"Anorexic" redirects here. For the use of the term as an appetite suppressant, see Anorectic.
This article has multiple issues. Please help improve it or discuss these issues on the talk page.
This article needs more medical references for verification or relies too heavily on primary sources. Please review the contents of the article and add the appropriate references if you can. Unsourced or poorly sourced material may be removed.(December 2013)
This article may lend undue weight to certain ideas, incidents, controversies or matters relative to the article subject as a whole. Please help to create a more balanced presentation. Discuss and resolve this issue before removing this message.(December 2013)
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
Anorexia nervosa is an eating disorder characterized by immoderate food restriction and irrational fear of gaining weight, as well as a distorted body self-perception. It typically involves excessive weight loss and usually occurs more in females than in males. Because of the fear of gaining weight, people 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 people with anorexia nervosa do not, in fact, lose their appetites. Patients with anorexia nervosa may experience dizziness, headaches, drowsiness and a lack of energy.
Anorexia nervosa is characterized by low body weight, inappropriate eating habits, obsession with having a thin figure, and the fear of gaining weight. It 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 her or his body, food and eating. People with anorexia often view themselves as "too fat" even if they are already underweight.
Anorexia nervosa most often has its onset in adolescence and is more prevalent among adolescent females than adolescent males.
People with anorexia nervosa continue to feel hunger, but they deny themselves all but very small quantities of food. The average caloric intake of a person with anorexia nervosa is 600–800 calories per day, but extreme cases of complete self-starvation are known. It is a serious health condition with a high incidence of comorbidity and similarly high mortality rates to serious psychiatric disorders. People with anorexia have extremely high levels of ghrelin (the hunger hormone that signals a physiological need for food) in their blood. The high levels of ghrelin suggests that their bodies are desperately trying to make them hungry; however, that hunger call is being suppressed, ignored, or overridden.
Anorexia nervosa is an eating disorder that is characterized by attempts to lose weight, sometimes to the point of 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.
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.
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.
Perception of self to be overweight despite being told by others they are too thin and, in most cases, underweight.
Becomes intolerant to cold and frequently complains of being cold from loss of insulating body fat or poor circulation resulting from extremely low blood pressure; body temperature lowers (hypothermia) in effort to conserve energy
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 could distract them from their desire for food (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.
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 prior to attaining 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 been frequently 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
Death (Anorexia nervosa has the highest rate of mortality of any psychological disorder)
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.
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 dopaminergicneurotransmission and Atrial natriuretic peptidehomeostasis 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.
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.
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.
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.
Sociocultural studies have highlighted the role of cultural factors, such as the promotion of thinness as the ideal female form in Western industrialized nations, particularly through the media. There is a necessary connection between anorexia nervosa and culture and whether culture is a cause, a trigger, or merely a kind of social address or envelope which determines in which segments of society or in which cultures anorexia nervosa will appear. The strong thesis of this connection is that culture acts as a cause by providing a blueprint for anorexia nervosa. A moderate thesis is that a specific cultural factors trigger the illness which is determined by many factors including family interactions, individual psychology, or biological predisposition. Culture change can trigger the emergence of anorexia in adolescent girls from immigrant families living in highly industrialized Western Societies. 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.
Anorexia nervosa is more likely to occur in a person's pubertal years, especially for girls. Female students are 10 times more likely to suffer from anorexia nervosa than male students. According to a survey of 1799 Japanese female high school students, "85% who were a normal weight wanted to be thinner and 45% who were 10–20% underweight wanted to be thinner." Teenage girls concerned about their weight and who believe that slimness is more attractive among peers trend to weight-control behaviors. Teen girls are learning from each other to consume low-caloric, low-fat foods and diet pills. This results in lack of nutrition and a greater chance of developing anorexia nervosa.
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 sexual abuse or dysfunctional families. Some studies reported a high rate of reported child sexual abuse experiences in clinical groups of who have been diagnosed with anorexia. One found that women with a history of eating disorders were twice as likely to have reported childhood sexual abuse compared to women with no history of eating disorders. The joint effect of both physical and sexual abuse resulted in a nearly 4-fold risk of eating disorders that met DSM-IV criteria. The conclusion was that links between childhood abuse and sexual abuse are complex, such as by influencing psychologic processes that increase a woman's susceptibility to the development of an eating disorder, or perhaps by producing changes in psychobiologic process and neurotransmitting function, associated with eating behaviour.
In contrast to the above, a metastudy of published research examining causes of anorexia find no conclusive link between abuse, parenting and eating disorders. The American Psychiatric Association writes: "No evidence exists to prove that families cause eating disorders."
Efforts have been made to dispel some of the myths around anorexia nervosa and eating disorders, such as the misconception that families, in particular mothers, are responsible for their daughter developing an eating disorder.
There is no evidence that the media is a cause of eating disorders, and advances in neuroscience point to a more complex combination of genetic and environmental influences.
