Share on Facebook Share on Twitter Email
Answers.com

anorexia nervosa

 
American Heritage Dictionary:

anorexia ner·vo·sa

(nûr-vō') pronunciation
n.
A psychophysiological disorder usually occurring in young women that is characterized by an abnormal fear of becoming obese, a distorted self-image, a persistent unwillingness to eat, and severe weight loss. It is often accompanied by self-induced vomiting, excessive exercise, malnutrition, amenorrhea, and other physiological changes.

[New Latin anorexia nervōsa : anorexia, anorexia + nervōsa, feminine of nervōsus, nervous.]


Search unanswered questions...
Enter a question here...
Search: All sources Community Q&A Reference topics
Britannica Concise Encyclopedia:

anorexia nervosa

Top

Eating disorder, mostly in young women, characterized by a failure to maintain body weight at a normal level because of an intense desire to be thin, a fear of gaining weight, or a disturbance in body image. Anorexia nervosa typically begins in late adolescence. In women a usual symptom is amenorrhea. A person with anorexia nervosa will often go to great lengths to resist eating in order to lose weight, and medical complications can be life-threatening. Treatment can include psychological and social therapy.

For more information on anorexia nervosa, visit Britannica.com.

A psychiatric disorder in which a dramatic reduction in caloric intake consequent to excessive dieting leads to significant bodily, physiological, biochemical, emotional, psychological, and behavioral disturbances. Anorexia nervosa is typically an illness of adolescent females: 90% of all cases begin in girls who are between 12 and 20 years of age. Nevertheless, this disorder can also occur in males, in prepubertal girls, and in women well into their third decade. Moreover, if the illness becomes chronic, it can persist into mid-life and beyond. Anorexia nervosa literally means “nervous loss of appetite” but appears to have little to do with such. Rather, there is usually a conscious decision made by a teen-age girl, most commonly around the ages of 14 or 18 years, to embark upon a diet. The amount of weight lost can vary considerably. The usual criterion for making a diagnosis of anorexia nervosa is a weight change of at least 25% from premorbid weight (to at least 15% below ideal weight in persons who were overweight at the onset). But this figure should be viewed as only a rule of thumb. In addition to these core disturbances, there is an array of associated symptoms and practices that characterize most persons with anorexia nervosa. Amenorrhea (absence of menstruation); increased physical activity; insomnia; use of emetics, cathartics, and diuretics; difficulty in recognizing satiation; and obsessional thinking and depression. The course and prognosis of anorexia nervosa is highly variable. While a high recovery rate, perhaps above 67%, is found in those persons whose illness begins acutely in their early teens and who quickly receive treatment, the outlook is considerably bleaker in those persons who develop the disorder later, who do not receive early treatment, and who develop bulimia.

Perhaps as many as 40–50% of anorectic patients whose illness persists for more than 1–2 years will develop the additional eating disturbance known as bulimia. Literally meaning “oxhunger,” bulimia refers to binge eating or compulsive overeating wherein thousands of calories are consumed in a relatively brief period of time (for example, 2 h). The binge characteristically involves carbohydrates and will usually culminate in self-induced vomiting. The precise nature of the relationship of bulimia to anorexia nervosa remains unclear. Not all anorectics become bulimic and not all bulimics were anorectic. But dieting is common as a precursor to bulimia, and high premorbid weight and chronicity of weight loss seem to predispose the anorectic to developing bulimia.

Although there is a broad range of symptoms, personality styles, precipitants, and outcomes that characterize anorexia nervosa, there is no simple explanation of its origins. In one widely accepted conception, the illness is viewed as a desperate struggle by the vulnerable female adolescent to establish a sense of identity separate from that of her domineering, overbearing, controlling, and intrusive mother. There is considerable emphasis on viewing the family system as the matrix in which the illness develops and for which the illness must have significance. Anorexia is viewed as both a response to the lack of “living space” that the adolescent experiences and as a defense against the threats to the stability of the family system that the girl's normal development implies. Development of anorexia is thus a function of both individual and family. It should be noted, however, that these formulations suffer from a common problem. They are based on assessments of anorectic patients—and their families—after the illness has become established. Thus, these theories cannot very well differentiate among predisposing, precipitating, and sustaining factors.

There are numerous physical, physiological, and biochemical changes that reflect primarily, although not solely, the ravages of starvation. In addition to the general bodily emaciation they manifest, anorectic individuals show brittle nails, thinning hair, cold extremities, a slow pulse, a small heart, and a hypometabolic state. In anorectic women who also binge and vomit, tooth decay and enlargement of the salivary glands are common. A mild-to-moderate anemia and a diminished white blood cell count develop with progressive malnutrition. Diabetes insipidus can also occur in advanced cases. In addition, abnormalities in glucose tolerance and blood electrolytes have been observed. Particularly in women who vomit, the blood potassium level can be significantly low. See also Malnutrition.

Because of the prominence of amenorrhea in its symptomatology, there has been a long-standing interest in the endocrinology of anorexia nervosa. A number of reliable hormonal abnormalities have been documented. Most prominent among these are diminished hypothalamic-pituitary-gonadal axis function and elevated hypothalamic-pituitary-adrenal axis function. Reversal of these endocrine aberrations usually occurs with clinical improvement, although considerable time may be required for full normalization.

As with virtually all psychiatric conditions for which the etiology is unknown and where no single empirically effective treatment exists, the therapeutic approaches to anorexia nervosa are diverse and reflect the different disciplines, training biases, and experiences of their proponents. Individual, insight-oriented psychotherapy directed toward increasing confidence in identifying and accepting bodily feelings, and understanding the sources of one's low self-esteem and poor sense of self, has generally been the essence of treatment for nonhospitalized individuals, particularly before chronicity has set in. Individual psychotherapy still remains a critical part of any approach to treatment, but the recovery rate can be increased, perhaps beyond 80%, by the inclusion of regular family therapy as part of the treatment approach. In the hospital, the first priority of treatment is directed toward correcting the biological abnormalities created by the extreme dieting (and, when present, the vomiting). If the individual appears unable or unwilling to resume adequate caloric intake, despite firm but supportive nursing and concomitant individual and family psychotherapy, more extreme measures may have to be instituted, including behavior modification or intravenous hyperalimentation. There is some evidence that, particularly in anorectics who are also characterized by depression and bulimia, antidepressant or possibly anticonvulsant medication may be helpful in damping down the binging and thereby gradually normalizing eating behavior in general. See also Psychopharmacology; Psychotherapy.


A psychological disturbance resulting in a refusal to eat, possibly with restriction to a very limited range of foods, and often accompanied by a rigid programme of vigorous physical exercise, to the point of exhaustion. Anorectic subjects generally do not feel sensations of hunger. The result is a very considerable loss of weight, with tissue atrophy and a fall in basal metabolic rate. It is especially prevalent among adolescent girls; when body weight falls below about 45 kg there is a cessation of menstruation. See also bulimia nervosa.

Oxford Food & Fitness Dictionary:

anorexia nervosa

Top

Anorexia nervosa is usually abbreviated to anorexia, and is sometimes referred to as self-starvation syndrome. It is a potentially fatal eating disorder in which there is a loss of appetite or desire for food, leading to severe loss of body weight. Clinical diagnosis is usually based on the following criteria:

weight less than 85 per cent ideal weight
intense fear of becoming obese, even when underweight
disturbance of body image (i.e. feeling fat even when thin)
in women, cessation of periods for three or more consecutive cycles when not on the contraceptive pill.

Anorexia is often associated with other eating disorders, such as bulimia nervosa. Although it can affect adults, both male and female, it occurs most frequently in adolescent girls. Anorexics are ten times more likely to be female than male.

Anorexia is now recognized as a serious psychological illness and is on the increase in Western societies (one estimate gives a 360 per cent increase over the last 9 years). Anorexics are usually emotionally disturbed and have a distorted body image. They are often convinced that they should be thinner even when their body weight is well below average. They will go to extreme lengths to restrict eating and to lose weight because they have a phobia about becoming obese. This phobia is expressed as an intense fear of gaining weight even when they are dangerously underweight.

There are many suggested causes of anorexia. It has been linked to dietary problems in early life, parental obsessions with food, problems within the family, and rejection of adult sexuality. Some psychologists see the relentless pursuit of thinness as a desire to be autonomous, to have control over one's own body, and to gain an identity. It is also seen as an attempt constantly to please others. Anorexia has been linked with participation in certain types of sports. Gymnasts, distance runners, and dancers are believed to be prone to eating disorders because of the pressure on them to remain slim, but it is generally agreed that these disorders rarely develop into the full condition. Some sport psychologists and sports nutritionists believe that high levels of physical activity can lead to the development of anorexia nervosa. They contend that strenuous exercise can suppress appetite resulting in a reduced food intake and weight loss. Many people who perceive themselves as being overweight exercise in order to slim. Any weight loss associated with their activity encourages them to exercise even more. This may initiate a cycle of exercise and weight loss that can lead to anorexia. However, although excessive exercise may contribute to anorexia, most experts believe that it is only one contributory factor, and does not explain the majority of cases.

Whatever the cause, the effects of anorexia are dramatic and potentially very dangerous. The persistent anorexic becomes malnourished, may suffer a variety of medical complications (including hair loss, cessation of periods, and cardiovascular abnormalities), and risks death due to starvation. One recent study reported a mortality rate of 6.6 per cent during a ten-year follow-up period.

Anorexia is much more than dieting gone wrong. It requires medical treatment and may respond to psychotherapy. The more chronic the condition, the more difficult it is to treat. If treated early, most of the physical symptoms can be corrected through adequate nutrition and the gradual restoration of normal weight. However, the underlying psychological problems may be more resistant to treatment.

Definition

Anorexia nervosa is an eating disorder characterized by self-starvation, unrealistic fear of weight gain, and conspicuous distortion of body image.

Description

The term anorexia nervosa comes from two Latin words that mean "nervous inability to eat." Anorexics have the following characteristics in common:

  • inability to maintain weight at or above what is normally expected for age or height
  • intense fear of becoming fat
  • distorted body image
  • in females who have begun to menstruate, the absence of at least three menstrual periods in a row, a condition called amenorrhea

There are two subtypes of anorexia nervosa: a restricting type, characterized by strict dieting and exercise without binge eating; and a binge-eating/purging type, marked by episodes of compulsive eating with or without self-induced vomiting and/or the use of laxatives or enemas. A binge is defined as a time-limited (usually under two hours) episode of compulsive eating in which the individual consumes a significantly larger amount of food than most people would eat in similar circumstances.

Demographics

Anorexia nervosa was not officially classified as a psychiatric disorder until the third edition of Diagnostic and Statistical Manual of Mental Disorders (DSM) in 1980. It is, however, a growing problem in the early 2000s among adolescent females. Its incidence in the United States has doubled since 1970. The rise in the number of reported cases reflects a genuine increase in the number of persons affected by the disorder and not simply earlier or more accurate diagnosis. Estimates of the incidence of anorexia range between 0.5 percent and 1 percent of Caucasian female adolescents. Over 90 percent of patients diagnosed with the disorder as of 2001 are female. The peak age range for onset of the disorder is 14 to 18 years. In the 1970s and 1980s, anorexia was regarded as a disorder of upper- and middle-class women, but that generalization is as of 2004 also changing. Studies indicate that anorexia is increasingly common among females of all races and social classes in the United States.

Causes and Symptoms

While the precise cause of the disease is not known, anorexia is a disorder that results from the interaction of cultural and interpersonal as well as biological factors.

Social Influences

The rising incidence of anorexia is thought to reflect the present idealization of thinness as a badge of upper-class status as well as of female beauty. In addition, the increase in cases of anorexia includes "copycat" behavior, with some patients developing the disorder from imitating other girls.

The onset of anorexia in adolescence is attributed to a developmental crisis caused by girls' changing bodies coupled with society's overemphasis on female appearance. The increasing influence of the mass media in spreading and reinforcing gender stereotypes has also been noted.

Occupational Goals

The risk of developing anorexia is higher among adolescents preparing for careers that require attention to weight and/or appearance. These high-risk groups include dancers, fashion models, professional athletes (including gymnasts, skaters, long-distance runners, and jockeys), and actresses.

Genetic and Biological Influences

Girls whose biological mothers or sisters have or have had anorexia nervosa appear to be at increased risk of developing the disorder.

Psychological Factors

A number of theories have been advanced to explain the psychological aspects of the disorder. No single explanation covers all cases. Anorexia nervosa has been given the following interpretations:

  • Overemphasis on control, autonomy, and independence: Some anorexics come from achievement-oriented families that stress physical fitness and dieting. Many anorexics are perfectionists who are driven about schoolwork and other matters in addition to weight control.
  • Evidence of family dysfunction: In some families, a daughter's eating disorder serves as a distraction from marital discord or other family tensions.
  • A rejection of female sexual maturity: This rejection is variously interpreted as a desire to remain a child or as a desire to resemble males.
  • A reaction to sexual abuse or assault.
  • A desire to appear as fragile and nonthreatening as possible: This hypothesis reflects the idea that female passivity and weakness are attractive to males.
  • Inability to interpret the body's hunger signals accurately due to early experiences of inappropriate feeding.

Male Anorexics

Although anorexia nervosa largely affects females, its incidence in the male population is rising in the early 2000s. Less is known about the causes of anorexia in males, but some risk factors are the same as for females. These include certain occupational goals and increasing media emphasis on external appearance in men. Homosexual males are under pressure to conform to an ideal body weight that is about 20 pounds lighter than the standard attractive weight for heterosexual males.

When to Call the Doctor

A healthcare professional should be contacted if a child or adolescent is suspected of having anorexia nervosa or displays early signs of the disorder, such as the following:

  • fear of gaining weight
  • distorted body image
  • recent weight loss
  • restrictive or abnormal eating patterns such as skipping meals or eliminating once-liked foods
  • preoccupation with food and dieting
  • compulsive exercising
  • purging behaviors such as vomiting or using laxatives
  • withdrawal from friends and family
  • wearing baggy clothes to hide weight loss

Diagnosis

Diagnosis of anorexia nervosa is complicated by a number of factors. One is that the disorder varies somewhat in severity from patient to patient. A second factor is denial, which is regarded as an early sign of the disorder. Many anorexics deny that they are ill and are usually brought to treatment by a family member.

Anorexia nervosa is a serious public health problem not only because of its rising incidence, but also because it has one of the highest mortality rates of any psychiatric disorder. Moreover, the disorder may cause serious long-term health complications, including congestive heart failure, sudden death, growth retardation, dental problems, constipation, stomach rupture, swelling of the salivary glands, anemia and other abnormalities of the blood, loss of kidney function, and osteoporosis.

