Eating Disorders

Eating Disorders



Kathleen N. Franco



DEFINITION AND ETOLOGY


Eating disorders are syndromes characterized by severe disturbances in eating behavior and by distress or excessive concern about body shape or weight. Presentation varies, but eating disorders often occur with severe medical or psychiatric comorbidity. Denial of symptoms and reluctance to seek treatment make treatment especially challenging.



CLASSIFICATION


Major eating disorders can be classified as anorexia nervosa (Box 1), bulimia nervosa (Box 2), and eating disorder not otherwise specified (Box 3). Although criteria of the Diagnostic and Statistical Manual of Mental Disorders, fourth edition, text revision (DSM IV-TR1), allow diagnosis of a specific eating disorder, many patients demonstrate a mixture of both anorexia and bulimia. Up to 50% of patients with anorexia nervosa develop bulimic symptoms, and a smaller percentage of patients who are initially bulimic develop anorexic symptoms.2



Box 1 DSM IV-TR Criteria for Anorexia Nervosa*


Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th ed, text rev. Washington, DC, American Psychiatric Association, 2000.



Criteria



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

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

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

Amenorrhea (at least three consecutive cycles) in postmenarchal girls and women. Amenorrhea is defined as periods occurring only following hormone (e.g., estrogen) administration.


Type



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

Binge-eating-purging type: During the current episode of anorexia nervosa, the person has regularly engaged in binge-eating or purging behavior (self-induced vomiting or the misuse of laxatives, diuretics, or enemas).


* See also Box 3.



Box 2 DSM IV-TR Criteria for Bulimia Nervosa*


Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th ed, text rev. Washington, DC, American Psychiatric Association, 2000.



Criteria



Recurrent episodes of binge eating characterized by both:

Eating, in a discrete period of time (e.g., within any 2-hour period), an amount of food that is definitely larger than most people would eat during a similar period of time and under similar circumstances

A sense of lack of control over eating during the episode, defined by a feeling that one cannot stop eating or control what or how much one is eating

Recurrent inappropriate compensatory behavior to prevent weight gain

Self-induced vomiting

Misuse of laxatives, diuretics, enemas, or other medications

Fasting

Excessive exercise

The binge eating and inappropriate compensatory behavior both occur, on average, at least twice a week for 3 months.

Self evaluation is unduly influenced by body shape and weight.

The disturbance does not occur exclusively during episodes of anorexia nervosa.


Type



Purging type: During the current episode of bulimia nervosa, the person has regularly engaged in self-induced vomiting or the misuse of laxatives, diuretics, or enemas.

Nonpurging type: During the current episode of bulimia nervosa, the person has used inappropriate compensatory behavior but has not regularly engaged in self-induced vomiting or misused laxatives, diuretics, or enemas.


* See also Box 3.



Box 3 DSM IV-TR Criteria for Eating Disorder Not Otherwise Specified*


Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th ed, text rev. Washington, DC, American Psychiatric Association, 2000.



Eating disorder not otherwise specified includes disorders of eating that do not meet the criteria for any specific eating disorder.

For female patients, all of the criteria for anorexia nervosa are met except that the patient has regular menses.

All of the criteria for anorexia nervosa are met except that, despite significant weight loss, the patient’s current weight is in the normal range.

All of the criteria for bulimia nervosa are met except that the binge eating and inappropriate compensatory mechanisms occur less than twice a week or for less than 3 months.

The patient has normal body weight and regularly uses inappropriate compensatory behavior after eating small amounts of food (e.g., self-induced vomiting after consuming two cookies).

Repeatedly chewing and spitting out, but not swallowing, large amounts of food.

Binge-eating disorder is recurrent episodes of binge eating in the absence if regular inappropriate compensatory behavior characteristic of bulimia nervosa.


* See also Boxes 1 and 2.


Anorexia nervosa has two subtypes: restrictive eating and binge eating alternating with restrictive eating at different periods of the illness. Patients with bulimia nervosa can be subclassified into purging and nonpurging. Many patients have a combination of eating disorder symptoms that cannot be strictly categorized as either anorexia nervosa or bulimia nervosa and are technically diagnosed as eating disorder not otherwise specified. Obesity alone is not considered an eating disorder.


Listed in the DSM IV-TR appendix, binge eating disorder is defined as uncontrolled binge eating without emesis or laxative abuse. It is often, but not always, associated with obesity symptoms. Night eating syndrome includes morning anorexia, increased appetite in the evening, and insomnia. Often obese, these patients can have complete or partial amnesia for eating during the night.


Eating disorders before puberty include food avoidance emotional disorder, which is similar to anorexia; selective eating of only a few foods; pervasive refusal syndrome, with reduced intake and added behavioral problems; and functional dysphagia with no organic etiology. Unpleasant mealtimes and conflicts over eating can precede these conditions of childhood. Pica and rumination are not considered eating disorders, but rather are feeding disorders of infancy and childhood.



