Anorexia nervosa

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Anorexia nervosa
Gull - Anorexia Miss A.jpg
"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
Classification and external resources
ICD-10 F50.0-F50.1
ICD-9 307.1
OMIM 606788
DiseasesDB 749
MedlinePlus 000362
eMedicine emerg/34 med/144
Patient UK Anorexia nervosa
MeSH D000856

Anorexia nervosa is an eating disorder characterized by food restriction, inappropriate eating habits or rituals, obsession with having a thin figure, and an irrational fear of weight gain.[citation needed] 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 and the majority of individuals afflicted with anorexia nervosa do not, in fact, lose their appetites.[1]

Anorexia nervosa is often coupled with a distorted self image[2][3] which may be maintained by various cognitive biases[4] that alter how the affected individual evaluates and thinks about their body, food, and eating.[5] People with anorexia nervosa often view themselves as overweight or "big" even when they are already underweight.[6] While the majority of people with anorexia nervosa continue to feel hunger, they deny themselves all but very small quantities of food.[5]

Anorexia nervosa is diagnosed approximately nine times more often in females than in males.[7] In 2013 it resulted in about 600 deaths globally up from 400 deaths in 1990.[8] It is a serious health condition with a high incidence of comorbidity and similarly high mortality rate to serious psychiatric disorders.[6]

Signs and symptoms[edit]

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.[9] Anorexia nervosa, and the associated malnutrition that results from self-imposed starvation, can cause severe complications in every major organ system in the body.[10][11][12]

Hypokalaemia, a drop in the level of potassium in the blood, is a sign of anorexia nervosa. A significant drop in potassium can cause abnormal heart rhythms, constipation, fatigue, muscle damage and paralysis.

Symptoms of a person with anorexia nervosa may include:

Dermatological signs of anorexia nervosa[29]
xerosis cutis telogen effluvium carotenoderma acne vulgaris hyperpigmentation
seborrhoeic dermatitis acrocyanosis chilblains 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[30] diarrhea[31] electrolyte imbalance[32] cavities[33] tooth loss[34]
cardiac arrest[35] amenorrhoea[36] edema[37] osteoporosis[38] osteopenia[39]
hyponatremia[40] hypokalemia[41] optic neuropathy[42] brain atrophy[43][44] leukopenia[45][46]

The prevalent symptoms for anorexia nervosa (as discussed above) such as decreased body temperature, obsessive-compulsivity, and changes in psychological state, can actually be attributed to symptoms of starvation. This theory can be supported by a study by Routtenberg in 1968 involving rats who were deprived of food; these rats showed dramatic increases in their activity on the wheel in their cage at times when not being fed.[47] These findings could explain why those with anorexia nervosa are often seen excessively exercising; their overactivity is the result of fasting, and by increasing their activity they could raise their body temperature, increase their chances of stumbling upon food, or become distracted from their desire for nourishment (because they do not, in fact, lose their appetite). While it is commonly believed that those with AN do not have a normal appetite, this is not the case. Those with AN are typically obsessive about food, cooking often for others, but not eating the food themselves. Despite the fact that the physiological cause behind each case of anorexia nervosa is different, the most common theme seen across the board is the element of self-control. The underlying cause behind the disorder is rarely about the food itself; it is about the individual attempting to gain complete control over an aspect of their lives, in order to prove themselves, and distract them from another aspect of their lives they wish they could control. For example, a child with a destructive family life who restricts food intake in order to compensate for the chaos occurring at home.[47]

Not only does starvation result in physical complications, but mental complications as well.[48]


Between 50% and 75% of individuals with an eating disorder experience depression. In addition, one in every four individuals who are diagnosed with anorexia nervosa also exhibit obsessive-compulsive disorder.[49]

Relationship to autism[edit]

A summary of the strategy Zucker et al. (2007) used to assess the relationship between anorexia nervosa and the autism spectrum.[50]

