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m addition of Neuroendocrine Dysregulation in the 'Biological' sub-section under 'Causes' to expand on orexin which was already mentioned
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* [[Addiction]] to the chemicals released in the brain during starving and physical activity:<ref name="Bergh1996">{{cite journal | author = Bergh C, Södersten P | title = Anorexia nervosa, self–starvation and the reward of stress | journal = Nature Medicine | volume = 2 | issue = 1 | pages = 21–22 | year = 1996 | pmid = 8564826 | pmc = | doi = 10.1038/nm0196-21 }}</ref><ref name="Keating">{{cite journal | author = Keating C | title = Sex differences precipitating anorexia nervosa in females: the estrogen paradox and a novel framework for targeting sex-specific neurocircuits and behavior | journal = Curr Top Behav Neurosci | volume = 8 | issue = | pages = 189–207| year = 2011 | pmid = 21769727 | doi = 10.1007/7854_2010_99}}{{vn|date=March 2015}}</ref> people affected with anorexia often report getting some sort of high from not eating. The effect of food restriction and intense activity causes symptoms similar to anorexia in female rats,<ref name="Bergh1996"/> though it is not explained why this addiction affects only females.
* [[Addiction]] to the chemicals released in the brain during starving and physical activity:<ref name="Bergh1996">{{cite journal | author = Bergh C, Södersten P | title = Anorexia nervosa, self–starvation and the reward of stress | journal = Nature Medicine | volume = 2 | issue = 1 | pages = 21–22 | year = 1996 | pmid = 8564826 | pmc = | doi = 10.1038/nm0196-21 }}</ref><ref name="Keating">{{cite journal | author = Keating C | title = Sex differences precipitating anorexia nervosa in females: the estrogen paradox and a novel framework for targeting sex-specific neurocircuits and behavior | journal = Curr Top Behav Neurosci | volume = 8 | issue = | pages = 189–207| year = 2011 | pmid = 21769727 | doi = 10.1007/7854_2010_99}}{{vn|date=March 2015}}</ref> people affected with anorexia often report getting some sort of high from not eating. The effect of food restriction and intense activity causes symptoms similar to anorexia in female rats,<ref name="Bergh1996"/> though it is not explained why this addiction affects only females.
* [[Obstetric]] complications: prenatal and perinatal complications may factor into the development of anorexia nervosa, such as maternal [[anemia]], [[diabetes mellitus]], [[preeclampsia]], [[placental]] [[infarction]], and [[neonatal]] [[cardiac]] abnormalities. Neonatal complications may also have an influence on [[harm avoidance]], one of the [[personality traits]] associated with the development of AN.{{mcn|date=March 2015}}
* [[Obstetric]] complications: prenatal and perinatal complications may factor into the development of anorexia nervosa, such as maternal [[anemia]], [[diabetes mellitus]], [[preeclampsia]], [[placental]] [[infarction]], and [[neonatal]] [[cardiac]] abnormalities. Neonatal complications may also have an influence on [[harm avoidance]], one of the [[personality traits]] associated with the development of AN.{{mcn|date=March 2015}}
* Neuroendocrine dysregulation: altered signalling of peptides that facilitate communication between the gut, brain and adipose tissue, such as [[ghrelin]], [[leptin]], [[neuropeptide Y]] and [[orexin]], may contribute to the pathogenesis of anorexia nervosa by disrupting regulation of hunger and satiety.<ref name=Davis>{{ cite book | chapter = 24. Orexigenic Hypothalamic Peptides Behavior and Feeding - 24.5 Orexin | url = http://books.google.com/books?id=KuAEPOPbW6MC&pg=PA361 | pages = 361–2 | author = Davis JF, Choi DL, Benoit SC | title = Handbook of Behavior, Food and Nutrition | editor = Preedy VR, Watson RR, Martin CR | publisher = Springer | year = 2011 | isbn = 9780387922713 }}</ref><ref>{{Cite journal|url = |title = The Role of ‘‘Mixed’’ Orexigenic and Anorexigenic Signals and Autoantibodies Reacting with Appetite-Regulating