Mass media interventions frequently offer a distorted vision of the world, and it may be difficult for children and adolescents to distinguish whether what they see is real or not, so that they are more vulnerable to the messages transmitted. Field, Cheung, et al.'s survey of 548 preadolescent and adolescent girls found that 69% acknowledged that images in magazines had influenced their conception of the ideal body, while 47% reported that they wanted to lose weight after seeing such images. There was also the survey by Utter et al. who studied 4,746 adolescent boys and girls demonstrating the tendency of magazine articles and advertisements to activate weight concerns and weight management behaviour. He discovered that girls who frequently read fashion and glamour magazines and girls who frequently read articles about diets and issues related to weight loss were seven times more likely to practice a range of unhealthy weight control behaviours and six times more likely to engage in extremely unhealthy weight control behaviours (e.g., taking diet pills, vomiting, using laxatives, and using diuretics) from magazines, websites that stress the message of thinness as the ideal have surfaced the internet and has managed to embed itself as an increasing source of influence. The possibility that pro-anorexia websites may reinforce restrictive eating and exercise behaviours is an area of concern. Pro-anorexia websites contain images and writing that support the pursuit of an ideal thin body image. Research has shown that these websites stress thinness as the ideal choice for women and in some websites ideal images of muscularity and thinness for men It has also been shown that women who had viewed these websites at least once had a decrease in self-esteem and reports also show an increased likelihood of future engagement in many negative behaviours related to food, exercise, and weight. Evidence of the value of thinness in majority U.S culture is found in Hollywood's elite and the media promotion of waif models in fashion and celebrity circles (e.g. Nicole Richie, Mary Kate Olsen, Kate Moss, and Lady Gaga).
Relationship to autism
A summary of the strategy Zucker et al. (2007) used to assess the relationship between anorexia nervosa and the autism spectrum.
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 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.
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, Crohn's Disease
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 used primarily to test kidney function. A low BUN level may indicate the effects of malnutrition.
Not only does starvation result in physical complications, but mental complications as well. 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.
Anorexia nervosa is classified as an Axis I disorder in the Diagnostic and Statistical Manual of Mental Health Disorders (DSM-IV), published by the American Psychiatric Association. The DSM-IV should not be used by laypersons to diagnose themselves.
DSM-IV has now been replaced by DSM-5 DSM-5. There are important changes to the criteria for anorexia nervosa and other eating disorders. Note that the following discussion concerns DSM-IV.
DSM-IV-TR: diagnostic criteria for AN includes intense fear of gaining weight, a refusal to maintain body weight above 85% of the expected weight for a given age and height, and three consecutive missed periods and either refusal to admit the seriousness of the weight loss, or undue influence of shape or weight on one's self-image, or a disturbed experience in one's shape or weight. There are two types: the binge-eating/purging type is characterized by overeating or purging, and the restricting type is not.
Criticism of DSM-IV There have been criticisms over various aspects of the diagnostic criteria utilized for anorexia nervosa in the DSM-IV. Including the requirement of maintaining a body weight below 85% of the expected weight and the requirement of amenorrhea for diagnosis; some women have all the symptoms of AN and continue to menstruate. Those who do not meet these criteria are usually classified as eating disorder not otherwise specified; this may affect treatment options and insurance reimbursments. The validity of the AN subtype classification has also been questioned because of the considerable diagnostic overlap between the binge-eating/purging type and the restricting type and the propensity of the patient to switch between the two.
Criticisms of DSM-IV and Diagnosing Adolescents with Anorexia Nervosa – There have been criticisms over the diagnostic criteria utilized for anorexia nervosa in the DSM- IV and its applicability in diagnosing adolescents with anorexia nervosa. Several criticisms of the DSM-IV in diagnosing adolescents with anorexia nervosa are:
Fulfillment of DSM- IV criteria B and C for anorexia nervosa are dependent on complex abstract reasoning, the capacity to describe internal experiences, and the ability to perceive risk. While formal thought emerges between ages 11–13, complex abstract reasoning continues to develop late into adolescence. The ability to perceive risk also continues to develop through adolescence, as some preadolescents have difficult perceiving the relative risk of alternative outcomes. Adolescents and children must first develop these internal thought processes in order to then endorse fear of weight gain or distortion of body image, and deny the seriousness of low body weight despite their behaviors that contribute to harmful weight loss, which are necessary to fulfill criteria B and C. These developmental factors may impede an adolescent or child from receiving a diagnosis of anorexia nervosa. It is the hope of certain professionals that the DSM-V will take the unique developmental stages of children and adolescents into account when revising the current criteria. One proposed amendment would be to allow behavioral indicators as a means of substituting internally referenced cognitive criteria.
Another criticism focuses on the current weight criteria specified to receive a diagnosis of anorexia nervosa. Critics state that there is wide variability in the rate, timing and magnitude of both height and weight gain during normal puberty. Physical development varies greatly during puberty, making it a challenge to define an optimal weight range for a growing child or adolescents.
ICD-10: The criteria are similar, but in addition, specifically mention:
The ways that individuals might induce weight-loss or maintain low body weight (avoiding fattening foods, self-induced vomiting, self-induced purging, excessive exercise, excessive use of appetite suppressants or diuretics).
If onset is before puberty, that development is delayed or arrested.
There are various medical and psychological conditions that have been misdiagnosed as anorexia nervosa, in some cases the correct diagnosis was not made for more than ten years. In a reported case of achalasia misdiagnosed as AN, the patient spent two months confined to a psychiatric hospital.
There are various other psychological issues that may factor into anorexia nervosa, some fulfill the criteria for a separate Axis I diagnosis or a personality disorder which is coded Axis II and thus are considered comorbid to the diagnosed eating disorder. Axis II disorders are subtyped into 3 "clusters", A, B and C.The causality between personality disorders and eating disorders has yet to be fully established. 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 adolescents as well as in adults.
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. It is not unusual for a person with an eating disorder to "move through" various diagnoses as his or her behavior and beliefs change over time.
There is no conclusive evidence that any particular treatment for anorexia nervosa work 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% of the patients develop anorexia nervosa as a chronic disorder. If anorexia nervosa is not treated, serious complications such as heart conditions and kidney failure can initiate and eventually lead to death. "As many as 6 percent of people with the disorder die from causes related to it."