Since Gillberg's (1983 & 1985)[51][52] and others' initial suggestion of relationship between anorexia nervosa and autism,[53][54] 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.[55][56][57][58][59][60][61] Those on the autism spectrum tend to have a worse outcome,[62] but may benefit from the combined use of behavioural and pharmacological therapies tailored to ameliorate autism rather than anorexia nervosa per se.[63][64] Other studies, most notably research conducted at the Maudsley Hospital, 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.[65][66][67][68][69][70]

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).[50] A pilot study into the effectiveness of 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.[71]

Some autistic traits are more prominent during the acute phase of AN.[72]


A diagnostic assessment may be conducted by a suitably trained general practitioner, or by a psychiatrist or psychologist, who records 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, focussing on views on weight and patterns of eating. 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.

DSM-5 and ICD-10 criteria[edit]

Anorexia nervosa is classified as an Axis I disorder in the Diagnostic and Statistical Manual of Mental Health Disorders (DSM 5), published by the American Psychiatric Association. The DSM 5 has replaced the previously used volume DSM-IV-TR, and there have been several changes made to the criteria in the new DSM 5 for anorexia nervosa, most notably that of the amenorrhea criterion being removed. However, significant changes in wording have also been made to each remaining criterion.

  • Persistent restriction of energy intake leading to significantly low body weight (in context of what is minimally expected for age, sex, developmental trajectory, and physical health).
  • Either an intense fear of gaining weight or of becoming fat, or persistent behaviour that interferes with weight gain (even though significantly low in weight).
  • Disturbance in the way one's body weight or shape is experienced, undue influence of body shape and weight on self-evaluation, or persistent lack of recognition of the seriousness of the current low body weight.[73]


  • Restricting type: Individual does not utilize binge eating nor displays purging behavior as their main strategy for weight loss. Instead, the individual uses restricting food intake, fasting, diet pills, and/or exercise as a means for losing weight.[74]
  • Binge-eating/purging type: Individual utilizes binge eating or displays purging behavior as a means for losing weight.[74]

Levels of severity[edit]

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:

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

F 50.0[edit]

A disorder characterized by deliberate weight loss, induced and sustained by the patient. It occurs most commonly in adolescent girls and young women, but adolescent boys and young men may also be affected, as may children approaching puberty and older women up to the menopause. The disorder is associated with a specific psychopathology whereby a dread of fatness and flabbiness of body contour persists as an intrusive overvalued idea, and the patients impose a low weight threshold on themselves. There is usually undernutrition of varying severity with secondary endocrine and metabolic changes and disturbances of bodily function. The symptoms include restricted dietary choice, excessive exercise, induced vomiting and purgation, and use of appetite suppressants and diuretics.[75]


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


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.[95][96][97][98] Studies have suggested 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 reported 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.[99][100] Even though anorexia does not affect males as often in comparison to females, studies have shown that males with a female twin have a higher chance of getting anorexia. Therefore anorexia may be linked to intrauterine exposure to female hormones.[101]