* Neuroendocrine dysregulation: altered signalling of peptides that facilitate communication between the gut, brain and adipose tissue, such as [[ghrelin]], [[leptin]], [[neuropeptide Y]] and [[orexin]], may contribute to the pathogenesis of anorexia nervosa by disrupting regulation of hunger and satiety.<ref name=Davis>{{ cite book | chapter = 24. Orexigenic Hypothalamic Peptides Behavior and Feeding - 24.5 Orexin | pages = [http://books.google.com/books?id=KuAEPOPbW6MC&pg=PA361 361–2] | author = Davis JF, Choi DL, Benoit SC | title = Handbook of Behavior, Food and Nutrition | editor = Preedy VR, Watson RR, Martin CR | publisher = Springer | year = 2011 | isbn = 9780387922713 }}</ref><ref>{{cite journal |author=Smitka K, Papezova H, Vondra K, Hill M, Hainer V, Nedvidkova J |title=The role of "mixed" orexigenic and anorexigenic signals and autoantibodies reacting with appetite-regulating neuropeptides and peptides of the adipose tissue-gut-brain axis: relevance to food intake and nutritional status in patients with anorexia nervosa and bulimia nervosa |journal=Int J Endocrinol |volume=2013 |issue= |pages=483145 |year=2013 |pmid=24106499 |pmc=3782835 |doi=10.1155/2013/483145}}</ref>
Neuropeptides and Peptides of the Adipose Tissue-Gut-Brain Axis: Relevance to Food Intake and Nutritional Status in Patients with Anorexia Nervosa and Bulimia Nervosa|last = |first = |date = 2013-07-11|journal = International Journal of Endocrinology|doi = 10.1155/2013/483145|pmid = |access-date = }}</ref>
* Infections: Some people are hypothesized to have developed anorexia abruptly as a reaction to a streptococcus or mycoplasma infection. [[Pediatric acute-onset neuropsychiatric syndrome]] (PANS) is a hypothesis describing children who have abrupt, dramatic onset of [[obsessive-compulsive disorder]] (OCD) or anorexia nervosa coincident with the presence of two or more neuropsychiatric symptoms.<ref name=Swedo2012>{{Cite journal|doi=10.4172/2161-0665.1000113|author= Swedo SE, Leckman JF, Rose NR |title= From Research Subgroup to Clinical Syndrome: Modifying the PANDAS Criteria to Describe PANS (Pediatric Acute-onset Neuropsychiatric Syndrome)|journal=Pediatr Therapeut. |year= 2012|volume=2|issue= 2| url=http://pandasnetwork.org/wp-content/uploads/2012/02/2161-0665-2-113.pdf |format=PDF}}</ref>
* Infections: Some people are hypothesized to have developed anorexia abruptly as a reaction to a streptococcus or mycoplasma infection. [[Pediatric acute-onset neuropsychiatric syndrome]] (PANS) is a hypothesis describing children who have abrupt, dramatic onset of [[obsessive-compulsive disorder]] (OCD) or anorexia nervosa coincident with the presence of two or more neuropsychiatric symptoms.<ref name=Swedo2012>{{Cite journal|doi=10.4172/2161-0665.1000113|author= Swedo SE, Leckman JF, Rose NR |title= From Research Subgroup to Clinical Syndrome: Modifying the PANDAS Criteria to Describe PANS (Pediatric Acute-onset Neuropsychiatric Syndrome)|journal=Pediatr Therapeut. |year= 2012|volume=2|issue= 2| url=http://pandasnetwork.org/wp-content/uploads/2012/02/2161-0665-2-113.pdf |format=PDF}}</ref>
* [[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&nbsp;mg per day) doubled the rate of body mass increase compared to patients receiving the placebo.<ref name="Zincappetitereview">{{cite journal | author = Shay NF, Mangian HF | title = Neurobiology of zinc-influenced eating behavior | journal = The Journal of Nutrition | volume = 130 | issue = 5S Suppl | pages = 1493S–9S | year = 2000 | pmid = 10801965 }}</ref>
* [[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&nbsp;mg per day) doubled the rate of body mass increase compared to patients receiving the placebo.<ref name="Zincappetitereview">{{cite journal | author = Shay NF, Mangian HF | title = Neurobiology of zinc-influenced eating behavior | journal = The Journal of Nutrition | volume = 130 | issue = 5S Suppl | pages = 1493S–9S | year = 2000 | pmid = 10801965 }}</ref>

