Eating disorder

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Eating disorders
Classification and external resources
Specialty Psychiatry
ICD-10 F50
ICD-9-CM 307.5
Patient UK Eating disorder
MeSH D001068
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Eating disorders are mental disorders defined by abnormal eating habits that negatively affect a person's physical or mental health. They include binge eating disorder where people eat a large amount in a short period of time, anorexia nervosa where people eat very little and thus have a low body weight, bulimia nervosa where people eat a lot and then try to rid themselves of the food, pica where people eat non-food items, rumination disorder where people regurgitate food, avoidant/restrictive food intake disorder where people have a lack of interest in food, and a group of other specified feeding or eating disorders. Anxiety disorders, depression, and substance abuse are common among people with eating disorders. These disorders do not include obesity.[1]

The cause of eating disorders is not clear.[2] Both genetic and environmental factors appear to play a role.[2][3] Cultural idealization of thinness is believed to contribute.[2] Eating disorders for example affect about 12% of dancers.[4] Those who have experienced sexual abuse are also more likely to develop eating disorders.[5] Some disorders such as pica and rumination disorder occur more often in people with intellectual disabilities. Only one eating disorder can be diagnosed at a given time.[1]

Treatment can be effective for many eating disorders. This typically involves counselling, a proper diet, and the reduction of efforts to eliminate food. Hospitalization is occasionally needed. Medications may be used to help with some of the associated symptoms.[3] At five years about 70% of people with anorexia and 50% of people with bulimia recover. Recovery from binge eating disorder is less clear and estimated at 20% to 60%. Both anorexia and bulimia increase the risk of death.[6]

In the developed world binge eating disorder affects about 1.6% of women and 0.8% of men in a given year. Anorexia affects about 0.4% and bulimia affects about 1.3% of young women in a given year.[1] During the entire life up to 4% of women have anorexia, 2% have bulimia, and 2% have binge eating disorder.[6] Anorexia and bulimia occur nearly ten times more often in females than males.[1] Typically they begin in late childhood or early adulthood.[3] Rates of other eating disorders are not clear.[1] Rates of eating disorders appear to be lower in less developed countries.[7]


Bulimia nervosa is a disorder characterized by binge eating and purging, as well as excessive evaluation of one's self-worth in terms of body weight or shape.[8] Purging can include self-induced vomiting, over-exercising, and the use of diuretics, enemas, and laxatives. Anorexia nervosa is characterized by extreme food restriction and excessive weight loss, accompanied by the fear of being fat.[9] The extreme weight loss often causes women and girls who have begun menstruating to stop having menstrual periods, a condition known as amenorrhea. Although amenorrhea was once a required criterion for the disorder, it is no longer required to meet criteria for anorexia nervosa due to its exclusive nature for sufferers who are male, post-menopause, or who do not menstruate for other reasons.[10] The DSM-5 specifies two subtypes of anorexia nervosa—the restricting type and the binge/purge type. Those who suffer from the restricting type of anorexia nervosa restrict food intake and do not engage in binge eating, whereas those suffering from the binge/purge type lose control over their eating at least occasionally and may compensate for these binge episodes.[11] The most notable difference between anorexia nervosa binge/purge type and bulimia nervosa is the body weight of the person. Those diagnosed with anorexia nervosa binge/purge type are underweight, while those with bulimia nervosa may have a body weight that falls within the range from normal to obese.[12][13]


These eating disorders are specified as mental disorders in standard medical manuals, such as in the ICD-10,[14] the DSM-5, or both.

  • Anorexia nervosa (AN), characterized by lack of maintenance of a healthy body weight, an obsessive fear of gaining weight or refusal to do so, and an unrealistic perception, or non-recognition of the seriousness, of current low body weight.[15] Anorexia can cause menstruation to stop, and often leads to bone loss, loss of skin integrity, etc. It greatly stresses the heart, increasing the risk of heart attacks and related heart problems. The risk of death is greatly increased in individuals with this disease.[16] The most underlining factor researchers are starting to take notice of is that it may not just be a vanity, social, or media issue, but it could also be related to biological and or genetic components.[17] The DSM-5 contains many changes that better represent patients with these conditions. The DSM-IV required amenorrhea (the absence of the menstrual cycle) to be present in order to diagnose a patient with anorexia.[18] This is no longer a requirement in the DSM-5.
  • Bulimia nervosa (BN), characterized by recurrent binge eating followed by compensatory behaviors such as purging (self-induced vomiting, excessive use of laxatives/diuretics, or excessive exercise). Fasting and over-exercising may also be used as a method of purging following a binge.
  • Binge Eating Disorder (BED), characterized by recurring binge eating at least once a week for over a period of 3 months while experiencing lack of control[19] and guilt after overeating.[20] The disorder can develop within individuals of a wide range of ages and socioeconomic classes.[21][22]
  • Other Specified Feeding or Eating Disorder (OSFED) is an eating or feeding disorder that does not meet full DSM-5 criteria for AN, BN, or BED. Examples of otherwise-specified eating disorders include individuals with atypical anorexia nervosa, who meet all criteria for AN except being underweight, despite substantial weight loss; atypical bulimia nervosa, who meet all criteria for BN except that bulimic behaviors are less frequent or have not been ongoing for long enough; purging disorder; and night eating syndrome.


  • Compulsive overeating, (COE), in which individuals habitually graze on large quantities of food rather than binging, as would be typical of binge eating disorder.
  • Prader-Willi syndrome
  • Diabulimia, characterized by the deliberate manipulation of insulin levels by diabetics in an effort to control their weight.
  • Food maintenance, characterized by a set of aberrant eating behaviors of children in foster care.[23]
  • Orthorexia nervosa, a term used by Steven Bratman to characterize an obsession with a "pure" diet, in which people develop an obsession with avoiding unhealthy foods to the point where it interferes with a person's life.[24]
  • Selective eating disorder, also called picky eating, is an extreme sensitivity to how something tastes. A person with SED may or may not be a supertaster.
  • Drunkorexia, commonly characterized by purposely restricting food intake in order to reserve food calories for alcoholic calories, exercising excessively in order to burn calories consumed from drinking, and over-drinking alcohols in order to purge previously consumed food.[25]
  • Pregorexia, characterized by extreme dieting and over-exercising in order to control pregnancy weight gain. Under-nutrition during pregnancy is associated with low birth weight, coronary heart disease, type 2 diabetes, stroke, hypertension, cardiovascular disease risk, and depression.[26]
  • Gourmand syndrome, a rare condition occurring after damage to the frontal lobe, resulting in an obsessive focus on fine foods.[27]

Signs and symptoms

Symptoms and complications vary according to the nature and severity of the eating disorder:[28]

Possible Symptoms and Complications of Eating Disorders
acne xerosis amenorrhoea tooth loss, cavities
constipation diarrhea water retention and/or edema lanugo
telogen effluvium cardiac arrest hypokalemia death
osteoporosis[29] electrolyte imbalance hyponatremia brain atrophy[30][31]
pellagra[32] scurvy kidney failure suicide[33][34][35]

Some physical symptoms of eating disorders are weakness, fatigue, sensitivity to cold, reduced beard growth in men, reduction in waking erections, reduced libido, weight loss and failure of growth.[36] Unexplained hoarseness may be a symptom of an underlying eating disorder, as the result of acid reflux, or entry of acidic gastric material into the laryngoesophageal tract. Patients who induce vomiting, such as those with anorexia nervosa, binge eating-purging type or those with purging-type bulimia nervosa are at risk for acid reflux.[37] Polycystic ovary syndrome (PCOS) is the most common endocrine disorder to affect women. Though often associated with obesity it can occur in normal weight individuals. PCOS has been associated with binge eating and bulimic behavior.[38][39][40][41][42][43]

Pro-Ana subculture

Several websites promote eating disorders, and can provide a means for individuals to communicate in order to maintain eating disorders. Members of these websites typically feel that their eating disorder is the only aspect of a chaotic life that they can control.[44] These websites are often interactive and have discussion boards where individuals can share strategies, ideas, and experiences, such as diet and exercise plans that achieve extremely low weights.[45] A study comparing the personal web-blogs that were pro-eating disorder with those focused on recovery found that the pro-eating disorder blogs contained language reflecting lower cognitive processing, used a more closed-minded writing style, contained less emotional expression and fewer social references, and focused more on eating-related contents than did the recovery blogs.[46]


The psychopathology of eating disorders centers around body image disturbance, such as concerns with weight and shape; self-worth being too dependent on weight and shape; fear of gaining weight even when underweight; denial of how severe the symptoms are and a distortion in the way the body is experienced.[36]


The cause of eating disorder is not clear.

Many people with eating disorders suffer also from body dysmorphic disorder, altering the way a person sees himself or herself.[47][48] Studies have found that a high proportion of individuals diagnosed with body dysmorphic disorder also had some type of eating disorder, with 15% of individuals having either anorexia nervosa or bulimia nervosa.[47] This link between body dysmorphic disorder and anorexia stems from the fact that both BDD and anorexia nervosa are characterized by a preoccupation with physical appearance and a distortion of body image.[48] There are also many other possibilities such as environmental, social and interpersonal issues that could promote and sustain these illnesses.}[49] Also, the media are oftentimes blamed for the rise in the incidence of eating disorders due to the fact that media images of idealized slim physical shape of people such as models and celebrities motivate or even force people to attempt to achieve slimness themselves. The media are accused of distorting reality, in the sense that people portrayed in the media are either naturally thin and thus unrepresentative of normality or unnaturally thin by forcing their bodies to look like the ideal image by putting excessive pressure on themselves to look a certain way. While past findings have described the causes of eating disorders as primarily psychological, environmental, and sociocultural, new studies have uncovered evidence that there is a prevalent genetic/heritable aspect of the causes of eating disorders.[50]


  • Genetic: Numerous studies have been undertaken that show a possible genetic predisposition toward eating disorders as a result of Mendelian inheritance.[51][51][52] It has also been shown that eating disorders can be heritable. Recent twin studies have found slight instances of genetic variance when considering the different criterion of both anorexia nervosa and bulimia nervosa as endophenotypes contributing to the disorders as a whole.[49] In another recent study, twin and family studies led researchers to discover a genetic link on chromosome 1 that can be found in multiple family members of an individual with anorexia nervosa, indicating an inheritance pattern found between family members of others that have been previously diagnosed with an eating disorder.[50] A study found that an individual who is a first degree relative of someone who has suffered or currently suffers from an eating disorder is seven to twelve times more likely to suffer from an eating disorder themselves.[53] Twin studies also have shown that at least a portion of the vulnerability to develop eating disorders can be inherited, and there has been sufficient evidence to show that there is a genetic locus that shows susceptibility for developing anorexia nervosa.[53]
  • Epigenetics: Epigenetic mechanisms are means by which environmental effects alter gene expression via methods such as DNA methylation; these are independent of and do not alter the underlying DNA sequence. They are heritable, but also may occur throughout the lifespan, and are potentially reversible. Dysregulation of dopaminergic neurotransmission due to epigenetic mechanisms has been implicated in various eating disorders.[54][55] One study has found that "epigenetic mechanisms may contribute to the known alterations of ANP homeostasis in women with eating disorders."[54][56] Other candidate genes for epigenetic studies in eating disorders include leptin, pro-opiomelanocortin (POMC) and brain-derived neurotrophic factor (BDNF).[57]


Eating disorders are classified as Axis I[58] disorders in the Diagnostic and Statistical Manual of Mental Health Disorders (DSM-IV) published by the American Psychiatric Association. There are various other psychological issues that may factor into eating disorders, 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.[59] Some people have a previous disorder which may increase their vulnerability to developing an eating disorder.[60][61][62] Some develop them afterwards.[63] The severity and type of eating disorder symptoms have been shown to affect comorbidity.[64] The DSM-IV should not be used by laypersons to diagnose themselves, even when used by professionals there has been considerable controversy over the diagnostic criteria used for various diagnoses, including eating disorders. There has been controversy over various editions of the DSM including the latest edition, DSM-V, due in May 2013.[65][66][67][68][69]

Cognitive attentional bias issues

Attentional bias may have an effect on eating disorders. Many studies have been performed to test this theory. These studies include Shafran, Lee, Cooper, Palmer & Fairburn (2007), Veenstra and de Jong (2012) and Smeets, Jansen, & Roefs (2005).

  • Evidence of the Effect of Attentional Bias on Eating Disorders

Shafran, Lee, Cooper, Palmer and Fairburn (2007) studied the effect of attentional bias on eating disorders in women with anorexia, bulimia, and ED-NOS (Eating Disorder Not Otherwise Specified) compared to a control group and found that those affected by an eating disorder were quicker to identify "bad" eating scenarios than "good" ones.

  • Attentional Bias in Anorexia Nervosa

A study of a more specific section of eating disorders has been performed by Veenstra and de Jong (2012). It found that both the control and the eating disorder patients showed attentional bias against high fat foods and negative eating pictures. The eating disorder patients showed a larger attentional bias against the foods that are considered "bad". From this study it was hypothesized that a negative attentional bias might facilitate the restricted food intake of the eating disorder patients.

  • Attentional bias in body dissatisfaction

Smeets, Jansen, & Roefs (2005) studied body dissatisfaction and its relation to attentional bias and found that induced bias for unattractive body parts made the participants feel worse about themselves and their body satisfaction decreased, as well as the reverse when a positive bias was induced.