Most anorexics are diagnosed by pediatricians or family practitioners. Anorexics develop emaciated bodies, dry or yellowish skin, and abnormally low blood pressure. There is usually a history of amenorrhea in female patients, and sometimes of abdominal pain, constipation, or lack of energy. The patient may feel chilly or have developed lanugo, a growth of downy body hair. If the patient has been self-inducing vomiting, she may have eroded tooth enamel or Russell's sign (scars on the back of the hand). The second step in diagnosis is measurement of the patient's weight loss. DSM-IV specifies a weight loss leading to a body weight 15 percent below normal, with some allowance for body build and weight history.

Criteria

SOURCE: Diagnostic and Statistical Manual of Mental Disorders IV.
1. Refusal to maintain body weight at or above a minimally normal weight for age and height. Body weight is less than 85 percent of what is expected.
2. Intense fear of gaining weight or becoming fat, even though patient is underweight.
3. Undue influence of body weight or shape on self-evaluation, or denial of the seriousness of current underweight condition.
4. Absence of at least three consecutive menstrual cycles in previously menstruating females.
Restricting type: No regular episodes of binge-eating or purging (self-induced vomiting or misuse of laxatives, diuretics, or enemas).
Binge-eating/purging type: Regular episodes of binge-eating or purging (self-induced vomiting or misuse of laxatives, diuretics, or enemas).

The doctor will need to rule out other physical conditions that can cause weight loss or vomiting after eating, including metabolic disorders, brain tumors (especially hypothalamus and pituitary gland lesions), diseases of the digestive tract, and a condition called superior mesenteric artery syndrome. Persons with this condition sometimes vomit after meals because the blood supply to the intestine is blocked. The doctor will usually order blood tests, an electrocardiogram, urinalysis, and bone densitometry (bone density test) in order to exclude other diseases and to assess the patient's nutritional status.

The doctor will also need to distinguish between anorexia and other psychiatric disorders, including depression, schizophrenia, social phobia, obsessive-compulsive disorder, and body dysmorphic disorder. Two diagnostic tests that are often used are the Eating Attitudes Test (EAT) and the Eating Disorder Inventory (EDI).

Treatment

Treatment of anorexia nervosa includes both short- and long-term measures and requires assessment by dietitians and psychiatrists as well as medical specialists. Therapy is often complicated by the patient's resistance or failure to carry out a treatment plan.

Hospital Treatment

Hospitalization is recommended for anorexics with any of the following characteristics:

  • weight of 40 percent or more below normal or weight loss over a three-month period of more than 30 lbs (13.6 kg)
  • severely disturbed metabolism
  • severe binging and purging
  • signs of psychosis
  • severe depression or risk of suicide
  • family in crisis

Hospital treatment includes individual and group therapy as well as refeeding and monitoring of the patient's physical condition. Treatment usually requires two to four months in the hospital. In extreme cases, hospitalized patients may be force-fed through a tube inserted in the nose (nasogastric tube) or into a vein (hyperalimentation).

Outpatient Treatment

Anorexics who are not severely malnourished can be treated by outpatient psychotherapy. The types of treatment recommended are supportive rather than insight-oriented and include behavioral approaches as well as individual or group therapy. Family therapy is often recommended when the patient's eating disorder is closely tied to family dysfunction. Self-help groups are often useful in helping anorexics find social support and encouragement. Psychotherapy with anorexics is a slow and difficult process; about 50 percent of patients continue to have serious psychiatric problems after their weight has stabilized.

Medications

Anorexics have been treated with a variety of medications, including antidepressants, antianxiety drugs, selective serotonin reuptake inhibitors, and lithium carbonate. The effectiveness of medications in treatment regimens is as of 2004 debated. However, at least one study of fluoxetine (Prozac) showed it helped the patient maintain weight gained while in the hospital.

Nutritional Concerns

A key focus of treatment for anorexia nervosa is teaching the principles of healthy eating and improving disordered eating behaviors. A dietician or nutritionist plays an important role in forming a nutrition plan for the patient; such plans are individualized and ensure that the patient is consuming enough food to gain or maintain weight as needed and stabilize medically. The anorexic's weight and food intake are closely monitored to ensure that the plan is being followed.

Prognosis

Figures for long-term recovery vary from study to study, but reliable estimates are that 40 to 60 percent of anorexics make a good physical and social recovery, and 75 percent gain weight. The long-term mortality rate for anorexia is estimated at around 10 percent, although some studies give a lower figure of 3 to 4 percent. The most frequent causes of death associated with anorexia are starvation, electrolyte imbalance, heart failure, and suicide.

Prevention

Short of major long-term changes in the larger society, the best strategy for prevention of anorexia is the cultivation of healthy attitudes toward food, weight control, and beauty (or body image) within families. Early treatment such as counseling may help to prevent early signs of disordered eating from progressing into more serious behaviors.

Parental Concerns

There are many strategies that parents can undertake to help encourage healthy attitudes toward weight, food, and exercise in their children. These include the following:

  • teaching children the importance of healthy eating and exercise
  • avoiding using food as a punishment or reward
  • instilling healthy eating and exercise habits by example
  • being a good role model by promoting healthy body image and encouraging children and adolescents to find role models in the media who do the same
  • encouraging children or teens who wish to diet to talk to a healthcare professional about healthy strategies to lose weight

See also Binge eating disorder; Bulimia nervosa.

Resources

Books

"Anorexia Nervosa." In The Merck Manual of Diagnosis and Therapy, 17th ed. Edited by Mark H. Beers and Robert Berkow. Whitehouse Station, NJ: Merck & Co. Inc., 2004.

Knowles, Jarol B. "Eating Disorders." In Textbook of Primary Care Medicine, 3rd ed. Edited by John Noble. St. Louis: Mosby Inc., 2001.

Litt, Iris F. "Anorexia Nervosa and Bulimia." In Nelson Textbook of Pediatrics, 17th ed. Edited by Richard E. Behrman, Robert M. Kliegman, and Hal B. Jenson. Philadelphia: Saunders, 2004.

Smith, Delia. "The Eating Disorders." In Cecil Textbook of Medicine, 21st ed. Edited by Lee Goldman and J. Claude Bennett. Philadelphia: Saunders, 2000.

Periodicals

American Academy of Pediatrics Committee on Adolescence. "Identifying and Treating Eating Disorders." Pediatrics 111, no. 1 (January 1, 2003): 204–11.

Pritts, Sarah D., and Jeffrey Susman. "Diagnosis of Eating Disorders in Primary Care." American Family Physician 67, no. 2 (January 15, 2003): 297–304.

Rome, E. S. "Eating Disorders." Obstetrics and Gynecology Clinics of North America 30, no. 2 (June 1, 2003): 353–77.

Rosen, David S. "Eating Disorders in Children and Young Adolescents: Etiology, Classification, Clinical Features, and Treatment." Adolescent Medicine 14, no. 1 (February 1, 2003): 49–59.

——. "Eating Disorders in Adolescent Males." Adolescent Medicine 14, no. 3 (October 1, 2003): 677–89.

Sigman, Gary S. "Eating Disorders in Children and Adolescents." Pediatric Clinics of North America 50, no. 5 (October 2003): 1139–77.

Organizations

American Anorexia/Bulimia Association. 418 East 76th St., New York, NY 10021. Telephone: 212/734–1114.

National Association of Anorexia Nervosa and Associated Disorders. Web site: www.anad.org.

National Institute of Mental Health Eating Disorders Program. Building 10, Room 3S231. 9000 Rockville Pike, Bethesda, MD 20892. Telephone: 301/496–1891.

[Article by: Rebecca J. Frey, PhD Stephanie Dionne Sherk]



An eating disorder (usually abbreviated as anorexia and sometimes called self-starvation syndrome) characterized by loss of appetite and desire for food, a refusal to maintain body weight over minimal weight for age and height, an intense fear of becoming fat or gaining weight, a distorted body image, and (in females) amenorrhoea. A persistent anorexic may suffer serious medical complications and the condition can be fatal. Anorexia nervosa occurs in males and females, but is most frequent in adolescent girls. Gymnasts, cheerleaders, and dancers may be particularly prone to anorexia because of the pressures on them to remain slim The illness requires medical treatment and may respond to psychotherapy. See also eating disorder.

Gale Nutrition Encyclopedia:

Anorexia Nervosa

Top
Anorexia nervosa is an eating disorder characterized by an extreme reduction in food intake leading to potentially life-threatening weight loss. This syndrome is marked by an intense, irrational fear of weight gain or excess body fat, accompanied by a distorted perception of body weight and shape. The onset is usually in the middle to late teens and is rarely seen in females over age forty. Among women of menstruating age with this disorder, amenorrhea is common.

A clinical diagnosis of anorexia nervosa necessitates body weight less than 85 percent of average for weight and height. Subtypes of this disorder include the binge eating/purging type (bingeing and purging are present) or the restricting type (bingeing and purging are absent).

See also Addiction, food; Body image; Bulimia nervosa; Eating disorders; Eating disturbances.

Bibliography
American Dietetic Association (1998). Nutrition Intervention in the Treatment of Anorexia Nervosa, Bulimia Nervosa, and Eating Disorder Not Otherwise Specified (EDNOS). Chicago: Author.

American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders, 4th edition. Washington, DC: Author.
Escott-Stump, Sylvia, and Mahan, L. Kathleen (1996). Krause's Food, Nutrition, and Diet Therapy, 9th edition. Philadelphia: W. B. Saunders.
Olson, James A.; Shike, Moshe; Shils, Maurice E. (1994). Modern Nutrition in Health and Disease. Media, PA: Williams & Wilkins.

Gale Encyclopedia of Diets:

Anorexia nervosa

Top

    Demographics
    Causes and symptoms
    Diagnosis
    Treatment
    Nutrition concerns
    Therapy
    Prognosis
    Prevention
    Resources

What is Anorexia nervosa?

Anorexia nervosa is an eating disorder that involves self-imposed starvation. The individual is obsessed with becoming increasingly thinner and limits food intake to the point where health is compromised. Anorexia nervosa can be fatal.

Description of Anorexia nervosa

Anorexia is often thought of as a modern problem, but the English physician Richard Morton first described it in 1689. In the twenty-first century anorexia nervosa is recognized as a psychiatric disorder in the Diagnostic and Statistical Manual for Mental Disorders Fourth Edition (DSM-IV-TR) published by the American Psychiatric Association.

Individuals with anorexia are on an irrational, unrelenting quest to lose weight, and no matter how much they lose and how much their health is compromised, they want to lose more weight. Recognizing the development of anorexia can be difficult, especially in a society that values and glamorizes thinness. Dieting is often the trigger that starts a person down the road to anorexia. The future anorectic may begin by skipping meals or taking only tiny portions. She (most anorectics are female) always has an excuse for why she does not want to eat, whether it is not feeling hungry, feeling ill, having just eaten with someone else, or not liking the food served. She also begins to read food labels and knows exactly how many calories and how much fat are in everything she eats. Many anorectics practically eliminate fat and sugar from their diets and seem to live on diet soda and lettuce. Some future anorectics begin to exercise compulsively to burn extra calories. Eventually these practices have serious health consequences. At some point, the line between problem eating and an eating disorder is crossed.

Anorexia nervosa is diagnosed when most of the following conditions are present:

  • an overriding obsession with food and thinness that controls activities and eating patterns every hour of every day
  • the individual weighs less than 85% of the average weight for his or her age and height group and willfully and intentionally refuses to maintain an appropriate body weight
  • extreme fear of gaining weight or becoming fat, even when the individual is significantly underweight
  • a distorted self-image that fuels a refusal to admit to being underweight, even when this is demonstrably true
  • refusal to admit that being severely underweight is dangerous to health
  • for women, three missed menstrual periods in a row after menstruation has been established
Anorectics spend a lot of time looking in the mirror, obsessing about clothing size, and practicing negative self-talk about their bodies. Some are secretive about eating and will avoid eating in front of other people. They may develop strange eating habits such as chewing their food and then spitting it out, or they may have rigid ideas about “good” and “bad” food. Anorectics will lie about their eating habits and their weight to friends, family, and healthcare providers. Many anorectics experience depression and anxiety disorders.

There are two major subtypes of anorectics. Restrictive anorectics control their weight by rigorously limiting the amount of calories they eat or by fasting. They may exercise excessively or abuse drugs or herbal remedies claim to increase the rate at which the body burns calories. Purge-type anorectics eat and then get rid of the calories and weight by self-induced vomiting, excessive laxative use, and abuse of diuretics or enemas.

Gale Dictionary of Psychoanalysis:

Anorexia Nervosa

Top

The term "anorexia nervosa" was coined by William Gull in 1873. Although the term has existed for little more than a century, the clinical description of the syndrome is much older. Among other works, we can find a description in Avicenna in the eleventh century, and we have no difficulty recognizing it in Richard Morton's 1694 account of "nervous consumption." The first complete description in terms identical to those of Gull can be found in an article written by Dr. Louis Victor Marcé in 1860.

The classic clinical picture of anorexia brings together three factors: weight loss of more than 10 percent, amenorrhea, and the absence of a manifest melancholic or delusional mental disturbance. But the emphasis has changed from these classic symptoms to more specific symptoms, such as a confused body image, denial of being thin, desperate desire to be thin, and fear of putting on weight. Also, two major types of anorexia nervosa have been distinguished: purely restrictive forms and forms associated with bulimic episodes accompanied by weight monitoring, self-induced vomiting, and excessive use of laxatives and diuretics. Anorexia nervosa frequently occurs during adolescence, especially among females (ten girls for every one boy). It affects between 1 and 2 percent of the female adolescent population.

Without ever dealing specifically with eating disorders, Freud did in fact establish all of the perspectives—hysteria, melancholia, and "actual" neurosis—around which the pathological manifestations of anorexia can be understood metapsychologically. As a hysteria, anorexia involves a double polarity: oral fixations of the libido serve as a point of regression, and sexual fantasies become oral and are then repressed. As a melancholia, anorexia involves melancholy over the issue of object loss and a loss of instinctual needs. Freud speaks of an anesthesia that leads to melancholic thinking, which opens up a research path related to the next perspective. As an "actual" neurosis, anorexia poses a threefold question about the importance of the current situation, of somatic and infrarepresentational factors, and of the inadequacy of the ego and capacities for working matters out.

Melanie Klein and her students have stressed the importance of archaic fantasies of sadistic devouring, destruction, and poisoning in anorexia. Psychoanalysts dealing specifically with eating disorders initially considered them to be primarily a symptom and took little interest in the organization of the personality. But because of the complexity of cases and the frequent severity of the evolution of the disorder, the pathology of the personality assumed a growing importance in their work. The Göttingen symposium, organized by J. E. Meyer and H. Feldmann (1965), recognized anorexia nervosa as having a specific structure and viewed it not so much as an attempt toward compromise formation but rather as an attempt to deal with psychotic failures in the organization of the ego by reestablishing the mother-child unit.