  • Obstetric complications: various 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.[102][103]
  • Genetics: anorexia nervosa is believed to be highly heritable, with estimated inheritance rates ranging from 56% to 84%.[104][105][106] Twin studies have shown a heritability rate of 56%.[107][108] Association studies have been performed, studying 128 different polymorphisms related to 43 genes including genes involved in regulation of eating behavior, motivation and reward mechanics, personality traits and emotion. Consistent associations have been identified for polymorphisms associated with agouti-related peptide, brain derived neurotrophic factor, catechol-o-methyl transferase, SK3 and opioid receptor delta-1.[109] In one study, variations in the norepinephrine transporter gene promoter were associated with restrictive anorexia nervosa, but not binge-purge anorexia.[110]
    • epigenetics: Epigenetic mechanisms: are means by which genetic mutations are caused by environmental effects that alter gene expression via methods such as DNA methylation, these are independent of and do not alter the underlying DNA sequence. They are heritable, as was shown in the Överkalix study, but also may occur throughout the lifespan, and are potentially reversible. Dysregulation of dopaminergic neurotransmission and Atrial natriuretic peptide homeostasis resulting from epigenetic mechanisms has been implicated in various eating disorders.[111] "We conclude that epigenetic mechanisms may contribute to the known alterations of ANP homeostasis in women with eating disorders."[111][112]
      alt = 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.
  • Addiction to the chemicals released in the brain during starving and physical activity;[117] 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,[117] though it is not explained why this addiction affects only females.
  • Serotonin dysregulation; brain imaging studies implicate alterations of 5-HT1A and 5-HT2A receptors and the 5-HT transporter. Alterations of these circuits may affect mood and impulse control as well as the motivating and hedonic aspects of feeding behavior.[118] Starvation has been hypothesized to be a response to these effects, as it is known to lower tryptophan and steroid hormone metabolism, which might reduce serotonin levels at these critical sites and ward off anxiety.[118] Other studies of the 5HT2A serotonin receptor (linked to regulation of feeding, mood, and anxiety), suggest that serotonin activity is decreased at these sites. There is evidence that both personality characteristics associated with AN and disturbances to the serotonin system are still apparent after patients have recovered from anorexia.[119] Another study found AN to be significantly associated with the S allele and S carrier (SS + LS) genotype.[120]
  • Brain-derived neurotrophic factor (BDNF) is a protein that regulates neuronal development and neuroplasticity, it also plays a role in learning, memory and in the hypothalamic pathway that controls eating behavior and energy homeostasis. BDNF amplifies neurotransmitter responses and promotes synaptic communication in the enteric nervous system. Low levels of BDNF are found in patients with AN and some comorbid disorders such as major depression.[121][122] Exercise increases levels of BDNF[123]
  • Leptin and ghrelin; leptin is a hormone produced primarily by the fat cells in white adipose tissue of the body it has an inhibitory (anorexigenic) effect on appetite, by inducing a feeling of satiety. Ghrelin is an appetite inducing (orexigenic) hormone produced in the stomach and the upper portion of the small intestine. Circulating levels of both hormones are an important factor in weight control. While often associated with obesity both have been implicated in the pathophysiology of anorexia nervosa and bulimia nervosa.[124] A 2013 study revealed that anorectic subjects may have reduced ghrelin bioactivity due to altered carrier-antibody affinity, leading to less efficient transport of ghrelin to the brain and thus reduced hunger sensation.[125]
  • Orexin; orexin is a neurotransmitter that regulates appetite and is responsible for increasing the craving for food.[126]
  • Cerebral blood flow (CBF); neuroimaging studies have shown reduced CBF in the temporal lobes of anorectic patients, which may be a predisposing factor in the onset of AN.[127]
  • Autoimmune system; Autoantibodies against neuropeptides such as melanocortin have been shown to affect personality traits associated with eating disorders such as those that influence appetite and stress responses.[128]
  • Infections: Some people are hypothesized to have developed anorexia abruptly as a reaction to a streptococcus or mycoplasma infection. PANS is an acronym for Pediatric acute-onset neuropsychiatric syndrome, 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.[129]
  • 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.[130]