Comorbid Disorders
Axis I Axis II
depression[70] obsessive compulsive personality disorder[71]
substance abuse, alcoholism[72] borderline personality disorder[73]
anxiety disorders[74] narcissistic personality disorder[75]
obsessive compulsive disorder[76][77] histrionic personality disorder[78]
Attention-deficit hyperactivity disorder[79][80][81][82] avoidant personality disorder[83]

Personality traits

There are various childhood personality traits associated with the development of eating disorders.[84] During adolescence these traits may become intensified due to a variety of physiological and cultural influences such as the hormonal changes associated with puberty, stress related to the approaching demands of maturity and socio-cultural influences and perceived expectations, especially in areas that concern body image. Many personality traits have a genetic component and are highly heritable. Maladaptive levels of certain traits may be acquired as a result of anoxic or traumatic brain injury, neurodegenerative diseases such as Parkinson's disease, neurotoxicity such as lead exposure, bacterial infection such as Lyme disease or viral infection such as Toxoplasma gondii as well as hormonal influences. While studies are still continuing via the use of various imaging techniques such as fMRI; these traits have been shown to originate in various regions of the brain[85] such as the amygdala[86][87] and the prefrontal cortex.[88] Disorders in the prefrontal cortex and the executive functioning system have been shown to affect eating behavior.[89][90]

Environmental influences

Child maltreatment

Child abuse which encompasses physical, psychological and sexual abuse, as well as neglect has been shown by innumerable studies to be a precipitating factor in a wide variety of psychiatric disorders, including eating disorders. Children who are subjected to abuse may develop eating disorders in an effort to gain some sense of control or for a sense of comfort, or they may be in an environment where the diet is unhealthy or insufficient. Child abuse and neglect can cause profound changes in both the physiological structure and the neurochemistry of the developing brain. Children who, as wards of the state, were placed in orphanages or foster homes are especially susceptible to developing a disordered eating pattern. In a study done in New Zealand 25% of the study subjects in foster care exhibited an eating disorder (Tarren-Sweeney M. 2006). An unstable home environment is detrimental to the emotional well-being of children, even in the absence of blatant abuse or neglect the stress of an unstable home can contribute to the development of an eating disorder.[91][92][93][94][95][96][97][98][99]

Social isolation

Social isolation has been shown to have a deleterious effect on an individual's physical and emotional well-being. Those that are socially isolated have a higher mortality rate in general as compared to individuals that have established social relationships. This effect on mortality is markedly increased in those with pre-existing medical or psychiatric conditions, and has been especially noted in cases of coronary heart disease. "The magnitude of risk associated with social isolation is comparable with that of cigarette smoking and other major biomedical and psychosocial risk factors." (Brummett et al.)

Social isolation can be inherently stressful, depressing and anxiety-provoking. In an attempt to ameliorate these distressful feelings an individual may engage in emotional eating in which food serves as a source of comfort. The loneliness of social isolation and the inherent stressors thus associated have been implicated as triggering factors in binge eating as well.[100][101][102][103]

Waller, Kennerley and Ohanian (2007) argued that both bingeing–vomiting and restriction are emotion suppression strategies, but they are just utilized at different times. For example, restriction is used to pre-empt any emotion activation, while bingeing–vomiting is used after an emotion has been activated.[104]

Parental influence

Parental influence has been shown to be an intrinsic component in the development of eating behaviors of children. This influence is manifested and shaped by a variety of diverse factors such as familial genetic predisposition, dietary choices as dictated by cultural or ethnic preferences, the parents' own body shape and eating patterns, the degree of involvement and expectations of their children's eating behavior as well as the interpersonal relationship of parent and child. This is in addition to the general psychosocial climate of the home and the presence or absence of a nurturing stable environment. It has been shown that maladaptive parental behavior has an important role in the development of eating disorders. As to the more subtle aspects of parental influence, it has been shown that eating patterns are established in early childhood and that children should be allowed to decide when their appetite is satisfied as early as the age of two. A direct link has been shown between obesity and parental pressure to eat more.

Coercive tactics in regard to diet have not been proven to be efficacious in controlling a child's eating behavior. Affection and attention have been shown to affect the degree of a child's finickiness and their acceptance of a more varied diet.[105][106][107][108][109][110]

Hilde Bruch, a pioneer in the field of studying eating disorders, asserts that anorexia nervosa often occurs in girls who are high achievers, obedient, and always trying to please their parents. Their parents have a tendency to be over-controlling and fail to encourage the expression of emotions, inhibiting daughters from accepting their own feelings and desires. Adolescent females in these overbearing families lack the ability to be independent from their families, yet realize the need to, often resulting in rebellion. Controlling their food intake may make them feel better, as it provides them with a sense of control.[111]

Peer pressure

In various studies such as one conducted by The McKnight Investigators, peer pressure was shown to be a significant contributor to body image concerns and attitudes toward eating among subjects in their teens and early twenties.

Eleanor Mackey and co-author, Annette M. La Greca of the University of Miami, studied 236 teen girls from public high schools in southeast Florida. "Teen girls' concerns about their own weight, about how they appear to others and their perceptions that their peers want them to be thin are significantly related to weight-control behavior", says psychologist Eleanor Mackey of the Children's National Medical Center in Washington and lead author of the study. "Those are really important."

According to one study, 40% of 9- and 10-year-old girls are already trying to lose weight.[112] Such dieting is reported to be influenced by peer behavior, with many of those individuals on a diet reporting that their friends also were dieting. The number of friends dieting and the number of friends who pressured them to diet also played a significant role in their own choices.[113][114][115][116]

Elite athletes have a significantly higher rate in eating disorders. Female athletes in sports such as gymnastics, ballet, diving, etc. are found to be at the highest risk among all athletes. Women are more likely than men to acquire an eating disorder between the ages of 13–30. 0–15% of those with bulimia and anorexia are men.[117]

Cultural pressure

There is a cultural emphasis on thinness which is especially pervasive in western society. There is an unrealistic stereotype of what constitutes beauty and the ideal body type as portrayed by the media, fashion and entertainment industries. "The cultural pressure on men and women to be 'perfect' is an important predisposing factor for the development of eating disorders".[118][119] Further, when women of all races base their evaluation of their self upon what is considered the culturally ideal body, the incidence of eating disorders increases.[120] Eating disorders are becoming more prevalent in non-Western countries where thinness is not seen as the ideal, showing that social and cultural pressures are not the only causes of eating disorders.[121] For example, observations of anorexia in all of the non-Western regions of the world point to the disorder not being "culture-bound" as once thought.[122] However, studies on rates of bulimia suggest that it might be culturally bound. In non-Western countries, bulimia is less prevalent than anorexia, but these non-Western countries where it is observed can be said to have probably or definitely been influenced or exposed to Western culture and ideology.[123]

Socioeconomic status (SES) has been viewed as a risk factor for eating disorders, presuming that possessing more resources allows for an individual to actively choose to diet and reduce body weight.[124] Some studies have also shown a relationship between increasing body dissatisfaction with increasing SES.[125] However, once high socioeconomic status has been achieved, this relationship weakens and, in some cases, no longer exists.[122]

The media plays a major role in the way in which people view themselves. Countless magazine ads and commercials depict thin celebrities like Lindsay Lohan, Nicole Richie and Mary Kate Olsen, who appear to gain nothing but attention from their looks. Society has taught people that being accepted by others is necessary at all costs.[126] Unfortunately this has led to the belief that in order to fit in one must look a certain way. Televised beauty competitions such as the Miss America Competition contribute to the idea of what it means to be beautiful because competitors are evaluated on the basis of their opinion.[127]

In addition to socioeconomic status being considered a cultural risk factor so is the world of sports. Athletes and eating disorders tend to go hand in hand, especially the sports where weight is a competitive factor. Gymnastics, horse back riding, wrestling, body building, and dancing are just a few that fall into this category of weight dependent sports. Eating disorders among individuals that participate in competitive activities, especially women, often lead to having physical and biological changes related to their weight that often mimic prepubescent stages. Oftentimes as women's bodies change they lose their competitive edge which leads them to taking extreme measures to maintain their younger body shape. Men often struggle with binge eating followed by excessive exercise while focusing on building muscle rather than losing fat, but this goal of gaining muscle is just as much an eating disorder as obsessing over thinness. The following statistics taken from Susan Nolen-Hoeksema's book, (ab)normal psychology, shows the estimated percentage of athletes that struggle with eating disorders based on the category of sport.

  • Aesthetic sports (dance, figure skating, gymnastics) – 35%
  • Weight dependent sports (judo, wrestling) – 29%
  • Endurance sports (cycling, swimming, running) – 20%
  • Technical sports (golf, high jumping) – 14%
  • Ball game sports (volleyball, soccer) – 12%

Although most of these athletes develop eating disorders to keep their competitive edge, others use exercise as a way to maintain their weight and figure. This is just as serious as regulating food intake for competition. Even though there is mixed evidence showing at what point athletes are challenged with eating disorders, studies show that regardless of competition level all athletes are at higher risk for developing eating disorders that non-athletes, especially those that participate in sports where thinness is a factor.[128]

Pressure from society is also seen within the homosexual community. Homosexual men are at greater risk of eating disorder symptoms than heterosexual men.[129] Within the gay culture, muscularity gives the advantages of both social and sexual desirability and also power.[130] These pressures and ideas that another homosexual male may desire a mate who is thinner or muscular can possibly lead to eating disorders. The higher eating disorder symptom score reported, the more concern about how others perceive them and the more frequent and excessive exercise sessions occur.[130] High levels of body dissatisfaction are also linked to external motivation to working out and old age; however, having a thin and muscular body occurs within younger homosexual males than older.[129][130]

It is important to realize some of the limitations and challenges of many studies that try to examine the roles of culture, ethnicity, and SES. For starters, most of the cross-cultural studies use definitions from the DSM-IV-TR, which has been criticized as reflecting a Western cultural bias. Thus, assessments and questionnaires may not be constructed to detect some of the cultural differences associated with different disorders. Also, when looking at individuals in areas potentially influenced by Western culture, few studies have attempted to measure how much an individual has adopted the mainstream culture or retained the traditional cultural values of the area. Lastly, the majority of the cross-cultural studies on eating disorders and body image disturbances occurred in Western nations and not in the countries or regions being examined.[131]

While there are many influences to how an individual processes their body image, the media does play a major role. Along with the media, parental influence, peer influence, and self-efficacy beliefs also play a large role in an individual's view of themselves. The way the media presents images can have a lasting effect on an individual's perception of their body image. Eating disorders are a worldwide issue and while women are more likely to be affected by an eating disorder it still affects both genders (Schwitzer 2012). The media has an impact on eating disorders whether shown in a positive or negative light, it then has a responsibility to use caution when promoting images that projects an ideal that many turn to eating disorders to attain.[132]

To combat unhealthy body image in the fashion world, in 2015, France passed a law requiring models to be declared healthy by a doctor to participate in fashion shows. It also requires re-touched images to be marked as such in magazines.[133]