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 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 adapted 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, a hormone regulating hunger and metabolism, levels decrease from zinc deficiency and even more with patients 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. Unfortunately, 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) 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.
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 rate of BMI growth in patients with anorexia.
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
There are various forms of family-based treatment that have been proven to work in the treatment of adolescent AN including "conjoint family therapy" (CFT), in which the parents and child are seen together by the same therapist, "separated family therapy" (SFT) in which parents and child attend therapy separately with different therapists. "Eisler's cohort show that, irrespective of the type of FBT, 75% of patients have a good outcome, 15% an intermediate outcome ...". Proponents of Family therapy for adolescents with AN assert that it is important to include parents in the adolescent's treatment. A 4 to 5 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 in an intimate relationship to create power struggles 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, 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."
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, the results found that the average duration of anorexia nervosa is 1.7 years. "Contrary to what people may believe, anorexia is not necessarily a chronic illness; in many cases, it runs its course and people get better ..." 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 to the body.
In cases of adolescent anorexia nervosa that utilize family-based treatment 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", which prohibits the patient from many basic rights, such as using the bathroom independently, has been seen as catalysts in increasing weight and pushing patients away from the path to recovery.
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 1.8–14.1%. 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.
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-behaviorial therapy, as well as, 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 0.3–1% in women and 0.1% in men for the diagnosis in developed countries. The condition largely affects young adolescent women, with between 15 and 19 years old making up 40% of all cases. Approximately 75% of people with anorexia are female. 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. Hence changes in incidence reported before 1970 should be taken with some caution.
Two images of an anorexic female patient published in 1900 in "Nouvelle Iconographie de la Salpêtrière". The case was entitiled "Un cas de anorexia hysterique" (A case of hysteria anorexia).
The term anorexia nervosa was established 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 orexe (όρεξη, "appetite"), thus meaning a lack of desire to eat. However, while the term anorexia nervosa literally means "neurotic loss of appetite", the literal meaning of the term is somewhat misleading. Many anorexics enjoy eating and have not lost their appetites as the term loss of appetite is normally understood; it is more accurate to regard anorexia nervosa as a compulsion similar to fasting, rather than as a literal loss of appetite.
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 century. 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 to be widely accepted by the medical profession as a recognised condition. In 1873, Sir William Gull, one of Queen Victoria's personal physicians, published a seminal paper which established the term anorexia nervosa and provided a number of detailed case descriptions and treatments. However, Gull was unable to provide an explanation for anorexia nervosa. 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". In spite of major advances, in neuroscience, Bruch's theories tend to dominate popular thinking. A further important event was the death of the popular singer 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 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 on her 5'3 frame and she was hospitalized,Mary-Kate Olsen,Alanis Morissette, and French model Isabelle Caro, who died due to complications connected to anorexia.
^Hockenbury, Don and Hockenbury, Sandra (2008) Psychology, p. 593. Worth Publishers, New York. ISBN 978-1-4292-0143-8.
^ abCarlson 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. ISBN978-0-205-64524-4.
^Rosen JC, Reiter J, Orosan P (1995). "Assessment of body image in eating disorders with the body dysmorphic disorder examination". Behaviour Research and Therapy33 (1): 77–84. doi:10.1016/0005-7967(94)E0030-M. PMID7872941.
^Cooper MJ (2005). "Cognitive theory in anorexia nervosa and bulimia nervosa: progress, development and future directions". Clinical Psychology Review25 (4): 511–31. doi:10.1016/j.cpr.2005.01.003. PMID15914267.
^Brooks S, Prince A, Stahl D, Campell IC, Treasure J (2010). "A systematic review & meta-analysis of cognitive bias to food stimuli in people with disordered eating behaviour". Clinical Psychology31 (1): 37. doi:10.1016/j.cpr.2010.09.006.
^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 Psychology41 (Pt 3): 321–6. doi:10.1348/014466502760379172. PMID12396259.
^Kovacs D, Palmer RL (2004). "The associations between laxative abuse and other symptoms among adults with anorexia nervosa". The International Journal of Eating Disorders36 (2): 224–8. doi:10.1002/eat.20024. PMID15282693.
^Friedman EJ (1984). "Death from ipecac intoxication in a patient with anorexia nervosa". The American Journal of Psychiatry141 (5): 702–3. PMID6143508.
^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 Disorders31 (4): 370–5. doi:10.1002/eat.10042. PMID11948642.
^Lucka I (2004). "[Depression syndromes in patients suffering from anorexia nervosa]". Psychiatria Polska (in Polish) 38 (4): 621–9. PMID15518310.
^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-laryngology265 (9): 1095–102. doi:10.1007/s00405-008-0598-8. PMID18253742.
^McClure, G.M.; Timimi, Westman (1995). "Anorexia nervosa in early adolescence following illness — the importance of the sick role". Journal of Adolescence18 (3): 359. doi:10.1006/jado.1995.1025.Cite uses deprecated parameters (help)
^Chiarioni, Giuseppe; Bassotti, Gabrio; Monsignori, Antonella; Menegotti, Monica; Salandini, Lara; Di Matteo, Giorgio; Vantini, Italo; Whitehead, William E. (2000). "Anorectal dysfunction in constipated women with anorexia nervosa". Mayo Clinic Proceedings75 (10): 1015–9. doi:10.4065/75.10.1015. PMID11040849.
^Waldholtz BD, Andersen AE (1990). "Gastrointestinal symptoms in anorexia nervosa. A prospective study". Gastroenterology98 (6): 1415–9. PMID2338185.
^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. PMID11441717.