Increased incidence of anorexia nervosa has been linked to vulnerability and internalization of body ideals.[131] There is a common connection between anorexia nervosa and the dominant culture in the West, which is a Eurocentric culture. Studies have shown than this Eurocentric culture includes a drive for thinness and thinness as a beauty ideal. Typically, young women of color are thought to be protected from this destructive beauty ideal because the ideals of their own ethnic groups, in which thinness is not favored, have stronger influence. Increasingly, studies show that this notion of women of color as "protected" is antiquated.[132] A 2008 meta-analysis included research in which significant differences in eating disorder symptoms were not found between Asian, Black, Hispanic, and White female subjects with a possible explanation being that the dominant Eurocentric culture has permeated ethnic boundaries.[133] Thinness has become a requirement to one’s acceptance into mainstream Eurocentric society. Where thinness is not the perceived norm in a certain group, such as amongst black women, these women might develop certain restrictive behaviors in order to combat the negative stereotypes held by members of the dominant culture, namely whites.[134] Specific cultural factors, such as family interactions, individual psychology, and media influence one’s likelihood of developing anorexia. Disparities might exist between ethnic groups and which of these cultural factors is most influential; according to a 2003 review article of women of color and eating disorders, black adolescents females reported being primarily influenced by family and adult role models, while their white counterparts reported being primarily influenced by the media and by peers.[135] Culture change can trigger the emergence of anorexia in adolescent girls from immigrant families living in highly industrialized Western Societies.[136] According to a study published in 1980, 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,[137] and further research has suggested that those with anorexia have much higher contact with cultural sources that promote weight-loss.[138]

Certain subcultures have been found to have higher rates of eating disorders than the general population including ballet dancers, models, skaters, gymnasts, rowers, jockeys and wrestlers.[139] 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.[140]

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." [131]

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.[141]

There is also evidence to suggest that patients who have anorexia nervosa can be characterised by alexithymia[70] 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.[142]

Early theories of the cause of anorexia linked it to childhood sexual abuse or dysfunctional families. Some studies reported a high rate of reported child sexual abuse experiences in clinical groups of people who have been diagnosed with anorexia. Evidence is conflicting regarding the comorbidity of childhood sexual abuse and anorexia nervosa and is in need of further research.[143][144]

No one factor alone is responsible for the onset of anorexia nervosa; however it is clear that certain circumstances increase incidence and pose significant risk factors.

Eating disorders vary in white women just as they vary in women of color. Theories now include many factors for the development of eating disorders like anorexia such as: sociocultural, environmental, and even genetic factors. All of these factors apply to women of every ethnic and racial group. A very common sociocultural reason for why anorexia has grown so common in the United States of America is because of how the women portrays women’s bodies and how they should look, even if it is not the most realistic model. Sometimes if women of color are more acculturated they will show more symptoms of having the disorder than those who reject certain “mainstream” ideals of beauty. This can be the case in white women as well who do not wish to follow the media’s perception of beauty, this can all vary depending on the person, not the race or ethnicity. In actuality, the disorder has more to do with the embodiment of the person and their environment than a racial or ethnic aspect. While the sociocultural aspect is an incredibly important part of the disorder, there is more to consider. For example stress can lead to anorexia nervosa. This too can vary in different ethnic and racial groups, but there are definitely aspects of racism and acculturation that can lead to stress and an eventual eating disorder. This data could go against the literature and argue that women of color are even more susceptible to get an eating disorder.[145]

Media effects[edit]

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 of the 10 magazines most popular among people aged 18 to 24 years the magazines read by men, unlike those read by women, were more likely to feature ads and articles on shape than on diet.[146] Body image research suggests that male body dissatisfaction is now comparable in prevalence to the rates reported in females.[147] Body dissatisfaction and internalization of body ideals are risk factors for anorexia nervosa that threaten the health of both male and female populations.

Furthermore, websites that stress the importance of attainment of body ideals have surfaced on the Internet. Such sites 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).[148] Pro-anorexia websites reinforce internalization of body ideals and the importance of their attainment.