  • Biochemical: Eating behavior is a complex process controlled by the neuroendocrine system, of which the Hypothalamus-pituitary-adrenal-axis (HPA axis) is a major component. Dysregulation of the HPA axis has been associated with eating disorders,[134][135] such as irregularities in the manufacture, amount or transmission of certain neurotransmitters, hormones[136] or neuropeptides[137] and amino acids such as homocysteine, elevated levels of which are found in AN and BN as well as depression.[138]
    • Serotonin: a neurotransmitter involved in depression also has an inhibitory effect on eating behavior.[139][140][141][142][143]
    • Norepinephrine is both a neurotransmitter and a hormone; abnormalities in either capacity may affect eating behavior.[144][145]
    • Dopamine: which in addition to being a precursor of norepinephrine and epinephrine is also a neurotransmitter which regulates the rewarding property of food.[146][147]
    • Neuropeptide Y also known as NPY is a hormone that encourages eating and decreases metabolic rate.[148] Blood levels of NPY are elevated in patients with anorexia nervosa, and studies have shown that injection of this hormone into the brain of rats with restricted food intake increases their time spent running on a wheel. Normally the hormone stimulates eating in healthy patients, but under conditions of starvation it increases their activity rate, probably to increase the chance of finding food.[148] The increased levels of NPY in the blood of patients with eating disorders can in some ways explain the instances of extreme over-exercising found in most anorexia nervosa patients.
  • Leptin and ghrelin: leptin is a hormone produced primarily by the fat cells in the body; it has an inhibitory effect on appetite by inducing a feeling of satiety. Ghrelin is an appetite inducing 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 hormones and their respective effects have been implicated in the pathophysiology of anorexia nervosa and bulimia nervosa.[149] Leptin can also be used to distinguish between constitutional thinness found in a healthy person with a low BMI and an individual with anorexia nervosa.[49][150]
  • Gut bacteria and immune system: studies have shown that a majority of patients with anorexia and bulimia nervosa have elevated levels of autoantibodies that affect hormones and neuropeptides that regulate appetite control and the stress response. There may be a direct correlation between autoantibody levels and associated psychological traits.[151][152] Later study revealed that autoantibodies reactive with alpha-MSH are, in fact, generated against ClpB, a protein produced by certain gut bacteria e.g. Escherichia coli. ClpB protein was identified as a conformational antigen-mimetic of alpha-MSH. In patients with eating disorders plasma levels of anti-ClpB IgG and IgM correalated with patients' psychological traits[153]
  • Infection: PANDAS, is an abbreviation for Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections. Children with PANDAS "have obsessive-compulsive disorder (OCD) and/or tic disorders such as Tourette syndrome, and in whom symptoms worsen following infections such as "strep throat" and scarlet fever". (NIMH) There is a possibility that PANDAS may be a precipitating factor in the development of anorexia nervosa in some cases, (PANDAS AN).[154]
  • Lesions: studies have shown that lesions to the right frontal lobe or temporal lobe can cause the pathological symptoms of an eating disorder.[155][156][157]
  • Tumors: tumors in various regions of the brain have been implicated in the development of abnormal eating patterns.[158][159][160][161][162]
  • Brain calcification: a study highlights a case in which prior calcification of the right thalumus may have contributed to development of anorexia nervosa.[163]
  • somatosensory homunculus: is the representation of the body located in the somatosensory cortex, first described by renowned neurosurgeon Wilder Penfield. The illustration was originally termed "Penfield's Homunculus", homunculus meaning little man. "In normal development this representation should adapt as the body goes through its pubertal growth spurt. However, in AN it is hypothesized that there is a lack of plasticity in this area, which may result in impairments of sensory processing and distortion of body image". (Bryan Lask, also proposed by VS Ramachandran)
  • Obstetric complications: There have been studies done which show maternal smoking, obstetric and perinatal complications such as maternal anemia, very pre-term birth (less than 32 weeks), being born small for gestational age, neonatal cardiac problems, preeclampsia, placental infarction and sustaining a cephalhematoma at birth increase the risk factor for developing either anorexia nervosa or bulimia nervosa. Some of this developmental risk as in the case of placental infarction, maternal anemia and cardiac problems may cause intrauterine hypoxia, umbilical cord occlusion or cord prolapse may cause ischemia, resulting in cerebral injury, the prefrontal cortex in the fetus and neonate is highly susceptible to damage as a result of oxygen deprivation which has been shown to contribute to executive dysfunction, ADHD, and may affect personality traits associated with both eating disorders and comorbid disorders such as impulsivity, mental rigidity and obsessionality. The problem of perinatal brain injury, in terms of the costs to society and to the affected individuals and their families, is extraordinary. (Yafeng Dong, PhD)[164][165][166][167][168][169][170][171][172][173][174]
  • Symptom of starvation: Evidence suggests that the symptoms of eating disorders are actually symptoms of the starvation itself, not of a mental disorder. In a study involving thirty-six healthy young men that were subjected to semi-starvation, the men soon began displaying symptoms commonly found in patients with eating disorders.[148][175] In this study, the healthy men ate approximately half of what they had become accustomed to eating and soon began developing symptoms and thought patterns (preoccupation with food and eating, ritualistic eating, impaired cognitive ability, other physiological changes such as decreased body temperature) that are characteristic symptoms of anorexia nervosa.[148] The men used in the study also developed hoarding and obsessive collecting behaviors, even though they had no use for the items, which revealed a possible connection between eating disorders and obsessive compulsive disorder.[148]


The initial diagnosis should be made by a competent medical professional. "The medical history is the most powerful tool for diagnosing eating disorders"(American Family Physician).[176] There are many medical disorders that mimic eating disorders and comorbid psychiatric disorders. All organic causes should be ruled out prior to a diagnosis of an eating disorder or any other psychiatric disorder. In the past 30 years eating disorders have become increasingly conspicuous and it is uncertain whether the changes in presentation reflect a true increase.[citation needed] Anorexia nervosa and bulimia nervosa are the most clearly defined subgroups of a wider range of eating disorders. Many patients present with subthreshold expressions of the two main diagnoses: others with different patterns and symptoms.[177]


The diagnostic workup typically includes complete medical and psychosocial history and follows a rational and formulaic approach to the diagnosis. Neuroimaging using fMRI, MRI, PET and SPECT scans have been used to detect cases in which a lesion, tumor or other organic condition has been either the sole causative or contributory factor in an eating disorder. "Right frontal intracerebral lesions with their close relationship to the limbic system could be causative for eating disorders, we therefore recommend performing a cranial MRI in all patients with suspected eating disorders" (Trummer M et al. 2002), "intracranial pathology should also be considered however certain is the diagnosis of early-onset anorexia nervosa. Second, neuroimaging plays an important part in diagnosing early-onset anorexia nervosa, both from a clinical and a research prospective".(O'Brien et al. 2001).[157][178]


Eating Disorder Specific Psychometric Tests
Eating Attitudes Test[179] SCOFF questionnaire[180]
Body Attitudes Test[181] Body Attitudes Questionnaire[182]
Eating Disorder Inventory[183] Eating Disorder Examination Interview[184]

After ruling out organic causes and the initial diagnosis of an eating disorder being made by a medical professional, a trained mental health professional aids in the assessment and treatment of the underlying psychological components of the eating disorder and any comorbid psychological conditions. The clinician conducts a clinical interview and may employ various psychometric tests. Some are general in nature while others were devised specifically for use in the assessment of eating disorders. Some of the general tests that may be used are the Hamilton Depression Rating Scale[185] and the Beck Depression Inventory.[186][187] longitudinal research showed that there is an increase in chance that a young adult female would develop bulimia due to their current psychological pressure and as the person ages and matures, their emotional problems change or are resolved and then the symptoms decline.[188]

Differential diagnoses

There are multiple medical conditions which may be misdiagnosed as a primary psychiatric disorder, complicating or delaying treatment. These may have a synergistic effect on conditions which mimic an eating disorder or on a properly diagnosed eating disorder.

  • Lyme disease which is known as the "great imitator", as it may present as a variety of psychiatric or neurological disorders including anorexia nervosa.[189][190]
  • Addison's Disease is a disorder of the adrenal cortex which results in decreased hormonal production. Addison's disease, even in subclinical form may mimic many of the symptoms of anorexia nervosa.[191]
  • Gastric adenocarcinoma is one of the most common forms of cancer in the world. Complications due to this condition have been misdiagnosed as an eating disorder.[192]
  • Helicobacter pylori is a bacterium which causes stomach ulcers and gastritis and has been shown to be a precipitating factor in the development of gastric carcinomas. It also has an effect on circulating levels of leptin and ghrelin, two hormones which help regulate appetite. Upon successful treatment of helicobacter pylori associated gastritis in pre-pubertal children they showed "significant increase in BMI, lean and fat mass along with a significant decrease in circulating ghrelin levels and an increase in leptin levels" (Pacifico, L). "SUMMARY: H. pylori has an influence on the release of gastric hormones and therefore plays a role in the regulation of body weight, hunger and satiety",(Weigt J, Malfertheiner P).[193][194]
  • Hypothyroidism, hyperthyroidism, hypoparathyroidism and hyperparathyroidism may mimic some of the symptoms of, can occur concurrently with, be masked by or exacerbate an eating disorder.[195][196][197][198][199][200][201][202]
  • Lupus: 19 psychiatric conditions have been associated with systemic lupus erythematosus (SLE), including depression and bipolar disorder.[203]
  • Toxoplasma seropositivity: even in the absence of symptomatic toxoplasmosis, toxoplasma gondii exposure has been linked to changes in human behavior and psychiatric disorders including those comorbid with eating disorders such as depression. In reported case studies the response to antidepressant treatment improved only after adequate treatment for toxoplasma.[204]
  • Neurosyphilis: It is estimated that there may be up to one million cases of untreated syphilis in the US alone. "The disease can present with psychiatric symptoms alone, psychiatric symptoms that can mimic any other psychiatric illness". Many of the manifestations may appear atypical. Up to 1.3% of short term psychiatric admissions may be attributable to neurosyphilis, with a much higher rate in the general psychiatric population. (Ritchie, M Perdigao J,)[205]
  • Dysautonomia: a wide variety of autonomic nervous system (ANS) disorders may cause a wide variety of psychiatric symptoms including anxiety, panic attacks and depression. Dysautonomia usually involves failure of sympathetic or parasympathetic components of the ANS system but may also include excessive ANS activity. Dysautonomia can occur in conditions such as diabetes and alcoholism.

Psychological disorders which may be confused with an eating disorder, or be co-morbid with one:

  • Emetophobia is an anxiety disorder characterized by an intense fear of vomiting. A person so afflicted may develop rigorous standards of food hygiene, such as not touching food with their hands. They may become socially withdrawn to avoid situations which in their perception may make them vomit. Many who suffer from emetophobia are diagnosed with anorexia or self-starvation. In severe cases of emetophobia they may drastically reduce their food intake.[206][207]
  • Phagophobia is an anxiety disorder characterized by a fear of eating, it is usually initiated by an adverse experience while eating such as choking or vomiting. Persons with this disorder may present with complaints of pain while swallowing.[208]
  • 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 39% of eating disorder cases. BDD is a chronic and debilitating condition which may lead to social isolation, major depression and 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 a new atrophy in the frontotemporal region.[209][210][211][212]


Prevention aims to promote a healthy development before the occurrence of eating disorders. It also intends early identification of an eating disorder before it is too late to treat. Children as young as ages 5–7 are aware of the cultural messages regarding body image and dieting. Prevention comes in bringing these issues to the light. The following topics can be discussed with young children (as well as teens and young adults).

  • Emotional Bites: a simple way to discuss emotional eating is to ask children about why they might eat besides being hungry. Talk about more effective ways to cope with emotions, emphasizing the value of sharing feelings with a trusted adult.
  • Say No to Teasing: another concept is to emphasize that it is wrong to say hurtful things about other people's body sizes.
  • Body Talk: emphasize the importance of listening to one's body. That is, eating when you are hungry (not starving) and stopping when you are satisfied (not stuffed). Children intuitively grasp these concepts.
  • Fitness Comes in All Sizes: educate children about the genetics of body size and the normal changes occurring in the body. Discuss their fears and hopes about growing bigger. Focus on fitness and a balanced diet.[213]

Internet and modern technologies provide new opportunities for prevention. On-line programs have the potential to increase the use of prevention programs. The development and practice of prevention programs via on-line sources make it possible to reach a wide range of people at minimal cost.[214] Such an approach can also make prevention programs to be sustainable.


Treatment varies according to type and severity of eating disorder, and usually more than one treatment option is utilized.[215] There is no well-established treatment for eating disorders, meaning that current views about treatment are based mainly on clinical experience. Family doctors play an important role in early treatment of people with eating disorders by encourages those who are also reluctant to see a psychiatrist.[216] Treatment can take place in a variety of different settings such as community programs, hospitals, day programs, and groups.[217] That said, some treatment methods are:

There are few studies on the cost-effectiveness of the various treatments.[249] Treatment can be expensive;[250][251] due to limitations in health care coverage, people hospitalized with anorexia nervosa may be discharged while still underweight, resulting in relapse and rehospitalization.[252]

For children with anorexia, the only well-established treatment is the family treatment-behavior.[253] For other eating disorders in children, however, there is no well-established treatments, though family treatment-behavior has been used in treating bulimia.[253]


Outcome estimates are complicated by non-uniform criteria used by various studies, but for anorexia nervosa, bulimia nervosa, and binge eating disorder, there seems to be general agreement that full recovery rates are in the 50% to 85% range, with larger proportions of people experiencing at least partial remission.[247][254][255][256] The outcomes of eating disorders (ED) vary among the cases. For many, it can be a lifelong struggle or it can be overcome within months. In the United States, twenty million women and ten million men have an eating disorders at least once in their lifetime.[257] Depending on the type of eating disorder, the age that it began, previous psychiatric disorders, etc., the severity of the outcomes differ.

  • Miscarriages: Pregnant women with a Binge Eating Disorder have shown to have a greater chance of having a miscarriage compared to pregnant women with any other eating disorders. According to a study done, out of a group of pregnant women being evaluated, 46.7% of the pregnancies ended with a miscarriage in women that were diagnosed with BED, with 23.0% in the control. In the same study, 21.4% of women diagnosed with Bulimia Nervosa had their pregnancies end with miscarriages and only 17.7% of the controls.[258]
  • Relapse: An individual who is in remission from BN and EDNOS (Eating Disorder Not Otherwise Specified) is at a high risk of falling back into the habit of self-harming themselves. Factors such as high stress regarding their job, pressures from society, as well as other occurrences that inflict stress on a person, can push a person back to what they feel will ease the pain. A study tracked a group of selected people that were either diagnosed with BN or EDNOS for 60 months. After the 60 months were complete, the researchers recorded whether or not the patients were suffering from a relapse. The results found that the probability of a person previously diagnosed with EDNOS had a 41% chance of relapsing; a person with BN had a 47% chance.[259]
  • Attachment insecurity: People who are showing signs of attachment anxiety will most likely have trouble communicating their emotional status as well as having trouble seeking effective social support. Signs that a person has adopted this symptom include not showing recognition to their caregiver or when he/she is feeling pain. In a clinical sample, it is clear that at the pretreatment step of a patient's recovery, more severe eating disorder symptoms directly corresponds to higher attachment anxiety. The more this symptom increases, the more difficult it is to achieve eating disorder reduction prior to treatment.[260]

Anorexia Nervosa symptoms include the increasing chance of getting osteoporosis. This disease causes the bones of an individual to become brittle, weak, and low in density. Thinning of the hair as well as dry hair and skin is also very common. The muscles of the heart will also start to change if no treatment is inflicted on the patient. This causes the heart to have an abnormally slow heart rate along with low blood pressure. Heart failure becomes a major consideration when this begins to occur. Muscles throughout the body begin to lose their strength. This will cause the individual to begin feeling faint, drowsy, and weak. Along with these symptoms, the body will begin to grow a layer of hair called lanugo. The human body does this in response to the lack of heat and insulation due to the low percentage of body fat.[257]