^Demaerel P, Daele MC, De Vuysere S, Wilms G, Baert AL (1996). "Orbital fat edema in anorexia nervosa: a reversible finding". American Journal of Neuroradiology17 (9): 1782–4. PMID8896638.
^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 Medicine31 (3): 325–31. PMID2308003.
^Golden NH (2003). "Osteopenia and osteoporosis in anorexia nervosa". Adolescent Medicine14 (1): 97–108. PMID12529194.
^Bahia A, Chu ES, Mehler PS (2010). "Polydipsia and hyponatremia in a woman with anorexia nervosa". The International Journal of Eating Disorders44 (2): 186–8. doi:10.1002/eat.20792. PMID20127934.
^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 Disorders44 (3): 281–3. doi:10.1002/eat.20806. PMID20186722.
^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". Neuroradiology43 (10): 838–40. doi:10.1007/s002340100589. PMID11688699.
^ abcPrabhakaran, R.; Misra, M.; Miller, K. K.; Kruczek, K.; Sundaralingam, S.; Herzog, D. B.; Katzman, D. K.; Klibanski, A. (2008). "Determinants of Height in Adolescent Girls with Anorexia Nervosa". Pediatrics121 (6): e1517–e1523. doi:10.1542/peds.2007-2820. PMID18519455. edit
^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 Psychiatry63 (1): 82–8. doi:10.1001/archpsyc.63.1.82. PMID16389201.
^Favaro A, Tenconi E, Santonastaso P (2008). "The relationship between obstetric complications and temperament in eating disorders: a mediation hypothesis". Psychosomatic Medicine70 (3): 372–7. doi:10.1097/PSY.0b013e318164604e. PMID18256341.
^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 Medicine31 (4): 737–40. doi:10.1017/S0033291701003725. PMID11352375.
^Kortegaard LS, Hoerder K, Joergensen J, Gillberg C, Kyvik KO (2001). "A preliminary population-based twin study of self-reported eating disorder". Psychological Medicine31 (2): 361–365. doi:10.1017/S0033291701003087. PMID11232922.
^Wade TD, Bulik CM, Neale M, Kendler KS (2000). "Anorexia nervosa and major depression: shared genetic and environmental risk factors". Am J Psychiatry157 (3): 469–71. doi:10.1176/appi.ajp.157.3.469. PMID10698830.
^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 Rev62 (2): 147–64. doi:10.1016/j.brainresrev.2009.10.007. PMID19931559.
^Urwin, R E; Bennetts, B; Wilcken, B; Lampropoulos, B; Beumont, P; Clarke, S; Russell, J; Tanner, S; Nunn, K P (2002). "Anorexia nervosa (restrictive subtype) is associated with a polymorphism in the novel norepinephrine transporter gene promoter polymorphic region". Molecular Psychiatry7 (6): 652–7. doi:10.1038/sj.mp.4001080. PMID12140790.
^ abFrieling, Helge; Römer, Konstanze D.; Scholz, Sarah; Mittelbach, Franziska; Wilhelm, Julia; De Zwaan, Martina; Jacoby, Georg E.; Kornhuber, Johannes et al. (2009). "Epigenetic dysregulation of dopaminergic genes in eating disorders". The International Journal of Eating Disorders43 (7): 577–83. doi:10.1002/eat.20745. PMID19728374.
^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". The International Journal of Eating Disorders. 37. Suppl (S1): S15–9; discussion S20–1. doi:10.1002/eat.20109. PMID15852312.
^Bergen, Andrew W; Yeager, Meredith; Welch, Robert A; Haque, Kashif; Ganjei, J Kelly; Van Den Bree, Marianne B M; Mazzanti, Chiara; Nardi, Irma et al. (2005). "Association of multiple DRD2 polymorphisms with anorexia nervosa". Neuropsychopharmacology30 (9): 1703–10. doi:10.1038/sj.npp.1300719. PMID15920508.
^Kaye, W; Bailer, U; Frank, G; Wagner, A (2006). "Persistent alterations of serotonin and dopamine activity after recovery from anorexia and bulimia nervosa". Psychosomatic Medicine1287: 45–48. doi:10.1016/j.ics.2005.12.038.
^Bosanac P, Norman T, Burrows G, Beumont P (2005). "Serotonergic and dopaminergic systems in anorexia nervosa: a role for atypical antipsychotics?". The Australian and New Zealand Journal of Psychiatry39 (3): 146–53. doi:10.1111/j.1440-1614.2005.01536.x. PMID15701063.
^ abBergh, C.; Södersten, P. (1996). "Anorexia nervosa, self–starvation and the reward of stress". Nature Medicine2 (1): 21–22. doi:10.1038/nm0196-21. PMID8564826.edit
^ abKaye, W.; Frank, G.; Bailer, U.; Henry, S.; Meltzer, C.; Price, J.; Mathis, C.; Wagner, A. (2005). "Serotonin alterations in anorexia and bulimia nervosa: New insights from imaging studies". Physiology & Behavior85: 73. doi:10.1016/j.physbeh.2005.04.013.edit
^Lee, Y.; Lin, P. Y. (2010). "Association between serotonin transporter gene polymorphism and eating disorders: A meta-analytic study". International Journal of Eating Disorders43 (6): 498–504. doi:10.1002/eat.20732. PMID19708070.edit
^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 Medicine35 (6): 897–905. doi:10.1017/S0033291704003368. PMID15997610.
^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 Physiology293 (3): R992–1002. doi:10.1152/ajpregu.00516.2006. PMID17567712.
^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 Exercise39 (4): 728–34. doi:10.1249/mss.0b013e31802f04c7. PMID17414812.