Revision as of 06:51, 20 May 2015

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"Anorexic" redirects here. For the use of the term as an appetite suppressant, see Anorectic.
Anorexia nervosa
SpecialtyPsychiatry, clinical psychology Edit this on Wikidata

Anorexia nervosa is an eating disorder characterized by food restriction, odd eating habits or rituals, obsession with having a thin figure, and an irrational fear of weight gain. It is accompanied by a distorted body self-perception, and typically involves excessive weight loss.

Due to their fear of gaining weight, individuals with this disorder restrict the amount of food they consume. Outside of medical literature, the terms anorexia nervosa and anorexia are often used interchangeably; however, anorexia is simply a medical term for lack of appetite; in AN, appetite dysregulation or alterations in the sensation of fullness are suspected.[1]

Anorexia nervosa is often coupled with a distorted self image[2] which may be maintained by various cognitive biases[3] that alter how individuals evaluate and think about their body, food, and eating. People with anorexia nervosa often view themselves as overweight or not thin enough even when they are underweight.[4]

Anorexia nervosa is diagnosed predominantly in women.[5] In 2013 it resulted in about 600 deaths globally up from 400 deaths in 1990.[6] It is a serious health condition with a high incidence of comorbidity and similarly high mortality rate to serious psychiatric disorders.[4]

Signs and symptoms

Anorexia nervosa is an eating disorder that is characterized by attempts to lose weight, to the point of self-starvation. A person with anorexia nervosa may exhibit a number of signs and symptoms, the type and severity of which may vary in each case and may be present but not readily apparent.[7]

Anorexia nervosa, and the associated malnutrition that results from self-imposed starvation, can cause severe complications in every major organ system in the body.[8] Hypokalaemia, a drop in the level of potassium in the blood, is a sign of anorexia nervosa.[1][9] A significant drop in potassium can cause abnormal heart rhythms, constipation, fatigue, muscle damage and paralysis.[10]

Symptoms of AN may include:

  • Refusal to maintain a normal body mass index for one's age
  • Amenorrhea, a symptom that occurs after prolonged weight loss; causes menses to stop, hair becomes brittle, and skin becomes yellow and unhealthy.
  • Fearful of even the slightest weight gain and takes all precautionary measures to avoid weight gain and becoming overweight[11]
  • Obvious, rapid, dramatic weight loss to at least 15% under normal body weight[12]
  • Lanugo: soft, fine hair growing on the face and body[9]
  • Obsession with calories and fat content of food
  • Preoccupation with food, recipes, or cooking; may cook elaborate dinners for others, but not eat the food themselves
  • Food restriction despite being underweight
  • Food rituals, such as cutting food into tiny pieces, refusing to eat around others, hiding or discarding food
  • Purging: May use laxatives, diet pills, ipecac syrup, or water pills; may engage in self-induced vomiting; may run to the bathroom after eating in order to vomit and quickly get rid of ingested calories
  • Excessive exercise[13]
  • Perception of self as overweight despite being told by others they are too thin
  • Intolerance to cold and frequent complaints of being cold; body temperature may lower (hypothermia) in an effort to conserve energy[14]
  • Hypotension or orthostatic hypotension
  • Bradycardia or tachycardia
  • Depression
  • Solitude: may avoid friends and family; becomes withdrawn and secretive
  • Abdominal distension
  • Halitosis (from vomiting or starvation-induced ketosis)
  • Dry hair and skin, as well as hair thinning
  • Chronic fatigue[11]
  • Rapid mood swings

Causes

There is evidence for biological, psychological, developmental, and sociocultural risk factors, but the exact cause of eating disorders is unknown.[15]

Biological

Dysregulation of the serotonin pathways has been implicated in the etiology, pathogenesis and pathophysiology of anorexia nervosa.[15]

Studies have hypothesized the continuance of disordered eating patterns may be epiphenomena of starvation. The results of the Minnesota Starvation Experiment showed normal controls exhibit many of the behavioral patterns of anorexia nervosa (AN) when subjected to starvation. This may be due to the numerous changes in the neuroendocrine system, which results in a self-perpetuating cycle.[25][26][27]

Another hypothesis is that anorexia nervosa is more likely to occur in populations in which obesity is more prevalent, and results from a sexually selected evolutionary drive to appear youthful in populations in which size becomes the primary indicator of age.[28]

