|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
|Patient UK||Anorexia nervosa|
Anorexia nervosa is an eating disorder characterized by immoderate food restriction, inappropriate 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. Anorexia nervosa is diagnosed approximately nine times more often in females than in males. 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.
Anorexia nervosa is often coupled with a distorted self image which may be maintained by various cognitive biases that alter how the affected individual evaluates and thinks about their body, food, and eating. People with anorexia nervosa often view themselves as overweight or "big" even when they are already underweight.
While the majority of people with anorexia nervosa continue to feel hunger, they deny themselves all but very small quantities of food. The caloric intake of people with anorexia nervosa can vary significantly between individuals and over time, depending on whether they engage in binging and/or purging behavior. Extreme cases of complete self-starvation are known. It is a serious health condition with a high incidence of comorbidity and similarly high mortality rate to serious psychiatric disorders.
- 1 Signs and symptoms
- 2 Diagnosis
- 3 Causes
- 4 Treatment
- 5 Prognosis
- 6 Epidemiology
- 7 History
- 8 See also
- 9 References
- 10 External links
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. Anorexia nervosa, and the associated malnutrition that results from self-imposed starvation, can cause severe complications in every major organ system in the body.
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:
- Refusal to maintain a normal body mass index for their 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
- Obvious, rapid, dramatic weight loss at least 15% under normal body weight
- Lanugo: soft, fine hair growing on the face and body – one theory is that this is related to hypothyroidism, as there are several reports of a similar hypertrichosis occurring in hypothyroidism
- 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, or 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 (see also bulimia nervosa)
- May engage in frequent, strenuous, or compulsive exercise
- 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
- Hypotension and/or orthostatic hypotension
- Bradycardia or tachycardia
- Depression: may frequently be in a sad, lethargic state
- Solitude: may avoid friends and family; becomes withdrawn and secretive
- Cheeks may become swollen because of enlargement of the salivary glands caused by excessive vomiting
- Swollen joints
- Abdominal distension
- Halitosis (from vomiting or starvation-induced ketosis)
- Dry hair and skin, as well as hair thinning
- Rapid mood swings
|constipation||diarrhea||electrolyte imbalance||cavities||tooth loss|
|hyponatremia||hypokalemia||optic neuropathy||brain atrophy||leukopenia|
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. 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.
Not only does starvation result in physical complications, but mental complications as well.
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.
Relationship to autism
Since Gillberg's (1983 & 1985) and others' initial suggestion of relationship between anorexia nervosa and autism, 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. Those on the autism spectrum tend to have a worse outcome, but may benefit from the combined use of behavioural and pharmacological therapies tailored to ameliorate autism rather than anorexia nervosa per se. 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.
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). 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.
Some autistic traits are more prominent during the acute phase of AN.
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
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.
- 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.
- Binge-eating/purging type: Individual utilizes binge eating or displays purging behavior as a means for losing weight.
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:
- Mild: BMI of 17-17.99
- Moderate: BMI of 16-16.99
- Severe: BMI of 15-15.99
- Extreme: BMI of less than 15
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.
Medical tests to check for signs of physical deterioration in anorexia nervosa may be performed by a general physician or psychiatrist, including:
- Complete Blood Count (CBC): a test of the white blood cells, red blood cells and platelets used to assess the presence of various disorders such as leukocytosis, leukopenia, thrombocytosis and anemia which may result from malnutrition.
- Urinalysis: a variety of tests performed on the urine used in the diagnosis of medical disorders, to test for substance abuse, and as an indicator of overall health
- Chem-20: Chem-20 also known as SMA-20 a group of twenty separate chemical tests performed on blood serum. Tests include cholesterol, protein and electrolytes such as potassium, chlorine and sodium and tests specific to liver and kidney function.
- Glucose tolerance test: Oral glucose tolerance test (OGTT) used to assess the body's ability to metabolize glucose. Can be useful in detecting various disorders such as diabetes, an insulinoma, Cushing's Syndrome, hypoglycemia and polycystic ovary syndrome
- Serum cholinesterase test: a test of liver enzymes (acetylcholinesterase and pseudocholinesterase) useful as a test of liver function and to assess the effects of malnutrition
- Liver Function Test: A series of tests used to assess liver function some of the tests are also used in the assessment of malnutrition, protein deficiency, kidney function, bleeding disorders, and Crohn's Disease.
- Lh response to GnRH: Luteinizing hormone (Lh) response to gonadotropin-releasing hormone (GnRH): Tests the pituitary glands' response to GnRh a hormone produced in the hypothalamus. Central hypogonadism is often seen in anorexia nervosa cases.
- Creatine Kinase Test (CK-Test): measures the circulating blood levels of creatine kinase an enzyme found in the heart (CK-MB), brain (CK-BB) and skeletal muscle (CK-MM).
- Blood urea nitrogen (BUN) test: urea nitrogen is the byproduct of protein metabolism first formed in the liver then removed from the body by the kidneys. The BUN test is primarily used to test kidney function. A low BUN level may indicate the effects of malnutrition.
- BUN-to-creatinine ratio: A BUN to creatinine ratio is used to predict various conditions. A high BUN/creatinine ratio can occur in severe hydration, acute kidney failure, congestive heart failure, and intestinal bleeding. A low BUN/creatinine ratio can indicate a low protein diet, celiac disease, rhabdomyolysis, or cirrhosis of the liver.
- Electrocardiogram (EKG or ECG): measures electrical activity of the heart. It can be used to detect various disorders such as hyperkalemia
- Electroencephalogram (EEG): measures the electrical activity of the brain. It can be used to detect abnormalities such as those associated with pituitary tumors
- Thyroid Screen TSH, t4, t3 :test used to assess thyroid functioning by checking levels of thyroid-stimulating hormone (TSH), thyroxine (T4), and triiodothyronine (T3)
- Parathyroid hormone (PTH) test: tests the functioning of the parathyroid by measuring the amount of (PTH) in the blood. It is used to diagnose parahypothyroidism. PTH also controls the levels of calcium and phosphorus in the blood (homeostasis).