^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 Medicine139 (2): 72–9. doi:10.1067/mlc.2002.121014. PMID11919545.
^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 Communications4. doi:10.1038/ncomms3685. PMID24158035. 2685.
^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. PMID15852320.
^Shay NF, Mangian HF (2000). "Neurobiology of zinc-influenced eating behavior". The Journal of Nutrition130 (5S Suppl): 1493S–9S. PMID10801965.
^Dinicola, V. F. (1990). "Anorexia Multiforme: Self-Starvation in Historical and Cultural Context: Part II: Anorexia Nervosa as a Culture-Reactive Syndrome1". Transcultural Psychiatry27 (4): 245–226. doi:10.1177/136346159002700401.edit
^Schmidt, U.; Treasure, J. (2006). "Anorexia nervosa: Valued and visible. A cognitive-interpersonal maintenance model and its implications for research and practice". The British journal of clinical psychology / the British Psychological Society45 (Pt 3): 343–366. doi:10.1348/014466505X53902. PMID17147101. edit
^Mukai, T; Crago, M; Shisslak, CM (1994). "Eating attitudes and weight preoccupation among female high school students in Japan". Journal of child psychology and psychiatry, and allied disciplines35 (4): 677–88. doi:10.1111/j.1469-7610.1994.tb01213.x. PMID8040220.
^Levine et al. 1994, Shisslak et al. 1998, Stice 1998, Wertheim et al. 1997
^Harrison, A.; Sullivan, S.; Tchanturia, K.; Treasure, J. (2009). "Emotion recognition and regulation in anorexia nervosa". Clinical Psychology & Psychotherapy16 (4): 348–356. doi:10.1002/cpp.628. PMID19517577. edit
^Zonnevijlle-Bender, M. J.; Van Goozen, S. H.; Cohen-Kettenis, P. T.; Van Elburg, A.; Van Engeland, H. (2002). "Do adolescent anorexia nervosa patients have deficits in emotional functioning?". European Child & Adolescent Psychiatry11 (1): 38–42. doi:10.1007/s007870200006. PMID11942427. edit
^Daniel Le Grange, James Lock, Katharine Loeb and Dasha Nicholls: Academy for Eating Disorders Position Paper: The Role of the Family in Eating Disorders. International Journal of Eating Disorders 2010 Jan;43(1) 1-5. doi:10.1002/eat.20751
^ abCarrie Arnold: Decoding Anorexia: How Breakthroughs in Science Offer Hope for Eating Disorders",Routledge Press
^ abLópez-Guimerà, G.; Levine, M. P.; Sánchez-Carracedo, D.; Fauquet, J. (2010). "Influence of Mass Media on Body Image and Eating Disordered Attitudes and Behaviors in Females: A Review of Effects and Processes". Media Psychology13 (4): 387. doi:10.1080/15213269.2010.525737.edit
^Gillberg, C. (1983). "Are autism and anorexia nervosa related?". The British Journal of Psychiatry142 (4): 428b. doi:10.1192/bjp.142.4.428b.
^Gillberg, C. (1985). "Autism and anorexia nervosa: Related conditions". Nordisk Psykiatrisk Tidskrift39 (4): 307–312. doi:10.3109/08039488509101911.
^Rothery, D.J.; D.M.F. Garden (1988-01-11). "Anorexia nervosa and infantile autism". The British journal of psychiatry : the journal of mental science153 (5): 714. doi:10.1192/bjp.153.5.714. PMID3255470.Cite uses deprecated parameters (help)
^Gillberg, I. Carina; Maria Råstam, Christopher Gillberg (February 1995). "Anorexia nervosa 6 years after onset: Part I. Personality disorders". Comprehensive Psychiatry36 (1): 61–69. doi:10.1016/0010-440X(95)90100-A. PMID7705090.Cite uses deprecated parameters (help)
^Gillberg, I. Carina; Christopher Gillberg, Maria Råstam, Maria Johansson (February 1996). "The cognitive profile of anorexia nervosa: A comparative study including a community-based sample". Comprehensive Psychiatry37 (1): 23–30. doi:10.1016/S0010-440X(96)90046-2. PMID8770522.Cite uses deprecated parameters (help)
^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 Adolescence25 (4): 439–453. doi:10.1007/BF01537541.Cite uses deprecated parameters (help)
^Nilsson, E. W; C. Gillberg, I. C Gillberg (November 1999). "Ten-year follow-up of adolescent-onset anorexia nervosa: personality disorders". Journal of the American Academy of Child and Adolescent Psychiatry38 (11): 1389–95. doi:10.1097/00004583-199911000-00013. PMID10560225.Cite uses deprecated parameters (help)
^Wentz, Elisabet; Christopher Gillberg, I. Carina Gillberg, Maria Råstam (2001). "Ten-Year Follow-up of Adolescent-Onset Anorexia Nervosa: Psychiatric Disorders and Overall Functioning Scales". The Journal of Child Psychology and Psychiatry and Allied Disciplines42 (5): 613–622. doi:10.1017/S0021963001007284.Cite uses deprecated parameters (help)
^Råstam, Maria; Christopher Gillberg, Elisabet Wentz (2003-01-01). "Outcome of teenage-onset anorexia nervosa in a Swedish community-based sample". European Child & Adolescent Psychiatry12 (1): I78–90. doi:10.1007/s00787-003-1111-y. PMID12567219.Cite uses deprecated parameters (help)