Evelyne Kestemberg et al. (1974) have provided a remarkable description of the specific modes of the regression and instinctual organization in anorexia. This organization is characterized by recourse to a primary erogenous masochism in which pleasure is linked directly to a refusal to satisfy a need. Pleasure does not accompany the feeling of having something inside oneself; rather, anorexia eroticizes not satisfying a vital need. Similarly, relationships become dominated by pleasure in their being not satisfied. The hedonization of refusal becomes the guardian of the feeling of being or existing in one's own right, corporeal activity and the body being thus liberated from all external holds. The most complete form of this hedonization of refusal is "hunger orgasm."

Different studies stress the importance of the dependence/autonomy conflict and the fundamental vulnerability of anorexics. This vulnerability is associated with powerful passive desires and, as a consequence, a constant fear of intrusion, particularly an invasion of the body by the object on which these desires depend. To pose the problem in terms that highlight the paradox of anorexia: anorexics destroy themselves to prove their own existence. The destructive effect is not sought after for its own sake, and in this respect anorexia is not a suicidal behavior, although it can be seen as the result of unleashing aggression and turning against the self an incorporation fantasy of an object experienced as destructive for the self. Anorexia is the consequence of using a physiological need indispensable for survival to preserve a feeling of autonomy. In doing so—and this is the second paradox—anorexics find themselves in fact more dependent on an environment from which they sought to free themselves. By making refusal the instrument of their liberation, they alienate themselves from the object of the refusal, which they can neither lose nor interiorize.

The anorexia-bulimia tandem leads to questions about whether a problem of dependence underlies other behaviors grouped under the label "addictive behaviors": drug addiction, alcoholism, pathological gambling, and shopping, as well as abuse of psychotropic drugs and kleptomania. The fragile narcissistic bases of such addicts makes their object relations difficult to manage, because these object relations become too exciting and too dangerous. Addiction to products or behavioral practices offers addicts a need-satisfying relational substitute that is always accessible and which they believe they can control, while in fact they fall into its grip.

The eating disorder represents a substitute for the object whose loss could plunge these patients into a collapse. This attempt to find a substitute object in addictive behavior represents a perverse organization of a relationship to the object in which the object is not recognized as having its own desires and differences, but is acknowledged only for purposes of narcissistic reassurance. An analogy exists among these patients' relationship with food, their relationship with their own bodies, and their object relations, as well as their modes of emotional investment in general.

Family-therapy approaches illustrate the sensitivity of these patients to the influences of their environment. These eating disorders can be seen as existing at an intersection between individual psychology, family interactions, the body in its most biological aspect, and society in general. An essentially mental disorder may thus have grave somatic consequences, and these consequences may in turn affect the anorexic's psychic state and thus contribute to maintaining the disorder.

Addictive behaviors raise questions about the type of society in which we live, particularly with the increase in the frequency of these disorders accompanying the increase in consumerism in our societies.

Bibliography

Agman, Gilles; Corcos, Maurice; and Jeammet, Philippe. (1994). Troubles des conduits alimentaires. In Encyclopédie medico-chirurgicale (Psychiatrie vol., fasc. 37-350-A-10). Paris: Encyclopédie medico-chirurgicale.

Brusset, Bernard. (1998). Psychopathologie de l'anorexie mentale. Paris: Dunod.

Kestemberg, Evelyne; Kestenberg, Jean; and Decobert, Simone. (1972). La faim et le corps: une étude psychanalytique de l'anorexie mentale. Paris: Presses Universitaires de France.

Venisse, Jean-Luc (Ed.). (1991). Les nouvelles addictions. Paris: Masson.

Further Reading

Aronson, Joyce K. (ed.) (1993). Insights in the dynamic psychotherapy of anorexia and bulimia: An introduction to the literature. Northvale, NJ: Jason Aronson.

Freedman, Norbert, et. al. (2002). Desymbolization: concept & observations on anorexia & bulimia. Psychoanalysis and Contemporary Thought, 25,165-200.

Sours, John. (1980). Starving to death in a sea of objects: the anorexia nervosa syndrome. New York: Jason Aronson.

Thoma, Helmut. (1967). Anorexia nervosa. New York: International Universities Press.

Wilson, Charles, Hogan, C., and Mintz, Ira. (1985). Fear of being fat: the treatment of anorexia and bulimia (2nd ed). Northvale, NJ: Aronson.

Young-Bruehl, Elisabeth. (1993). Feminism and psychoanalysis: in the case of anorexia nervosa. Psychoanalytical Psychology, 10, 317-330.

—PHILIPPE JEAMMET

(an-uh-rek-see-uh nur-voh-suh)

A psychosomatic disorder in which the sufferer refuses to eat and undertakes activities (such as self-induced vomiting) to bring about extreme weight loss. Anorexia, which is also characterized by a distorted self-image, occurs most often in young women aged twelve to twenty-one and may result in death if medical treatment is not obtained. Treatment for anorexia often includes extensive counseling to reveal underlying emotional problems.

Mosby's Dental Dictionary:

anorexia nervosa

Top

n

A psychoneurotic disorder characterized by a prolonged refusal to eat, resulting in emaciation, amenorrhea in women, emotional disturbance concerning body image, and an abnormal fear of becoming fat.

Random House Word Menu:

categories related to 'anorexia nervosa'

Top
Random House Word Menu by Stephen Glazier
For a list of words related to anorexia nervosa, see:
  • Afflictions and Conditions - anorexia nervosa: extreme loss of appetite, esp. in adolescent females, causing severe weight loss and starvation
  • Syndromes, Disorders, and Conditions - anorexia nervosa: pathological fear of obesity, esp. in young women, leading to inability to retain food, loss of appetite, malnutrition, and sometimes death


Wikipedia on Answers.com:

Anorexia nervosa

Top
Anorexia nervosa
Classification and external resources

"Miss A—” pictured in 1866 and in 1870 after treatment. She was one of the earliest Anorexia nervosa case studies. From the published medical papers of Sir William Gull.
ICD-10 F50.0-F50.1
ICD-9 307.1
OMIM 606788
DiseasesDB 749
eMedicine emerg/34 med/144
MeSH D000856

Anorexia nervosa is an eating disorder characterized by an obsessive fear of gaining weight. The terms anorexia nervosa and anorexia are often used interchangeably, however anorexia is simply a medical term for lack of appetite. Anorexia nervosa has many complicated implications and may be thought of as a lifelong illness that may never be truly cured, but only managed over time.

Anorexia nervosa is often coupled with a distorted self image[1][2] which may be maintained by various cognitive biases[3] that alter how the affected individual evaluates and thinks about her or his body, food and eating. Persons with anorexia nervosa continue to feel hunger, but deny themselves all but very small quantities of food. The average caloric intake of a person with anorexia nervosa is 600–800 calories per day, but extreme cases of complete self-starvation are known.[4] It is a serious mental illness with a high incidence of comorbidity and the highest mortality rate of any psychiatric disorder.[5]

Anorexia most often has its onset in adolescence and is most prevalent among adolescent girls. [6] However, more recent studies show that the onset age of anorexia decreased from an average of 13 to 17 years of age to 9 to 12. [7] While it can affect men and women of any age, race, and socioeconomic and cultural background,[8] Anorexia nervosa occurs in females 10 times more than in males.[9] While anorexia nervosa is quite commonly (in lay circles) believed to be a woman 's illness, it should not be forgotten than ten per cent of people with anorexia nervosa are male.

The term anorexia nervosa was established in 1873 by Sir William Gull, one of Queen Victoria's personal physicians.[10] The term is of Greek origin: an- (ἀν-, prefix denoting negation) and orexis (ὄρεξις, "appetite"), thus meaning a lack of desire to eat.[11] However, while the term "anorexia nervosa" literally means "neurotic loss of appetite" the literal meaning of the term is somewhat misleading. Many anorexics do enjoy eating and have certainly not lost their appetite as the term "loss of appetite" is normally understood; it is better to regard anorexia nervosa as a self-punitive addiction to fasting, rather than a literal loss of appetite.

Contents

Signs and symptoms

A person with anorexia nervosa may exhibit a number of signs and symptoms, some of which are listed below. The type and severity vary in each case and may be present but not readily apparent. Anorexia nervosa and the associated malnutrition that results from self-imposed starvation, can cause severe complications in every major organ system in the body.[12][13][14]

Dermatologic signs of anorexia nervosa[24]
xerosis telogen effluvium carotenoderma acne hyperpigmentation
seborrheic dermatitis acrocyanosis perniosis petechiae livedo reticularis
interdigital intertrigo paronychia generalized pruritus acquired striae distensae angular stomatitis
prurigo pigmentosa edema linear erythema craquele acrodermatitis enteropathica pellagra
Possible medical complications of anorexia nervosa
constipation[25] diarrhea[26] electrolyte imbalance[27] cavities[28] tooth loss[29]
cardiac arrest[30] amenorrhoea[31] edema[32] osteoporosis[33] osteopenia[34]
hyponatremia[35] hypokalemia[36] optic neuropathy[37] brain atrophy[38][39] leukopenia[40][41]

Causes

Studies have hypothesized that the continuance of disordered eating patterns may be epiphenomena of starvation. The results of the Minnesota Starvation Experiment showed that normal controls exhibit many of the behavioral patterns of anorexia nervosa when subjected to starvation. This may be due to the numerous changes in the neuroendocrine system, which results in a self perpetuating cycle.[42][43][44][45] Studies have suggested that the initial weight loss such as dieting may be the triggering factor in developing AN in some cases, possibly because of an already inherent predisposition toward AN. One study reports cases of AN resulting from unintended weight loss that resulted from varied causes such as a parasitic infection, medication side effects, and surgery. The weight loss itself was the triggering factor.[46][47]

Biological

Dysregulation of the neurogenic pathways of serotonin and dopamine, two important neurotransmitters have been implicated in the etiology, pathogenesis and pathophsiology of various neuropsychiatric disorders, including anorexia nervosa.
Dysregulation of the dopamine and serotonin pathways has been implicated in the etiology, pathogenesis and pathophysiology of anorexia nervosa.[59][60][61][62]
  • Nutritional deficiencies
    • Zinc deficiency may play a role in anorexia. It is not thought responsible for causation of the initial illness but there is evidence that it may be an accelerating factor that deepens the pathology of the anorexia. A 1994 randomized, double-blind, placebo-controlled trial showed that zinc (14 mg per day) doubled the rate of body mass increase compared to patients receiving the placebo.[71]

Environmental

Sociocultural studies have highlighted the role of cultural factors, such as the promotion of thinness as the ideal female form in Western industrialized nations, particularly through the media.[72] A recent epidemiological study of 989,871 Swedish residents indicated that gender, ethnicity and socio-economic status were large influences on the chance of developing anorexia, with those with non-European parents among the least likely to be diagnosed with the condition, and those in wealthy, white families being most at risk.[73] People in professions where there is a particular social pressure to be thin (such as models and dancers) were much more likely to develop anorexia during the course of their career,[74] and further research has suggested that those with anorexia have much higher contact with cultural sources that promote weight-loss.[75]

Anorexia nervosa is more likely to occur in a person’s pubertal years, especially for girls.[76] Female students are 10 times more likely to suffer from anorexia nervosa than male students. According to a survey of 1799 Japanese female high school students, “85% who were a normal weight wanted to be thinner and 45% who were 10–20% underweight wanted to be thinner.”[77] Teenage girls concerned about their weight and who believe that slimness is more attractive among peers trend to weight-control behaviors. Teen girls are learning from each other to consume low-caloric, low-fat foods and diet pills. This results in lack of nutrition and a greater chance of developing anorexia nervosa.[78]

It has also been noted that anorexia nervosa is more likely to occur in populations in which obesity is more prevalent. It has been suggested that anorexia nervosa results from a sexually selected evolutionary drive to appear youthful in populations in which size becomes the primary indicator of age.[79]

There is also evidence to suggest that patients who have anorexia nervosa can be characterised by alexithymia[80] and also a deficit in certain emotional functions. A research study showed that this was the case in both adult and adolescent anorexia nervosa patients.[81]

There is a high rate of reported child sexual abuse experiences in clinical groups of who have been diagnosed with anorexia. The connection between eating disorders and abuse has been convincingly evidenced by a number of studies, including one published in Epidemiology (and strengthened by blind hypothesis survey), which showed in a comparison of women with no history of eating disorders, women with a history of eating disorders were twice as likely to have reported childhood sexual abuse.[82] While the joint effect of both physical and sexual abuse resulted in a nearly 4-fold risk of eating disorders that met DSM-IV criteria.[82] It is thought that links between childhood abuse and sexual abuse are complex, such as by influencing psychologic processes that increase a woman's susceptibility to the development of an eating disorder, or perhaps by producing changes in psychobiologic process and neurotransmitting function, associated with eating behaviour.[82]

Recent efforts have been made to dispel some of the myths around anorexia nervosa and eating disorders, such as the misconception that families, in particular mothers, are responsible for their daughter developing an eating disorder.[83]

Relationship to autism

A summary of the strategy Zucker et al. (2007) used to assess the relationship between anorexia nervosa and the autism spectrum.[84]

Since Gillberg's (1983 & 1985)[85][86] and others' initial suggestion of relationship between anorexia nervosa and autism,[87][88] a large-scale longitudinal study into teenage-onset anorexia nervosa conducted in Sweden confirmed that 23% of people with a long-standing eating disorder are on the autism spectrum.[89][90][91][92][93][94][95] Those on autism spectrum tend to have a worse outcome,[96] but may benefit from the combined use of behavioural and pharmacological therapies tailored to ameliorate autism rather than anorexia nervosa per se.[97][98] Other studies, most notably research conducted at the Maudsley Hospital, UK, furthermore suggest that autistic traits are common in people with anorexia nervosa; shared traits include, e.g., poor executive function, autism quotient score, central coherence, theory of mind, cognitive-behavioural flexibility, emotion regulation and understanding facial expressions.[99][100][101][102][103][104]

Zucker et al. (2007) proposed that conditions on the autism spectrum make up the cognitive endophenotype underlying anorexia nervosa and appealed for increased interdisciplinary collaboration (see figure to right).[84] A pilot study into the effectiveness Cognitive Behaviour Therapy, which based its treatment protocol on the hypothesised relationship between anorexia nervosa and an underlying autistic like condition, reduced perfectionism and rigidity in 17 out of 19 participants.[105]

Diagnosis

Medical

The initial diagnosis should be made by a competent medical professional. There are multiple medical conditions, such as viral or bacterial infections, hormonal imbalances, neurodegenerative diseases and brain tumors which may mimic psychiatric disorders including anorexia nervosa. According to an in depth study conducted by psychiatrist Richard Hall as published in the Archives of General Psychiatry:

  • Medical illness often presents with psychiatric symptoms.
  • It is difficult to distinguish physical disorders from functional psychiatric disorders on the basis of psychiatric symptoms alone.
  • Detailed physical examination and laboratory screening are indicated as a routine procedure in the initial evaluation of psychiatric patients.
  • Most patients are unaware of the medical illness that is causative of their psychiatric symptoms.
  • The conditions of patients with medically induced symptoms are often initially misdiagnosed as a functional psychosis.[106][107]

Psychological

Anorexia nervosa is classified as an Axis I[134] disorder in the Diagnostic and Statistical Manual of Mental Health Disorders (DSM-IV), published by the American Psychiatric Association. The DSM-IV should not be used by laypersons to diagnose themselves.