RISK FACTORS AND PREVALENCE


Eating disorders have been reported in up to 4% of adolescents and young adults. The most common age at onset for anorexia nervosa is the mid teens; in 5% of the patients, the onset of the disorder is in the early twenties. The onset of bulimia nervosa is usually in adolescence but may be as late as early adulthood.2–3



Gender Prevalence


Both anorexia nervosa and bulimia nervosa are more commonly seen in girls and women. Estimates of female-to-male ratio range from 6 : 1 to 10 : 1.



Lifetime Prevalence


The reported lifetime prevalence of anorexia nervosa among women has ranged from 0.5% when narrowly defined to 3.7% for more broadly defined anorexia nervosa. With regard to bulimia nervosa, estimates of lifetime prevalence among women range from 1.1% to 4.2%. Prevalence of eating disorders in young children is unknown. However, children as young as 5 years have reported awareness of dieting and know that inducing vomiting can produce weight loss. Eating disorder not otherwise specified is the most prevalent eating disorder.



Cultural Considerations


Eating disorders are more common in industrialized societies where there is an abundance of food and being thin, especially for women, is considered attractive.3 Eating disorders are most common in the United States, Canada, Europe, Australia, New Zealand, and South Africa. However, rates are increasing in Asia, especially in Japan and China, where women are exposed to cultural change and modernization. In the United States, eating disorders are common in young Latin American, Native American, and African American women, but the rates are still lower than in white women. African American women are more likely to develop bulimia and more likely to purge. Female athletes involved in running, gymnastics, or ballet and male body builders or wrestlers are at increased risk.



PATHOPHYSIOLOGY AND NATURAL HISTORY


Biologic and psychosocial factors are implicated in the pathophysiology, but the causes and mechanisms underlying eating disorders remain uncertain.2–4



Biologic Factors


First-degree female relatives and monozygotic twin offspring of patients with anorexia nervosa have higher rates of anorexia nervosa and bulimia nervosa. Children of patients with anorexia nervosa have a lifetime risk for anorexia nervosa that is tenfold that of the general population (5%). Families of patients with bulimia nervosa have higher rates of substance abuse, particularly alcoholism, affective disorders, and obesity.


Endogenous opioids might contribute to denial of hunger in patients with anorexia nervosa. Some hypothesize that dieting can increase the risk for developing an eating disorder. Increased endorphin levels have been described in patients with bulimia nervosa after purging and may be likely to induce feelings of well being. Diminished norepinephrine turnover and activity are suggested by reduced levels of 3-methoxy-4-hydroxyphenylglycol in the urine and cerebrospinal fluid of some patients with anorexia nervosa. Antidepressants often benefit patients with bulimia nervosa and support a pathophysiologic role for serotonin and norepinephrine.


Starvation results in many biochemical changes such as hypercortisolemia, nonsuppression of dexamethasone, suppression of thyroid function, and amenorrhea. Several computed tomography (CT) studies of the brain have revealed enlarged sulci and ventricles, a finding that is reversed with weight gain. In one study using positron emission tomography (PET), metabolism was higher in the caudate nucleus during the anorectic state than after hyperalimentation.


Anorexia risk may increase with a polymorphism of the promoter region of serotonin 2a receptor. The melanocortin 4 receptor gene is hypothesized to regulate weight and appetite. Polymorphism in the gene for agouti-related peptide might also play a role at the melancortin receptor. In bulimia nervosa there is excessive secretion of ghrelin. Ghrelin receptor gene polymorphism is associated with both hyperphagia of bulimia and Prader-Willi syndrome.


Perhaps some of the most fascinating new research addresses the overlap between uncontrolled compulsive eating and compulsive drug seeking in drug addiction.4 Reduction in ventral striatal dopamine is found in both of these groups. The lower the frequency of dopamine D2 receptors, the higher the body mass index. Obese persons might eat to temporarily increase activity in these reward circuits. Frequent visual food stimuli paired with increased sensitivity of right orbitofrontal brain activity is likely to initiate eating behavior. Marijuana’s well-known appetite stimulant effect is likely due to its agonist activity at cannabinoid receptors, and cannabinoid receptor antagonism has been associated with reduced binge eating (Fig. 1).


image

Figure 1 Comprehensive treatment plan for the patient with an eating disorder.

Related posts:

  1. Anaphylaxis
  2. Chronic Nonmalignant Pain
  3. Polymyalgia Rheumatica and Giant Cell Arteritis
  4. Systemic Scleroderma

Stay updated, free articles. Join our Telegram channel
Tags:
Jul 18, 2017 | Posted by in GENERAL SURGERY | Comments Off on Eating Disorders

Full access? Get Clinical Tree
Get Clinical Tree app for offline access