Anorexia nervosa is more likely to occur in a person's pubertal years. Some explanatory hypotheses for the rising prevalence of eating disorders in adolescence are "increase of adipose tissue in girls, hormonal changes of puberty, societal expectations of increased independence and autonomy that are particularly difficult for anorexic adolescents to meet; [and] increased influence of the peer group and its values." [29]

Psychological

Early theories of the cause of anorexia linked it to childhood sexual abuse or dysfunctional families;[30][31] evidence is conflicting, and well-designed research is needed.[15]

Sociological

Anorexia nervosa has been increasingly diagnosed since 1950;[32] the increase has been linked to vulnerability and internalization of body ideals.[29] People in professions where there is a particular social pressure to be thin (such as models and dancers) were more likely to develop anorexia,

and those with anorexia have much higher contact with cultural sources that promote weight loss.

This trend can also be observed for people who partake in certain sports, such as jockeys and wrestlers.[33] There is a higher incidence and prevalence of anorexia nervosa in sports with an emphasis on aesthetics, where low body fat is advantageous, and sports in which one has to make weight for competition.[34]

Media effects

Constant exposure to media that presents body ideals may constitute a risk factor for body dissatisfaction and anorexia nervosa. The cultural ideal for body shape for men versus women continues to favor slender women and athletic, V-shaped muscular men. A 2002 review found that the magazines most popular among people aged 18 to 24 years, those read by men, unlike those read by women, were more likely to feature ads and articles on shape than on diet.[unreliable medical source?][35] Body dissatisfaction and internalization of body ideals are risk factors for anorexia nervosa that threaten the health of both male and female populations.

Websites that stress the importance of attainment of body ideals extol and promote anorexia nervosa through the use of religious metaphors, lifestyle descriptions, "thinspiration" or "fitspiration" (inspirational photo galleries and quotes that aim to serve as motivators for attainment of body ideals).[36] Pro-anorexia websites reinforce internalization of body ideals and the importance of their attainment.[36]

Diagnosis

A diagnostic assessment includes the person's current circumstances, biographical history, current symptoms, and family history. The assessment also includes a mental state examination, which is an assessment of the person's current mood and thought content, focusing on views on weight and patterns of eating.

DSM-5

Anorexia nervosa is classified as an Axis I disorder in the latest revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM 5).

Relative to the previous version of the DSM (DSM-IV-TR) the 2013 revision (DSM5) reflects changes in the criteria for anorexia nervosa, most notably that of the amenorrhea criterion being removed.[37][38] Amenorrhea was removed for several reasons: it doesn't apply to males, it isn't applicable for females before or after the age of menstruation or taking birth control pills, and some women who meet the other criteria for AN still report some menstrual activity.[38]

Subtypes

There are two subtypes of AN:[8][39]

  • Binge-eating/purging type: the individual utilizes binge eating or displays purging behavior as a means for losing weight.[39] It is different from bulima nervosa in terms of the individual's weight. An individual with binge-eating/purging type anorexia does not maintain a healthy or normal weight but is significantly underweight. People with bulima nervosa on the other hand can sometimes be overweight.[11]
  • Restricting type: the individual uses restricting food intake, fasting, diet pills, or exercise as a means for losing weight;[8] they may exercise excessively to keep off weight or prevent weight gain, and some individuals eat only enough to stay alive.[8][11]

Levels of severity

Body mass index (BMI) is used by the DSM-V as an indicator of the level of severity of anorexia nervosa. The DSM-V states these as follows:[40]

  • Mild: BMI of 17–17.99
  • Moderate: BMI of 16–16.99
  • Severe: BMI of 15–15.99
  • Extreme: BMI of less than 15

Investigations

Medical tests to check for signs of physical deterioration in anorexia nervosa may be performed by a general physician or psychiatrist, including:

Differential diagnoses

Main article: Anorexia nervosa (differential diagnoses)

A variety of medical and psychological conditions have been misdiagnosed as anorexia nervosa; in some cases the correct diagnosis was not made for more than ten years.

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. A main factor differentiating binge-purge anorexia from bulimia is the gap in physical weight. Someone with bulimia nervosa is ordinarily at a healthy weight, or slightly overweight. Someone with binge-purge anorexia is commonly underweight.[54] People with the binge purging subtype of AN may be significantly underweight and typically do not binge eat large amounts of food, yet they purge the small amount of food they eat.[54] In contrast, those with bulimia nervosa, tend to be normal weight or overweight and binge large amounts of food.[54] It is not unusual for a person with an eating disorder to "move through" various diagnoses as their behavior and beliefs change over time.[55]

Comorbidity

Other psychological issues 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. Some people have a previous disorder which may increase their vulnerability to developing an eating disorder and some develop them afterwards.