Differential diagnoses[edit]

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. In a reported case of achalasia misdiagnosed as AN, the patient spent two months confined to a psychiatric hospital.[149]

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. 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.[150] Some people have a previous disorder which may increase their vulnerability to developing an eating disorder.[151][152][153] Some develop them afterwards.[154] The presence of Axis I and/or Axis II psychiatric comorbidity has been shown to affect the severity and type of anorexia nervosa symptoms in both adolescents and adults.[155][156] In particular, substance abuse and borderline personality appear more frequent among anorexics who binge or purge.[157][158] And obsessive-compulsive personality disorder—according to some studies, the most common personality disorder among anorexics—and particular traits of this diagnosis such as perfectionism are linked with more severe symptomatology and worse prognosis.[159][160]

Comorbid Disorders
Axis I Axis II
depression[161] obsessive compulsive personality disorder[162]
substance abuse, alcoholism[163] borderline personality disorder[164]
anxiety disorders[165]
obsessive compulsive disorder[166][167]
  • 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.[172]

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.[173][174][175][175][176]

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.[177] It is not unusual for a person with an eating disorder to "move through" various diagnoses as their behavior and beliefs change over time.[50]


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.[178] 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.[179]

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.[13] Not all anorexia nervosa patients recover completely; About 20% develop anorexia nervosa as a chronic disorder.[180] If anorexia nervosa is not treated, serious complications such as heart conditions and kidney failure can arise and eventually lead to death. "As many as 6 percent of people with the disorder die from causes related to it."[181]


P. Sodersten and colleagues suggest that effective treatment of this disorder depends on re-establishing reinforcement for normal eating behaviours instead of unhealthy weight loss.[1]

Diet is the most essential factor to work on in patients with anorexia nervosa, and must be tailored to each patient's needs. Initial meal plans may be low in calories, about 1200, in order to build comfort in eating, and then food amount can gradually be increased. Food variety is important when establishing meal plans as well as foods that are higher in energy density. Other more specific dietary treatments are listed below.[182]

  • Zinc: 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. Patients with anorexia nervosa have a high likelihood of being zinc deficient, and this probability increases if they are vegetarians. Vegetarianism is adopted by many patients with eating disorders because it is widely acclaimed as healthy and easy to manage calorie intake.[183] Sufficient Zinc must be available during recovery, and normal zinc levels were seen in the Notre Dame study to increase weight gain at a faster rate. Zinc supplementation can also help reduce reproductive issues for patients with anorexia nervosa. Leptin levels, which regulate hunger and metabolism, decrease from zinc deficiency and even more with AN sufferers due to the reduction in size of adipose tissue. Reproductive tissues have been discovered to contain leptin receptors, thus a decrease in leptin concentration would lead to a lower rate of fertility. Despite the connection to weight gain and reproduction, zinc supplementation seems to be largely under-appreciated and many do not consider zinc deficiency as an important factor in regard to anorexia nervosa.[184]
  • Calories: Patients must be fed adequate calories at a measured pace for improvement of their condition to occur. The best level for calorie intake is to start by providing 1200 to 1500 calories daily and increasing this amount by 500 each day. This process should continue until the level of 4000 calories (for male patients) or 3500 calories (for female patients) is achieved. This system should also decrease effects such as apathy, lethargy, and food-related obsessions.[185]
  • 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.[186] 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),[187] 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.[188][189]
  • Nutritional counseling.[190][191]
  • 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.[192][193][194]


  • Olanzapine: There have been some claims that olanzapine is effective in treating certain aspects of AN including helping raise the body mass index and reducing obsessionality, including obsessional thoughts about food.[195][196] Olanzapine does not increase the rate of body mass index growth in patients with anorexia.[197]


Family-based treatment

Family-based treatment (FBT) has been shown in randomized controlled trials to be more successful than individual therapy in most treatment trials.[13] Several components of family therapy for patients with AN are:

  • the family is seen as a resource for the adolescent[198]
  • anorexia nervosa is reframed in benign, non blaming terms[198]
  • directives are provided to parents so that they may take charge of their child or adolescent's eating routine[198]
  • a structured behavioral weight gain program is implemented[198]
  • after weight gain, control over eating is gradually returned to the child or adolescent[198]
  • as the child or adolescent begins to eat and gain weight, the therapeutic focus broadens to include family interaction problems, growth and autonomy issues and parent–child conflicts[198]