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. 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. 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.
- 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.
- Genetics: anorexia nervosa is believed to be highly heritable, with estimated inheritance rates ranging from 56% to 84%. Twin studies have shown a heritability rate of 56%. 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. In one study, variations in the norepinephrine transporter gene promoter were associated with restrictive anorexia nervosa, but not binge-purge anorexia.
- 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. "We conclude that epigenetic mechanisms may contribute to the known alterations of ANP homeostasis in women with eating disorders."
- 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. "We conclude that epigenetic mechanisms may contribute to the known alterations of ANP homeostasis in women with eating disorders."
- Addiction to the chemicals released in the brain during starving and physical activity; 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, 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. 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. 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. Another study found AN to be significantly associated with the S allele and S carrier (SS + LS) genotype.
- 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. Exercise increases levels of BDNF
- 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. 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.
- Orexin; orexin is a neurotransmitter that regulates appetite and is responsible for increasing the craving for food.
- 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.
- 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.
- 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.
- 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.
Increased incidence of anorexia nervosa has been linked to vulnerability and internalization of body ideals. 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. 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. 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. 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. Culture change can trigger the emergence of anorexia in adolescent girls from immigrant families living in highly industrialized Western Societies. 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, and further research has suggested that those with anorexia have much higher contact with cultural sources that promote weight-loss.
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. 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.
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." 
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.
There is also evidence to suggest that patients who have anorexia nervosa can be characterised by alexithymia 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.
Early theories of the cause of anorexia linked it to childhoodsexual 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.
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.
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. Body image research suggests that male body dissatisfaction is now comparable in prevalence to the rates reported in females. 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). Pro-anorexia websites reinforce internalization of body ideals and the importance of their attainment.
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.
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. Some people have a previous disorder which may increase their vulnerability to developing an eating disorder. Some develop them afterwards. 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. In particular, substance abuse and borderline personality appear more frequent among anorexics who binge or purge. 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.
- 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.
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.
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. It is not unusual for a person with an eating disorder to "move through" various diagnoses as their behavior and beliefs change over time.
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. 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.
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. Not all anorexia nervosa patients recover completely; About 20% develop anorexia nervosa as a chronic disorder. 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."
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.
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.
- 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. 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.
- 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.
- 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. 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), 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.
- Nutritional counseling.
- 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.
- 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. Olanzapine does not increase the rate of body mass index growth in patients with anorexia.
- 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. Several components of family therapy for patients with AN are:
- the family is seen as a resource for the adolescent
- anorexia nervosa is reframed in benign, non blaming terms
- directives are provided to parents so that they may take charge of their child or adolescent's eating routine
- a structured behavioral weight gain program is implemented
- after weight gain, control over eating is gradually returned to the child or adolescent
- 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
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 ...". Proponents of Family therapy for adolescents with AN assert that it is important to include parents in the adolescent's treatment.
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%. Although this model is recommended by the NIMH, critics claim that it has the potential to create power struggles in an intimate relationship and may disrupt equal partnerships.
- 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. 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
- 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
- cognitive techniques such as restructuring, problem solving, and identification and expression of affect
- 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. 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.
- 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."
- 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 and in Poland with adolescents CRT was proven to be beneficial in treating anorexia nervosa, in the United States clinical trials are still being conducted by the National Institute of Mental Health on adolescents age 10–17 and Stanford University in subjects over 16 as a conjunctive therapy with Cognitive behavioral therapy.
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 ..." 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.
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. In a five-year post treatment follow-up of Maudsley Family Therapy the full recovery rate was between 75% and 90%.
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.
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. 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.
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%. Recovery can be lifelong for some; energy intake and eating habits may never return to normal. 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.
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:
- 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. 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. 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.
- 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. 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. 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. In some cases, especially where onset is pre-pubertal, physical consequences such as stunted growth and pubertal delay are usually fully reversible.
- 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.
- Hepatic steatosis – fatty infiltration of the liver is an indicator of malnutrition in children.
- Heart disease and arrythmias
- Neurological disorders- seizures, tremors
- Acute gastric dilation, infarction and perforation,
- Death (Anorexia nervosa has the highest rate of mortality of any psychological disorder): [5-9 percent]
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. Relapse, binging or starving after initial weight gain, occurs in 40–70% of anorexia patients. Prevention of relapse can be helped by cognitive-behavioral therapy and pharmacological therapies. Link of OCD with anorexia shows treatments for OCD such as serotonin re-uptake inhibitors (SSRI) helps in preventing relapse.
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.
Anorexia has an average prevalence of 0.9% in women and 0.3% in men for the diagnosis in developed countries. The condition largely affects young adolescent women, with those between 15 and 19 years old making up 40% of all cases. Anorexia nervosa is more prevalent in the upper social classes and it is thought to be rare in less-developed countries. Anorexia is more prevalent in females and males born after 1945. 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%.
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. 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.
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.  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.
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. 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. 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. 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. 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. 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. In a Canadian study, 4% of boys in grade nine used anabolic steroids. 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.
The term anorexia nervosa was coined in 1873 by Sir William Gull, one of Queen Victoria's personal physicians. The term is of Greek origin: an- (ἀν-, prefix denoting negation) and orexis (ὄρεξις, "appetite"), thus meaning a lack of desire to eat.
The history of anorexia nervosa begins with descriptions of religious fasting dating from the Hellenistic era 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.
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.
The earliest medical descriptions of anorexic illnesses are generally credited to English physician Richard Morton in 1689. 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. Noah Webster writes of an instructor at Yale College in the 1770s who refused to eat because he believed food was "dulling his mind."
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. 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, 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 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, Portia de Rossi, Calista Flockhart, Tracey Gold, 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, Mary-Kate Olsen, Alanis Morissette, and French model Isabelle Caro, who died due to complications related to anorexia.