  • DSM-IV-TR: diagnostic criteria for AN includes intense fear of gaining weight, a refusal to maintain body weight above 85% of the expected weight for a given age and height, and three consecutive missed periods and either refusal to admit the seriousness of the weight loss, or undue influence of shape or weight on one's self image, or a disturbed experience in one's shape or weight. There are two types: the binge-eating/purging type is characterized by overeating or purging, and the restricting type is not.[135]
    • Criticism of DSM-IV There has been criticisms over various aspects of the diagnostic criteria utilized for anorexia nervosa in the DSM-IV. Including the requirement of maintaining a body weight below 85% of the expected weight and the requirement of amenorrhea for diagnosis; some women have all the symptoms of AN and continue to menstruate.[136] Those who do not meet these criteria are usually classified as eating disorder not otherwise specified this may affect treatment options and insurance reimbursments.[137] The validity of the AN subtype classification has also been questioned because of the considerable diagnostic overlap between the binge eating/ purging type and the restricting type and the propensity of the patient to switch between the two.[138][139]
  • ICD-10: The criteria are similar, but in addition, specifically mention:
  1. The ways that individuals might induce weight-loss or maintain low body weight (avoiding fattening foods, self-induced vomiting, self-induced purging, excessive exercise, excessive use of appetite suppressants or diuretics).
  2. If onset is before puberty, that development is delayed or arrested.
  3. Certain physiological features, including "widespread endocrine disorder involving hypothalamic-pituitary-gonadal axis is manifest in women as amenorrhoea and in men as loss of sexual interest and potency. There may also be elevated levels of growth hormones, raised cortisol levels, changes in the peripheral metabolism of thyroid hormone and abnormalities of insulin secretion".

Differential diagnoses

There are various medical and psychological conditions that have been misdiagnosed as anorexia nervosa, in some cases the correct diagnosis was not made for more than ten years. In a reported case of achalasia misdiagnosed as AN, the patient spent two months confined to a psychiatric hospital.[140]

There are various other psychological issues that may factor into anorexia nervosa, some fulfill the criteria for a separate Axis I diagnosis or a personality disorder which is coded Axis II and thus are considered comorbid to the diagnosed eating disorder. Axis II disorders are subtyped into 3 "clusters", A, B and C.The causality between personality disorders and eating disorders has yet to be fully established.[141] Some people have a previous disorder which may increase their vulnerability to developing an eating disorder.[142][143][144] Some develop them afterwards.[145] The severity and type of eating disorder symptoms have been shown to affect comorbidity.[146]

Comorbid Disorders
Axis I Axis II
depression[147] obsessive compulsive personality disorder[148]
substance abuse, alcoholism[149] borderline personality disorder[150]
anxiety disorders[151] narcissistic personality disorder[152]
obsessive compulsive disorder[153][154] histrionic personality disorder[155]
Attention-Deficit-Hyperactivity-Disorder[156][157][158][159] avoidant personality disorder[160]
  • Body dysmorphic disorder (BDD) is listed as a somatoform disorder that affects up to 2% of the population. BDD is characterized by excessive rumination over an actual or perceived physical flaw. BDD has been diagnosed equally among men and women. While BDD has been misdiagnosed as anorexia nervosa, it also occurs comorbidly in 25% to 39% of AN cases.[161]

BDD is a chronic and debilitating condition which may lead to social isolation, major depression, suicidal ideation and attempts. Neuroimaging studies to measure response to facial recognition have shown activity predominately in the left hemisphere in the left lateral prefrontal cortex, lateral temporal lobe and left parietal lobe showing hemispheric imbalance in information processing. There is a reported case of the development of BDD in a 21 year old male following an inflammatory brain process. Neuroimaging showed the presence of new atrophy in the frontotemporal region.[162][163][164][164][165]

The distinction between the diagnoses of anorexia nervosa, bulimia nervosa and eating disorder not otherwise specified (EDNOS) is often difficult to make as there is considerable overlap between patients diagnosed with these conditions. Seemingly minor changes in a patient's overall behavior or attitude can change a diagnosis from "anorexia: binge-eating type" to bulimia nervosa. It is not unusual for a person with an eating disorder to "move through" various diagnoses as his or her behavior and beliefs change over time.[84]

Treatment

Treatment for anorexia nervosa tries to address three main areas. 1) Restoring the person to a healthy weight; 2) Treating the psychological disorders related to the illness; 3) Reducing or eliminating behaviours or thoughts that originally led to the disordered eating.[166] If anorexia nervosa is not treated, serious complications such as heart conditions and kidney failure can initiate and eventually lead to death.

Dietary

  • Zinc supplementation has been shown in various studies to be beneficial in the treatment of AN even in patients not suffering from zinc deficiency, by helping to increase weight gain.[167][168][169]
  • Essential fatty acids:The omega-3 fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) have been shown to benefit various neuropsychiatric disorders. There was reported rapid improvement in a case of severe AN treated with ethyl-eicosapentaenoic acid (E-EPA) and micronutrients.[170] DHA and EPA supplementation has been shown to be a benefit in many of the comorbid disorders of AN including: attention deficit/hyperactivity disorder (ADHD), autism, major depressive disorder (MDD),[171] bipolar disorder, and borderline personality disorder. Accelerated cognitive decline and mild cognitive impairment (MCI) correlate with lowered tissue levels of DHA/EPA, and supplementation has improved cognitive function.[172][173]
  • Nutrition counseling[174][175]
  • Medical Nutrition Therapy;(MNT) also referred to as Nutrition Therapy is the development and provision of a nutritional treatment or therapy based on a detailed assessment of a person's medical history, psychosocial history, physical examination, and dietary history.[176][177][178]

Medication

  • Olanzapine: has been shown to be effective in treating certain aspects of AN including to help raise the body mass index and reduce obsessionality, including obsessional thoughts about food.[179][180]

Therapy

  • Cognitive behavioral therapy (CBT) CBT is an evidence based approach which in studies to date has shown to be useful in adolescents and adults with anorexia nervosa.[181][182][183]
  • Acceptance and commitment therapy: A type of CBT, has shown promise in the treatment of AN" participants experienced clinically significant improvement on at least some measures; no participants worsened or lost weight even at 1-year follow-up."[184]
  • Cognitive Remediation Therapy (CRT): is a cognitive rehabilitation therapy developed at King's College in London designed to improve neurocognitive abilities such as attention, working memory, cognitive flexibility and planning, and executive functioning which leads to improved social functioning. Neuropsychological studies have shown that patients with AN have difficulties in cognitive flexibility. In studies conducted at Kings College[185] and in Poland with adolescents CRT was proven to be beneficial in treating anorexia nervosa,[185] in the United States clinical trials are still being conducted by the National Institute of Mental Health[186] on adolescents age 10–17 and Stanford University in subjects over 16 as a conjunctive therapy with Cognitive behavioral therapy.[187]
  • Family therapy: The most effective form of therapy for adolescents with anorexia is family therapy.[188] There are various forms of family therapy that have been proven to work in the treatment of adolescent AN including "conjoint family therapy" (CFT), in which the parents and child are seen together by the same therapist, "separated family therapy" (SFT) in which parents and child attend therapy separately with different therapists. "Eisler's cohort show that, irrespective of the type of FBT, 75% of patients have a good outcome, 15% an intermediate outcome... ".[189][190]
  • Maudsley Family Therapy: A 4 to 5 year follow up study of the Maudsley approach, a manualized model, that shows full recovery at rates up to 90%.[191]

Alternative medicine

  • Yoga: In preliminary studies indivualized yoga treatment has shown positive results for use as an adjunctive therapy to standard care. The treatment was shown to reduce eating disorder symptoms, including food preoccupation, which decreased immediately after each session. Scores on the Eating Disorder Examination decreased consistently over the course of treatment.[192]

Prognosis

The long term prognosis of anorexia is more on the favorable side. The National Comorbidity Replication Survey was conducted among more than 9,282 participants throughout the United States, the results found that the average duration of anorexia nervosa is 1.7 years. "Contrary to what people may believe, anorexia is not necessarily a chronic illness; in many cases, it runs its course and people get better..."[193]

In cases of adolescent anorexia nervosa that utilize Family treatment 75% of patients have a good outcome and an additional 15% show an intermediate yet more positive outcome.[189] In a five year post treatment follow-up of Maudsley Family Therapy the full recovery rate was between 75% and 90%.[194] Even in severe cases of AN, despite a noted 30% relapse rate after hospitalization, and a lengthy time to recovery ranging from 57 to 79 months, the full recovery rate was still 76%. There were minimal cases of relapse even at the long term follow-up conducted between 10–15 years.[195] The long-term prognosis of anorexia nervosa is changeable: a fifth of patients stay severely ill, another fifth of patients recover fully and three fifths of patients have a fluctuating and chronic course (Gelder, Mayou and Geddes 2005).

Epidemiology

Anorexia has an average prevalence of 0.3–1% in women and 0.1% in men for the diagnosis in developed countries.[196] The condition largely affects young adolescent women, with between 15 and 19 years old making up 40% of all cases. Approximately 75% of people with anorexia are female.[197] Anorexia nervosa is more prevalent in the upper social classes and it is declared to be rare in less developed countries (Gelder, Mayou and Geddes 2005).

History

Two images of an anorexic female patient published in 1900 in "Nouvelle Iconographie de la Salpêtrière". The case was entitiled "Un cas de anorexia hysterique" (A case of hysteria anorexia).

The history of anorexia nervosa begins with descriptions of religious fasting dating from the Hellenistic era [198] and continuing into the medieval period. A number of well known historical figures, including Catherine of Siena and Mary, Queen of Scots are believed to have suffered from the condition.[199][200]

Of interest in terms of anorexia nervosa is the medieval practice of self-starvation by women, including some young women, in the name of religious piety and purity. This is sometimes referred to as anorexia mirabilis. By the thirteenth century, it was increasingly common for women to participate in religious life . Many women who ultimately became saints engaged in self-starvation, including Saint Hedwig of Andechs in the thirteenth century and Catherine of Siena in the fourteenth century. By the time of Catherine of Siena, however, the Church became concerned about extreme fasting as an indicator of spirituality and as a criterion for sainthood. Indeed, Catherine of Siena was told by Church authorities to pray that she would be able to eat again, but was unable to give up fasting.[199]

The earliest medical descriptions of anorexic illnesses are generally credited to English physician Richard Morton, in 1689.[198]

However it was not until the late 19th century that anorexia nervosa was to be widely accepted by the medical profession as a recognised condition. In 1873, Sir William Gull, one of Queen Victoria’s personal physicians, published a seminal paper which established the term anorexia nervosa and provided a number of detailed case descriptions and treatments. In the same year, French physician Ernest-Charles Lasègue similarly published details of a number of cases in a paper entitled De l’Anorexie Histerique.

Awareness of the condition was largely limited to the medical profession until the latter part of the 20th century, when German-American psychoanalyst Hilde Bruch published her popular work The Golden Cage: the Enigma of Anorexia Nervosa in 1978. This book created a wider awareness of anorexia nervosa among lay readers. A further important event was the death of the popular singer Karen Carpenter in 1983, which prompted widespread ongoing media coverage of eating disorders.

