4-3) has greatly
replaced VBG as the operation of choice. The procedure involves dividing the stomach
into two pouches—a small upper pouch and a larger lower “remnant” pouch—and then
rearranging the small intestine to connect to both. The expected weight loss averages 70
percent of excess body weight with the maximum weight loss occurring by 3 years
postoperatively (Fig. 15.4-4). The main complications of gastric bypass surgery are
primarily seen during the perioperative period. Mortality is less than 0.5 percent and is
mainly due to pulmonary emboli or sepsis secondary to anastomotic leakage. Vitamin
B12 and iron deficiencies may present and may require oral supplementation. All
patients need to take multivitamins postoperatively and need to be followed at regular
intervals for nutritional assessment. About 10 to 15 percent of patients will either fail to
achieve significant weight loss or regain a significant amount of their loss after 2 or 3
years. This is usually due to consumption of carbohydrates, such as potato chips or other
snack foods. Psychological treatment of abnormal eating behaviors is essential to
prevent weight gain.
FIGURE 15.4-3
Roux-en Y gastric bypass. (From Sadock BJ, Sadock VA, Ruiz P, eds. Kaplan & Sadock’s
Comprehensive Textbook of Psychiatry. 9th ed. Philadelphia: Lippincott Williams &
Wilkins; 2009, with permission.)
FIGURE 15.4-4
A. Preoperative photograph of a woman who lost 140 pounds after laparoscopic gastric
bypass surgery with significant deflation and poor skin quality. B. Postoperative
photograph after extended vertical thigh lift demonstrates tightening of the skin and
dramatic improvement of the thigh appearance. (From Sadock BJ, Sadock VA, Ruiz P,
eds. Kaplan & Sadock’s Comprehensive Textbook of Psychiatry. 9th ed. Philadelphia:
Lippincott Williams & Wilkins; 2009, with permission.)
Gastric Banding.
Laparoscopic adjustable gastric band was approved by the FDA
in 2002 and is one of the least invasive operations for obesity because it does not
involve cutting the stomach or the intestine. It involves placing a band around the
upper part of the stomach, creating a smaller stomach above the band and a larger
stomach below the band (Fig. 15.4-5). The smaller stomach allows the patient to feel
fuller quicker, thus reducing the amount of food intake. Average weight loss is
approximately 37 to 50 percent of excess body weight. Complications involve band
movement, erosion, malfunction, and slippage (stomach herniating through the band).
Improvements in the design of the band and newer placement techniques appear to be
reducing complications.
FIGURE 15.4-5
Laparoscopic adjustable gastric band. (From Sadock BJ, Sadock VA, Ruiz P, eds. Kaplan
& Sadock’s Comprehensive Textbook of Psychiatry. 9th ed. Philadelphia: Lippincott
Williams & Wilkins; 2009, with permission.)
Other Methods.
The surgical removal of fat (lipectomy) has no effect on weight
loss in the long run nor does liposuction, which has value only for cosmetic reasons.
Bariatric surgery is now recommended in individuals who have serious obesity-related
health complications and a BMI of greater than 35 kg/m2 (or a BMI greater than 40
kg/m2 in the absence of major health complications). Before surgery, candidates should
have tried to lose weight using the safer, more traditional options of diet, exercise, and
weight loss medication.
Psychotherapy
The psychological problems of obese persons vary, and there is no particular personality
type that is more prone to obesity. Some patients may respond to insight-oriented
psychodynamic therapy with weight loss, but this treatment has not had much success.
Uncovering the unconscious causes of overeating may not alter the behavior of persons
who overeat in response to stress, although it may serve to augment other treatment
methods. Years after successful psychotherapy many persons who overeat under stress
continue to do so. Obese persons seem particularly vulnerable to overdependency on a
therapist, and the inordinate regression that may occur during the uncovering
psychotherapies should be carefully monitored.
Behavior modification has been the most successful of the therapeutic approaches for
obesity and is considered the method of choice. Patients are taught to recognize external
cues that are associated with eating and to keep diaries of foods consumed in particular
circumstances, such as at the movies or while watching television, or during certain
emotional states, such as anxiety or depression. Patients are also taught to develop new
eating patterns, such as eating slowly, chewing food well, not reading while eating, and
not eating between meals or when not seated. Operant conditioning therapies that use
rewards such as praise or new clothes to reinforce weight loss have also been successful.
Group therapy helps to maintain motivation, to promote identification among members
who have lost weight, and to provide education about nutrition.
Comprehensive Approach
The National Heart, Lung, and Blood Institute formulated key recommendations for
patients and the public regarding weight loss. These are listed in Table 15.4-7.
Table 15.4-7
Key Recommendations for Healthy Weight
METABOLIC SYNDROME
The metabolic syndrome consists of a cluster of metabolic abnormalities associated with
obesity and that contribute to an increased risk of cardiovascular disease and type 2
diabetes. The syndrome is diagnosed when a patient has three or more of the following
five risk factors: (1) abdominal obesity, (2) high triglyceride level, (3) low HDL
cholesterol level, (4) hypertension, and (5) an elevated fasting blood glucose level.
Table 15.4-8 lists the criteria as set forth by the World Health Organization (WHO). The
syndrome is believed to occur in about 30 percent of the American population, but is
also well known in other industrialized countries around the world.
Table 15.4-8
World Health Organization Clinical Criteria for Metabolic Syndrome
The cause of the syndrome is unknown, but obesity, insulin resistance, and a genetic
vulnerability are involved. Treatment involves weight loss, exercise, and the use of
statins and antihypertensives as needed to lower lipid levels and blood pressure,
respectively. Because of the increased risk of mortality, it is important that the
syndrome be recognized early and treated.
Second-generation (atypical) antipsychotic medications have been implicated as a
cause of metabolic syndrome. In patients with schizophrenia, treatment with these
medications can cause a rapid increase in body weight in the first few months of
therapy, which may continue on for more than a year. In addition, insulin resistance
leading to type 2 diabetes has been associated with an atherogenic lipid profile.
Clozapine (Clozaril) and olanzapine (Zyprexa) are the two drugs most implicated, but
other atypical antipsychotics may also be involved.
Patients prescribed second-generation antipsychotic medications should be monitored
periodically with hemoglobin A1c, fasting blood glucose levels at the beginning of
treatment and during its course. Lipid profiles should also be obtained. Table 15.4-9 lists
screening procedures for patients taking these medications.
Table 15.4-9
Screen Patients Before Prescribing Antipsychotics
Psychological reactions to the metabolic syndrome depend on the signs and symptoms
experienced by the patient. Those who suffer primarily from obesity must deal with selfesteem issues from being overweight as well as the stress of participating in weight loss
programs. In many cases of obesity, eating is a way of satisfying deep-seated
dependency needs. As weight is lost, some patients become depressed or anxious. Cases
of psychosis have been reported in a few markedly obese patients during or after the
process of losing a vast amount of weight. Other metabolic discrepancies, particularly
variations in blood sugar, may be accompanied by irritability or other mood changes.
Finally, fatigue is a common occurrence in patients with this syndrome. As the condition
improves, especially if exercise is part of the regimen, fatigue eventually diminishes; but
patients may be misdiagnosed as having a dysthymic disorder or chronic fatigue
syndrome if metabolic causes of fatigue are not considered.
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