^Wentz, Elisabet; J. Lacey, Glenn Waller, Maria Råstam, Jeremy Turk, Christopher Gillberg (2005-12-01). "Childhood onset neuropsychiatric disorders in adult eating disorder patients". European Child & Adolescent Psychiatry14 (8): 431–437. doi:10.1007/s00787-005-0494-3. PMID16341499.Cite uses deprecated parameters (help)
^Wentz, Elisabet; I. Carina Gillberg, Henrik Anckarsater, Christopher Gillberg, Maria Rastam (2009-02-01). "Adolescent-onset anorexia nervosa: 18-year outcome". The British Journal of Psychiatry194 (2): 168–174. doi:10.1192/bjp.bp.107.048686. PMID19182181.Cite uses deprecated parameters (help)
^Fisman, S; M Steele, J Short, T Byrne, C Lavallee (July 1996). "Case study: anorexia nervosa and autistic disorder in an adolescent girl". Journal of the American Academy of Child and Adolescent Psychiatry35 (7): 937–940. doi:10.1097/00004583-199607000-00021. PMID8768355.Cite uses deprecated parameters (help)
^Kerbeshian, Jacob; Larry Burd (2008). "Is anorexia nervosa a neuropsychiatric developmental disorder? An illustrative case report". World Journal of Biological Psychiatry10 (4 Pt 2): 648–57. doi:10.1080/15622970802043117. PMID18609437.Cite uses deprecated parameters (help)
^Gillberg, I. C; M. Raastam, E. Wentz, C. Gillberg (2007). "Cognitive and executive functions in anorexia nervosa ten years after onset of eating disorder". Journal of Clinical and Experimental Neuropsychology29 (2): 170–178. doi:10.1080/13803390600584632. PMID17365252.Cite uses deprecated parameters (help)
^Hambrook, D.; K. Tchanturia, U. Schmidt, T. Russell, J. Treasure (2008). "Empathy, systemizing, and autistic traits in anorexia nervosa: a pilot study". The British journal of clinical psychology/the British Psychological Society47 (Pt 3): 335–9. doi:10.1348/014466507X272475. PMID18208640.Cite uses deprecated parameters (help)
^Lopez, C.; K. Tchanturia, D. Stahl, R. Booth, J. Holliday, J. Treasure (2008). "An examination of the concept of central coherence in women with anorexia nervosa". International Journal of Eating Disorders41 (2): 143–152. doi:10.1002/eat.20478. PMID17937420.Cite uses deprecated parameters (help)
^Russell, Tamara Anne; Ulrike Schmidt, Liz Doherty, Vicky Young, Kate Tchanturia (2009). "Aspects of social cognition in anorexia nervosa: Affective and cognitive theory of mind". Psychiatry Research168 (3): 181–185. doi:10.1016/j.psychres.2008.10.028. PMID19467562.Cite uses deprecated parameters (help)
^Zastrow, Arne; Kaiser; Kaiser, Christoph Stippich, Stephan Walther, Wolfgang Herzog, Kate Tchanturia, Aysenil Belger, Matthias Weisbrod, Janet Treasure, Hans-Christoph Friederich (2009-05-01). "Neural Correlates of Impaired Cognitive-Behavioral Flexibility in Anorexia Nervosa". Am J Psychiatry166 (5): 608–616. doi:10.1176/appi.ajp.2008.08050775. PMID19223435.Cite uses deprecated parameters (help)
^Harrison, Amy; Sarah Sullivan, Kate Tchanturia, Janet Treasure (2009). "Emotion recognition and regulation in anorexia nervosa". Clinical Psychology & Psychotherapy16 (4): 348–356. doi:10.1002/cpp.628. PMID19517577.Cite uses deprecated parameters (help)
^Whitney, Jenna; Abigail Easter, Kate Tchanturia (2008). "Service users' feedback on cognitive training in the treatment of anorexia nervosa: A qualitative study". International Journal of Eating Disorders41 (6): 542–550. doi:10.1002/eat.20536. PMID18433016.Cite uses deprecated parameters (help)
^Treasure, J. (2013). "Coherence and other autistic spectrum traits and eating disorders: Building from mechanism to treatment. The Birgit Olsson lecture". Nordic Journal of Psychiatry67 (1): 38–42. doi:10.3109/08039488.2012.674554. PMID22468644.edit
^Hall RC, Gardner ER, Stickney SK, LeCann AF, Popkin MK (1980). "Physical illness manifesting as psychiatric disease. II. Analysis of a state hospital inpatient population". Archives of General Psychiatry37 (9): 989–95. doi:10.1001/archpsyc.1980.01780220027002. PMID7416911.
^"CBC". MedlinePlus : U.S. National Library of Medicine. Retrieved 31 May 2013.
^Kawabata M, Kubo N, Arashima Y, Yoshida M, Kawano K (1991). "[Serodiagnosis of Lyme disease by ELISA using Borrelia burgdorferi flagellum antigen]". Rinsho Byori (in Japanese) 39 (8): 891–4. PMID1920889.
^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". Endocrine36 (2): 326–32. doi:10.1007/s12020-009-9226-7. PMID19688613.
^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. PMID3525245.
^Rolny P, Lukes PJ, Gamklou R, Jagenburg R, Nilson A (1978). "A comparative evaluation of endoscopic retrograde pancreatography and secretin-CCK test in the diagnosis of pancreatic disease". Scandinavian Journal of Gastroenterology13 (7): 777–81. doi:10.3109/00365527809182190. PMID725498.
^Glasbrenner, B; Malfertheiner, P; Pieramico, O; Klatt, S; Riepl, R; Friess, H; Ditschuneit, H (1993). "Gallbladder dynamics in chronic pancreatitis. Relationship to exocrine pancreatic function, CCK, and PP release". Digestive Diseases and Sciences38 (3): 482–9. doi:10.1007/BF01316503. PMID8444080.