Research

Notable cases

See also

References

  1. ^ Rosen JC, Reiter J, Orosan P (1995). "Assessment of body image in eating disorders with the body dysmorphic disorder examination". Behaviour Research and Therapy 33 (1): 77–84. doi:10.1016/0005-7967(94)E0030-M. PMID 7872941. 
  2. ^ Cooper MJ (2005). "Cognitive theory in anorexia nervosa and bulimia nervosa: progress, development and future directions". Clinical Psychology Review 25 (4): 511–31. doi:10.1016/j.cpr.2005.01.003. PMID 15914267. 
  3. ^ Brooks S, Prince A, Stahl D, Campell IC, Treasure J (2010). "A systematic review & meta-analysis of cognitive bias to food stimuli in people with disordered eating behaviour". Clinical Psychology 31 (1): 37. doi:10.1016/j.cpr.2010.09.006. 
  4. ^ Neil Frude (1998). Understanding abnormal psychology. Wiley-Blackwell. ISBN 978-0-631-16195-0. http://books.google.com/books?id=rVMMj4Y7Xm8C. Retrieved 4 February 2012. 
  5. ^ Attia E (2010). "Anorexia Nervosa: Current Status and Future Directions". Annual Review of Medicine 61 (1): 425–35. doi:10.1146/annurev.med.050208.200745. PMID 19719398. 
  6. ^ "Society of Clinical Child and Adolescent Psychology – What is Anorexia Nervosa?". http://www.abct.org/sccap/?m=sPublic&fa=pub_AnorexiaNervosa. 
  7. ^ The scary trend of tweens with anorexia. CNN.com (2011-08-08). Retrieved on 2012-02-04.
  8. ^ Bennett J (2008). "It's not just white girls. Anorexics can be male, old, Latino, black or pregnant. A new book undercuts old stereotypes". Newsweek 152 (11): 96. PMID 18800573. 
  9. ^ Woodside, DB; Garfinkel, PE; Lin, E; Goering, P; Kaplan, AS; Goldbloom, DS; Kennedy, SH (2001). "Comparisons of Men With Full or Partial Eating Disorders, Men Without Eating Disorders, and Women With Eating Disorders in the Community". The American journal of psychiatry 158 (4): 570–4. PMID 11282690. http://homepage.psy.utexas.edu/homepage/class/Psy394Q/Behavior%20Therapy%20Class/Assigned%20Readings/Eating%20Disorders/Woodside2001.pdf. 
  10. ^ Gull WW (1997). "Anorexia nervosa (apepsia hysterica, anorexia hysterica). 1868". Obesity Research 5 (5): 498–502. PMID 9385628. 
  11. ^ Costin, Carolyn (1999). The Eating Disorder Sourcebook. Linconwood: Lowell House. p. 6. ISBN 0585189226. 
  12. ^ Abell, TL; Malagelada, JR; Lucas, AR; Brown, ML; Camilleri, M; Go, VL; Azpiroz, F; Callaway, CW et al (1987). "Gastric electromechanical and neurohormonal function in anorexia nervosa". Gastroenterology 93 (5): 958–65. PMID 3653645. 
  13. ^ Ulger Z, Gürses D, Ozyurek AR, Arikan C, Levent E, Aydoğdu S (2006). "Follow-up of cardiac abnormalities in female adolescents with anorexia nervosa after refeeding". Acta Cardiologica 61 (1): 43–9. doi:10.2143/AC.61.1.2005139. PMID 16485732. 
  14. ^ Støving RK, Hangaard J, Hagen C; Hangaard; Hagen (2001). "Update on endocrine disturbances in anorexia nervosa". Journal of Pediatric Endocrinology & Metabolism 14 (5): 459–80. doi:10.1515/JPEM.2001.14.5.459. PMID 11393567. 
  15. ^ a b c Attia, E. and Walsh, B. T. (2007). "Anorexia Nervosa". American Journal of Psychiatry 164 (12): 1805–1810. doi:10.1176/appi.ajp.2007.07071151. PMID 18056234. 
  16. ^ Walsh JM, Wheat ME, Freund K (2000). "Detection, Evaluation, and Treatment of Eating Disorders: The Role of the Primary Care Physician". Journal of General Internal Medicine 15 (8): 577–90. doi:10.1046/j.1525-1497.2000.02439.x. PMC 1495575. PMID 10940151. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1495575. 
  17. ^ Pietrowsky R, Krug R, Fehm HL, Born J (2002). "Food deprivation fails to affect preoccupation with thoughts of food in anorectic patients". The British Journal of Clinical Psychology 41 (Pt 3): 321–6. doi:10.1348/014466502760379172. PMID 12396259. 
  18. ^ Kovacs D, Palmer RL (2004). "The associations between laxative abuse and other symptoms among adults with anorexia nervosa". The International Journal of Eating Disorders 36 (2): 224–8. doi:10.1002/eat.20024. PMID 15282693. 
  19. ^ Friedman EJ (1984). "Death from ipecac intoxication in a patient with anorexia nervosa". The American Journal of Psychiatry 141 (5): 702–3. PMID 6143508. 
  20. ^ Peñas-Lledó E, Vaz Leal FJ, Waller G (2002). "Excessive exercise in anorexia nervosa and bulimia nervosa: relation to eating characteristics and general psychopathology". The International Journal of Eating Disorders 31 (4): 370–5. doi:10.1002/eat.10042. PMID 11948642. 
  21. ^ Haller E (1992). "Eating disorders. A review and update". The Western Journal of Medicine 157 (6): 658–62. PMC 1022101. PMID 1475950. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1022101. 
  22. ^ Lucka I (2004). "[Depression syndromes in patients suffering from anorexia nervosa]" (in Polish). Psychiatria Polska 38 (4): 621–9. PMID 15518310. 
  23. ^ Bozzato A, Burger P, Zenk J, Uter W, Iro H (2008). "Salivary gland biometry in female patients with eating disorders". European Archives of Oto-rhino-laryngology 265 (9): 1095–102. doi:10.1007/s00405-008-0598-8. PMID 18253742. 
  24. ^ Strumia R (2005). "Dermatologic signs in patients with eating disorders". American Journal of Clinical Dermatology 6 (3): 165–73. doi:10.2165/00128071-200506030-00003. PMID 15943493. 
  25. ^ Chiarioni, Giuseppe; Bassotti, Gabrio; Monsignori, Antonella; Menegotti, Monica; Salandini, Lara; Di Matteo, Giorgio; Vantini, Italo; Whitehead, William E. (2000). "Anorectal dysfunction in constipated women with anorexia nervosa". Mayo Clinic Proceedings 75 (10): 1015–9. doi:10.4065/75.10.1015. PMID 11040849. 
  26. ^ Waldholtz BD, Andersen AE (1990). "Gastrointestinal symptoms in anorexia nervosa. A prospective study". Gastroenterology 98 (6): 1415–9. PMID 2338185. 
  27. ^ Olson AF (2005). "Outpatient management of electrolyte imbalances associated with anorexia nervosa and bulimia nervosa". Journal of Infusion Nursing 28 (2): 118–22. doi:10.1097/00129804-200503000-00005. PMID 15785332. 
  28. ^ van Nieuw Amerongen A, Vissink A (2001). "[Oral complications of anorexia nervosa, bulimia nervosa and other metabolic disorders]" (in Dutch). Nederlands Tijdschrift Voor Tandheelkunde 108 (6): 242–7. PMID 11441717. 
  29. ^ de Moor RJ (2004). "Eating disorder-induced dental complications: a case report". Journal of Oral Rehabilitation 31 (7): 725–32. doi:10.1111/j.1365-2842.2004.01282.x. PMID 15210036. 
  30. ^ García-Rubira JC, Hidalgo R, Gómez-Barrado JJ, Romero D, Cruz Fernández JM (1994). "Anorexia nervosa and myocardial infarction". International Journal of Cardiology 45 (2): 138–40. doi:10.1016/0167-5273(94)90270-4. PMID 7960253. 
  31. ^ Golden NH, Shenker IR (1994). "Amenorrhea in anorexia nervosa. Neuroendocrine control of hypothalamic dysfunction". The International Journal of Eating Disorders 16 (1): 53–60. doi:10.1002/1098-108X(199407)16:1<53::AID-EAT2260160105>3.0.CO;2-V. PMID 7920581. 
  32. ^ Demaerel P, Daele MC, De Vuysere S, Wilms G, Baert AL (1996). "Orbital fat edema in anorexia nervosa: a reversible finding". American Journal of Neuroradiology 17 (9): 1782–4. PMID 8896638. http://www.ajnr.org/cgi/pmidlookup?view=long&pmid=8896638. 
  33. ^ Joyce JM, Warren DL, Humphries LL, Smith AJ, Coon JS (1990). "Osteoporosis in women with eating disorders: comparison of physical parameters, exercise, and menstrual status with SPA and DPA evaluation". Journal of Nuclear Medicine 31 (3): 325–31. PMID 2308003. http://jnm.snmjournals.org/cgi/pmidlookup?view=long&pmid=2308003. 
  34. ^ Golden NH (2003). "Osteopenia and osteoporosis in anorexia nervosa". Adolescent Medicine 14 (1): 97–108. PMID 12529194. 
  35. ^ Bahia A, Chu ES, Mehler PS (2010). "Polydipsia and hyponatremia in a woman with anorexia nervosa". The International Journal of Eating Disorders 44 (2): 186–8. doi:10.1002/eat.20792. PMID 20127934. 
  36. ^ Bonne OB, Bloch M, Berry EM (1993). "Adaptation to severe chronic hypokalemia in anorexia nervosa: a plea for conservative management". The International Journal of Eating Disorders 13 (1): 125–8. doi:10.1002/1098-108X(199301)13:1<125::AID-EAT2260130115>3.0.CO;2–4. PMID 8477271. 
  37. ^ Mroczkowski MM, Redgrave GW, Miller NR, McCoy AN, Guarda AS (2010). "Reversible vision loss secondary to malnutrition in a woman with severe anorexia nervosa, purging type, and alcohol abuse". The International Journal of Eating Disorders 44 (3): 281–3. doi:10.1002/eat.20806. PMID 20186722. 
  38. ^ Drevelengas A, Chourmouzi D, Pitsavas G, Charitandi A, Boulogianni G (2001). "Reversible brain atrophy and subcortical high signal on MRI in a patient with anorexia nervosa". Neuroradiology 43 (10): 838–40. doi:10.1007/s002340100589. PMID 11688699. 
  39. ^ Addolorato G, Taranto C, Capristo E, Gasbarrini G (1998). "A case of marked cerebellar atrophy in a woman with anorexia nervosa and cerebral atrophy and a review of the literature". The International Journal of Eating Disorders 24 (4): 443–7. doi:10.1002/(SICI)1098-108X(199812)24:4<443::AID-EAT13>3.0.CO;2–4. PMID 9813771. 
  40. ^ Hütter G, Ganepola S, Hofmann WK (2009). "The hematology of anorexia nervosa". The International Journal of Eating Disorders 42 (4): 293–300. doi:10.1002/eat.20610. PMID 19040272. 
  41. ^ Allende, LM; Corell, A; Manzanares, J; Madruga, D; Marcos, A; Madrono, A; Lopez-Goyanes, A; Garcia-Perez, MA et al (1998). "Immunodeficiency associated with anorexia nervosa is secondary and improves after refeeding". Immunology 94 (4): 543–51. doi:10.1046/j.1365-2567.1998.00548.x. PMC 1364233. PMID 9767443. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1364233. 
  42. ^ Zandian M, Ioakimidis I, Bergh C, Södersten P (2007). "Cause and treatment of anorexia nervosa". Physiology & Behavior 92 (1–2): 283–90. doi:10.1016/j.physbeh.2007.05.052. PMID 17585973. 
  43. ^ Thambirajah, M. S. (2007). Case Studies in Child and Adolescent Mental Health. Radcliffe Publishing. p. 145. ISBN 978-1-85775-698-2. OCLC 84150452. 
  44. ^ Kaye W (2008). "Neurobiology of Anorexia and Bulimia Nervosa Purdue Ingestive Behavior Research Center Symposium Influences on Eating and Body Weight over the Lifespan: Children and Adolescents". Physiology & Behavior 94 (1): 121–35. doi:10.1016/j.physbeh.2007.11.037. PMC 2601682. PMID 18164737. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2601682. 
  45. ^ Støving RK, Hansen-Nord M, Hangaard J, Hagen C (1996). "[Neuroendocrine disorders in anorexia nervosa—primary or secondary?]" (in Danish). Ugeskrift for Laeger 158 (49): 7052–6. PMID 8999610. 
  46. ^ Brandenburg BM, Andersen AE (2007). "Unintentional onset of anorexia nervosa". Eating and Weight Disorders 12 (2): 97–100. PMID 17615494. http://www.kurtis.it/abs/index.cfm?id_articolo_numero=3749. 
  47. ^ Nygaard JA (1990). "Anorexia nervosa. Treatment and triggering factors". Acta Psychiatrica Scandinavica. Supplementum 361: 44–9. PMID 2291425. 
  48. ^ Favaro A, Tenconi E, Santonastaso P (2006). "Perinatal factors and the risk of developing anorexia nervosa and bulimia nervosa". Archives of General Psychiatry 63 (1): 82–8. doi:10.1001/archpsyc.63.1.82. PMID 16389201. 
  49. ^ Favaro A, Tenconi E, Santonastaso P (2008). "The relationship between obstetric complications and temperament in eating disorders: a mediation hypothesis". Psychosomatic Medicine 70 (3): 372–7. doi:10.1097/PSY.0b013e318164604e. PMID 18256341. 
  50. ^ Klump KL, Miller KB, Keel PK, McGue M, Iacono WG (2001). "Genetic and environmental influences on anorexia nervosa syndromes in a population-based twin sample". Psychological Medicine 31 (4): 737–40. doi:10.1017/S0033291701003725. PMID 11352375. 
  51. ^ Kortegaard LS, Hoerder K, Joergensen J, Gillberg C, Kyvik KO (2001). "A preliminary population-based twin study of self-reported eating disorder". Psychological Medicine 31 (2): 361–365. doi:10.1017/S0033291701003087. PMID 11232922. 
  52. ^ Wade TD, Bulik CM, Neale M, Kendler KS (2000). "Anorexia nervosa and major depression: shared genetic and environmental risk factors". Am J Psychiatry 157 (3): 469–71. doi:10.1176/appi.ajp.157.3.469. PMID 10698830. 
  53. ^ Rask-Andersen M, Olszewski PK, Levine AS, Schiöth HB (2009). "Molecular mechanisms underlying anorexia nervosa: Focus on human gene association studies and systems controlling food intake". Brain Res Rev 62 (2): 147–64. doi:10.1016/j.brainresrev.2009.10.007. PMID 19931559. 
  54. ^ Urwin, R E; Bennetts, B; Wilcken, B; Lampropoulos, B; Beumont, P; Clarke, S; Russell, J; Tanner, S et al (2002). "Anorexia nervosa (restrictive subtype) is associated with a polymorphism in the novel norepinephrine transporter gene promoter polymorphic region". Molecular Psychiatry 7 (6): 652–7. doi:10.1038/sj.mp.4001080. PMID 12140790. 
  55. ^ Young JK (2010). "Anorexia nervosa and estrogen: current status of the hypothesis". Neuroscience and Biobehavioral Reviews 34 (8): 1195–1200. doi:10.1016/j.neubiorev.2010.01.015. PMID 20138911. 
  56. ^ Versini, Audrey; Ramoz, Nicolas; Le Strat, Yann; Scherag, Susann; Ehrlich, Stefan; Boni, Claudette; Hinney, Anke; Hebebrand, Johannes et al (2010). "Estrogen Receptor 1 Gene (ESR1) is Associated with Restrictive Anorexia Nervosa". Neuropsychopharmacology 35 (8): 1–8. doi:10.1038/npp.2010.49. PMC 3055492. PMID 20375995. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3055492. 
  57. ^ a b Frieling, Helge; Römer, Konstanze D.; Scholz, Sarah; Mittelbach, Franziska; Wilhelm, Julia; De Zwaan, Martina; Jacoby, Georg E.; Kornhuber, Johannes et al (2009). "Epigenetic dysregulation of dopaminergic genes in eating disorders". The International Journal of Eating Disorders 43 (7): 577–83. doi:10.1002/eat.20745. PMID 19728374. 
  58. ^ Epigenetic Downregulation of Atrial Natriuretic Peptide but not Vasopressin mRNA Expression in Females with Eating Disorders is Related to Impulsivity
  59. ^ Kaye WH, Frank GK, Bailer UF, Henry SE (2005). "Neurobiology of anorexia nervosa: clinical implications of alterations of the function of serotonin and other neuronal systems". The International Journal of Eating Disorders. 37 Suppl (S1): S15–9; discussion S20–1. doi:10.1002/eat.20109. PMID 15852312. 
  60. ^ Bergen, Andrew W; Yeager, Meredith; Welch, Robert A; Haque, Kashif; Ganjei, J Kelly; Van Den Bree, Marianne B M; Mazzanti, Chiara; Nardi, Irma et al (2005). "Association of multiple DRD2 polymorphisms with anorexia nervosa". Neuropsychopharmacology 30 (9): 1703–10. doi:10.1038/sj.npp.1300719. PMID 15920508. 
  61. ^ Kaye, W; Bailer, U; Frank, G; Wagner, A (2006). "Persistent alterations of serotonin and dopamine activity after recovery from anorexia and bulimia nervosa". Psychosomatic Medicine 1287: 45–48. doi:10.1016/j.ics.2005.12.038. 
  62. ^ Bosanac P, Norman T, Burrows G, Beumont P (2005). "Serotonergic and dopaminergic systems in anorexia nervosa: a role for atypical antipsychotics?". The Australian and New Zealand Journal of Psychiatry 39 (3): 146–53. doi:10.1111/j.1440-1614.2005.01536.x. PMID 15701063. 
  63. ^ Kaye, W; Frank, G; Bailer, U; Henry, S; Meltzer, C; Price, J; Mathis, C; Wagner, A (2005). "Serotonin alterations in anorexia and bulimia nervosa: new insights from imaging studies". Physiology & Behavior 85 (1): 73–81. doi:10.1016/j.physbeh.2005.04.013. PMID 15869768. 
  64. ^ Kaye WH, Bailer UF, Frank GK, Wagner A, Henry SE (2005). "Brain imaging of serotonin after recovery from anorexia and bulimia nervosa". Physiology & Behavior 86 (1–2): 15–7. doi:10.1016/j.physbeh.2005.06.019. PMID 16102788. 
  65. ^ Monteleone P, Fabrazzo M, Martiadis V, Serritella C, Pannuto M, Maj M (2005). "Circulating brain-derived neurotrophic factor is decreased in women with anorexia and bulimia nervosa but not in women with binge-eating disorder: relationships to co-morbid depression, psychopathology and hormonal variables". Psychological Medicine 35 (6): 897–905. doi:10.1017/S0033291704003368. PMID 15997610. 
  66. ^ Wang C, Bomberg E, Billington C, Levine A, Kotz CM (2007). "Brain-derived neurotrophic factor in the hypothalamic paraventricular nucleus increases energy expenditure by elevating metabolic rate". American Journal of Physiology. Regulatory, Integrative and Comparative Physiology 293 (3): R992–1002. doi:10.1152/ajpregu.00516.2006. PMID 17567712. 