- List of people with anorexia nervosa
- Anti-fat bias
- Binge eating disorder
- Bulimia nervosa
- Caloric restriction
- Cigarette smoking for weight loss
- Eating disorders and development
- Eating Recovery
- Hungry: A Mother and Daughter Fight Anorexia (book)
- Life-Size (novel)
- Marya Hornbacher
- Muscle dysmorphia
- National Association of Anorexia Nervosa and Associated Disorders
- Orthorexia nervosa
- Weight phobia
- Sandra Lahire
- Hockenbury, Don and Hockenbury, Sandra (2008) Psychology, p. 593. Worth Publishers, New York. ISBN 978-1-4292-0143-8.
- Carlson N., Heth C., Miller Harold, Donahoe John, Buskist William, Martin G., Schmaltz Rodney (2007). Psychology: the science of behaviour-4th Canadian ed. Toronto, ON: Pearson Education Canada. pp. 414–415. ISBN 978-0-205-64524-4.
- 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.
- 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.
- Brooks S, Prince A, Stahl D, Campbell 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): 37–51. doi:10.1016/j.cpr.2010.09.006. PMID 21130935.
- Neil Frude (1998). Understanding abnormal psychology. Wiley-Blackwell. ISBN 978-0-631-16195-0.
- 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.
- Burd, C; Mitchell, J. E.; Crosby, R. D.; Engel, S. G.; Wonderlich, S. A.; Lystad, C; Le Grange, D; Peterson, C. B.; Crow, S (2009). "An assessment of daily food intake in participants with anorexia nervosa in the natural environment". International Journal of Eating Disorders 42 (4): 371–4. doi:10.1002/eat.20628. PMC 3584709. PMID 19040266.
- Surgenor LJ; Maguire S (2013). "Assessment of anorexia nervosa: an overview of". Journal of Eating Disorders 1 (1): 1–12. doi:10.1186/2050-2974-1-29.
- Abell TL, Malagelada JR, Lucas AR, Brown ML, Camilleri M, Go VL, Azpiroz F, Callaway CW, Kao PC, Zinsmeister AR (1987). "Gastric electromechanical and neurohormonal function in anorexia nervosa". Gastroenterology 93 (5): 958–65. PMID 3653645.
- 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.
- Støving RK, Hangaard J, Hagen C (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.
- Attia E, Walsh BT (2007). "Anorexia Nervosa". American Journal of Psychiatry 164 (12): 1805–1810. doi:10.1176/appi.ajp.2007.07071151. PMID 18056234.
- "Anorexia Nervosa". National Association of Anorexia Nervosa and Associated Disorders. Retrieved 15 April 2014.
- 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.
- Stern SR, Kelnar CJ (1985). "Hypertrichosis due to primary hypothyroidism". Archives of Disease in Childhood 60 (8): 763–766. doi:10.1136/adc.60.8.763. PMC 1777396. PMID 4037863.
- Sharma, D; Shanker, V; Tegta, G; Gupta, M; Verma, G. K. (2012). "Clinico-investigative Profile of Patients of Hirsutism in a Tertiary Level Institution". International Journal of Trichology 4 (2): 69–74. doi:10.4103/0974-7753.96904. PMC 3500076. PMID 23180912.
- Pietrowsky R, Krug R, Fehm HL, Born J (2002). "Food deprivation fails to affect preoccupation with thoughts of food in anorexic patients". The British Journal of Clinical Psychology 41 (Pt 3): 321–6. doi:10.1348/014466502760379172. PMID 12396259.
- 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.
- Friedman EJ (1984). "Death from ipecac intoxication in a patient with anorexia nervosa". The American Journal of Psychiatry 141 (5): 702–3. PMID 6143508.
- 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.
- Haller E (1992). "Eating disorders. A review and update". The Western Journal of Medicine 157 (6): 658–62. PMC 1022101. PMID 1475950.
- Lucka I (2004). "[Depression syndromes in patients suffering from anorexia nervosa]". Psychiatria Polska (in Polish) 38 (4): 621–9. PMID 15518310.
- 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.
- "Signs of Anorexia". anorexia.emedtv.com.
- "Noticing the Signs and Symptoms". The Something Fishy Website on Eating Disorders.
- "Anorexia Nervosa". National Eating Disorders Association
- McClure, G.M.; Timimi, Westman (1995). "Anorexia nervosa in early adolescence following illness — the importance of the sick role". Journal of Adolescence 18 (3): 359. doi:10.1006/jado.1995.1025.
- 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.
- Chiarioni G, Bassotti G, Monsignori A, Menegotti M, Salandini L, Di Matteo G, Vantini I, Whitehead WE (2000). "Anorectal dysfunction in constipated women with anorexia nervosa". Mayo Clinic Proceedings 75 (10): 1015–9. doi:10.4065/75.10.1015. PMID 11040849.
- Waldholtz BD, Andersen AE (1990). "Gastrointestinal symptoms in anorexia nervosa. A prospective study". Gastroenterology 98 (6): 1415–9. PMID 2338185.
- 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.
- van Nieuw Amerongen A, Vissink A (2001). "[Oral complications of anorexia nervosa, bulimia nervosa and other metabolic disorders]". Nederlands Tijdschrift Voor Tandheelkunde (in Dutch) 108 (6): 242–7. PMID 11441717.
- 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.
- 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.
- 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.
- 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.
- 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.
- Golden NH (2003). "Osteopenia and osteoporosis in anorexia nervosa". Adolescent Medicine 14 (1): 97–108. PMID 12529194.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- Allende LM, Corell A, Manzanares J, Madruga D, Marcos A, Madroño A, López-Goyanes A, García-Pérez MA, Moreno JM, Rodrigo M, Sanz F, Arnaiz-Villena A (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.
- Carlson, Neil R. (2011) Foundations of Behavioral Neuroscience. 8h ed. Boston, MA: Allyn & Bacon, ISBN 0-205-79035-6.
- Schleimer, Kari (1981). "Anorexia Nervosa". Nutrition Reviews 39 (2): 99. doi:10.1111/j.1753-4887.1981.tb06739.x.