Bulimia nervosa symptoms include heart problems like an irregular heartbeat that can lead to heart failure and death may occur. This occurs because of the electrolyte imbalance that is a result of the constant binge and purge process. The probability of a gastric rupture increases. A gastric rupture is when there is a sudden rupture of the stomach lining that can be fatal.The acids that are contained in the vomit can cause a rupture in the esophagus as well as tooth decay. As a result, to laxative abuse, irregular bowel movements may occur along with constipation. Sores along the lining of the stomach called peptic ulcers begin to appear and the chance of developing pancreatitis increases.[257]

Binge eating symptoms include high blood pressure, which can cause heart disease if it is not treated. Many patients recognize an increase in the levels of cholesterol. The chance of being diagnosed with gallbladder disease increases, which affects an individual’s digestive tract.[257]


Eating disorders result in about 7,000 deaths a year as of 2010, making them the mental illnesses with the highest mortality rate.[261]


  • Total costs in USA for hospital stays involving eating disorders rose from $165 million in 1999–2000 to $277 million in 2008–2009; this was a 68% increase. The mean cost per discharge of a person with an eating disorder rose by 29% over the decade, from $7,300 to $9,400.
  • Over the decade, hospitalizations involving eating disorders increased among all age groups. The greatest increases occurred among those 45 to 65 years of age (an 88% increase), followed by hospitalizations among people younger than 12 years of age (a 72% increase).
  • The majority of eating disorder inpatients were female. During 2008–2009, 88% of cases involved females, and 12% were males. The report also showed a 53% increase in hospitalizations for males with a principal diagnosis of an eating disorder, from 10% to 12% over the decade.[262]