  67. ^ Ferris LT, Williams JS, Shen CL (2007). "The effect of acute exercise on serum brain-derived neurotrophic factor levels and cognitive function". Medicine and Science in Sports and Exercise 39 (4): 728–34. doi:10.1249/mss.0b013e31802f04c7. PMID 17414812. 
  68. ^ Frederich R, Hu S, Raymond N, Pomeroy C (2002). "Leptin in anorexia nervosa and bulimia nervosa: importance of assay technique and method of interpretation". The Journal of Laboratory and Clinical Medicine 139 (2): 72–9. doi:10.1067/mlc.2002.121014. PMID 11919545. 
  69. ^ Lask B, Gordon I, Christie D, Frampton I, Chowdhury U, Watkins B (2005). "Functional neuroimaging in early-onset anorexia nervosa". The International Journal of Eating Disorders. 37 Suppl (S1): S49–51; discussion S87–9. doi:10.1002/eat.20117. PMID 15852320. 
  70. ^ Fetissov, S. O.; Harro, J; Jaanisk, M; Järv, A; Podar, I; Allik, J; Nilsson, I; Sakthivel, P et al (2005). "Autoantibodies against neuropeptides are associated with psychological traits in eating disorders". Proceedings of the National Academy of Sciences of the United States of America 102 (41): 14865–70. doi:10.1073/pnas.0507204102. PMC 1253594. PMID 16195379. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1253594. 
  71. ^ Shay NF, Mangian HF (2000). "Neurobiology of zinc-influenced eating behavior". The Journal of Nutrition 130 (5S Suppl): 1493S–9S. PMID 10801965. http://jn.nutrition.org/cgi/pmidlookup?view=long&pmid=10801965. 
  72. ^ Psychiatrists call for new ‘editorial code’ to end media promotion of a thin body ideal. Rcpsych.ac.uk (2010-02-23). Retrieved on 2012-02-04.
  73. ^ Lindberg L, Hjern A (2003). "Risk factors for anorexia nervosa: a national cohort study". The International Journal of Eating Disorders 34 (4): 397–408. doi:10.1002/eat.10221. PMID 14566927. 
  74. ^ Garner DM, Garfinkel PE (1980). "Socio-cultural factors in the development of anorexia nervosa". Psychological Medicine 10 (4): 647–56. doi:10.1017/S0033291700054945. PMID 7208724. 
  75. ^ Toro J, Salamero M, Martinez E (1994). "Assessment of sociocultural influences on the aesthetic body shape model in anorexia nervosa". Acta Psychiatrica Scandinavica 89 (3): 147–51. doi:10.1111/j.1600-0447.1994.tb08084.x. PMID 8178671. 
  76. ^ Schmidt U, Treasure J. Anorexia nervosa: valued and visible. A cognitive-interpersonal maintenance model and its implications for research and practice. Br J Clin Psychol 2006
  77. ^ Mukai, T; Crago, M; Shisslak, CM (1994). "Eating attitudes and weight preoccupation among female high school students in Japan". Journal of child psychology and psychiatry, and allied disciplines 35 (4): 677–88. PMID 8040220. 
  78. ^ Levine et al. 1994, Shisslak et al. 1998, Stice 1998, Wertheim et al. 1997
  79. ^ Lozano, GA (2008). "Obesity and sexually selected anorexia nervosa". Medical Hypotheses 71 (6): 933–940. doi:10.1016/j.mehy.2008.07.013. PMID 18760541. 
  80. ^ Harrison, A.; Sullivan, S.; Tchanturia, K.; Treasure, J. (2009). "Emotion recognition and regulation in anorexia nervosa". Clinical Psychology & Psychotherapy 16 (4): 348–356. doi:10.1002/cpp.628. PMID 19517577.  edit
  81. ^ Zonnevijlle-Bender, M. J.; Van Goozen, S. H.; Cohen-Kettenis, P. T.; Van Elburg, A.; Van Engeland, H. (2002). "Do adolescent anorexia nervosa patients have deficits in emotional functioning?". European Child & Adolescent Psychiatry 11 (1): 38–42. doi:10.1007/s007870200006. PMID 11942427.  edit
  82. ^ a b c Rayworth, B. B.; Wise, L. A.; Harlow, B. L. (2004). "Childhood Abuse and Risk of Eating Disorders in Women". Epidemiology 15 (3): 271–278. JSTOR 20485891. PMID 15097006. 
  83. ^ "Lessons for Parents of Anorexics" (2005) in BBC Health News, 22 October 2005 viewable at http://news.bbc.co.uk/1/hi/health/4363304.stm (Accessed 22 Aug, 2011)
  84. ^ a b c Zucker NL, Losh M, Bulik CM, LaBar KS, Piven J, Pelphrey KA (2007). "Anorexia nervosa and autism spectrum disorders: guided investigation of social cognitive endophenotypes". Psychological Bulletin 133 (6): 976–1006. doi:10.1037/0033-2909.133.6.976. PMID 17967091. http://www.duke.edu/web/mind/level2/faculty/labar/pdfs/Zucker_et_al_2007.pdf. 
  85. ^ Gillberg, C. (1983). "Are autism and anorexia nervosa related?". The British Journal of Psychiatry 142 (4): 428b. doi:10.1192/bjp.142.4.428b. 
  86. ^ Gillberg, C. (1985). "Autism and anorexia nervosa: Related conditions". Nordisk Psykiatrisk Tidskrift 39 (4): 307–312. doi:10.3109/08039488509101911. http://informahealthcare.com/doi/abs/10.3109/08039488509101911. 
  87. ^ Rothery, D.J.; D.M.F. Garden (1988-01-11). "Anorexia nervosa and infantile autism". The British journal of psychiatry : the journal of mental science 153 (5): 714. doi:10.1192/bjp.153.5.714. PMID 3255470. 
  88. ^ Gillberg, C.; M. Rastam (1992). "Do some cases of anorexia nervosa reflect underlying autistic-like conditions?". Behavioural neurology 5 (1): 27–32. http://psycnet.apa.org/?fa=main.doiLanding&uid=1993-02071-001. 
  89. ^ Gillberg, I. Carina; Maria Råstam, Christopher Gillberg (1995-02). "Anorexia nervosa 6 years after onset: Part I. Personality disorders". Comprehensive Psychiatry 36 (1): 61–69. doi:10.1016/0010-440X(95)90100-A. PMID 7705090. 
  90. ^ Gillberg, I. Carina; Christopher Gillberg, Maria Råstam, Maria Johansson (1996-02). "The cognitive profile of anorexia nervosa: A comparative study including a community-based sample". Comprehensive Psychiatry 37 (1): 23–30. doi:10.1016/S0010-440X(96)90046-2. PMID 8770522. 
  91. ^ Råstam, M.; C. Gillberg, I. C. Gillberg (1996). "A six-year follow-up study of anorexia nervosa subjects with teenage onset". Journal of Youth and Adolescence 25 (4): 439–453. doi:10.1007/BF01537541. 
  92. ^ Nilsson, E. W; C. Gillberg, I. C Gillberg (1999-11). "Ten-year follow-up of adolescent-onset anorexia nervosa: personality disorders". Journal of the American Academy of Child and Adolescent Psychiatry 38 (11): 1389–95. doi:10.1097/00004583-199911000-00013. PMID 10560225. 
  93. ^ Wentz, Elisabet; Christopher Gillberg, I. Carina Gillberg, Maria Råstam (2001). "Ten-Year Follow-up of Adolescent-Onset Anorexia Nervosa: Psychiatric Disorders and Overall Functioning Scales". The Journal of Child Psychology and Psychiatry and Allied Disciplines 42 (5): 613–622. doi:10.1017/S0021963001007284. 
  94. ^ Råstam, Maria; Christopher Gillberg, Elisabet Wentz (2003-01-01). "Outcome of teenage-onset anorexia nervosa in a Swedish community-based sample". European Child & Adolescent Psychiatry 12 (1): I78–90. doi:10.1007/s00787-003-1111-y. PMID 12567219. 
  95. ^ Wentz, Elisabet; J. Lacey, Glenn Waller, Maria Råstam, Jeremy Turk, Christopher Gillberg (2005-12-01). "Childhood onset neuropsychiatric disorders in adult eating disorder patients". European Child & Adolescent Psychiatry 14 (8): 431–437. doi:10.1007/s00787-005-0494-3. PMID 16341499. 
  96. ^ Wentz, Elisabet; I. Carina Gillberg, Henrik Anckarsater, Christopher Gillberg, Maria Rastam (2009-02-01). "Adolescent-onset anorexia nervosa: 18-year outcome". The British Journal of Psychiatry 194 (2): 168–174. doi:10.1192/bjp.bp.107.048686. PMID 19182181. 
  97. ^ Fisman, S; M Steele, J Short, T Byrne, C Lavallee (1996-07). "Case study: anorexia nervosa and autistic disorder in an adolescent girl". Journal of the American Academy of Child and Adolescent Psychiatry 35 (7): 937–940. doi:10.1097/00004583-199607000-00021. ISSN 0890-8567. PMID 8768355. 
  98. ^ Kerbeshian, Jacob; Larry Burd (2008). "Is anorexia nervosa a neuropsychiatric developmental disorder? An illustrative case report". World Journal of Biological Psychiatry 10 (4 Pt 2): 648–57. doi:10.1080/15622970802043117. ISSN 1562-2975. PMID 18609437. 
  99. ^ Gillberg, I. C; M. Raastam, E. Wentz, C. Gillberg (2007). "Cognitive and executive functions in anorexia nervosa ten years after onset of eating disorder". Journal of Clinical and Experimental Neuropsychology 29 (2): 170–178. doi:10.1080/13803390600584632. PMID 17365252. 
  100. ^ Hambrook, D.; K. Tchanturia, U. Schmidt, T. Russell, J. Treasure (2008). "Empathy, systemizing, and autistic traits in anorexia nervosa: a pilot study". The British journal of clinical psychology/the British Psychological Society 47 (Pt 3): 335–9. doi:10.1348/014466507X272475. PMID 18208640. http://openurl.ingenta.com/content?genre=article&issn=0144-6657&volume=47&issue=3&spage=335&epage=339. 
  101. ^ Lopez, C.; K. Tchanturia, D. Stahl, R. Booth, J. Holliday, J. Treasure (2008). "An examination of the concept of central coherence in women with anorexia nervosa". International Journal of Eating Disorders 41 (2): 143–152. doi:10.1002/eat.20478. PMID 17937420. 
  102. ^ Russell, Tamara Anne; Ulrike Schmidt, Liz Doherty, Vicky Young, Kate Tchanturia (2009). "Aspects of social cognition in anorexia nervosa: Affective and cognitive theory of mind". Psychiatry Research 168 (3): 181–185. doi:10.1016/j.psychres.2008.10.028. ISSN 01651781. PMID 19467562. 
  103. ^ Zastrow, Arne; Kaiser; Kaiser, Christoph Stippich, Stephan Walther, Wolfgang Herzog, Kate Tchanturia, Aysenil Belger, Matthias Weisbrod, Janet Treasure, Hans-Christoph Friederich (2009-05-01). "Neural Correlates of Impaired Cognitive-Behavioral Flexibility in Anorexia Nervosa". Am J Psychiatry 166 (5): 608–616. doi:10.1176/appi.ajp.2008.08050775. PMID 19223435. 
  104. ^ Harrison, Amy; Sarah Sullivan, Kate Tchanturia, Janet Treasure (2009). "Emotion recognition and regulation in anorexia nervosa". Clinical Psychology & Psychotherapy 16 (4): 348–356. doi:10.1002/cpp.628. PMID 19517577. 
  105. ^ Whitney, Jenna; Abigail Easter, Kate Tchanturia (2008). "Service users' feedback on cognitive training in the treatment of anorexia nervosa: A qualitative study". International Journal of Eating Disorders 41 (6): 542–550. doi:10.1002/eat.20536. PMID 18433016. 
  106. ^ Hall RC, Popkin MK, Devaul RA, Faillace LA, Stickney SK (1978). "Physical illness presenting as psychiatric disease". Archives of General Psychiatry 35 (11): 1315–20. doi:10.1001/archpsyc.1978.01770350041003. PMID 568461. http://archpsyc.ama-assn.org/cgi/pmidlookup?view=long&pmid=568461. 
  107. ^ Hall RC, Gardner ER, Stickney SK, LeCann AF, Popkin MK (1980). "Physical illness manifesting as psychiatric disease. II. Analysis of a state hospital inpatient population". Archives of General Psychiatry 37 (9): 989–95. doi:10.1001/archpsyc.1980.01780220027002. PMID 7416911. 
  108. ^ CBC at Medline. Nlm.nih.gov. Retrieved on 2012-02-04.
  109. ^ Urinalysis at Medline. Nlm.nih.gov (2012-01-26). Retrieved on 2012-02-04.
  110. ^ Kawabata M, Kubo N, Arashima Y, Yoshida M, Kawano K (1991). "[Serodiagnosis of Lyme disease by ELISA using Borrelia burgdorferi flagellum antigen]" (in Japanese). Rinsho Byori 39 (8): 891–4. PMID 1920889. 
  111. ^ Western Blot use in Lyme Disease. CDC
  112. ^ Chem-20 at Medline. Nlm.nih.gov. Retrieved on 2012-02-04.
  113. ^ Lee H, Oh JY, Sung YA, Chung H, Cho WY (2009). "The prevalence and risk factors for glucose intolerance in young Korean women with polycystic ovary syndrome". Endocrine 36 (2): 326–32. doi:10.1007/s12020-009-9226-7. PMID 19688613. 
  114. ^ Takeda, N; Yasuda, K; Horiya, T; Yamada, H; Imai, T; Kitada, M; Miura, K (1986). "[Clinical investigation on the mechanism of glucose intolerance in Cushing's syndrome]" (in Japanese). Nippon Naibunpi Gakkai Zasshi 62 (5): 631–48. PMID 3525245. 
  115. ^ Rolny P, Lukes PJ, Gamklou R, Jagenburg R, Nilson A (1978). "A comparative evaluation of endoscopic retrograde pancreatography and secretin-CCK test in the diagnosis of pancreatic disease". Scandinavian Journal of Gastroenterology 13 (7): 777–81. doi:10.3109/00365527809182190. PMID 725498. 
  116. ^ Glasbrenner, B; Malfertheiner, P; Pieramico, O; Klatt, S; Riepl, R; Friess, H; Ditschuneit, H (1993). "Gallbladder dynamics in chronic pancreatitis. Relationship to exocrine pancreatic function, CCK, and PP release". Digestive Diseases and Sciences 38 (3): 482–9. PMID 8444080. 
  117. ^ Montagnese C, Scalfi L, Signorini A, De Filippo E, Pasanisi F, Contaldo F (2007). "Cholinesterase and other serum liver enzymes in underweight outpatients with eating disorders". The International Journal of Eating Disorders 40 (8): 746–50. doi:10.1002/eat.20432. PMID 17610252. 
  118. ^ Narayanan V, Gaudiani JL, Harris RH, Mehler PS (2010). "Liver function test abnormalities in anorexia nervosa—cause or effect". The International Journal of Eating Disorders 43 (4): 378–81. doi:10.1002/eat.20690. PMID 19424979. 
  119. ^ Sherman BM, Halmi KA, Zamudio R (1975). "LH and FSH response to gonadotropin-releasing hormone in anorexia nervosa: Effect of nutritional rehabilitation". The Journal of Clinical Endocrinology and Metabolism 41 (1): 135–42. doi:10.1210/jcem-41-1-135. PMID 1097461. 
  120. ^ Salvadori A, Fanari P, Ruga S, Brunani A, Longhini E (1992). "Creatine kinase and creatine kinase-MB isoenzyme during and after exercise testing in normal and obese young people". Chest 102 (6): 1687–9. doi:10.1378/chest.102.6.1687. PMID 1446472. 
  121. ^ Walder A, Baumann P (2008). "Increased creatinine kinase and rhabdomyolysis in anorexia nervosa". The International Journal of Eating Disorders 41 (8): 766–7. doi:10.1002/eat.20548. PMID 18521917. 
  122. ^ BUN at Medline. Nlm.nih.gov (2012-01-26). Retrieved on 2012-02-04.
  123. ^ Ernst AA, Haynes ML, Nick TG, Weiss SJ (1999). "Usefulness of the blood urea nitrogen/creatinine ratio in gastrointestinal bleeding". The American Journal of Emergency Medicine 17 (1): 70–2. doi:10.1016/S0735-6757(99)90021-9. PMID 9928705. 
  124. ^ Sheridan AM, Bonventre JV (2000). "Cell biology and molecular mechanisms of injury in ischemic acute renal failure". Current Opinion in Nephrology and Hypertension 9 (4): 427–34. doi:10.1097/00041552-200007000-00015. PMID 10926180. 
  125. ^ Nelsen DA (2002). "Gluten-sensitive enteropathy (celiac disease): more common than you think". American Family Physician 66 (12): 2259–66. PMID 12507163. http://www.aafp.org/link_out?pmid=12507163. 
  126. ^ Pascual, M; Pascual, DA; Soria, F; Vicente, T; Hernández, AM; Tébar, FJ; Valdés, M (2003). "Effects of isolated obesity on systolic and diastolic left ventricular function". Heart 89 (10): 1152–6. doi:10.1136/heart.89.10.1152. PMC 1767886. PMID 12975404. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1767886. 
  127. ^ Esposito C, Bellotti N, Fasoli G, Foschi A, Plati AR, Dal Canton A (2004). "Hyperkalemia-induced ECG abnormalities in patients with reduced renal function". Clinical Nephrology 62 (6): 465–8. PMID 15630907. 
  128. ^ Electroencephalogram at Medline. Nlm.nih.gov (2012-01-26). Retrieved on 2012-02-04.
  129. ^ Kameda K, Itoh N, Nakayama H, Kato Y, Ihda S (1995). "Frontal intermittent rhythmic delta activity (FIRDA) in pituitary adenoma". Clinical EEG 26 (3): 173–9. PMID 7554305. 
  130. ^ Mashako, Mamba Nyenya Léonard; Cezard, Jean Pierre; Navarro, Jean; Mougenot, Jean Francois; Sonsino, Elise; Gargouri, Abdellatif; Maherzi, Ahmed (1989). "Crohn's disease lesions in the upper gastrointestinal tract: correlation between clinical, radiological, endoscopic, and histological features in adolescents and children". Journal of Pediatric Gastroenterology and Nutrition 8 (4): 442–6. doi:10.1097/00005176-198905000-00004. PMID 2723935. 
  131. ^ Kumar MS, Safa AM, Deodhar SD, Schumacher OP (1977). "The relationship of thyroid-stimulating hormone (TSH), thyroxine (T4), and triiodothyronine (T3) in primary thyroid failure". American Journal of Clinical Pathology 68 (6): 747–51. PMID 579717. 
  132. ^ Nilsson P, Melsen F, Malmaeus J, Danielson BG, Mosekilde L (1985). "Relationships between calcium and phosphorus homeostasis, parathyroid hormone levels, bone aluminum, and bone histomorphometry in patients on maintenance hemodialysis". Bone 6 (1): 21–7. doi:10.1016/8756-3282(85)90402-8. PMID 2581596. 
  133. ^ Barium Enema at Medline. Nlm.nih.gov (2012-01-26). Retrieved on 2012-02-04.
  134. ^ Westen D, Harnden-Fischer J (2001). "Personality profiles in eating disorders: rethinking the distinction between axis I and axis II". The American Journal of Psychiatry 158 (4): 547–62. doi:10.1176/appi.ajp.158.4.547. PMID 11282688. 