- "Anorexia, Bulimia" 1 (1). 2003. pp. 86–92.
- 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.
- Gillberg, C. (1983). "Are autism and anorexia nervosa related?". The British Journal of Psychiatry 142 (4): 428b. doi:10.1192/bjp.142.4.428b.
- Gillberg, C. (1985). "Autism and anorexia nervosa: Related conditions". Nordisk Psykiatrisk Tidskrift 39 (4): 307–312. doi:10.3109/08039488509101911.
- Rothery DJ, Garden GM (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.
- Gillberg, C. and Rastam, M. (1992). "Do some cases of anorexia nervosa reflect underlying autistic-like conditions?". Behavioural neurology 5 (1): 27–32. doi:10.1155/1992/259318. PMID 24487658.
- Gillberg IC, Råstam M, Gillberg C (February 1995). "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.
- Gillberg IC, Gillberg C, Råstam M, Johansson M (February 1996). "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.
- 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.
- Nilsson EW, Gillberg C, Gillberg IC, Råstam M (November 1999). "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.
- Wentz E, Gillberg C, Gillberg IC, Råstam M (July 2001). "Ten-year follow-up of adolescent-onset anorexia nervosa: psychiatric disorders and overall functioning scales". J Child Psychol Psychiatry 42 (5): 613–22. doi:10.1017/S0021963001007284. PMID 11464966.
- Råstam M, Gillberg C, Wentz E (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.
- Wentz E, Lacey JH, Waller G, Råstam M, Turk J, Gillberg C (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.
- Wentz E, Gillberg IC, Anckarsäter H, Gillberg C, Råstam M (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.
- Fisman S, Steele M, Short J, Byrne T, Lavallee C (July 1996). "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. PMID 8768355.
- Kerbeshian J, Burd L (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. PMID 18609437.
- Gillberg IC, Råstam M, Wentz E, Gillberg C (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.
- Hambrook D, Tchanturia K, Schmidt U, Russell T, Treasure J (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.
- Lopez C, Tchanturia K, Stahl D, Booth R, Holliday J, Treasure J (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.
- Russell TA, Schmidt U, Doherty L, Young V, Tchanturia K (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. PMID 19467562.
- Zastrow A, Kaiser S, Stippich C, Walther S, Herzog W, Tchanturia K, Belger A, Weisbrod M, Treasure J, Friederich HC (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.
- 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.
- Whitney J, Easter A, Tchanturia K (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.
- Treasure J (2013). "Coherence and other autistic spectrum traits and eating disorders: Building from mechanism to treatment. The Birgit Olsson lecture". Nordic Journal of Psychiatry 67 (1): 38–42. doi:10.3109/08039488.2012.674554. PMID 22468644.
- Diagnostic and Statistical Manual of Mental Disorders. eatingdisorders.org.au
- Yale, Susan Nolen-Hoeksema, (2014). Abnormal psychology (Sixth ed.). McGraw-Hill Humanities/Social Sciences/Languages. p. 339. ISBN 0078035384.
- "ICD-10:". who.int
- "CBC". MedlinePlus : U.S. National Library of Medicine. Retrieved 31 May 2013.
- Urinalysis at Medline. Nlm.nih.gov (2012-01-26). Retrieved on 2012-02-04.
- Chem-20 at Medline. Nlm.nih.gov. Retrieved on 2012-02-04.
- 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.
- 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]". Nippon Naibunpi Gakkai Zasshi (in Japanese) 62 (5): 631–48. PMID 3525245.
- 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.
- 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.
- 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.
- 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.
- 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.
- BUN at Medline. Nlm.nih.gov (2012-01-26). Retrieved on 2012-02-04.
- 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.
- 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.
- Nelsen DA (2002). "Gluten-sensitive enteropathy (celiac disease): more common than you think". American Family Physician 66 (12): 2259–66. PMID 12507163.
- 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. doi:10.5414/cnp62465. PMID 15630907.
- Electroencephalogram at Medline. Nlm.nih.gov (2012-01-26). Retrieved on 2012-02-04.
- 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. doi:10.1177/155005949502600309. PMID 7554305.
- 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.
- 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.
- 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.
- Thambirajah, M. S. (2007). Case Studies in Child and Adolescent Mental Health. Radcliffe Publishing. p. 145. ISBN 978-1-85775-698-2. OCLC 84150452.
- 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.
- Støving RK, Hansen-Nord M, Hangaard J, Hagen C (1996). "[Neuroendocrine disorders in anorexia nervosa—primary or secondary?]". Ugeskrift for Laeger (in Danish) 158 (49): 7052–6. PMID 8999610.
- Brandenburg BM, Andersen AE (2007). "Unintentional onset of anorexia nervosa". Eating and Weight Disorders 12 (2): 97–100. doi:10.1007/bf03327584. PMID 17615494.
- Nygaard JA (1990). "Anorexia nervosa. Treatment and triggering factors". Acta Psychiatrica Scandinavica. Supplementum 361: 44–9. doi:10.1111/j.1600-0447.1990.tb10754.x. PMID 2291425.
- Schacter et Al. Psychology 2nd Edition. 2011 p. 330.
- 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.
- 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.
- 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.
- 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.
- 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.
- Study with over 30,000 twins. (Bulik et al., 2006)
- Nolen-Hoeksema, Susan. Abnormal Psychology, 6/e. (p. 361) ISBN 978–0–07–803538–8 Yale University: McGraw-Hill Higher Education, 2014. Print.
- 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.
- Urwin RE, Bennetts B, Wilcken B, Lampropoulos B, Beumont P, Clarke S, Russell J, Tanner S, Nunn KP (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.
- Frieling H, Römer KD, Scholz S, Mittelbach F, Wilhelm J, De Zwaan M, Jacoby GE, Kornhuber J, Hillemacher T, Bleich S (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.