The presence of Axis I or Axis II psychiatric comorbidity has been shown to affect the severity and type of anorexia nervosa symptoms in both adolescents and adults.

Obsessive-compulsive disorder (OCD) and obsessive-compulsive personality disorder (OCPD) are highly comorbid with AN, particularly the restrictive subtype.[56] Obsessive-compulsive personality disorder is linked with more severe symptomatology and worse prognosis.[57] The causality between personality disorders and eating disorders has yet to be fully established.

Other comorbid conditions include depression,[58] alcoholism,[59] borderline and other personality disorders,[60][61] anxiety disorders,[62] attention deficit hyperactivity disorder,[63] and body dysmorphic disorder (BDD).[64] Depression and anxiety are the most common comorbidities,[65] and depression is associated with a worse outcome.[65]

Autism spectrum disorders have a higher prevalence among people with eating disorders than in the general population.[66] 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.[55]


Treatment

There is no conclusive evidence that any particular treatment for anorexia nervosa works better than others; however, there is enough evidence to suggest that early intervention and treatment are more effective.[67] Treatment for anorexia nervosa tries to address three main areas.

  • Restoring the person to a healthy weight;
  • Treating the psychological disorders related to the illness;
  • Reducing or eliminating behaviours or thoughts that originally led to the disordered eating.[68]

Although restoring the person's weight is the primary task at hand, optimal treatment also includes and monitors behavioral change in the individual as well.

Some remedies have little value in resolving anorexia; hospitalization is worse than voluntary treatment.[69]

Psychotherapy for individuals with AN is challenging as they may value being thin and may seek to maintain control and resist change.[70]

Diet

Diet is the most essential factor to work on in patients with anorexia nervosa, and must be tailored to each patient's needs. Food variety is important when establishing meal plans as well as foods that are higher in energy density.[71] Patients must consume adequate calories, starting slowly, and increasing at a measured pace.[13]

Medication

Pharmaceuticals have limited benefit for anorexia itself.[72]

Therapy

Family-based treatment (FBT) has been shown to be more successful than individual therapy.[73] Various forms of family-based treatment 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, and separated family therapy (SFT) in which the parents and child attend therapy separately with different therapists.[73] Proponents of Family therapy for adolescents with AN assert that it is important to include parents in the adolescent's treatment.[73]

A four- to five-year follow up study of the Maudsley family therapy, an evidence-based manualized model, showed full recovery at rates up to 90%.[74] Although this model is recommended by the NIMH,[75] critics claim that it has the potential to create power struggles in an intimate relationship and may disrupt equal partnerships.[76]

Cognitive behavioral therapy (CBT) is useful in adolescents and adults with anorexia nervosa;[77] acceptance and commitment therapy is a type of CBT, which has shown promise in the treatment of AN.[78] Cognitive remediation therapy (CRT) is used in treating anorexia nervosa.[79]

Prognosis

AN has the highest mortality rate of any psychological disorder.[73] The mortality rate is 11 to 12 times higher than expected, and the suicide risk is 56 times higher; half of women with AN achieve a full recovery, while an additional 20–30% may partially recover.[1] Not all anorexia nervosa patients recover completely: about 20% develop anorexia nervosa as a chronic disorder.[67] If anorexia nervosa is not treated, serious complications such as heart conditions[7] and kidney failure can arise and eventually lead to death.[80] The average number of years from onset to remission of AN is seven for women and three for men. After ten to fifteen years, 70% of people no longer meet the diagnostic criteria, but many still continue to have eating-related problems.[81]

Alexithymia has an impact on treatment outcome.[72] Recovery is also viewed on a spectrum rather than black and white. According to the Morgan-Russell criteria patients can have a good, intermediate, or poor outcome. Even when a patient is classified as having a "good" outcome, weight only has to be within 15% of average and normal menstruation must be present in females. The good outcome also excludes psychological health. Recovery for patients with anorexia nervosa is undeniably positive, but recovery does not mean a return to normal.