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, "separated family therapy" (SFT) in which the 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 ...".[199][200] Proponents of Family therapy for adolescents with AN assert that it is important to include parents in the adolescent's treatment.[201]
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%.[202] Although this model is recommended by the NIMH,[203] critics claim that it has the potential to create power struggles in an intimate relationship and may disrupt equal partnerships.[204]

Cognitive behavioral therapy

Cognitive behavioral therapy (CBT) is an evidence based approach which in studies to date has shown to be useful in adolescents and adults with anorexia nervosa.[205][206][207] Components of using CBT with adults and adolescents with anorexia nervosa have been outlined by several professionals as:

  • the therapist focuses on using cognitive restructuring to modify distorted beliefs and attitudes about the meaning of weight, shape and appearance[198]
  • specific behavioral techniques addressing the normalization of eating patterns and weight restorations, examples of this include the use of a food diary, meal plans, and incremental weight gain[198]
  • cognitive techniques such as restructuring, problem solving, and identification and expression of affect[198]
  • When using CBT with adolescents and children with AN, several professionals have expressed concerns about the minimum age and level of cognition necessary for implementing cognitive behavioral techniques.[198] Modified versions and elements of CBT can be implemented with children and adolescents with AN. Such modifications may include the use of behavioral experiments to disconfirm distorted beliefs and absolutistic thinking in children and adolescents.[198]
Acceptance and commitment therapy

Acceptance and commitment therapy is a type of CBT, which 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."[208]

Cognitive remediation therapy

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[209] and in Poland with adolescents CRT was proven to be beneficial in treating anorexia nervosa,[209] in the United States clinical trials are still being conducted by the National Institute of Mental Health[210] on adolescents age 10–17 and Stanford University in subjects over 16 as a conjunctive therapy with Cognitive behavioral therapy.[211]


The long-term prognosis of anorexia nervosa is more on the favorable side. The National Comorbidity Replication Survey was conducted among more than 9,282 participants throughout the United States; ` 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 ..."[212] However, 5–20% of people diagnosed with anorexia nervosa die from it, and the cause of death is mostly because of the direct health effects of the eating disorder on the body.[213]

In cases of adolescent anorexia nervosa where family-based treatment is used, 75% of patients have a good outcome and an additional 15% show an intermediate yet more positive outcome.[199] In a five-year post treatment follow-up of Maudsley Family Therapy the full recovery rate was between 75% and 90%.[214]

Some remedies, however, are proven to not have any value in resolving anorexia. "Incarceration in hospital" prohibits patients from many basic rights, such as using the bathroom independently. Therefore, it has been seen as catalytic in increasing weight and pushing patients away from the path to recovery.[215]

According to a 1997 study, 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.[216] 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.[217]

Although overall the prognosis may seem favorable, this is not the case for all patients of anorexia nervosa. Among psychiatric disorders, anorexia nervosa has one of the highest mortality rates because of side effects of the disorder, such as cardiac complications or suicide. In intermediate to long-term studies with juveniles, death rates, on average, have ranged anywhere from 1.8 to 14.1%.[218] Recovery can be lifelong for some; energy intake and eating habits may never return to normal.[182] Many studies have attempted to study relapse and recovery through longitudinal studies but this is difficult, time consuming, and costly. 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 normal.[218]


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.[219] Complications specific to adolescents and children with anorexia nervosa can include the following:

  • Growth retardation – height gain may slow and can stop completely with severe weight loss or chronic malnutrition. In such cases, provided that growth potential is preserved, height increase can resume and reach full potential after normal intake is resumed.[219] Height potential is normally preserved if the duration and severity of illness are not significant and/or if the illness is accompanied with delayed bone age (especially prior to a bone age of approximately 15 years), as hypogonadism may negate the deleterious effects of undernutrition on stature by allowing for a longer duration of growth compared to controls.[220] In such cases, appropriate early treatment can preserve height potential and may even help to increase it in some post-anorexic subjects due to the aforementioned reasons in addition to factors such as long-term reduced estrogen-producing adipose tissue levels compared to premorbid levels.[221][222][223][224]
  • Pubertal delay or arrest – both height gain and pubertal development are dependent on the release of growth hormone and gonadotrophins (LH and FSH) from the pituitary gland. Suppression of gonadotrophins in patients with anorexia nervosa has frequently been documented.[219] However, a study demonstrated that growth hormone levels were not a predictor of height measures in anorexic patients, which is suggestive of a resistance to growth hormone effects at the growth plate, similar to the resistance to growth hormone of bone-formation markers.[220] Instead, insulin-like growth factor had a larger effect, with lower IGF-I levels and longer durations of illness tending to result in lower height measures than vice versa, although IGF-I levels in anorexic subjects may not necessarily be low enough to affect height measures.[220] In some cases, especially where onset is pre-pubertal, physical consequences such as stunted growth and pubertal delay are usually fully reversible.[225]
  • Reduction of Peak Bone Mass – bone accretion is the highest during adolescence, and if onset of anorexia nervosa occurs during this time and stalls puberty, bone mass may remain low.[219]
  • Hepatic steatosis – fatty infiltration of the liver is an indicator of malnutrition in children.[219]
  • Heart disease and arrythmias
  • Neurological disorders- seizures, tremors
  • Acute gastric dilation, infarction and perforation,[226]
  • Death (Anorexia nervosa has the highest rate of mortality of any psychological disorder):[227] [5-9 percent][228]


According to the Eckert study, relapse is greatest in the first year after normal body weight is obtained. This includes right after release from inpatient institutions. Relapse includes a return to food restriction as well as a shift to binge eating habits.

As stated above, higher energy density in dietary plans is important. Patients with lower dietary energy density in their meals, prior to being discharged, had worse outcomes within the year, therefore a higher likelihood of relapse. This is speculated to be due to fat and fluid consumption. Patients whose dietary plans included fats and foods containing fats were forced to eat a more realistic and "normal" plan than those with lower energy density. Therefore, when released from inpatient treatment, the patients with higher dietary energy density plans had adopted healthier and more balanced eating habits. A greater food variety in inpatient dietary plans may help lower rates of relapse as well.[229] Relapse, binging or starving after initial weight gain, occurs in 40–70% of anorexia patients.[230] Prevention of relapse can be helped by cognitive-behavioral therapy and pharmacological therapies.[230] Link of OCD with anorexia shows treatments for OCD such as serotonin re-uptake inhibitors (SSRI) helps in preventing relapse.[230]

Several clinically significant variables that could predict relapse among AN patients were identified in a study conducted by a team at the University of Toronto. First, patients with binge-purge type AN were twice as likely to have a relapse as those with restricting subtype AN. The second predictor of relapse was the level of motivation to recover. When patients' motivation to recover fell during the first 4 weeks of inpatient treatment, the risk of relapse rose. The third predictor identified in the study was higher pre-treatment severity of checking behaviors, as reported on the Padua Inventory (PI) Checking Behavior scale, a measure of obsessive-compulsive disorder symptoms.[231]


Anorexia has an average prevalence of 0.9% in women and 0.3% in men for the diagnosis in developed countries.[232][233] The condition largely affects young adolescent women, with those between 15 and 19 years old making up 40% of all cases.[233] Anorexia nervosa is more prevalent in the upper social classes and it is thought to be rare in less-developed countries.[217] Anorexia is more prevalent in females and males born after 1945.[234] 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%.[235]

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.[236] 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.[237][238][239]

Only recently has there been extensive research on ethnic minorities and anorexia. This can be attributed to the assumption that anorexia is only a disorder for the white and wealthy. [240] Though anorexia is common among many groups in the United States, the disorder is more limited to the Western world. Because of the diversity of the United States of America, there is an element of acculturation involved in the prevalence of the disorder. While there is a belief that African American women have a different set of criteria for body image than white woman, these two criteria are actually being blended together to create a new standard of beauty.[241]