  135. ^ American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th, text revision (DSM-IV-TR) ed. 2000. ISBN 0-89042-025-4. Anorexia Nervosa.
  136. ^ Gendall KA, Joyce PR, Carter FA, McIntosh VV, Jordan J, Bulik CM (2006). "The psychobiology and diagnostic significance of amenorrhea in patients with anorexia nervosa". Fertility and Sterility 85 (5): 1531–5. doi:10.1016/j.fertnstert.2005.10.048. PMID 16600234. 
  137. ^ Smith, A. T.; Wolfe, B. E. (2008). "Amenorrhea as a Diagnostic Criterion for Anorexia Nervosa: A Review of the Evidence and Implications for Practice". Journal of the American Psychiatric Nurses Association 14 (3): 209–15. doi:10.1177/1078390308320288. PMID 21665766. 
  138. ^ Eddy KT, Dorer DJ, Franko DL, Tahilani K, Thompson-Brenner H, Herzog DB (2008). "Diagnostic crossover in anorexia nervosa and bulimia nervosa: implications for DSM-V". The American Journal of Psychiatry 165 (2): 245–50. doi:10.1176/appi.ajp.2007.07060951. PMID 18198267. 
  139. ^ Marlene Busko Diagnostic Criteria for Eating Disorders May Be Too Stringent. Medscape.com (2007-05-30). Retrieved on 2012-02-04.
  140. ^ Marshall JB, Russell JL (1993). "Achalasia mistakenly diagnosed as eating disorder and prompting prolonged psychiatric hospitalization". Southern Medical Journal 86 (12): 1405–7. doi:10.1097/00007611-199312000-00019. PMID 8272922. 
  141. ^ Rosenvinge JH, Martinussen M, Ostensen E (2000). "The comorbidity of eating disorders and personality disorders: a meta-analytic review of studies published between 1983 and 1998". Eating and Weight Disorders 5 (2): 52–61. PMID 10941603. 
  142. ^ Kaye WH, Bulik CM, Thornton L, Barbarich N, Masters K (2004). "Comorbidity of anxiety disorders with anorexia and bulimia nervosa". The American Journal of Psychiatry 161 (12): 2215–21. doi:10.1176/appi.ajp.161.12.2215. PMID 15569892. 
  143. ^ Thornton C, Russell J (1997). "Obsessive compulsive comorbidity in the dieting disorders". The International Journal of Eating Disorders 21 (1): 83–7. doi:10.1002/(SICI)1098-108X(199701)21:1<83::AID-EAT10>3.0.CO;2-P. PMID 8986521. 
  144. ^ Vitousek K, Manke F (1994). "Personality variables and disorders in anorexia nervosa and bulimia nervosa". Journal of Abnormal Psychology 103 (1): 137–47. doi:10.1037/0021-843X.103.1.137. PMID 8040475. 
  145. ^ Braun DL, Sunday SR, Halmi KA (1994). "Psychiatric comorbidity in patients with eating disorders". Psychological Medicine 24 (4): 859–67. doi:10.1017/S0033291700028956. PMID 7892354. 
  146. ^ Spindler A, Milos G (2007). "Links between eating disorder symptom severity and psychiatric comorbidity". Eating Behaviors 8 (3): 364–73. doi:10.1016/j.eatbeh.2006.11.012. PMID 17606234. 
  147. ^ Casper RC (1998). "Depression and eating disorders". Depression and Anxiety 8 (Suppl 1): 96–104. doi:10.1002/(SICI)1520-6394(1998)8:1+<96::AID-DA15>3.0.CO;2–4. PMID 9809221. 
  148. ^ Serpell L, Livingstone A, Neiderman M, Lask B (2002). "Anorexia nervosa: obsessive-compulsive disorder, obsessive-compulsive personality disorder, or neither?". Clinical Psychology Review 22 (5): 647–69. doi:10.1016/S0272-7358(01)00112-X. PMID 12113200. 
  149. ^ Bulik, Cynthia M.; Klump, Kelly L.; Thornton, Laura; Kaplan, Allan S.; Devlin, Bernie; Fichter, Manfred M.; Halmi, Katherine A.; Strober, Michael et al (2004). "Alcohol use disorder comorbidity in eating disorders: a multicenter study". The Journal of Clinical Psychiatry 65 (7): 1000–6. doi:10.4088/JCP.v65n0718. PMID 15291691. 
  150. ^ Larsson JO, Hellzén M (2004). "Patterns of personality disorders in women with chronic eating disorders". Eating and Weight Disorders 9 (3): 200–5. PMID 15656014. 
  151. ^ Swinbourne JM, Touyz SW (2007). "The co-morbidity of eating disorders and anxiety disorders: a review". European Eating Disorders Review : the Journal of the Eating Disorders Association 15 (4): 253–74. doi:10.1002/erv.784. PMID 17676696. 
  152. ^ Ronningstam E (1996). "Pathological narcissism and narcissistic personality disorder in Axis I disorders". Harvard Review of Psychiatry 3 (6): 326–40. doi:10.3109/10673229609017201. PMID 9384963. 
  153. ^ Anderluh MB, Tchanturia K, Rabe-Hesketh S, Treasure J (2003). "Childhood obsessive-compulsive personality traits in adult women with eating disorders: defining a broader eating disorder phenotype". The American Journal of Psychiatry 160 (2): 242–7. doi:10.1176/appi.ajp.160.2.242. PMID 12562569. 
  154. ^ Pinto A, Mancebo MC, Eisen JL, Pagano ME, Rasmussen SA (2006). "The Brown Longitudinal Obsessive Compulsive Study: clinical features and symptoms of the sample at intake". The Journal of Clinical Psychiatry 67 (5): 703–11. doi:10.4088/JCP.v67n0503. PMID 16841619. 
  155. ^ Lucka I, Cebella A (2004). "[Characteristics of the forming personality in children suffering from anorexia nervosa]" (in Polish). Psychiatria Polska 38 (6): 1011–8. PMID 15779665. 
  156. ^ Dukarm CP (2005). "Bulimia nervosa and attention deficit hyperactivity disorder: a possible role for stimulant medication". Journal of Women's Health 14 (4): 345–50. doi:10.1089/jwh.2005.14.345. PMID 15916509. 
  157. ^ Mikami, Amori Yee; Hinshaw, Stephen P.; Arnold, L. Eugene; Hoza, Betsy; Hechtman, Lily; Newcorn, Jeffrey H.; Abikoff, Howard B. (2010). "Bulimia nervosa symptoms in the multimodal treatment study of children with ADHD". The International Journal of Eating Disorders 43 (3): 248–59. doi:10.1002/eat.20692. PMID 19378318. 
  158. ^ Biederman J, Ball SW, Monuteaux MC, Surman CB, Johnson JL, Zeitlin S (2007). "Are girls with ADHD at risk for eating disorders? Results from a controlled, five-year prospective study". Journal of Developmental and Behavioral Pediatrics 28 (4): 302–7. doi:10.1097/DBP.0b013e3180327917. PMID 17700082. 
  159. ^ Cortese S, Bernardina BD, Mouren MC (2007). "Attention-deficit/hyperactivity disorder (ADHD) and binge eating". Nutrition Reviews 65 (9): 404–11. doi:10.1111/j.1753-4887.2007.tb00318.x. PMID 17958207. 
  160. ^ Bruce KR, Steiger H, Koerner NM, Israel M, Young SN (2004). "Bulimia nervosa with co-morbid avoidant personality disorder: behavioural characteristics and serotonergic function". Psychological Medicine 34 (1): 113–24. doi:10.1017/S003329170300864X. PMID 14971632. 
  161. ^ Grant JE, Kim SW, Eckert ED (2002). "Body dysmorphic disorder in patients with anorexia nervosa: Prevalence, clinical features, and delusionality of body image". International Journal of Eating Disorders 32 (3): 291–300. doi:10.1002/eat.10091. PMID 12210643. 
  162. ^ Gabbay V, Asnis GM, Bello JA, Alonso CM, Serras SJ, O'Dowd MA (2003). "New onset of body dysmorphic disorder following frontotemporal lesion". Neurology 61 (1): 123–5. PMID 12847173. 
  163. ^ Phillips, KA; McElroy, SL; Keck Jr, PE; Hudson, JI; Pope Jr, HG (1994). "A comparison of delusional and nondelusional body dysmorphic disorder in 100 cases". Psychopharmacol Bull. 30 (2): 179–86. PMID 7831453. 
  164. ^ a b Feusner JD, Townsend J, Bystritsky A, Bookheimer S (2007). "Visual Information Processing of Faces in Body Dysmorphic Disorder". Archives of General Psychiatry 64 (12): 1417–25. doi:10.1001/archpsyc.64.12.1417. PMID 18056550. 
  165. ^ Feusner JD, Yaryura-Tobias J, Saxena S (2008). "The pathophysiology of body dysmorphic disorder". Body Image 5 (1): 3–12. doi:10.1016/j.bodyim.2007.11.002. PMID 18314401. 
  166. ^ National Institute of Mental Health. http://www.nimh.nih.gov/health/publications/eating-disorders/anorexia-nervosa.shtml. 
  167. ^ Safai-Kutti S (1990). "Oral zinc supplementation in anorexia nervosa". Acta Psychiatrica Scandinavica. Supplementum 361: 14–7. PMID 2291418. 
  168. ^ Su JC, Birmingham CL (2002). "Zinc supplementation in the treatment of anorexia nervosa". Eating and Weight Disorders 7 (1): 20–2. PMID 11930982. 
  169. ^ Birmingham CL, Gritzner S (2006). "How does zinc supplementation benefit anorexia nervosa?". Eating and Weight Disorders 11 (4): e109–11. PMID 17272939. http://www.kurtis.it/abs/index.cfm?id_articolo_numero=3347. 
  170. ^ Ayton AK, Azaz A, Horrobin DF (2004). "Rapid improvement of severe anorexia nervosa during treatment with ethyl-eicosapentaenoate and micronutrients". European Psychiatry 19 (5): 317–9. doi:10.1016/j.eurpsy.2004.06.002. PMID 15276668. 
  171. ^ Lucas M, Asselin G, Mérette C, Poulin MJ, Dodin S (2009). "Ethyl-eicosapentaenoic acid for the treatment of psychological distress and depressive symptoms in middle-aged women: a double-blind, placebo-controlled, randomized clinical trial". The American Journal of Clinical Nutrition 89 (2): 641–51. doi:10.3945/ajcn.2008.26749. PMID 19116322. 
  172. ^ McNamara, R. K; Able, J.; Jandacek, R.; Rider, T.; Tso, P.; Eliassen, J. C; Alfieri, D.; Weber, W. et al (2010). "Docosahexaenoic acid supplementation increases prefrontal cortex activation during sustained attention in healthy boys: a placebo-controlled, dose-ranging, functional magnetic resonance imaging study". The American Journal of Clinical Nutrition 91 (4): 1060–7. doi:10.3945/ajcn.2009.28549. PMC 2844685. PMID 20130094. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2844685. 
  173. ^ Kidd PM (2007). "Omega-3 DHA and EPA for cognition, behavior, and mood: clinical findings and structural-functional synergies with cell membrane phospholipids". Alternative Medicine Review 12 (3): 207–27. PMID 18072818. http://www.thorne.com/altmedrev/.fulltext/12/3/207.pdf. 
  174. ^ Latner JD, Wilson GT (2000). "Cognitive-behavioral therapy and nutritional counseling in the treatment of bulimia nervosa and binge eating". Eating Behaviors 1 (1): 3–21. doi:10.1016/S1471-0153(00)00008-8. PMID 15001063. 
  175. ^ Breen HB, Espelage DL (2004). "Nutrition expertise in eating disorders". Eating and Weight Disorders 9 (2): 120–5. PMID 15330079. 
  176. ^ Perelygina L, Patrusheva I, Manes N, Wildes MJ, Krug P, Hilliard JK (2003). "Quantitative real-time PCR for detection of monkey B virus (Cercopithecine herpesvirus 1) in clinical samples". Journal of Virological Methods 109 (2): 245–51. doi:10.1016/S0166-0934(03)00078-8. PMID 12711069. 
  177. ^ Whisenant SL, Smith BA (1995). "Eating disorders: current nutrition therapy and perceived needs in dietetics education and research". Journal of the American Dietetic Association 95 (10): 1109–12. doi:10.1016/S0002-8223(95)00301-0. PMID 7560681. 
  178. ^ American Dietetic, Association (2006). "Position of the American Dietetic Association: Nutrition intervention in the treatment of anorexia nervosa, bulimia nervosa, and other eating disorders". Journal of the American Dietetic Association 106 (12): 2073–82. doi:10.1016/j.jada.2006.09.007. PMID 17186637. 
  179. ^ Brambilla, Francesca; Garcia, Cristina Segura; Fassino, Secondo; Daga, Giovanni Abbate; Favaro, Angela; Santonastaso, Paolo; Ramaciotti, Carla; Bondi, Emilia et al (2007). "Olanzapine therapy in anorexia nervosa: psychobiological effects". International Clinical Psychopharmacology 22 (4): 197–204. doi:10.1097/YIC.0b013e328080ca31. PMID 17519642. 
  180. ^ Bissada H, Tasca GA, Barber AM, Bradwejn J (2008). "Olanzapine in the treatment of low body weight and obsessive thinking in women with anorexia nervosa: a randomized, double-blind, placebo-controlled trial". The American Journal of Psychiatry 165 (10): 1281–8. doi:10.1176/appi.ajp.2008.07121900. PMID 18558642. 
  181. ^ Pike KM, Walsh BT, Vitousek K, Wilson GT, Bauer J (2003). "Cognitive behavior therapy in the posthospitalization treatment of anorexia nervosa". The American Journal of Psychiatry 160 (11): 2046–9. doi:10.1176/appi.ajp.160.11.2046. PMID 14594754. 
  182. ^ Bowers WA, Ansher LS (2008). "The effectiveness of cognitive behavioral therapy on changing eating disorder symptoms and psychopathology of 32 anorexia nervosa patients at hospital discharge and one year follow-up". Annals of Clinical Psychiatry 20 (2): 79–86. doi:10.1080/10401230802017068. PMID 18568579. 
  183. ^ Ball J, Mitchell P (2004). "A randomized controlled study of cognitive behavior therapy and behavioral family therapy for anorexia nervosa patients". Eating Disorders 12 (4): 303–14. doi:10.1080/10640260490521389. PMID 16864523. 
  184. ^ Berman MI, Boutelle KN, Crow SJ (2009). "A case series investigating acceptance and commitment therapy as a treatment for previously treated, unremitted patients with anorexia nervosa". European Eating Disorders Review 17 (6): 426–34. doi:10.1002/erv.962. PMID 19760625. 
  185. ^ a b Tchanturia K, Davies H, Campbell IC (2007). "Cognitive remediation therapy for patients with anorexia nervosa: preliminary findings". Annals of General Psychiatry 6 (1): 14. doi:10.1186/1744-859X-6-14. PMC 1892017. PMID 17550611. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1892017. 
  186. ^ NIMH · Eating Disorders. Nimh.nih.gov (2011-08-23). Retrieved on 2012-02-04.
  187. ^ Studies – Eating Disorders Program – Stanford University School of Medicine. Edresearch.stanford.edu (2008-06-20). Retrieved on 2012-02-04.
  188. ^ "Association for Behavioral and Cognitive Therapies – What is Family Therapy?". http://www.abct.org/sccap/?m=sPublic&fa=pub_WhatIsFT. 
  189. ^ a b Eisler I, Dare C, Hodes M, Russell G, Dodge E, Le Grange D (2000). "Family therapy for adolescent anorexia nervosa: the results of a controlled comparison of two family interventions". Journal of Child Psychology and Psychiatry, and Allied Disciplines 41 (6): 727–36. doi:10.1111/1469-7610.00660. PMID 11039685. 
  190. ^ Lock J, le Grange D (2005). "Family-based treatment of eating disorders". The International Journal of Eating Disorders. 37 Suppl (S1): S64–7; discussion S87–9. doi:10.1002/eat.20122. PMID 15852323. 
  191. ^ le Grange D, Eisler I (2009). "Family interventions in adolescent anorexia nervosa". Child and Adolescent Psychiatric Clinics of North America 18 (1): 159–73. doi:10.1016/j.chc.2008.07.004. PMID 19014864. 
  192. ^ Carei TR, Fyfe-Johnson AL, Breuner CC, Brown MA (2010). "Randomized Controlled Clinical Trial of Yoga in the Treatment of Eating Disorders". The Journal of Adolescent Health 46 (4): 346–51. doi:10.1016/j.jadohealth.2009.08.007. PMC 2844876. PMID 20307823. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2844876. 
  193. ^ Hudson JI, Hiripi E, Pope HG, Kessler RC (2007). "The Prevalence and Correlates of Eating Disorders in the National Comorbidity Survey Replication". Biological Psychiatry 61 (3): 348–58. doi:10.1016/j.biopsych.2006.03.040. PMC 1892232. PMID 16815322. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1892232. 
  194. ^ Eisler I, Le Grange D, Asen KE (2003). "Family interventions". In Treasure J, Schmidt U, van Furth E. Handbook of eating disorders (2nd ed.). Chichester: Wiley. pp. 291–310. 
  195. ^ Strober M, Freeman R, Morrell W (1997). "The long-term course of severe anorexia nervosa in adolescents: survival analysis of recovery, relapse, and outcome predictors over 10–15 years in a prospective study". The International Journal of Eating Disorders 22 (4): 339–60. doi:10.1002/(SICI)1098-108X(199712)22:4<339::AID-EAT1>3.0.CO;2-N. PMID 9356884. 
  196. ^ Treasure J, Claudino AM, Zucker N (2010). "Eating disorders". Lancet 375 (9714): 583–93. doi:10.1016/S0140-6736(09)61748-7. PMID 19931176. 
  197. ^ Gowers S, Bryant-Waugh R (2004). "Management of child and adolescent eating disorders: the current evidence base and future directions". Journal of Child Psychology and Psychiatry, and Allied Disciplines 45 (1): 63–83. doi:10.1046/j.0021-9630.2003.00309.x. PMID 14959803. 
  198. ^ a b Richard Morton: Origins of Anorexia nervosa. Content.karger.com. Retrieved on 2012-02-04.
  199. ^ a b Hepworth, Julie. 1999. The Social Construction of Anorexia Nervosa. Thousand Oaks, CA: Sage Publications ISBN 0761953094
  200. ^ McSherry, JA (1985). "Was Mary, Queen of Scots, anorexic?". Scottish medical journal 30 (4): 243–5. PMID 3912990. 
  201. ^ Cannabinoid Receptor (CB1) Agonist Treatment in Severe Chronic Anorexia Nervosa. clinicaltrials.gov. September 25, 2008
  202. ^ Hotta M, Ohwada R, Akamizu T, Shibasaki T, Takano K, Kangawa K (2009). "Ghrelin increases hunger and food intake in patients with restricting-type anorexia nervosa: a pilot study". Endocrine Journal 56 (9): 1119–28. doi:10.1507/endocrj.K09E-168. PMID 19755753. 