^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 Disorders40 (8): 746–50. doi:10.1002/eat.20432. PMID17610252.
^Narayanan V, Gaudiani JL, Harris RH, Mehler PS (2010). "Liver function test abnormalities in anorexia nervosa—cause or effect". The International Journal of Eating Disorders43 (4): 378–81. doi:10.1002/eat.20690. PMID19424979.
^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 Metabolism41 (1): 135–42. doi:10.1210/jcem-41-1-135. PMID1097461.
^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". Chest102 (6): 1687–9. doi:10.1378/chest.102.6.1687. PMID1446472.
^Walder A, Baumann P (2008). "Increased creatinine kinase and rhabdomyolysis in anorexia nervosa". The International Journal of Eating Disorders41 (8): 766–7. doi:10.1002/eat.20548. PMID18521917.
^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 Medicine17 (1): 70–2. doi:10.1016/S0735-6757(99)90021-9. PMID9928705.
^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 Nephrology62 (6): 465–8. PMID15630907.
^Mashako, Mamba Nyenya Léonard; Cezard, Jean Pierre; Navarro, Jean; Mougenot, Jean Francois; Sonsino, Elise; Gargouri, Abdellatif; Maherzi, Ahmed (1989). "Crohn's disease lesions in the upper gastrointestinal tract: correlation between clinical, radiological, endoscopic, and histological features in adolescents and children". Journal of Pediatric Gastroenterology and Nutrition8 (4): 442–6. doi:10.1097/00005176-198905000-00004. PMID2723935.
^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 Pathology68 (6): 747–51. PMID579717.
^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". Bone6 (1): 21–7. doi:10.1016/8756-3282(85)90402-8. PMID2581596.
^Westen D, Harnden-Fischer J (2001). "Personality profiles in eating disorders: rethinking the distinction between axis I and axis II". The American Journal of Psychiatry158 (4): 547–62. doi:10.1176/appi.ajp.158.4.547. PMID11282688.
^Gendall KA, Joyce PR, Carter FA, McIntosh VV, Jordan J, Bulik CM (2006). "The psychobiology and diagnostic significance of amenorrhea in patients with anorexia nervosa". Fertility and Sterility85 (5): 1531–5. doi:10.1016/j.fertnstert.2005.10.048. PMID16600234.
^Smith, A. T.; Wolfe, B. E. (2008). "Amenorrhea as a Diagnostic Criterion for Anorexia Nervosa: A Review of the Evidence and Implications for Practice". Journal of the American Psychiatric Nurses Association14 (3): 209–15. doi:10.1177/1078390308320288. PMID21665766.
^ abcWorkgroup for Classification of Eating Disorders in Children and Adolescents. "Classifications of Eating Disturbance in Children and Adolescents: Proposed Changes for the DSM-V". European Eating Disorders Review, 2010,p.81
^ abKnoll, S., Bulik, C., & Hebebrand, J. "Do the currently proposed DSM-5 criteria for anorexia nervosa adequately consider developmental aspects in children and adolescents?". Early Adolescent Psychiatry, 2011,p.96
^Journal of Adolescent Health. "Eating Disorders in Adolescents: Position Paper of the Society for Adolescent Medicine". 2003,33,p.496
^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 Disorders5 (2): 52–61. PMID10941603.
^Kaye WH, Bulik CM, Thornton L, Barbarich N, Masters K (2004). "Comorbidity of anxiety disorders with anorexia and bulimia nervosa". The American Journal of Psychiatry161 (12): 2215–21. doi:10.1176/appi.ajp.161.12.2215. PMID15569892.
^Gaudio S, Di Ciommo V (2011). "Prevalence of personality disorders and their clinical correlates in outpatient adolescents with anorexia nervosa". Psychosomatic Medicine73 (9): 769–74. doi:10.1097/PSY.0b013e318235b9b5. PMID22042882.
^Serpell L, Livingstone A, Neiderman M, Lask B (2002). "Anorexia nervosa: obsessive-compulsive disorder, obsessive-compulsive personality disorder, or neither?". Clinical Psychology Review22 (5): 647–69. doi:10.1016/S0272-7358(01)00112-X. PMID12113200.
^Bulik, Cynthia M.; Klump, Kelly L.; Thornton, Laura; Kaplan, Allan S.; Devlin, Bernie; Fichter, Manfred M.; Halmi, Katherine A.; Strober, Michael et al. (2004). "Alcohol use disorder comorbidity in eating disorders: a multicenter study". The Journal of Clinical Psychiatry65 (7): 1000–6. doi:10.4088/JCP.v65n0718. PMID15291691.
^Larsson JO, Hellzén M (2004). "Patterns of personality disorders in women with chronic eating disorders". Eating and Weight Disorders9 (3): 200–5. PMID15656014.
^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 Association15 (4): 253–74. doi:10.1002/erv.784. PMID17676696.
^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 Psychiatry160 (2): 242–7. doi:10.1176/appi.ajp.160.2.242. PMID12562569.
^Lucka I, Cebella A (2004). "[Characteristics of the forming personality in children suffering from anorexia nervosa]". Psychiatria Polska (in Polish) 38 (6): 1011–8. PMID15779665.
^Dukarm CP (2005). "Bulimia nervosa and attention deficit hyperactivity disorder: a possible role for stimulant medication". Journal of Women's Health14 (4): 345–50. doi:10.1089/jwh.2005.14.345. PMID15916509.