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.[242] Due to different standards of beauty for men and women, men are often not diagnosed as anorexic. Many men do not conform to the ideals of women to be thin and men that do try to alter their bodies often try to be lean and muscular. In addition they may not meet the DSM IV criteria for BMI since they have muscle weight, but have very little fat.[243] An article investigating the differences between beauty ideals in men and women found that in women’s magazines weight loss is advertised 10.5 times more than men’s, and in men’s magazines the advertisements were to change body shape rather than lose weight.[244] Often many men have been reluctant to participate in studies, and the data that is available today does not show the full picture. Men and women athletes often are often overlooked as anorexic however, estimates show that 33% of male athletes have an eating disorder, according to information from the National Athletic Trainers’ Association.[243] Research emphasizes the importance for strict watch over athletes diet, weight, and symptoms, which adhere to all of the defining characteristics of anorexia on the DSM, rather than just looking at weight and BMI. For athletes, ritualized activities such as weigh-ins place emphasis on weight, promoting the development of eating disorders among athletes.[242] 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.[245] In a Canadian study, 4% of boys in grade nine used anabolic steroids.[245] In addition, since anorexia is commonly thought of as something that afflicts women, anorexic men have their own title: “manorexia,” although it is the same condition.


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.[246] The term is of Greek origin: an- (ἀν-, prefix denoting negation) and orexis (ὄρεξις, "appetite"), thus meaning a lack of desire to eat.[247]

The history of anorexia nervosa begins with descriptions of religious fasting dating from the Hellenistic era[248] 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.[249][250]

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. By the thirteenth century, it was increasingly common for women to participate in religious life and to even be named as saints by the Catholic Church. 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. 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.[249]

The earliest medical descriptions of anorexic illnesses are generally credited to English physician Richard Morton in 1689.[248] Case descriptions fitting anorexic illnesses continued throughout the 17th, 18th and 19th centuries. They include the cases of an 18-year-old girl treated by Richard Morton in 1689 who refused to eat and died 3 months later.[251] Noah Webster writes of an instructor at Yale College in the 1770s who refused to eat because he believed food was "dulling his mind."[252]

However, it was not until the late 19th century that anorexia nervosa was 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 coined the term anorexia nervosa and provided a number of detailed case descriptions and treatments. However, Gull was unable to provide an explanation for the condition.[251] 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 The Golden Cage: the Enigma of Anorexia Nervosa in 1978. This book created a wider interest in anorexia nervosa among lay readers. Bruch postulated that anorexia nervosa is a "desperate struggle for a self-respecting identity". Despite major advances in neuroscience,[253] 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. Anorexia has the highest mortality rate of any mental illness[254] and continues to be in the public eye. "Pro-ana" websites range from those claiming to be a safe-space for anorexics to discuss their problems, to those supporting anorexia as a lifestyle choice and offering "thinspiration," or photos and videos of thin or emaciated women. A survey by Internet security firm Optenet found a 470% increase in pro-ana and pro-mia (as in bulimia) sites from 2006 to 2007. Many celebrities have come forward discussing their struggles with anorexia, increasing awareness of the disease. Celebrities who have come forward publicly to discuss their experiences with anorexia include singer Fiona Apple, who purposely lost weight to discourage unwanted sexual advances after being raped at age 12,[255] Portia de Rossi,[256] Calista Flockhart,[257] Tracey Gold,[258] whose difficult recovery was well publicized by the media after her weight dropped to 80 pounds (36 kg) on her 5 ft 3 in (1.60 m) frame and she was hospitalized,[259] Mary-Kate Olsen,[260] Alanis Morissette,[261] and French model Isabelle Caro, who died due to complications related to anorexia.

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