- Epigenetic Downregulation of Atrial Natriuretic Peptide but not Vasopressin mRNA Expression in Females with Eating Disorders is Related to Impulsivity
- 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". Int J Eat Disord. 37 Suppl (S1): S15–9; discussion S20–1. doi:10.1002/eat.20109. PMID 15852312.
- Bergen AW, Yeager M, Welch RA, Haque K, Ganjei JK, van den Bree MB, Mazzanti C, Nardi I, Fichter MM, Halmi KA, Kaplan AS, Strober M, Treasure J, Woodside DB, Bulik CM, Bacanu SA, Devlin B, Berrettini WH, Goldman D, Kaye WH (2005). "Association of multiple DRD2 polymorphisms with anorexia nervosa". Neuropsychopharmacology 30 (9): 1703–10. doi:10.1038/sj.npp.1300719. PMID 15920508.
- 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.
- Bosanac P, Norman T, Burrows G, Beumont P; Norman; Burrows; Beumont (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.
- Bergh C, Södersten P (1996). "Anorexia nervosa, self–starvation and the reward of stress". Nature Medicine 2 (1): 21–22. doi:10.1038/nm0196-21. PMID 8564826.
- Kaye WH, Frank GK, Bailer UF, Henry SE, Meltzer CC, Price JC, Mathis CA, Wagner A (2005). "Serotonin alterations in anorexia and bulimia nervosa: new insights from imaging studies". Physiol. Behav. 85 (1): 73–81. doi:10.1016/j.physbeh.2005.04.013. PMID 15869768.
- 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.
- Lee Y, Lin PY (2010). "Association between serotonin transporter gene polymorphism and eating disorders: A meta-analytic study". International Journal of Eating Disorders 43 (6): 498–504. doi:10.1002/eat.20732. PMID 19708070.
- 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.
- 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.
- 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.
- 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.
- Takagi K, Legrand R, Asakawa A, Amitani H, François M, Tennoune N, Coëffier M, Claeyssens S, do Rego JC, Déchelotte P, Inui A, Fetissov SO (2013). "Anti-ghrelin immunoglobulins modulate ghrelin stability and its orexigenic effect in obese mice and humans". Nature Communications 4: 2685. Bibcode:2013NatCo...4E2685T. doi:10.1038/ncomms3685. PMC 3826639. PMID 24158035. 2685.
- Davis JF, Choi DL, Benoit SC (2011). "24. Orexigenic Hypothalamic Peptides Behavior and Feeding - 24.5 Orexin". In Preedy VR, Watson RR, Martin CR. Handbook of Behavior, Food and Nutrition. Springer. pp. 361–2. ISBN 9780387922713.
- 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.
- Fetissov SO, Harro J, Jaanisk M, Järv A, Podar I, Allik J, Nilsson I, Sakthivel P, Lefvert AK, Hökfelt T (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. Bibcode:2005PNAS..10214865F. doi:10.1073/pnas.0507204102. PMC 1253594. PMID 16195379.
- Swedo SE, Leckman JF, Rose NR (2012). "From Research Subgroup to Clinical Syndrome: Modifying the PANDAS Criteria to Describe PANS (Pediatric Acute-onset Neuropsychiatric Syndrome)". Pediatr Therapeut. 2 (2). doi:10.4172/2161-0665.1000113.
- Shay NF, Mangian HF (2000). "Neurobiology of zinc-influenced eating behavior". The Journal of Nutrition 130 (5S Suppl): 1493S–9S. PMID 10801965.
- Herpertz-Dahlmann, B; Bühren, K; Remschmidt, H (2013). "Growing up is hard: Mental disorders in adolescence". Deutsches Arzteblatt international 110 (25): 432–9; quiz 440. doi:10.3238/arztebl.2013.0432 (inactive 2014-12-20). PMC 3705204. PMID 23840288.
- Williamson, L (1998). "Eating disorders and the cultural forces behind the drive for thinness: Are African American women really protected?". Social Work in Health Care 28 (1): 61–73. doi:10.1300/J010v28n01_04. PMID 9711686.
- Botelho, Linda J. (2008) "Risk factors contributing to the development and maintenance of Anorexia Nervosa: A meta-analysis." Thesis, University of the Rockies.
- Williamson, L (1998). "Eating disorders and the cultural forces behind the drive for thinness: Are African American women really protected?". Social Work in Health Care 28 (1): 61–73. doi:10.1300/J010v28n01_04. PMID 9711686.
- Gilbert, Stefanie C. (2006). "Eating Disorders in Women of Color". Clinical Psychology: Science and Practice 10 (4): 444. doi:10.1093/clipsy.bpg045.
- Dinicola, V. F. (1990). "Anorexia Multiforme: Self-Starvation in Historical and Cultural Context: Part II: Anorexia Nervosa as a Culture-Reactive Syndrome1". Transcultural Psychiatry 27 (4): 245–226. doi:10.1177/136346159002700401.
- 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.
- 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.
- Anderson-Fye, Eileen P. and Becker, Anne E. (2004) "Sociocultural Aspects of Eating Disorders" pp. 565-89 in Handbook of Eating Disorders and Obesity, J. Kevin (ed.). Thompson. Hoboken, NJ: John Wiley & Sons.
- Baum, Antonia (2006). "Eating Disorders in the Male Athlete". Sports medicine (Auckland, N.Z.) 36 (1): 1–6. PMID 16445307.
- 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.
- Zonnevijlle-Bender MJ, van Goozen SH, Cohen-Kettenis PT, 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.
- Wonderlich, Stephen A.; Brewerton, Timothy D.; Jocic, Zeljko; Dansky, Bonnie S.; Abbott, David W. (1997). "Relationship of Childhood Sexual Abuse and Eating Disorders". Journal of the American Academy of Child & Adolescent Psychiatry 36 (8): 1107. doi:10.1097/00004583-199708000-00018.
- Connors, M. E.; Morse, W (1993). "Sexual abuse and eating disorders: A review". The International journal of eating disorders 13 (1): 1–11. PMID 8477269.