Further reading

  • Anorexia Nervosa and Related Eating Disorders in Childhood and Adolescence By Bryan Lask, Rachel Bryant-Waugh Publisher: Psychology Press; 2 edition (October 12, 2000) ISBN 0863778046 ISBN 978-0863778049
  • Help Your Teenager Beat an Eating Disorder. James Lock MD PhD, Daniel le Grange PhD. Publisher: The Guilford Press; 1 edition (January 1, 2005) Language: English ISBN 1572309083 ISBN 978-1572309081
  • Too Fat or Too Thin?: A Reference Guide to Eating Disorders; Cynthia R. Kalodner. Publisher: Greenwood Press; 1 edition (August 30, 2003) Language: English ISBN 0313315817 ISBN 978-0313315817
  • Wasted: A Memoir of Anorexia and Bulimia Marya Hornbacher. Publisher: Harper Perennial; 1 edition (January 15, 1999) Language: English ISBN 0060930934 ISBN 978-0060930936
  • Cardboard: A woman left for dead. 1st ed Local Consumption Publications (1989). Winner of the National Book Council's Award for New Writers. 2nd ed January 2010 ISBN 9781450502023
  • Eating with Your Anorexic: How My Child Recovered Through Family-based Treatment and Yours Can Too by Laura Collins Publisher: McGraw-Hill; 1 edition (December 15, 2004) Language: English ISBN 0071445587 ISBN 978-0071445580

External links


 
 

 

Copyrights:

American Heritage Dictionary. The American Heritage® Dictionary of the English Language, Fourth Edition Copyright © 2007, 2000 by Houghton Mifflin Company. Updated in 2009. Published by Houghton Mifflin Company. All rights reserved.  Read more
Britannica Concise Encyclopedia. Britannica Concise Encyclopedia. © 1994-2012 Encyclopædia Britannica, Inc. All rights reserved.  Read more
McGraw-Hill Science & Technology Encyclopedia. McGraw-Hill Encyclopedia of Science and Technology. Copyright © 2005 by The McGraw-Hill Companies, Inc. All rights reserved.  Read more
Oxford Food & Nutrition Dictionary. A Dictionary of Food and Nutrition. Copyright © 1995, 2003, 2005 by A. E. Bender and D. A. Bender. All rights reserved.  Read more
Oxford Food & Fitness Dictionary. Food and Fitness: A Dictionary of Diet and Exercise. Copyright © 1997, 2003 by Oxford University Press. All rights reserved.  Read more
$copyright.smallImage.alttext Gale Encyclopedia of Children's Health. © 2006 by The Gale Group, Inc. All rights reserved.  Read more
Oxford Dictionary of Sports Science & Medicine. The Oxford Dictionary of Sports Science & Medicine. Copyright © Michael Kent 1998, 2006, 2007. All rights reserved.  Read more
Gale Nutrition Encyclopedia. Nutrition and Well-Being A-Z © 2004 The Gale Group, Inc. All rights reserved.  Read more
Gale Encyclopedia of Diets. The Gale Encyclopedia of Diets © 2008 The Gale Group, Inc. All rights reserved.  Read more
$copyright.smallImage.alttext Gale Dictionary of Psychoanalysis. International Dictionary of Psychoanalysis. Copyright © 2005 by The Gale Group, Inc. All rights reserved.  Read more
Dictionary of Cultural Literacy: Health. The New Dictionary of Cultural Literacy, Third Edition Edited by E.D. Hirsch, Jr., Joseph F. Kett, and James Trefil. Copyright © 2002 by Houghton Mifflin Company. Published by Houghton Mifflin. All rights reserved.  Read more
Mosby's Dental Dictionary. Mosby's Dental Dictionary. Copyright © 2004 by Elsevier, Inc. All rights reserved.  Read more
Random House Word Menu. © 2010 Write Brothers Inc. Word Menu is a registered trademark of the Estate of Stephen Glazier. Write Brothers Inc. All rights reserved.  Read more
 Rhymes. Oxford University Press. © 2006, 2007 All rights reserved.  Read more
Wikipedia on Answers.com. This article is licensed under the Creative Commons Attribution/Share-Alike License. It uses material from the Wikipedia article Anorexia nervosa Read more