See also


  1. 1.0 1.1 1.2 1.3 1.4 American Psychiatry Association (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington: American Psychiatric Publishing. pp. 329–354. ISBN 0890425558. 
  2. 2.0 2.1 2.2 Rikani, AA; Choudhry, Z; Choudhry, AM; Ikram, H; Asghar, MW; Kajal, D; Waheed, A; Mobassarah, NJ (October 2013). "A critique of the literature on etiology of eating disorders.". Annals of neurosciences. 20 (4): 157–61. PMC 4117136Freely accessible. PMID 25206042. doi:10.5214/ans.0972.7531.200409. 
  3. 3.0 3.1 3.2 "What are Eating Disorders?". NIMH. Retrieved 24 May 2015. 
  4. Arcelus, J; Witcomb, GL; Mitchell, A (March 2014). "Prevalence of eating disorders amongst dancers: a systemic review and meta-analysis.". European eating disorders review : the journal of the Eating Disorders Association. 22 (2): 92–101. PMID 24277724. doi:10.1002/erv.2271. 
  5. Chen, L; Murad, MH; Paras, ML; Colbenson, KM; Sattler, AL; Goranson, EN; Elamin, MB; Seime, RJ; Shinozaki, G; Prokop, LJ; Zirakzadeh, A (July 2010). "Sexual Abuse and Lifetime Diagnosis of Psychiatric Disorders: Systematic Review and Meta-analysis". Mayo Clinic Proceedings. 85 (7): 618–629. PMID 20458101. doi:10.4065/mcp.2009.0583. 
  6. 6.0 6.1 Smink, FR; van Hoeken, D; Hoek, HW (November 2013). "Epidemiology, course, and outcome of eating disorders.". Current opinion in psychiatry. 26 (6): 543–8. PMID 24060914. doi:10.1097/yco.0b013e328365a24f. 
  7. Pike, KM; Hoek, HW; Dunne, PE (November 2014). "Cultural trends and eating disorders.". Current opinion in psychiatry. 27 (6): 436–42. PMID 25211499. doi:10.1097/yco.0000000000000100. 
  8. American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders (5 ed.). Washington, D.C.: American Psychiatric Publishing. ISBN 978-0-89042-555-8. 
  9. "Anorexia Nervosa". Retrieved 2013-02-13. 
  10. Nolen-Hoeksma (2014). Abnormal Psychology (6th ed.). US: McGraw-Hill. p. 339. ISBN 1-308-21150-3. 
  11. Yale, Susan Nolen-Hoeksema, (2014). Abnormal psychology (6th ed.). New York, NY: McGraw Hill Education. pp. 340–341. ISBN 978-0-07-803538-8. 
  12. "Eating Disorders". American Psychiatric Association. Retrieved 4 December 2014. 
  13. "NAMI National Alliance on Mental Illness". Retrieved 4 December 2014. 
  14. "CD 10 Codes For Psychiatry". Priory Lodge Education Ltd. 2011. 
  15. Thompson, S.B.N. "Eating disorders: a guide for health professionals." London: Chapman & Hall 1993."
  16. Neumaker, K.J. (2000). "Morality rates and causes of death". European Eating Disorders Review. 8 (2): 181–187. doi:10.1002/(SICI)1099-0968(200003)8:2<181::AID-ERV336>3.0.CO;2-# (inactive 2015-04-04). 
  17. Psychology Second Edition 2009, chap. 8 Eating Disorders by Schacter, Daniel L.
  18. [1]
  19. Binge Eating2
  20. Binge Eating
  21. Striegel-Moore, RH; Franko, DL (2008). "Should binge eating disorder be included in the DSM-V? A critical review of the state of the evidence". Annual review of clinical psychology. 4: 305–24. PMID 18370619. doi:10.1146/annurev.clinpsy.4.022007.141149. 
  22. Teaching Students with Mental Health Disorders: Resources for Teachers. Victoria: British Columbia Ministry of Education, Special Programs Branch, 2001. Print.
  23. Tarren-Sweeney, M; Hazell, P (2006). "Mental health of children in foster and kinship care in New South Wales, Australia". Journal of paediatrics and child health. 42 (3): 89–97. PMID 16509906. doi:10.1111/j.1440-1754.2006.00804.x. 
  24. Too Much #Fitspo: When Healthy Eating Becomes an Eating Disorder,, 2015-4-29
  25. Barry, E; Piazza-Gardner, K (2012). "Drunkorexia: Understanding the Co-occurrence of Alcohol Consumption and Eating/Exercise Weight Management Behaviors". Journal of American College Health. 60 (3): 236–243. PMID 22420701. doi:10.1080/07448481.2011.587487. 
  26. Mathieu, J (2009). "What Is Pregorexia?". Journal of the American Dietetic Association. 109 (6): 976–979. PMID 19465173. doi:10.1016/j.jada.2009.04.021. 
  27. Regard, M; Landis, T (1997). ""Gourmand syndrome": Eating passion associated with right anterior lesions". Neurology. 48 (5): 1185–90. PMID 9153440. doi:10.1212/wnl.48.5.1185. 
  28. Strumia, R (2005). "Dermatologic signs in patients with eating disorders". American journal of clinical dermatology. 6 (3): 165–73. PMID 15943493. doi:10.2165/00128071-200506030-00003. 
  29. 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. 
  30. 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. PMID 11688699. doi:10.1007/s002340100589. 
  31. 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. PMID 9813771. doi:10.1002/(SICI)1098-108X(199812)24:4<443::AID-EAT13>3.0.CO;2-4. 
  32. Jagielska, G; Tomaszewicz-Libudzic, EC; Brzozowska, A (2007). "Pellagra: a rare complication of anorexia nervosa". European child & adolescent psychiatry. 16 (7): 417–20. PMID 17712518. doi:10.1007/s00787-007-0613-4. 
  33. Pompili, M; Mancinelli, I; Girardi, P; Accorrà, D; Ruberto, A; Tatarelli, R (2003). "Suicide and attempted suicide in anorexia nervosa and bulimia nervosa". Annali dell'Istituto Superiore di Sanità. 39 (2): 275–81. PMID 14587228. 
  34. Franko, DL; Keel, PK; Dorer, DJ; Blais, MA; Delinsky, SS (2004). "What predicts suicide attempts in women with eating disorders?". Psychological Medicine. 34 (5): 843–53. PMID 15500305. doi:10.1017/S0033291703001545. 
  35. Fedorowicz, VJ; Falissard, B; Foulon, C; Dardennes, R; Divac, SM (2007). "Factors associated with suicidal behaviors in a large French sample of inpatients with eating disorders". The International Journal of Eating Disorders. 40 (7): 589–95. PMID 17607699. doi:10.1002/eat.20415. 
  36. 36.0 36.1 Treasure, J; Claudino, AM; Zucker, N (2010). "Eating disorders". The Lancet. 375 (9714): 583–93. PMID 19931176. doi:10.1016/S0140-6736(09)61748-7. 
  37. "Unexplained Hoarseness: One Clue to an Eating Disorder". Eating Disorders Review. 24 (1). 2013. [author missing]
  38. Hirschberg, AL; Naessén, S; Stridsberg, M; Byström, B; Holtet, J (2004). "Impaired cholecystokinin secretion and disturbed appetite regulation in women with polycystic ovary syndrome". Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology. 19 (2): 79–87. PMID 15624269. doi:10.1080/09513590400002300. 
  39. Naessén, S; Carlström, K; Garoff, L; Glant, R; Hirschberg, AL (2006). "Polycystic ovary syndrome in bulimic women—an evaluation based on the new diagnostic criteria". Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology. 22 (7): 388–94. PMID 16864149. doi:10.1080/09513590600847421. 
  40. McCluskey, S; Evans, C; Lacey, JH; Pearce, JM; Jacobs, H (1991). "Polycystic ovary syndrome and bulimia". Fertility and Sterility. 55 (2): 287–91. PMID 1991526. 
  41. Jahanfar, S; Eden, JA; Nguyent, TV (1995). "Bulimia nervosa and polycystic ovary syndrome". Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology. 9 (2): 113–7. PMID 7502686. doi:10.3109/09513599509160199. 
  42. Morgan, JF; McCluskey, SE; Brunton, JN; Hubert Lacey, J (2002). "Polycystic ovarian morphology and bulimia nervosa: a 9-year follow-up study". Fertility and Sterility. 77 (5): 928–31. PMID 12009345. doi:10.1016/S0015-0282(02)03063-7. 
  43. Lujan, ME; Chizen, DR; Pierson, RA (2008). "Diagnostic Criteria for Polycystic Ovary Syndrome: Pitfalls and Controversies". Journal of obstetrics and gynaecology Canada : JOGC. 30 (8): 671–9. PMC 2893212Freely accessible. PMID 18786289. 
  44. Gailey, J (2009). "Starving is the most fun a girl can have: The Pro-Ana subculture as edgework". Critical Criminology. 17 (2): 93–108. doi:10.1007/s10612-009-9074-z. 
  45. Borzekowski, D; Schenk, S; Wilson, J; Peebles, R (2010). "E-Ana and e-mia: A content analysis of pro-eating disorder web sites". American Journal of Public Health. 100 (8): 1526–1534. PMC 2901299Freely accessible. PMID 20558807. doi:10.2105/AJPH.2009.172700. 
  46. Wolf, M; Theis, F; Kordy, H (2013). "Language Use in Eating Disorder Blogs: Psychological Implications of Social Online Activity". Journal of Language and Social Psychology. 32 (2): 212–226. doi:10.1177/0261927x12474278. 
  47. 47.0 47.1 Ruffolo, J; Phillips, K; Menard, W; Fay, C; Weisberg, R (2006). "Comorbidity of Body Dysmorphic Disorder and Eating Disorders: Severity of Psychopathology and Body Image Disturbance". The International Journal of Eating Disorders. 39 (1): 11–19. PMID 16254870. doi:10.1002/eat.20219. 
  48. 48.0 48.1 Grant, J; Kim, S; Eckert, E (November 2002). "Body Dysmorphic Disorder in Patients with Anorexia Nervosa: Prevalence, Clinical Features, and Delusionality of Body Image". Wiley Interscience. 32 (3): 291–300. PMID 12210643. doi:10.1002/eat.10091. 
  49. 49.0 49.1 49.2 Bulick, C; Hebebrand, J; Keski-Rahkonen, A; Klump, K; Reichborn, T; Mazzeo, SE; Wade, TD (2007). "Genetic Epidemiology, Endophenotypes, and Eating Disorder Classification". The International Journal of Eating Disorders. 40: S52–S60. PMID 17573683. doi:10.1002/eat.20398. 
  50. 50.0 50.1 DeAngelis, T (2002). "A genetic link to anorexia". American Psychological Association. 33 (3): 34. 
  51. 51.0 51.1 Klump, KL; Kaye, WH; Strober, M (2001). "The evolving genetic foundations of eating disorders". The Psychiatric clinics of North America. 24 (2): 215–25. PMID 11416922. doi:10.1016/S0193-953X(05)70218-5. 
  52. Mazzeo, SE; Bulik, CM (2009). "Environmental and genetic risk factors for eating disorders: What the clinician needs to know". Child and adolescent psychiatric clinics of North America. 18 (1): 67–82. PMC 2719561Freely accessible. PMID 19014858. doi:10.1016/j.chc.2008.07.003. 
  53. 53.0 53.1 Patel, P; Wheatcroft, R; Park, R; Stein, A (2002). "The Children of Mothers With Eating Disorders". Clinical Child and Family Psychology Review. 5 (1): 1–19. PMID 11993543. doi:10.1023/A:1014524207660. 
  54. 54.0 54.1 Frieling, H; Römer, KD; Scholz, S; Mittelbach, F; Wilhelm, J; De Zwaan, M; Jacoby, GE; Kornhuber, J; Hillemacher, T; Bleich, S (2010). "Epigenetic dysregulation of dopaminergic genes in eating disorders". The International Journal of Eating Disorders. 43 (7): 577–83. PMID 19728374. doi:10.1002/eat.20745. 
  55. Frieling, Helge; Römer, Konstanze D.; Scholz, Sarah; Mittelbach, Franziska; Wilhelm, Julia; De Zwaan, Martina; Jacoby, Georg E.; Kornhuber, Johannes; Hillemacher, Thomas (2010-11-01). "Epigenetic dysregulation of dopaminergic genes in eating disorders". International Journal of Eating Disorders. 43 (7): 577–583. ISSN 1098-108X. PMID 19728374. doi:10.1002/eat.20745. 
  56. Frieling, H; Bleich, S; Otten, J; Römer, KD; Kornhuber, J; et al. (2008). "Epigenetic downregulation of atrial natriuretic peptide but not vasopressin mRNA expression in females with eating disorders is related to impulsivity". Neuropsychopharmacology. 33 (11): 2605–9. PMID 18172431. doi:10.1038/sj.npp.1301662. 
  57. Campbell, Iain C.; Mill, Jonathan; Uher, Rudolf; Schmidt, Ulrike (2011-01-01). "Eating disorders, gene–environment interactions and epigenetics". Neuroscience & Biobehavioral Reviews. 35 (3): 784–793. PMID 20888360. doi:10.1016/j.neubiorev.2010.09.012. 
  58. Westen, D; Harnden-Fischer, J (2001). "Personality profiles in eating disorders: rethinking the distinction between axis I and axis II". The American Journal of Psychiatry. 158 (4): 547–62. PMID 11282688. doi:10.1176/appi.ajp.158.4.547. 
  59. Rosenvinge, JH; Martinussen, M; Ostensen, E (2000). "The comorbidity of eating disorders and personality disorders: a meta-analytic review of studies published between 1983 and 1998". Eating and weight disorders. 5 (2): 52–61. PMID 10941603. doi:10.1007/bf03327480. 
  60. 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. PMID 15569892. doi:10.1176/appi.ajp.161.12.2215. 
  61. Thornton, C; Russell, J (1997). "Obsessive compulsive comorbidity in the dieting disorders". The International Journal of Eating Disorders. 21 (1): 83–7. PMID 8986521. doi:10.1002/(SICI)1098-108X(199701)21:1<83::AID-EAT10>3.0.CO;2-P. 
  62. Vitousek, K; Manke, F (1994). "Personality variables and disorders in anorexia nervosa and bulimia nervosa". Journal of Abnormal Psychology. 103 (1): 137–47. PMID 8040475. doi:10.1037/0021-843X.103.1.137. 
  63. Braun, DL; Sunday, SR; Halmi, KA (1994). "Psychiatric comorbidity in patients with eating disorders". Psychological Medicine. 24 (4): 859–67. PMID 7892354. doi:10.1017/S0033291700028956. 
  64. Spindler, A; Milos, G (2007). "Links between eating disorder symptom severity and psychiatric comorbidity". Eating behaviors. 8 (3): 364–73. PMID 17606234. doi:10.1016/j.eatbeh.2006.11.012. 
  65. Collier, R (2010). "DSM revision surrounded by controversy". Canadian Medical Association Journal. 182 (1): 16–7. PMC 2802599Freely accessible. PMID 19920166. doi:10.1503/cmaj.109-3108. 
  66. Kutchins, H; Kirk, SA (1989). "DSM-III-R: the conflict over new psychiatric diagnoses". Health & social work. 14 (2): 91–101. PMID 2714710. 
  67. Busko, Marlene. "DSM-IV Diagnostic Criteria for Eating Disorders May Be Too Stringent". Medscape. 
  68. Murdoch, CJ (10 September 2009). "The Politics of Disease Definition: A Summer of DSM-V Controversy in Review. Stanford Center for Law and the Biosciences". 
  69. "Psychiatry manual's secrecy criticized". Los Angeles Times. 29 December 2008. 
  70. Casper, RC (1998). "Depression and eating disorders". Depression and Anxiety. 8 (Suppl 1): 96–104. PMID 9809221. doi:10.1002/(SICI)1520-6394(1998)8:1+<96::AID-DA15>3.0.CO;2-4. 
  71. 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. PMID 12113200. doi:10.1016/S0272-7358(01)00112-X. 
  72. Bulik, CM; Klump, KL; Thornton, L; Kaplan, AS; Devlin, B (2004). "Alcohol use disorder comorbidity in eating disorders: a multicenter study". The Journal of clinical psychiatry. 65 (7): 1000–6. PMID 15291691. doi:10.4088/JCP.v65n0718. 
  73. Larsson, JO; Hellzén, M (2004). "Patterns of personality disorders in women with chronic eating disorders". Eating and weight disorders : EWD. 9 (3): 200–5. PMID 15656014. doi:10.1007/bf03325067. 