^Mikami, Amori Yee; Hinshaw, Stephen P.; Arnold, L. Eugene; Hoza, Betsy; Hechtman, Lily; Newcorn, Jeffrey H.; Abikoff, Howard B. (2010). "Bulimia nervosa symptoms in the multimodal treatment study of children with ADHD". The International Journal of Eating Disorders43 (3): 248–59. doi:10.1002/eat.20692. PMID19378318.
^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 Pediatrics28 (4): 302–7. doi:10.1097/DBP.0b013e3180327917. PMID17700082.
^Bruce KR, Steiger H, Koerner NM, Israel M, Young SN (2004). "Bulimia nervosa with co-morbid avoidant personality disorder: behavioural characteristics and serotonergic function". Psychological Medicine34 (1): 113–24. doi:10.1017/S003329170300864X. PMID14971632.
^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 Disorders32 (3): 291–300. doi:10.1002/eat.10091. PMID12210643.
^Phillips, KA; McElroy, SL; Keck Jr, PE; Hudson, JI; Pope Jr, HG (1994). "A comparison of delusional and nondelusional body dysmorphic disorder in 100 cases". Psychopharmacol Bull.30 (2): 179–86. PMID7831453.
^ abFeusner JD, Townsend J, Bystritsky A, Bookheimer S (2007). "Visual Information Processing of Faces in Body Dysmorphic Disorder". Archives of General Psychiatry64 (12): 1417–25. doi:10.1001/archpsyc.64.12.1417. PMID18056550.
^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. ISBN978-0-205-64524-4.
^ abWhitnet, E. and Rolfes, S. R. (2011). Understanding Nutrition United States: Wadsworth Cengage Learning, ISBN 1-133-58752-6.
^Ayton AK, Azaz A, Horrobin DF (2004). "Rapid improvement of severe anorexia nervosa during treatment with ethyl-eicosapentaenoate and micronutrients". European Psychiatry19 (5): 317–9. doi:10.1016/j.eurpsy.2004.06.002. PMID15276668.
^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 Nutrition89 (2): 641–51. doi:10.3945/ajcn.2008.26749. PMID19116322.
^Breen HB, Espelage DL (2004). "Nutrition expertise in eating disorders". Eating and Weight Disorders9 (2): 120–5. PMID15330079.
^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 Methods109 (2): 245–51. doi:10.1016/S0166-0934(03)00078-8. PMID12711069.
^Whisenant SL, Smith BA (1995). "Eating disorders: current nutrition therapy and perceived needs in dietetics education and research". Journal of the American Dietetic Association95 (10): 1109–12. doi:10.1016/S0002-8223(95)00301-0. PMID7560681.
^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 Association106 (12): 2073–82. doi:10.1016/j.jada.2006.09.007. PMID17186637.
^Brambilla, Francesca; Garcia, Cristina Segura; Fassino, Secondo; Daga, Giovanni Abbate; Favaro, Angela; Santonastaso, Paolo; Ramaciotti, Carla; Bondi, Emilia et al. (2007). "Olanzapine therapy in anorexia nervosa: psychobiological effects". International Clinical Psychopharmacology22 (4): 197–204. doi:10.1097/YIC.0b013e328080ca31. PMID17519642.
^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 Psychiatry165 (10): 1281–8. doi:10.1176/appi.ajp.2008.07121900. PMID18558642.
^ abEisler 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 Disciplines41 (6): 727–36. doi:10.1111/1469-7610.00660. PMID11039685.
^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. PMID15852323.
^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. ISBN1-55798-758-0.edit
^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 Psychiatry160 (11): 2046–9. doi:10.1176/appi.ajp.160.11.2046. PMID14594754.
^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 Psychiatry20 (2): 79–86. doi:10.1080/10401230802017068. PMID18568579.
^Ball J, Mitchell P (2004). "A randomized controlled study of cognitive behavior therapy and behavioral family therapy for anorexia nervosa patients". Eating Disorders12 (4): 303–14. doi:10.1080/10640260490521389. PMID16864523.
^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 Review17 (6): 426–34. doi:10.1002/erv.962. PMID19760625.
^Schebendach, J.; Mayer, L. E. S.; Devlin, M. J.; Attia, E.; Walsh, B. T. (2012). "Dietary energy density and diet variety as risk factors for relapse in anorexia nervosa: A replication". International Journal of Eating Disorders45 (1): 79–84. doi:10.1002/eat.20922. PMID21448937. edit
^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 Disciplines45 (1): 63–83. doi:10.1046/j.0021-9630.2003.00309.x. PMID14959803.
^Bulik, C. M.; Sullivan, P. F.; Tozzi, F.; Furberg, H.; Lichtenstein, P.; Pedersen, N. L. (2006). "Prevalence, Heritability, and Prospective Risk Factors for Anorexia Nervosa". Archives of General Psychiatry63 (3): 305–312. doi:10.1001/archpsyc.63.3.305. PMID16520436.edit
^ abHepworth, 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 journal30 (4): 243–5. PMID3912990.
^ abSir 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. ISBN978-0-399-15699-1.
^Birmingham, C. L.; Su, J.; Hlynsky, J. A.; Goldner, E. M.; Gao, M. (2005). "The mortality rate from anorexia nervosa". International Journal of Eating Disorders38 (2): 143–146. doi:10.1002/eat.20164. PMID16134111. edit
^A survey by Internet security firm Optenet found a 470% increase in pro-ana and pro-mia sites from 2006 to 2007
^Heath, Chris (22 Jan 1998). "The Caged Birds Sings". Rolling Stone778.