- Garner, D. M.; Garfinkel, P. E. (1980). "Socio-cultural factors in the development of anorexia nervosa". Psychological medicine 10 (4): 647–56. PMID 7208724.
- Labre, M. P. (2002). "Adolescent boys and the muscular male body ideal". The Journal of adolescent health : official publication of the Society for Adolescent Medicine 30 (4): 233–42. PMID 11927235.
- Murray, Stuart B.; Rieger, Elizabeth; Hildebrandt, Tom; Karlov, Lisa; Russell, Janice; Boon, Evelyn; Dawson, Robert T.; Touyz, Stephen W. (2012). "A comparison of eating, exercise, shape, and weight related symptomatology in males with muscle dysmorphia and anorexia nervosa". Body Image 9 (2): 193. doi:10.1016/j.bodyim.2012.01.008. PMID 22391410.
- Norris, M. L.; Boydell, K. M.; Pinhas, L; Katzman, D. K. (2006). "Ana and the Internet: A review of pro-anorexia websites". International Journal of Eating Disorders 39 (6): 443–7. doi:10.1002/eat.20305. PMID 16721839.
- 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.
- 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. doi:10.1007/bf03327480. PMID 10941603.
- 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.
- 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.
- 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.
- 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.
- Gaudio S, Di Ciommo V (2011). "Prevalence of personality disorders and their clinical correlates in outpatient adolescents with anorexia nervosa". Psychosomatic Medicine 73 (9): 769–74. doi:10.1097/PSY.0b013e318235b9b5. PMID 22042882.
- 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.
- Root TL, Pinheiro AP, Thornton L, Strober M, Fernandez-Aranda F, Brandt H, Crawford S, Fichter MM, Halmi KA, Johnson C, Kaplan AS, Klump KL, La Via M, Mitchell J, Woodside DB, Rotondo A, Berrettini WH, Kaye WH, Bulik CM (2010). "Substance Use Disorders in Women with Anorexia Nervosa". International Journal of Eating Disorders 43 (1): 14–21. doi:10.1002/eat.20670. PMC 2807480. PMID 19260043.
- Pérez, Inmaculada; Del Río Sánchez, C; Borda Mas, M (2008). "MCMI-II borderline personality disorder in anorexia and bulimia nervosa". Psicothema 20 (1): 138–143. PMID 18206076.
- Halmi, Katherine A.; Sunday, Suzanne R.; Strober, Michael; Kaplan, Alan; Woodside, D. Blake; Fichter, Manfred; Treasure, Janet; Berrettini, Wade H.; Kaye, Walter H. (2000). "Perfectionism in Anorexia Nervosa: Variation by Clinical Subtype, Obsessionality, and Pathological Eating Behavior". Am J Psychiatry 157 (11): 1799–805. doi:10.1176/appi.ajp.157.11.1799. PMID 11058477.
- Crane, Anna (2007). "Are Obsessive-Compulsive Personality Traits Associated with a Poor Outcome in Anorexia Nervosa? A Systematic Review of Randomized Controlled Trials and Naturalistic Outcome Studies". International Journal of Eating Disorders. doi:10.1002/eat (inactive 2014-12-20). PMID 17607713.
- 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.
- 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.
- Bulik CM, Klump KL, Thornton L, Kaplan AS, Devlin B, Fichter MM, Halmi KA, Strober M, Woodside DB, Crow S, Mitchell JE, Rotondo A, Mauri M, Cassano GB, Keel PK, Berrettini WH, Kaye WH (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.
- Larsson JO, Hellzén M (2004). "Patterns of personality disorders in women with chronic eating disorders". Eating and Weight Disorders 9 (3): 200–5. doi:10.1007/bf03325067. PMID 15656014.
- 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.
- 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.
- 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. PMC 3272757. PMID 16841619.
- 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.
- Mikami AY, Hinshaw SP, Arnold LE, Hoza B, Hechtman L, Newcorn JH, Abikoff HB (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.
- 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.
- 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.
- 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.
- 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. doi:10.1212/01.WNL.0000069607.30528.D5. PMID 12847173.
- Phillips KA, McElroy SL, Keck PE, Hudson JI, Pope HG (1994). "A comparison of delusional and nondelusional body dysmorphic disorder in 100 cases". Psychopharmacol Bull. 30 (2): 179–86. PMID 7831453.
- 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.
- 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. PMC 3836287. PMID 18314401.
- Nolen-Hoeksema, Susan (2014). Abnormal Psychology (6th edition). New York: McGraw-Hill Education. p. 341. ISBN 978-0-07-803538-8.
- Lock JD, Fitzpatrick KK (2009). "Anorexia nervosa". Clinical evidence 2009: 1011. PMC 2907776. PMID 19445758.
- National Institute of Mental Health. "Anorexia Nervosa".
- Lock JD, Fitzpatrick KK (10 March 2009). "Anorexia nervosa". Clinical Evidence 2009 (3): 1011. PMC 2907776. PMID 19445758.
- Carlson N., Heth C., Miller Harold, Donahoe John, Buskist William, Martin G., Schmaltz Rodney (2007). Psychology: the science of behaviour-4th Canadian ed. Toronto, ON: Pearson Education Canada. p. 297. ISBN 978-0-205-64524-4.
- Whitnet, E. and Rolfes, S. R. (2011). Understanding Nutrition United States: Wadsworth Cengage Learning, ISBN 1-133-58752-6.
- Bakan R, Birmingham CL, Aeberhardt L, Goldner EM (1993). "Dietary zinc intake of vegetarian and nonvegetarian patients with anorexia nervosa". The International Journal of Eating Disorders 13 (2): 229–233. doi:10.1002/1098-108X(199303)13:2<229::AID-EAT2260130211>3.0.CO;2-1. PMID 8477292.
- Shay NF, Mangian HF (2000). "Neurobiology of zinc-influenced eating behavior". The Journal of nutrition 130 (5S Suppl): 1493S–1499S. PMID 10801965.