  74. 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. PMID 17676696. doi:10.1002/erv.784. 
  75. Ronningstam, E (1996). "Pathological narcissism and narcissistic personality disorder in Axis I disorders". Harvard Review of Psychiatry. 3 (6): 326–40. PMID 9384963. doi:10.3109/10673229609017201. 
  76. 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. PMID 12562569. doi:10.1176/appi.ajp.160.2.242. 
  77. 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. PMC 3272757Freely accessible. PMID 16841619. doi:10.4088/JCP.v67n0503. 
  78. Lucka, I; Cebella, A (2004). "Characteristics of the forming personality in children suffering from anorexia nervosa". Psychiatria polska. 38 (6): 1011–8. PMID 15779665. 
  79. 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 : JDBP. 28 (4): 302–7. PMID 17700082. doi:10.1097/DBP.0b013e3180327917. 
  80. Dukarm, CP (May 2005). "Bulimia nervosa and attention deficit hyperactivity disorder: a possible role for stimulant medication". Journal of Women's Health. 14 (4): 345–50. PMID 15916509. doi:10.1089/jwh.2005.14.345. 
  81. Mikami, AY; Hinshaw, SP; Arnold, LE; Hoza, B; Hechtman, L (2010). "Bulimia nervosa symptoms in the multimodal treatment study of children with ADHD". The International Journal of Eating Disorders. 43 (3): 248–59. PMID 19378318. doi:10.1002/eat.20692. 
  82. Cortese, S; Bernardina, BD; Mouren, MC (2007). "Attention-deficit/hyperactivity disorder (ADHD) and binge eating". Nutrition Reviews. 65 (9): 404–11. PMID 17958207. doi:10.1111/j.1753-4887.2007.tb00318.x. 
  83. Bruce, KR; Steiger, H; Koerner, NM; Israel, M; Young, SN (2004). "Bulimia nervosa with co-morbid avoidant personality disorder: behavioural characteristics and serotonergic function". Psychological Medicine. 34 (1): 113–24. PMID 14971632. doi:10.1017/S003329170300864X. 
  84. Podar, I; Hannus, A; Allik, J (1999). "Personality and affectivity characteristics associated with eating disorders: a comparison of eating disordered, weight-preoccupied, and normal samples". Journal of Personality Assessment. 73 (1): 133–47. PMID 10497805. doi:10.1207/S15327752JPA730109. 
  85. Gardini, S; Cloninger, CR; Venneri, A (2009). "Individual differences in personality traits reflect structural variance in specific brain regions". Brain Research Bulletin. 79 (5): 265–70. PMID 19480986. doi:10.1016/j.brainresbull.2009.03.005. 
  86. Marsh, AA; Finger, EC; Mitchell, DG; Reid, ME; Sims, C (2008). "Reduced amygdala response to fearful expressions in children and adolescents with callous-unemotional traits and disruptive behavior disorders". The American Journal of Psychiatry. 165 (6): 712–20. PMID 18281412. doi:10.1176/appi.ajp.2007.07071145. 
  87. Iidaka, T; Matsumoto, A; Ozaki, N; Suzuki, T; Iwata, N (2006). "Volume of left amygdala subregion predicted temperamental trait of harm avoidance in female young subjects. A voxel-based morphometry study". Brain Research. 1125 (1): 85–93. PMID 17113049. doi:10.1016/j.brainres.2006.09.015. 
  88. Rubino, V; Blasi, G; Latorre, V; Fazio, L; D'errico, I (2007). "Activity in medial prefrontal cortex during cognitive evaluation of threatening stimuli as a function of personality style". Brain Research Bulletin. 74 (4): 250–7. PMID 17720547. doi:10.1016/j.brainresbull.2007.06.019. 
  89. Spinella, M; Lyke, J (2004). "Executive personality traits and eating behavior". The International journal of neuroscience. 114 (1): 83–93. PMID 14660070. doi:10.1080/00207450490249356. 
  90. Sinai, C; Hirvikoski, T; Vansvik, ED; Nordström, AL; Linder, J (2009). "Thyroid hormones and personality traits in attempted suicide". Psychoneuroendocrinology. 34 (10): 1526–32. PMID 19525070. doi:10.1016/j.psyneuen.2009.05.009. 
  91. Horesh, N; Apter, A; Ishai, J; Danziger, Y; Miculincer, M (1996). "Abnormal psychosocial situations and eating disorders in adolescence". Journal of the American Academy of Child and Adolescent Psychiatry. 35 (7): 921–7. PMID 8768353. doi:10.1097/00004583-199607000-00019. 
  92. Köpp, W; Rost, F; Kiesewetter, S; Deter, HC (2010). "The fatal outcome of an individual with anorexia nervosa and Sheehan's syndrome as a result of acute enterocolitis: a case report". The International Journal of Eating Disorders. 43 (1): 93–6. PMID 19247986. doi:10.1002/eat.20652. 
  93. Rayworth, BB; Wise, LA; Harlow, BL (2004). "Childhood abuse and risk of eating disorders in women". Epidemiology (Cambridge, Mass.). 15 (3): 271–8. PMID 15097006. doi:10.1097/01.ede.0000120047.07140.9d. 
  94. Wonderlich, SA; Brewerton, TD; Jocic, Z; Dansky, BS; Abbott, DW (1997). "Relationship of childhood sexual abuse and eating disorders". Journal of the American Academy of Child and Adolescent Psychiatry. 36 (8): 1107–15. PMID 9256590. doi:10.1097/00004583-199708000-00018. 
  95. Feldman, MB; Meyer, IH (2007). "Childhood Abuse and Eating Disorders in Gay and Bisexual Men". The International Journal of Eating Disorders. 40 (5): 418–23. PMC 2042584Freely accessible. PMID 17506080. doi:10.1002/eat.20378. 
  96. Rohde, P; Ichikawa, L; Simon, GE; Ludman, EJ; Linde, JA (2008). "Associations of child sexual and physical abuse with obesity and depression in middle-aged women". Child abuse & neglect. 32 (9): 878–87. PMC 2609903Freely accessible. PMID 18945487. doi:10.1016/j.chiabu.2007.11.004. 
  97. Williamson, DF; Thompson, TJ; Anda, RF; Dietz, WH; Felitti, V (2002). "Body weight and obesity in adults and self-reported abuse in childhood". International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity. 26 (8): 1075–82. PMID 12119573. doi:10.1038/sj.ijo.0802038. 
  98. Waller, G (1992). "Sexual abuse and the severity of bulimic symptoms". The British journal of psychiatry : the journal of mental science. 161: 90–3. PMID 1638336. doi:10.1192/bjp.161.1.90. 
  99. Waller, G; Halek, C; Crisp, AH (1993). "Sexual abuse as a factor in anorexia nervosa: evidence from two separate case series". Journal of psychosomatic research. 37 (8): 873–9. PMID 8301627. doi:10.1016/0022-3999(93)90176-G. 
  100. Troop, NA; Bifulco, A (2002). "Childhood social arena and cognitive sets in eating disorders". The British journal of clinical psychology. The British Psychological Society. 41 (Pt 2): 205–11. PMID 12034006. doi:10.1348/014466502163976. 
  101. Nonogaki, K; Nozue, K; Oka, Y (2007). "Social isolation affects the development of obesity and type 2 diabetes in mice". Endocrinology. 148 (10): 4658–66. PMID 17640995. doi:10.1210/en.2007-0296. 
  102. Esplen, MJ; Garfinkel, P; Gallop, R (2000). "Relationship between self-soothing, aloneness, and evocative memory in bulimia nervosa". The International Journal of Eating Disorders. 27 (1): 96–100. PMID 10590454. doi:10.1002/(SICI)1098-108X(200001)27:1<96::AID-EAT11>3.0.CO;2-S. 
  103. Larson, R; Johnson, C (1985). "Bulimia: disturbed patterns of solitude". Addictive behaviors. 10 (3): 281–90. PMID 3866486. doi:10.1016/0306-4603(85)90009-7. 
  104. Fox, John (July 2009). "Eating Disorders and Emotions" (PDF). Clinical Psychology & Psychotherapy. 16 (237–239): 237–239. doi:10.1002/cpp.625. 
  105. Johnson, JG; Cohen, P; Kasen, S; Brook, JS (2002). "Childhood adversities associated with risk for eating disorders or weight problems during adolescence or early adulthood". The American Journal of Psychiatry. 159 (3): 394–400. PMID 11870002. doi:10.1176/appi.ajp.159.3.394. 
  106. Klesges, RC; Coates, TJ; Brown, G; Sturgeon-Tillisch, J; Moldenhauer-Klesges, LM (1983). "Parental influences on children's eating behavior and relative weight". Journal of applied behavior analysis. 16 (4): 371–8. PMC 1307898Freely accessible. PMID 6654769. doi:10.1901/jaba.1983.16-371. 
  107. Galloway, AT; Fiorito, L; Lee, Y; Birch, LL (2005). "Parental Pressure, Dietary Patterns, and Weight Status among Girls Who Are "Picky Eaters"". Journal of the American Dietetic Association. 105 (4): 541–8. PMC 2530930Freely accessible. PMID 15800554. doi:10.1016/j.jada.2005.01.029. 
  108. Jones, C; Harris, G; Leung, N (2005). "Parental rearing behaviours and eating disorders: the moderating role of core beliefs". Eating behaviors. 6 (4): 355–64. PMID 16257809. doi:10.1016/j.eatbeh.2005.05.002. 
  109. Brown, R; Ogden, J (2004). "Children's eating attitudes and behaviour: a study of the modelling and control theories of parental influence". Health education research. 19 (3): 261–71. PMID 15140846. doi:10.1093/her/cyg040. 
  110. Savage, JS; Fisher, JO; Birch, LL (2007). "Parental Influence on Eating Behavior: Conception to Adolescence". The Journal of law, medicine & ethics : a journal of the American Society of Law, Medicine & Ethics. 35 (1): 22–34. PMC 2531152Freely accessible. PMID 17341215. doi:10.1111/j.1748-720X.2007.00111.x. 
  111. Nolen-Hoeksema, Susan. Abnormal Psychology, 6e. McGraw-Hill Education, 2014. p. 359-360.
  112. Schreiber, GB; Robins, M; Striegel-Moore, R; Obarzanek, E (1996). "Weight modification efforts reported by black and white preadolescent girls: National Heart, Lung, and Blood Institute Growth and Health Study". Pediatrics. 98 (1): 63–70. PMID 8668414. 
  113. Page, RM; Suwanteerangkul, J (2007). "Dieting among Thai adolescents: having friends who diet and pressure to diet". Eating and weight disorders : EWD. 12 (3): 114–24. PMID 17984635. doi:10.1007/bf03327638. 
  114. McKnight, Investigators (2003). "Risk factors for the onset of eating disorders in adolescent girls: results of the McKnight longitudinal risk factor study". The American Journal of Psychiatry. 160 (2): 248–54. PMID 12562570. doi:10.1176/appi.ajp.160.2.248. 
  115. Paxton, SJ; Schutz, HK; Wertheim, EH; Muir, SL (1999). "Friendship clique and peer influences on body image concerns, dietary restraint, extreme weight-loss behaviors, and binge eating in adolescent girls". Journal of Abnormal Psychology. 108 (2): 255–66. PMID 10369035. doi:10.1037/0021-843X.108.2.255. 
  116. Rukavina, T; Pokrajac-Bulian, A (2006). "Thin-ideal internalization, body dissatisfaction and symptoms of eating disorders in Croatian adolescent girls". Eating and weight disorders : EWD. 11 (1): 31–7. PMID 16801743. doi:10.1007/bf03327741. 
  117. [ Nolen-Hoeksema, Susan (2014). (Ab)normal psychology. New York, NY: McGraw Hill. p. 323. ISBN 978-0-07-803538-8.
  118. Garner, DM; Garfinkel, PE (2009). "Socio-cultural factors in the development of anorexia nervosa". Psychological Medicine. 10 (4): 647–56. PMID 7208724. doi:10.1017/S0033291700054945. 
  119. Eisenberg, ME; Neumark-Sztainer, D; Story, M; Perry, C (2005). "The role of social norms and friends' influences on unhealthy weight-control behaviors among adolescent girls". Social Science & Medicine. 60 (6): 1165–73. PMID 15626514. doi:10.1016/j.socscimed.2004.06.055. 
  120. Jung, J; Lennon, SJ (2003). "Body Image, Appearance Self-Schema, and Media Images". Family and Consumer Sciences Research Journal. 32: 27–51. doi:10.1177/1077727X03255900. 
  121. Simpson, KJ (2002). "Anorexia nervosa and culture". Journal of Psychiatric and Mental Health Nursing. 9 (1): 65–71. PMID 11896858. doi:10.1046/j.1351-0126.2001.00443.x. 
  122. 122.0 122.1 Soh, NL; Touyz, SW; Surgenor, LJ (2006). "Eating and body image disturbances across cultures: A review". European Eating Disorders Review. 14 (1): 54–65. doi:10.1002/erv.678. 
  123. Keel, PK; Klump, KL (2003). "Are eating disorders culture-bound syndromes? Implications for conceptualizing their etiology". Psychological Bulletin. 129 (5): 747–69. PMID 12956542. doi:10.1037/0033-2909.129.5.747. 
  124. Nevonen, L; Norring, C (2004). "Socio-economic variables and eating disorders: A comparison between patients and normal controls". Eating and Weight Disorders. 9 (4): 279–84. PMID 15844400. doi:10.1007/BF03325082. 
  125. Polivy, J; Herman, CP (2002). "Causes of eating disorders". Annual Review of Psychology. 53: 187–213. PMID 11752484. doi:10.1146/annurev.psych.53.100901.135103. 
  126. Essick, Ellen (2006). "Eating Disorders and Sexuality". In Steinberg, Shirley R.; Parmar, Priya; Richard, Birgit. Contemporary Youth Culture: An International Encyclopedia. Greenwood. pp. 276–80. ISBN 978-0-313-33729-1. 
  127. DeMonte, Alexandria. "Beauty Pageants". M.E. Sharpe. Archived from the original on December 9, 2013. Retrieved 24 September 2013. 
  128. Nolen-Hoeksema, Susan (2014). abnormal psychology (6th ed.). New York: McGraw-Hill Education. pp. 353–354. ISBN 978-0-07-803538-8. 
  129. 129.0 129.1 Harrell, WA; Boisvert, JA (2009). "Homosexuality as a Risk Factor for Eating Disorder Symptomatology in Men". The Journal of Men's Studies. 17 (3): 210–25. doi:10.3149/jms.1703.210. 
  130. 130.0 130.1 130.2 Burton, CL; Allomong, TW; Halkitis, PN; Siconolfi, D (2009). "Body Dissatisfaction and Eating Disorders in a Sample of Gay and Bisexual Men". International Journal of Men's Health. 8 (3): 254–64. doi:10.3149/jmh.0803.254. 
  131. Mash, Eric Jay; Wolfe, David Allen (2010). "Eating Disorders and Related Conditions". Abnormal Child Psychology. Belmont, CA: Wadsworth: Cengage Learning. pp. 415–26. ISBN 978-0-495-50627-0. 
  132. Schwitzer, AM (2012). "Diagnosing, Conceptualizing, and Treating Eating Disorders Not Otherwise Specified: A Comprehensive Practice Model". Journal of Counseling & Development. 90 (3): 281–9. doi:10.1002/j.1556-6676.2012.00036.x. 
  133. Kim Willsher, Models in France must provide doctor's note to work, The Guardian, 18 December.
  134. Gross, MJ; Kahn, JP; Laxenaire, M; Nicolas, JP; Burlet, C (1994). "Corticotropin-releasing factor and anorexia nervosa: reactions of the hypothalamus-pituitary-adrenal axis to neurotropic stress". Annales d'endocrinologie. 55 (6): 221–8. PMID 7864577. 
  135. Licinio, J; Wong, ML; Gold, PW (1996). "The hypothalamic-pituitary-adrenal axis in anorexia nervosa". Psychiatry Research. 62 (1): 75–83. PMID 8739117. doi:10.1016/0165-1781(96)02991-5. 