Complications

Anorexia nervosa can have serious implications if its duration and severity are significant and if onset occurs before the completion of growth, pubertal maturation, or the attainment of peak bone mass.

Complications specific to adolescents and children with anorexia nervosa can include the following:

Relapse

Relapse occurs in approximately a third of inpatients, and is greatest in the first half-year to year-and-a-half after release from inpatient institutions.[5]

Epidemiology

Though anorexia is common among many groups in the United States, the disorder is more limited to the Western world.

Anorexia has an average prevalence of 0.9% in women and 0.3% in men for the diagnosis in developed countries.[84] About three times as many women as men are affected.[5] The lifetime incidence of atypical anorexia nervosa, a form of ED-NOS in which not all of the diagnostic criteria for AN are met, is much higher, at 5–12%.[85]

The question of whether the incidence of AN is on the rise has been under debate. Most studies show that since at least 1970 the incidence of AN in adult women is fairly constant, while there is some indication that the incidence may have been increasing for girls aged between 14 and 20.[86] It is difficult to compare incidence rates at different times and possibly different locations due to changes in methods of diagnosing, reporting and changes in the population numbers, as evidenced on data from after 1970.[87][88]

Underrepresentation

Eating disorders are less reported in preindustrial, non-westernized countries than in Western countries. In Africa, not including South Africa, the only data presenting information about eating disorders occurs in case reports and isolated studies, not studies investigating prevalence. Data shows in research that in westernized civilizations, ethnic minorities have very similar rates of eating disorders, contrary to the belief that eating disorders predominantly occur in Caucasian people.

Due to different standards of beauty for men and women, men are often not diagnosed as anorexic. Generally men who alter their bodies do so to be lean and muscular rather than thin. In addition, men who might otherwise be diagnosed with anorexia may not meet the DSM IV criteria for BMI since they have muscle weight, but have very little fat.[89] Men and women athletes are often overlooked as anorexic.[89] Research emphasizes the importance to take athletes' diet, weight and symptoms into account when diagnosing anorexia, instead of just looking at weight and BMI. For athletes, ritualized activities such as weigh-ins place emphasis on weight, which may promote the development of eating disorders among them.[citation needed] While women use diet pills, which is an indicator of unhealthy behavior and an eating disorder, men use steroids, which contextualizes the beauty ideals for genders. This also shows men having a preoccupation with their body, which is an indicator of an eating disorder.[15] In a Canadian study, 4% of boys in grade nine used anabolic steroids.[15] Anorexic men are sometimes referred to as manorexic.[90]

History

Main article: History of anorexia nervosa
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 term anorexia nervosa was coined in 1873 by Sir William Gull, one of Queen Victoria's personal physicians.[91] The term is of Greek origin: an- (ἀν-, prefix denoting negation) and orexis (ὄρεξις, "appetite"), translating literally to a nervous loss of appetite.[92]

The history of anorexia nervosa begins with descriptions of religious fasting dating from the Hellenistic era[93] and continuing into the medieval period. The medieval practice of self-starvation by women, including some young women, in the name of religious piety and purity also concerns anorexia nervosa; it is sometimes referred to as anorexia mirabilis.[94][95]

The earliest medical descriptions of anorexic illnesses are generally credited to English physician Richard Morton in 1689.[93] Case descriptions fitting anorexic illnesses continued throughout the 17th, 18th and 19th centuries.[96]

In the late 19th century anorexia nervosa became widely accepted by the medical profession as a recognized condition. In 1873, Sir William Gull, one of Queen Victoria's personal physicians, published a seminal paper which coined the term anorexia nervosa and provided a number of detailed case descriptions and treatments.[96] 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.[97]

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 The Golden Cage: the Enigma of Anorexia Nervosa in 1978. Despite major advances in neuroscience,[98] Bruch's theories tend to dominate popular thinking. A further important event was the death of the popular singer and drummer Karen Carpenter in 1983, which prompted widespread ongoing media coverage of eating disorders.[citation needed]

See also

References

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  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.
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  6. ^ GBD 2013 Mortality and Causes of Death Collaborators (17 December 2014). "Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013". Lancet. 385 (9963): 117–171. doi:10.1016/S0140-6736(14)61682-2. PMC 4340604. PMID 25530442. {{cite journal}}: |author= has generic name (help)CS1 maint: numeric names: authors list (link)
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Further reading

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