- Yager J, Andersen AE (2005). "Anorexia Nervosa". New England Journal of Medicine 353 (14): 1481–1488. doi:10.1056/NEJMcp050187. PMID 16207850.
- 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.
- 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.
- McNamara RK, Able J, Jandacek R, Rider T, Tso P, Eliassen JC, Alfieri D, Weber W, Jarvis K, DelBello MP, Strakowski SM, Adler CM (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.
- 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.
- 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.
- Breen HB, Espelage DL (2004). "Nutrition expertise in eating disorders". Eating and Weight Disorders 9 (2): 120–5. doi:10.1007/bf03325055. PMID 15330079.
- 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.
- 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.
- 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.
- Brambilla F, Garcia CS, Fassino S, Daga GA, Favaro A, Santonastaso P, Ramaciotti C, Bondi E, Mellado C, Borriello R, Monteleone P (2007). "Olanzapine therapy in anorexia nervosa: psychobiological effects". International Clinical Psychopharmacology 22 (4): 197–204. doi:10.1097/YIC.0b013e328080ca31. PMID 17519642.
- 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.
- Maglione M, Maher AR, Hu J et al. (2011). "Off-Label Use of Atypical Antipsychotics: An Update". PMID 22132426.
- Robin AL, Gilroy M, Dennis AB (1998). "Treatment of eating disorders in children and adolescents". Clinical Psychology Review 18 (4): 421–446. doi:10.1016/S0272-7358(98)00013-0. PMID 9638356.
- 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.
- 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.
- Gore, S. A.; Vander Wal, J. S.; Thelen, M. H. (2001). "Treatment of eating disorders in children and adolescents". Body image, eating disorders, and obesity in youth: Assessment, prevention, and treatment. p. 293. doi:10.1037/10404-012. ISBN 1-55798-758-0.
- 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.
- "Eating Disorders". National Institute of Mental Health (NIMH). 2011. Retrieved 29 September 2013.
- "Couples Therapy Helps Combat Anorexia Nervosa". Eating Disorders Review 23 (6). 2012.
- 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.
- 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.
- 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.
- 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.
- 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.
- NIMH · Eating Disorders. Nimh.nih.gov (2011-08-23). Retrieved on 2012-02-04.
- Studies – Eating Disorders Program – Stanford University School of Medicine. Edresearch.stanford.edu (2008-06-20). Retrieved on 2012-02-04.
- 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.
- Shaw, Gina. Anorexia: The Body Neglected. Webmd.com. Retrieved on 2013-04-29.
- 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.
- Morris J, Twaddle S (2007). "Anorexia nervosa". BMJ 334 (7599): 894–898. doi:10.1136/bmj.39171.616840.BE. PMC 1857759. PMID 17463461.
- 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.
- Gelder, Michael; Mayou, Richard and Geddes, John (2005) Psychiatry, Oxford; New York: Oxford University Press, ISBN 0-19-852863-9.
- 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". International Journal of Eating Disorders 22 (4): 339–360. doi:10.1002/(SICI)1098-108X(199712)22:4<339::AID-EAT1>3.0.CO;2-N. PMID 9356884.
- Nicholls, Dasha; Stanhope, Richard (2000). "Medical complications of anorexia nervosa in children and young adolescents". European Eating Disorders Review 8 (2): 170. doi:10.1002/(SICI)1099-0968(200003)8:2<170::AID-ERV338>3.0.CO;2-Y.
- Prabhakaran R, Misra M, Miller KK, Kruczek K, Sundaralingam S, Herzog DB, Katzman DK, Klibanski A (2008). "Determinants of Height in Adolescent Girls with Anorexia Nervosa". Pediatrics 121 (6): e1517–e1523. doi:10.1542/peds.2007-2820. PMID 18519455.
- Nelson LR, Bulun SE (2001). "Estrogen production and action". J. Am. Acad. Dermatol. 45 (3 Suppl): S116–24. doi:10.1067/mjd.2001.117432. PMID 11511861.
- Carter, Shea L. (2008). "The genetic basis of human height : the role of estrogen".
- "Anorexia nervosa may not stunt growth, short term". Reuters. 2008-06-06.
- Pfeiffer, R. J.; Lucas, A. R.; Ilstrup, D. M. (1986). "Effect of anorexia nervosa on linear growth". Clinical pediatrics 25 (1): 7–12. PMID 3943254.
- "Core interventions in the treatment and management of anorexia nervosa, bulimia nervosa and related eating disorders". National Collaborating Centre for Mental Health. 2004.
- Saul, S. H.; Dekker, A; Watson, C. G. (1981). "Acute gastric dilatation with infarction and perforation. Report of fatal outcome in patient with anorexia nervosa". Gut 22 (11): 978–83. PMC 1419461. PMID 7308853.
- Eating disorders – Complications of Anorexia. University of Maryland Medical Center (2012-12-03). Retrieved on 2013-04-29.
- Nolen-Hoeksema, Susan. (2013). Abnormal psychology (6th ed.). New York, NY: McGraw-Hill Education.
- Schebendach J, Mayer LE, Devlin MJ, Attia E, Walsh BT (2012). "Dietary energy density and diet variety as risk factors for relapse in anorexia nervosa: A replication". International Journal of Eating Disorders 45 (1): 79–84. doi:10.1002/eat.20922. PMID 21448937.
- Halmi, K. A.; Mitchell, J.; Agras, S. (1996). "Anorexia nervosa: Prevention of relapse". Biological Psychiatry 39 (7): 666. doi:10.1016/0006-3223(96)84502-1.
- "Tackling Relapse Among Anorexia Nervosa Patients". Eating Disorders Review 24 (1). 2013.
- Treasure J, Claudino AM, Zucker N (2010). "Eating disorders". Lancet 375 (9714): 583–93. doi:10.1016/S0140-6736(09)61748-7. PMID 19931176.
- 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.