  136. Chaudhri, O; Small, C; Bloom, S (2006). "Gastrointestinal hormones regulating appetite". Philosophical Transactions of the Royal Society B. 361 (1471): 1187–209. PMC 1642697Freely accessible. PMID 16815798. doi:10.1098/rstb.2006.1856. 
  137. Gendall, KA; Kaye, WH; Altemus, M; McConaha, CW; La Via, MC (1999). "Leptin, neuropeptide Y, and peptide YY in long-term recovered eating disorder patients". Biological Psychiatry. 46 (2): 292–9. PMID 10418705. doi:10.1016/S0006-3223(98)00292-3. 
  138. Wilhelm, J; Müller, E; De Zwaan, M; Fischer, J; Hillemacher, T; Kornhuber, J; Bleich, S; Frieling, H (2010). "Elevation of homocysteine levels is only partially reversed after therapy in females with eating disorders". Journal of neural transmission (Vienna, Austria : 1996). 117 (4): 521–7. PMID 20191295. doi:10.1007/s00702-010-0379-6. 
  139. Jimerson, DC; Lesem, MD; Kaye, WH; Hegg, AP; Brewerton, TD (1990). "Eating disorders and depression: is there a serotonin connection?". Biological Psychiatry. 28 (5): 443–54. PMID 2207221. doi:10.1016/0006-3223(90)90412-U. 
  140. Leibowitz, SF (1990). "The role of serotonin in eating disorders". Drugs. 39 Suppl 3: 33–48. PMID 2197074. doi:10.2165/00003495-199000393-00005. 
  141. Blundell, JE; Lawton, CL; Halford, JC (1995). "Serotonin, eating behavior, and fat intake". Obesity research. 3 Suppl 4: 471S–476S. PMID 8697045. doi:10.1002/j.1550-8528.1995.tb00214.x. 
  142. Kaye, WH (1997). "Anorexia nervosa, obsessional behavior, and serotonin". Psychopharmacology bulletin. 33 (3): 335–44. PMID 9550876. 
  143. Bailer, UF; Price, JC; Meltzer, CC; Mathis, CA; Frank, GK; Weissfeld, L; McConaha, CW; Henry, SE; Brooks-Achenbach, S; Barbarich, NC; Kaye, WH (2004). "Altered 5-HT(2A) receptor binding after recovery from bulimia-type anorexia nervosa: relationships to harm avoidance and drive for thinness". Neuropsychopharmacology. 29 (6): 1143–55. PMID 15054474. doi:10.1038/sj.npp.1300430. 
  144. Hainer, V; Kabrnova, K; Aldhoon, B; Kunesova, M; Wagenknecht, M (2006). "Serotonin and norepinephrine reuptake inhibition and eating behavior". Annals of the New York Academy of Sciences. 1083: 252–69. Bibcode:2006NYASA1083..252H. PMID 17148744. doi:10.1196/annals.1367.017. 
  145. George, DT; Kaye, WH; Goldstein, DS; Brewerton, TD; Jimerson, DC (July 1990). "Altered norepinephrine regulation in bulimia: effects of pharmacological challenge with isoproterenol". Psychiatry Res. 33 (1): 1–10. PMID 2171006. doi:10.1016/0165-1781(90)90143-S. 
  146. Wang, GJ; Volkow, ND; Logan, J; Pappas, NR; Wong, CT; Zhu, W; Netusil, N; Fowler, JS (2001). "Brain dopamine and obesity". Lancet. 357 (9253): 354–7. PMID 11210998. doi:10.1016/S0140-6736(00)03643-6. 
  147. Zhulenko, VN; Georgieva, GN; Smirnova, LA (1975). "Mercury content in the organs and tissues of slaughter animals". Veterinariia (4): 96–8. PMID 1216579. 
  148. 148.0 148.1 148.2 148.3 148.4 Carlson, Neil (2013). "Ingestive Behavior". Physiology of Behavior. University of Massachusetts, Amherst: Pearson. pp. 428–432. ISBN 0-205-23939-0. 
  149. 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. PMID 11919545. doi:10.1067/mlc.2002.121014. 
  150. Ferron, F; Considine, R; Peino, R; Lado; I (1997). "Serum leptin concentrations in patients with anorexia nervosa, bulimia nervosa, and non-specific eating disorders correlate with the body mass index but are independent of the respective disease". Clinical Endocrinology. 46 (3): 289–293. PMID 9156037. doi:10.1046/j.1365-2265.1997.1260938.x. 
  151. Fetissov, SO; Harro, J; Jaanisk, M; Järv, A; Podar, I; Nilsson, I; Sakthivel, P; Lefvert, AK; et al. (2005). "Autoantibodies against neuropeptides are associated with psychological traits in eating disorders". Proceedings of the National Academy of Sciences of the United States of America. 102 (41): 14865–70. Bibcode:2005PNAS..10214865F. PMC 1253594Freely accessible. PMID 16195379. doi:10.1073/pnas.0507204102. 
  152. Sinno, MH; Do Rego, JC; Coëffier, M; Bole-Feysot, C; Ducrotté, P; Gilbert, D; Tron, F; Costentin, J; Hökfelt, T; Déchelotte, P; Fetissov, SO (2009). "Regulation of feeding and anxiety by alpha-MSH reactive autoantibodies". Psychoneuroendocrinology. 34 (1): 140–9. PMID 18842346. doi:10.1016/j.psyneuen.2008.08.021. 
  153. Translational Psychiatry (2014) 4, e458; doi:10.1038/tp.2014.98
  154. Sokol, MS (2000). "Infection-triggered anorexia nervosa in children: clinical description of four cases". Journal of child and adolescent psychopharmacology. 10 (2): 133–45. PMID 10933123. doi:10.1089/cap.2000.10.133. 
  155. Uher, R; Treasure, J (2005). "Brain lesions and eating disorders". Journal of neurology, neurosurgery, and psychiatry. 76 (6): 852–7. PMC 1739667Freely accessible. PMID 15897510. doi:10.1136/jnnp.2004.048819. 
  156. Houy, E; Debono, B; Dechelotte, P; Thibaut, F (2007). "Anorexia nervosa associated with right frontal brain lesion". The International Journal of Eating Disorders. 40 (8): 758–61. PMID 17683096. doi:10.1002/eat.20439. 
  157. 157.0 157.1 Trummer, M; Eustacchio, S; Unger, F; Tillich, M; Flaschka, G (2002). "Right hemispheric frontal lesions as a cause for anorexia nervosa report of three cases". Acta neurochirurgica. 144 (8): 797–801. PMID 12181689. doi:10.1007/s00701-002-0934-5. 
  158. Winston, AP; Barnard, D; D'souza, G; Shad, A; Sherlala, K (2006). "Pineal germinoma presenting as anorexia nervosa: Case report and review of the literature". The International Journal of Eating Disorders. 39 (7): 606–8. PMID 17041920. doi:10.1002/eat.20322. 
  159. Chipkevitch, E; Fernandes, AC (1993). "Hypothalamic tumor associated with atypical forms of anorexia nervosa and diencephalic syndrome". Arquivos de neuro-psiquiatria. 51 (2): 270–4. PMID 8274094. doi:10.1590/S0004-282X1993000200022. 
  160. Rohrer, TR; Fahlbusch, R; Buchfelder, M; Dörr, HG (2006). "Craniopharyngioma in a female adolescent presenting with symptoms of anorexia nervosa". Klinische Padiatrie. 218 (2): 67–71. PMID 16506105. doi:10.1055/s-2006-921506. 
  161. Chipkevitch, E (1994). "Brain tumors and anorexia nervosa syndrome". Brain & development. 16 (3): 175–9. PMID 7943600. doi:10.1016/0387-7604(94)90064-7. 
  162. Lin, L; Liao, SC; Lee, YJ; Tseng, MC; Lee, MB (2003). "Brain tumor presenting as anorexia nervosa in a 19-year-old man". Journal of the Formosan Medical Association, Taiwan yi zhi. 102 (10): 737–40. PMID 14691602. 
  163. Conrad, R; Wegener, I; Geiser, F; Imbierowicz, K; Liedtke, R (2008). "Nature against nurture: calcification in the right thalamus in a young man with anorexia nervosa and obsessive-compulsive personality disorder". CNS spectrums. 13 (10): 906–10. PMID 18955946. 
  164. Burke, CJ; Tannenberg, AE; Payton, DJ (1997). "Ischaemic cerebral injury, intrauterine growth retardation, and placental infarction". Developmental medicine and child neurology. 39 (11): 726–30. PMID 9393885. doi:10.1111/j.1469-8749.1997.tb07373.x. 
  165. Cnattingius, S; Hultman, CM; Dahl, M; Sparén, P (1999). "Very preterm birth, birth trauma, and the risk of anorexia nervosa among girls". Archives of General Psychiatry. 56 (7): 634–8. PMID 10401509. doi:10.1001/archpsyc.56.7.634. 
  166. 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. PMID 16389201. doi:10.1001/archpsyc.63.1.82. 
  167. 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. PMID 18256341. doi:10.1097/PSY.0b013e318164604e. 
  168. Decker, MJ; Hue, GE; Caudle, WM; Miller, GW (2003). "Episodic neonatal hypoxia evokes executive dysfunction and regionally specific alterations in markers of dopamine signaling". Neuroscience. 117 (2): 417–25. PMID 12614682. doi:10.1016/S0306-4522(02)00805-9. 
  169. Decker, MJ; Rye, DB (2002). "Neonatal intermittent hypoxia impairs dopamine signaling and executive functioning". Sleep & breathing. 6 (4): 205–10. PMID 12524574. doi:10.1007/s11325-002-0205-y. 
  170. Scher, MS (2003). "Fetal and neonatal neurologic case histories: assessment of brain disorders in the context of fetal-maternal-placental disease. Part 1: Fetal neurologic consultations in the context of antepartum events and prenatal brain development". Journal of child neurology. 18 (2): 85–92. PMID 12693773. doi:10.1177/08830738030180020901. 
  171. Scher, MS; Wiznitzer, M; Bangert, BA (2002). "Cerebral infarctions in the fetus and neonate: maternal-placental-fetal considerations". Clinics in perinatology. 29 (4): 693–724, vi–vii. PMID 12516742. doi:10.1016/S0095-5108(02)00055-6. 
  172. Burke, CJ; Tannenberg, AE (1995). "Prenatal brain damage and placental infarction- an autopsy study". Developmental medicine and child neurology. 37 (6): 555–62. PMID 7789664. doi:10.1111/j.1469-8749.1995.tb12042.x. 
  173. Squier, M; Keeling, JW (1991). "The incidence of prenatal brain injury". Neuropathology and applied neurobiology. 17 (1): 29–38. PMID 2057048. doi:10.1111/j.1365-2990.1991.tb00691.x. 
  174. Al Mamun, A; Lawlor, DA; Alati, R; O'Callaghan, MJ (2006). "Does maternal smoking during pregnancy have a direct effect on future offspring obesity? Evidence from a prospective birth cohort study". American Journal of Epidemiology. 164 (4): 317–25. PMID 16775040. doi:10.1093/aje/kwj209. 
  175. Keys, A; Brozek, J; Henschel, A; Mickelsen, O; Taylor, H (1950). The Biology of Human Starvation. University of Minnesota Press. 
  176. Pritts, SD; Susman, J (2003). "Diagnosis of eating disorders in primary care". American family physician. 67 (2): 297–304. PMID 12562151. 
  177. Gelder, Mayou, Geddes (2005). Psychiatry: Page 161. New York, NY; Oxford University Press Inc.
  178. O'Brien, A; Hugo, P; Stapleton, S; Lask, B (2001). ""Anorexia saved my life": coincidental anorexia nervosa and cerebral meningioma". The International Journal of Eating Disorders. 30 (3): 346–9. PMID 11746295. doi:10.1002/eat.1095. 
  179. Garfinkel, PE; Newman, A (2001). "The eating attitudes test: twenty-five years later". Eating and weight disorders : EWD. 6 (1): 1–24. PMID 11300541. doi:10.1007/bf03339747. 
  180. Rueda, GE; Díaz, LA; Campo, A; Barros, JA; Avila, GC (2005). "Validation of the SCOFF questionnaire for screening of eating disorders in university women". Biomedica : revista del Instituto Nacional de Salud. 25 (2): 196–202. PMID 16022374. 
  181. Probst, M; Pieters, G; Vanderlinden, J (2008). "Evaluation of body experience questionnaires in eating disorders in female patients (AN/BN) and nonclinical participants". The International Journal of Eating Disorders. 41 (7): 657–65. PMID 18446834. doi:10.1002/eat.20531. 
  182. Ben-Tovim, DI; Walker, MK (1992). "A quantitative study of body-related attitudes in patients with anorexia and bulimia nervosa". Psychological Medicine. 22 (4): 961–9. PMID 1488491. doi:10.1017/S0033291700038538. 
  183. Olson, MS; Williford, HN; Richards, LA; Brown, JA; Pugh, S (1996). "Self-reports on the Eating Disorder Inventory by female aerobic instructors". Perceptual and motor skills. 82 (3 Pt 1): 1051–8. PMID 8774050. doi:10.2466/pms.1996.82.3.1051. 
  184. Wilfley, DE; Schwartz, MB; Spurrell, EB; Fairburn, CG (2000). "Using the eating disorder examination to identify the specific psychopathology of binge eating disorder". The International Journal of Eating Disorders. 27 (3): 259–69. PMID 10694711. doi:10.1002/(SICI)1098-108X(200004)27:3<259::AID-EAT2>3.0.CO;2-G. 
  185. Ehle, G; Wahlstab, A; Ott, J (1982). "Psychodiagnostic findings in anorexia nervosa and post-pill amenorrhea". Psychiatrie, Neurologie, und medizinische Psychologie. 34 (11): 647–56. PMID 7170321. 
  186. Kennedy, SH; Kaplan, AS; Garfinkel, PE; Rockert, W (1994). "Depression in anorexia nervosa and bulimia nervosa: discriminating depressive symptoms and episodes". Journal of psychosomatic research. 38 (7): 773–82. PMID 7877132. doi:10.1016/0022-3999(94)90030-2. 
  187. Camargo, EE (2001). "Brain SPECT in neurology and psychiatry". Journal of Nuclear Medicine. 42 (4): 611–23. PMID 11337551. 
  188. Abebe, D; Lein, L; von Soest (2012). "The development of bulimic symptoms from adolescence to young adulthood in females and males: A population‐based longitudinal cohort study". International Journal of Eating Disorders. 45 (6): 737–745. PMID 22886952. doi:10.1002/eat.20950. 
  189. Fallon, BA; Nields, JA (1994). "Lyme disease: a neuropsychiatric illness". The American Journal of Psychiatry. 151 (11): 1571–83. PMID 7943444. doi:10.1176/ajp.151.11.1571. 
  190. Pachner, AR (1988). "Borrelia burgdorferi in the nervous system: the new "great imitator"". Annals of the New York Academy of Sciences. 539: 56–64. Bibcode:1988NYASA.539...56P. PMID 3190104. doi:10.1111/j.1749-6632.1988.tb31838.x. 
  191. Adams, R; Hinkebein, MK; McQuillen, M; Sutherland, S (1998). "Prompt differentiation of Addison's disease from anorexia nervosa during weight loss and vomiting". Southern Medical Journal. 91 (2): 208–11. PMID 9496878. doi:10.1097/00007611-199802000-00017. 
  192. Siew, LC; Huang, C; Fleming, J (2010). "Gastric adenocarcinoma mistakenly diagnosed as an eating disorder: case report". The International Journal of Eating Disorders. 43 (3): 286–8. PMID 19365820. doi:10.1002/eat.20678. 
  193. Pacifico, L; Anania, C; Osborn, JF; Ferrara, E; Schiavo, E (2008). "Long-term effects of Helicobacter pylori eradication on circulating ghrelin and leptin concentrations and body composition in prepubertal children". European Journal of Endocrinology. 158 (3): 323–32. PMID 18299465. doi:10.1530/EJE-07-0438. 
  194. Weigt, J; Malfertheiner, P (2009). "Influence of Helicobacter pylori on gastric regulation of food intake". Current Opinion in Clinical Nutrition and Metabolic Care. 12 (5): 522–5. PMID 19584718. doi:10.1097/MCO.0b013e32832eb56e. 
  195. Mannucci, E; Ricca, V; Filetti, S; Boldrini, M; Rotella, CM (2003). "Eating behavior and thyroid disease in female obese patients". Eating behaviors. 4 (2): 173–9. PMID 15000980. doi:10.1016/S1471-0153(03)00012-6. 
  196. Byerley, B; Black, DW; Grosser, BI (1983). "Anorexia nervosa with hyperthyroidism: case report". The Journal of clinical psychiatry. 44 (8): 308–9. PMID 6874653. 
  197. Krahn, D (1990). "Thyrotoxicosis and bulimia nervosa". Psychosomatics. 31 (2): 222–4. PMID 2330406. doi:10.1016/S0033-3182(90)72201-3. 
  198. Tiller, J; MacRae, A; Schmidt, U; Bloom, S; Treasure, J (1994). "The prevalence of eating disorders in thyroid disease: a pilot study". Journal of psychosomatic research. 38 (6): 609–16. PMID 7990069. doi:10.1016/0022-3999(94)90058-2. 
  199. Fonseca, V; Wakeling, A; Havard, CW (1990). "Hyperthyroidism and eating disorders". BMJ (Clinical research ed.). 301 (6747): 322–3. PMC 1663651Freely accessible. PMID 2393739. doi:10.1136/bmj.301.6747.322. 
  200. Birmingham, CL; Gritzner, S; Gutierrez, E (2006). "Hyperthyroidism in anorexia nervosa: case report and review of the literature". The International Journal of Eating Disorders. 39 (7): 619–20. PMID 16958126. doi:10.1002/eat.20308. 
  201. Mattingly, D; Bhanji, S (April 1995). "Hypoglycaemia and anorexia nervosa". J R Soc Med. 88 (4): 191–195. PMC 1295161Freely accessible. PMID 7745563. 
  202. Ozawa, Y; Koyano, H; Akama, T (1999). "Complete recovery from intractable bulimia nervosa by the surgical cure of primary hyperparathyroidism". The International Journal of Eating Disorders. 26 (1): 107–10. PMID 10349592. doi:10.1002/(SICI)1098-108X(199907)26:1<107::AID-EAT15>3.0.CO;2-U. 
  203. Alao, AO; Chlebowski, S; Chung, C (2009). "Neuropsychiatric systemic lupus erythematosus presenting as bipolar I disorder with catatonic features". Psychosomatics. 50 (5): 543–7. PMID 19855042. doi:10.1176/appi.psy.50.5.543. 
  204. Kar, N; Misra, B (2004). "Toxoplasma seropositivity and depression: a case report". BMC Psychiatry. 4: 1. PMC 356918Freely accessible. PMID 15018628. doi:10.1186/1471-244X-4-1. 
  205. Ritchie MA, Perdigao JA. Neurosyphilis: Considerations for a Psychiatrist. Louisiana State University School of Medicine Department of Psychiatry Neurosyphilis
  206. Lipsitz, JD; Fyer, AJ; Paterniti, A; Klein, DF (2001). "Emetophobia: preliminary results of an internet survey". Depression and anxiety. 14 (2): 149–52. PMID 11668669. doi:10.1002/da.1058. 
  207. Boschen, MJ (2007). "Reconceptualizing emetophobia: a cognitive-behavioral formulation and research agenda". Journal of anxiety disorders. 21 (3): 407–19. PMID 16890398. doi:10.1016/j.janxdis.2006.06.007. 
  208. Shapiro, J; Franko, DL; Gagne, A (1997). "Phagophobia: a form of psychogenic dysphagia. A new entity". Annals of Otology, Rhinology, and Laryngology. 106 (4): 286–90. PMID 9109717. 
  209. Gabbay, V; Asnis, GM; Bello, JA; Alonso, CM (2003). "New onset of body dysmorphic disorder following frontotemporal lesion". Neurology. 61 (1): 123–5. PMID 12847173. doi:10.1212/01.WNL.0000069607.30528.D5. 
  210. 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". Psychopharmacology bulletin. 30 (2): 179–86. PMID 7831453. 
  211. 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. PMID 18056550. doi:10.1001/archpsyc.64.12.1417. 
  212. Feusner, JD; Yaryura-Tobias, J; Saxena, S (2008). "The pathophysiology of body dysmorphic disorder". Body Image. 5 (1): 3–12. PMID 18314401. doi:10.1016/j.bodyim.2007.11.002. 
  213. Zeckhausen, Dina (2005). "Prevention: It's never too young to start". Eating Disoreders Recovery Today. 3 (2). 
  214. National Research Council & Institute of Medicine. (2009b). Preventing mental, emotional, and behavioral disorders among young people: Progress and possibilities (M. E. O'Connell, T. Boat, & K. E. Warner,Eds.).Washington, DC: National Academies Press.[page needed]
  215. Halmi, KA (2005). "The multimodal treatment of eating disorders". World Psychiatry. World Psychiatric Association. 4 (2): 69–73. PMC 1414734Freely accessible. PMID 16633511. 
  216. Gelder, Mayou, Geddes (2005). Psychiatry. New York, NY: Oxford University Press Inc.[page needed]
  217. (Downey, 2014)
  218. 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. PMID 14594754. doi:10.1176/appi.ajp.160.11.2046. 
  219. Yeh, HW; Tzeng, NS; Lai, TJ; Chou, KR (2006). "Cognitive behavioral therapy for eating disorders". Hu li za zhi the journal of nursing. 53 (4): 65–73. PMID 16874604. 
  220. 220.0 220.1 Schmidt, U; Lee, S; Beecham, J; Perkins, S; Treasure, J (2007). "A randomized controlled trial of family therapy and cognitive behavior therapy guided self-care for adolescents with bulimia nervosa and related disorders". The American Journal of Psychiatry. 164 (4): 591–8. PMID 17403972. doi:10.1176/appi.ajp.164.4.591. 
  221. 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. PMID 19760625. doi:10.1002/erv.962. 
  222. Wykes, T; Brammer, M; Mellers, J; Bray, P; Reeder, C; et al. (2002). "Effects on the brain of a psychological treatment: cognitive remediation therapy: functional magnetic resonance imaging in schizophrenia". The British journal of psychiatry. 181: 144–52. PMID 12151286. doi:10.1192/bjp.181.2.144. 
  223. Cognitive Remediation Therapy for Anorexia Nervosa by Kate Tchanturia Publisher: Cambridge University Press; 1 edition (April 30, 2010) Language: English ISBN 0-521-74816-X ISBN 978-0-521-74816-2
  224. Tchanturia, K; Davies, H; Campbell, IC (2007). "Cognitive remediation therapy for patients with anorexia nervosa: preliminary findings". Annals of General Psychiatry. 6 (1): 14. PMC 1892017Freely accessible. PMID 17550611. doi:10.1186/1744-859X-6-14. 
  225. Cwojdzińska, A; Markowska-Regulska, K; Rybakowski, F (2009). "Cognitive remediation therapy in adolescent anorexia nervosa—case report". Psychiatria polska. 43 (1): 115–24. PMID 19694406. 
  226. Safer, DL; Telch, CF; Agras, WS (2001). "Dialectical behavior therapy for bulimia nervosa". The American Journal of Psychiatry. 158 (4): 632–4. PMID 11282700. doi:10.1176/appi.ajp.158.4.632. 
  227. Eisler, I; Dare, C; Hodes, M; Russell, G (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. PMID 11039685. doi:10.1111/1469-7610.00660. 
  228. Rhodes, P; Brown, J; Madden, S (2009). "The Maudsley model of family-based treatment for anorexia nervosa: a qualitative evaluation of parent-to-parent consultation". Journal of marital and family therapy. 35 (2): 181–92. PMID 19302516. doi:10.1111/j.1752-0606.2009.00115.x. 
  229. Wallis, A; Rhodes, P; Kohn, M; Madden, S (2007). "Five-years of family based treatment for anorexia nervosa: the Maudsley Model at the Children's Hospital at Westmead". International journal of adolescent medicine and health. 19 (3): 277–83. PMID 17937144. doi:10.1515/IJAMH.2007.19.3.277. 
  230. Gray, JJ; Hoage, CM (1990). "Bulimia nervosa: group behavior therapy with exposure plus response prevention". Psychological reports. 66 (2): 667–74. PMID 1971954. doi:10.2466/PR0.66.2.667-674. 
  231. McIntosh, VV; Bulik, CM; McKenzie, JM; Luty, SE; Jordan, J (2000). "Interpersonal psychotherapy for anorexia nervosa". The International Journal of Eating Disorders. 27 (2): 125–39. PMID 10657886. doi:10.1002/(SICI)1098-108X(200003)27:2<125::AID-EAT1>3.0.CO;2-4. 
  232. Corstorphine, E (2006). "Cognitive Emotional Behavioural Therapy for the eating disorders; working with beliefs about emotions". European Eating Disorders Review. 14 (6): 448–461. doi:10.1002/erv.747. 
  233. Frisch, MJ; Franko, DL; Herzog, DB (2006). "Arts-based therapies in the treatment of eating disorders". Eating disorders. 14 (2): 131–42. PMID 16777810. doi:10.1080/10640260500403857. 
  234. 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. PMID 15001063. doi:10.1016/S1471-0153(00)00008-8. 
  235. Perelygina, L; Patrusheva, I; Manes, N; Wildes, MJ (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. PMID 12711069. doi:10.1016/S0166-0934(03)00078-8. 
  236. 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. PMID 7560681. doi:10.1016/S0002-8223(95)00301-0. 
  237. 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. PMID 17186637. doi:10.1016/j.jada.2006.09.007. 
  238. Casper, RC (2002). "How useful are pharmacological treatments in eating disorders?". Psychopharmacology bulletin. 36 (2): 88–104. PMID 12397843. 
  239. Goldberg, SC; Halmi, KA; Eckert, ED; Casper, RC; Davis, JM (1979). "Cyproheptadine in anorexia nervosa". The British journal of psychiatry. 134: 67–70. PMID 367480. doi:10.1192/bjp.134.1.67. 
  240. Walsh, BT; Wilson, GT; Loeb, KL; Devlin, MJ; Pike, KM (1997). "Medication and psychotherapy in the treatment of bulimia nervosa". The American Journal of Psychiatry. 154 (4): 523–31. PMID 9090340. 
  241. Marrazzi, MA; Markham, KM; Kinzie, J; Luby, ED (1995). "Binge eating disorder: response to naltrexone". International journal of obesity and related metabolic disorders. International Association for the Study of Obesity. 19 (2): 143–5. PMID 7735342. 
  242. Vandereycken, W; Pierloot, R (1982). "Pimozide combined with behavior therapy in the short-term treatment of anorexia nervosa. A double-blind placebo-controlled cross-over study". Acta Psychiatrica Scandinavica. 66 (6): 445–50. PMID 6758492. doi:10.1111/j.1600-0447.1982.tb04501.x. 
  243. Birmingham, CL; Gritzner, S (2006). "How does zinc supplementation benefit anorexia nervosa?". Eating and weight disorders : EWD. 11 (4): e109–11. PMID 17272939. 
  244. Perkins, SJ; Murphy, R; Schmidt, U; Williams, C; Schmidt, UUS (2006). "Self-help and guided self-help for eating disorders". Cochrane database of systematic reviews (Online). 3 (3): CD004191. PMID 16856036. doi:10.1002/14651858.CD004191.pub2. 
  245. Carter, JC; Olmsted, MP; Kaplan, AS; McCabe, RE (2003). "Self-help for bulimia nervosa: a randomized controlled trial". The American Journal of Psychiatry. 160 (5): 973–8. PMID 12727703. doi:10.1176/appi.ajp.160.5.973. 
  246. Thiels, C; Schmidt, U; Treasure, J; Garthe, R (2003). "Four-year follow-up of guided self-change for bulimia nervosa". Eating and weight disorders : EWD. 8 (3): 212–7. PMID 14649785. doi:10.1007/bf03325016. 
  247. 247.0 247.1 Peterson, CB; Mitchell, JE; Crow, SJ; Crosby, RD; Wonderlich, SA (2009). "The Efficacy of Self-Help Group Treatment and Therapist-Led Group Treatment for Binge Eating Disorder". The American Journal of Psychiatry. 166 (12): 1347–54. PMC 3041988Freely accessible. PMID 19884223. doi:10.1176/appi.ajp.2009.09030345. 
  248. Delinsky, SS; Latner, JD; Wilson, GT (2006). "Binge eating and weight loss in a self-help behavior modification program". Obesity. 14 (7): 1244–9. PMID 16899805. doi:10.1038/oby.2006.141. 
  249. Bulik, CM; Berkman, ND; Brownley, KA; Sedway, JA; Lohr, KN (2007). "Anorexia nervosa treatment: a systematic review of randomized controlled trials". The International Journal of Eating Disorders. 40 (4): 310–20. PMID 17370290. doi:10.1002/eat.20367. 
  250. Agras, WS (2001). "The consequences and costs of the eating disorders". The Psychiatric clinics of North America. 24 (2): 371–9. PMID 11416936. doi:10.1016/S0193-953X(05)70232-X. 
  251. Palmer, RL; Birchall, H; Damani, S; Gatward, N (2003). "A dialectical behavior therapy program for people with an eating disorder and borderline personality disorder—description and outcome". The International Journal of Eating Disorders. 33 (3): 281–6. PMID 12655624. doi:10.1002/eat.10141. 
  252. Baran, SA; Weltzin, TE; Kaye, WH (1995). "Low discharge weight and outcome in anorexia nervosa". The American Journal of Psychiatry. 152 (7): 1070–2. PMID 7793445. 
  253. 253.0 253.1 Lock, J (2015). "An Update on Evidence-Based Psychosocial Treatments for Eating Disorders in Children and Adolescents.". Journal of clinical child and adolescent psychology : the official journal for the Society of Clinical Child and Adolescent Psychology, American Psychological Association, Division 53. 44 (5): 707–21. PMID 25580937. doi:10.1080/15374416.2014.971458. 
  254. Vandereycken, W (2003). "Prognosis of anorexia nervosa". The American Journal of Psychiatry. 160 (9): 1708. PMID 12944354. doi:10.1176/appi.ajp.160.9.1708. 
  255. Bergh, C; Brodin, U; Lindberg, G; Södersten, P (2002). "Randomized controlled trial of a treatment for anorexia and bulimia nervosa". Proceedings of the National Academy of Sciences of the United States of America. 99 (14): 9486–91. Bibcode:2002PNAS...99.9486B. PMC 123167Freely accessible. PMID 12082182. doi:10.1073/pnas.142284799. 
  256. Herzog, DB; Dorer, DJ; Keel, PK; Selwyn, SE; Ekeblad, ER (1999). "Recovery and relapse in anorexia and bulimia nervosa: a 7.5-year follow-up study". Journal of the American Academy of Child and Adolescent Psychiatry. 38 (7): 829–37. PMID 10405500. doi:10.1097/00004583-199907000-00012. 
  257. 257.0 257.1 257.2 257.3 "Health Consequences of Eating Disorders". National Eating Disorder Association. 
  258. Linna, Milla S., Anu Raevuori, Jari Haukka, Jaana M. Suvisaari, Jaana T. Suokas, and Mika Gissler. "Reproductive Health Outcomes in Eating Disorders." International Journal of Eating Disorders 46.8 (2013): 826-33. Web.
  259. Grilo, Carlos M., Maria E. Pagano, Robert L. Stout, John C. Markowitz, Emily B. Ansell, Anthony Pinto, Mary C. Zanarini, Shirley Yen, and Andrew E. Skodol. "Stressful Life Events Predict Eating Disorder Relapse following Remission: Six‐year Prospective Outcomes." International Journal of Eating Disorders 45.2 (2012): 185-92. Web.
  260. Illing, Vanessa A., Giorgio Tasca, Louise Balfour, and Hany Bissada. "Attachment Insecurity Predicts Eating Disorder Symptoms and Treatment Outcomes in a Clinical Sample of Women." The Journal of Nervous and Mental Disease 198.9 (2010): 653-59. Web.
  261. Lozano, R; Naghavi, M; Foreman, K; Lim, S; Shibuya, K; Aboyans, V; Abraham, J; Adair, T; et al. (Dec 15, 2012). "Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010". Lancet. 380 (9859): 2095–128. PMID 23245604. doi:10.1016/S0140-6736(12)61728-0. 
  262. "Hospitalizations for Eating Disorders Rose Over the Past Decade". Eating Disorders Review. 24 (2). 2013. 

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