- Bulik CM, Sullivan PF, Tozzi F, Furberg H, Lichtenstein P, Pedersen NL (2006). "Prevalence, Heritability, and Prospective Risk Factors for Anorexia Nervosa". Archives of General Psychiatry 63 (3): 305–312. doi:10.1001/archpsyc.63.3.305. PMID 16520436.
- Zanetti, Tatiana (2013). "Epidemiology of Eating Disorders". Eating Disorders and the Skin. pp. 9–15. doi:10.1007/978-3-642-29136-4_2. ISBN 978-3-642-29135-7.
- Smink FR, van Hoeken D, Hoek HW (2012). "Epidemiology of Eating Disorders: Incidence, Prevalence and Mortality Rates". Current Psychiatry Reports 14 (4): 406–414. doi:10.1007/s11920-012-0282-y. PMC 3409365. PMID 22644309.
- Williams, P.; King, M. (1987). "The "epidemic" of Anorexia Nervosa: Another Medical Myth?". The Lancet 329 (8526): 205–7. doi:10.1016/S0140-6736(87)90015-8. PMID 2880028.
- Williams P, King M (1987). "The "epidemic" of anorexia nervosa: another medical myth?". Lancet 329 (8526): 205–7. doi:10.1016/S0140-6736(87)90015-8. PMID 2880028.
- Roux H, Chapelon E, Godart N (2013). "[Epidemiology of anorexia nervosa: a review]". L'Encéphale (in French) 39 (2): 85–93. doi:10.1016/j.encep.2012.06.001. PMID 23095584.
- The relationship between eating disordered behaviors, body image dissatisfaction, depression, and socioeconomic status among African-American women. ISBN 9780542160776
- "Potential Stressors Contributing to Eating Disorder Symptoms in African American Women: Implications for Mental Health Counselors". Journal of Mental Health Counseling. 28(4): 338-352.
- Becker, Anne E. "Sociocultural Aspects of Eating Disorders." Special Topics. By Eileen P. Anderson-Fye. N.p.: n.p., n.d. 565-80. Print.
- Bonci, C. M.; Bonci, L. J.; Granger, L. R.; Johnson, C. L.; Malina, R. M.; Milne, L. W.; Ryan, R. R.; Vanderbunt, E. M. (2008). "National athletic trainers' association position statement: Preventing, detecting, and managing disordered eating in athletes". Journal of Athletic Training 43 (1): 80–108. doi:10.4085/1062-6050-43.1.80. PMC 2231403. PMID 18335017.
- Andersen, Arnold E.; Didomenico, Lisa (1992). "Diet vs. Shape content of popular male and female magazines: A dose-response relationship to the incidence of eating disorders?". International Journal of Eating Disorders 11 (3): 283. doi:10.1002/1098-108X(199204)11:3<283::AID-EAT2260110313>3.0.CO;2-O.
- Rikani, A. A.; Choudhry, Z; Choudhry, A. M.; Ikram, H; Asghar, M. W.; Kajal, D; Waheed, A; Mobassarah Nj Ph, D (2013). "A critique of the literature on etiology of eating disorders". Annals of Neurosciences 20 (4): 157–161. doi:10.5214/ans.0972.7531.200409. PMC 4117136. PMID 25206042.
- Gull WW (1997). "Anorexia nervosa (apepsia hysterica, anorexia hysterica). 1868". Obesity Research 5 (5): 498–502. doi:10.1002/j.1550-8528.1997.tb00677.x. PMID 9385628.
- Costin, Carolyn (1999). The Eating Disorder Sourcebook. Linconwood: Lowell House. p. 6. ISBN 0-585-18922-6.
- Pearce JM (2004). "Richard Morton: Origins of Anorexia nervosa". European Neurology 52 (4): 191–192. doi:10.1159/000082033. PMID 15539770.
- Hepworth, Julie (1999) The Social Construction of Anorexia Nervosa. Thousand Oaks, CA: Sage Publications, ISBN 0-7619-5309-4.
- McSherry JA (1985). "Was Mary, Queen of Scots, anorexic?". Scottish medical journal 30 (4): 243–5. PMID 3912990.
- Sir William Withey Gull (1894). T D Acland, ed. Medical Papers. p. 309.
- Kendall, Joshua C. (2011). The Forgotten Founding Father: Noah Webster's Obsession and the Creation of an American Culture. Penguin. p. 368. ISBN 978-0-399-15699-1.
- Arnold, Carrie (2012) Decoding Anorexia: How Breakthroughs in Science Offer Hope for Eating Disorders, Routledge Press. ISBN 0415898676
- Birmingham CL, Su J, Hlynsky JA, Goldner EM, Gao M (2005). "The mortality rate from anorexia nervosa". International Journal of Eating Disorders 38 (2): 143–146. doi:10.1002/eat.20164. PMID 16134111.
- Heath, Chris (22 Jan 1998). "The Caged Birds Sings". Rolling Stone 778.
- Katrandjian, Olivia (3 Nov 2010). "Portia de Rossi: "I would strave myself daily"". ABC news. Retrieved 23 October 2012.
- Mirror.co.uk (7 April 2006). "Calista Flockhart Exclusive: I Did Have an Eating Problem". Daily Mirror, UK.
- Sporkin, Elizabeth (17 February 1992). "A Terrible Hunger". People Magazine 37 (6).
- Dumas, Daisy (29 November 2011). "Anorexia would have killed me". Daily Mail UK (London: Daily Mail UK).
- Soriano, César G. (2004-06-22). "Mary-Kate Olsen seeks treatment for eating disorder". USA Today. Retrieved 23 October 2012.
- Felts, Susannah. "How Alanis Morissette Beat Her Eating Disorder How Alanis Morissette Beat Her Eating Disorder". Health Magazine. Retrieved 23 October 2012.
- National Association of Anorexia Nervosa and Associated Disorders
- International Eating Disorder Referral and Information Center
- Anorexia nervosa
- Society of Clinical Child and Adolescent Psychology – What is Anorexia Nervosa?